Ortho Lecture Notes Combined
Ortho 2 - Head pain
Objectives
1. Describe the etiology, risk factors, pathogenesis, clinical manifestations & treatment of
mTBI/concussions
2. Identify the etiology for the causes of head pain presented
3. Describe the pathological changes for the causes of head pain
4. Identify the risk factors
5. Explain the clinical manifestations for the causes of head pain
6. Identify the appropriate diagnostic studies that will aid in ruling in the condition & explain what
they findings would be
7. Describe the management for the conditions presented.
Headache review:
RED FLAGS
 “Worst HA of life”,
 New or Sudden onset,
 Onset w/exertion
 Decreased mental capacity,
 Stiff neck
 Marked deterioration
 Changing characteristics
When to order imaging for HA
 New & atypical HA
 Change in HA frequency, severity, pattern
 Neuro symptom and/or exam findings
 Onset under 5 or over 50
When to refer to ER?
 Vomiting, sweating, pain
 Bladder problems
 Sudden severe onset “Thunderclap” - subarachnoid hemorrhage, thrombus
 Worst HA ever
 Increased Pn w/cough or strain (truly only if very bad HA too)
 Neuro signs – stroke
 Clinically it should be obvious
Migraine characteristics
 Unilateral
 Throbbing
 Auras & Prodrome
 Duration 4-72 hrs
 Mod – severe “incapacitating”
 ADL changes
 NV
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Photo/phono phobia
Cervicogenic HA
 Reproducible - usually mechanical origin, aggravated by motion
 Worse w/repetition
 Unilateral, top & back of head
 Dull achy
 Mod to severe
 Neck pain
Tension “Hat band”
 Pressure
 No NV (minimal associated Sx)
 Bilateral temporal or occipital
 Mild – Mod
Cluster HA
 Night, seasonal
 Clockwork timing
 Suicide HA
 Short duration, in clusters 15 – 180 min / 1-8x in 24 hrs
 Periorbital, Unilateral
 Severe
 Transient Horner Syndrome: Superior Cervical chain sympathetics
Sinus HA
 Face sinuses
Chronic Daily HA CDH
 15+ days/month @4+ hrs/day
 Majority are: chronic migraine, chronic tension HA, rebound HA
 Manifestations of CDH are dependent on the type of HA
o Migraines w/o Aura
 15x/month for 3+ mons
 At least 5+ attacks w/our aura, presenting:
 Unilateral
 Pulsating
 Mod-severe
 Loss of ADL/aggravated by ADL/avoidance
 At least 1+:
 NV
 Photo/phonophobia
 Can’t attribute to another cause
 Tx:
treat Prodrome phase w/Triptans, Ergot
o Migraines w/Aura
 Has visual, sensory, speech, sensory, language Sx that are fully reversible
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No motor, brainstem or retinal Sx
2+
 1+ aura spread over 5 min
 Or 2+ aura in succession
 Each aura 5-60 min
 1+ aura unilateral
 HA arrives w/in 60 min & aura associated
 TIA ruled out (from emboli, sympathetic vasoconstriction/spasm)
 Can’t attribute to another cause
o Rebound HA (med overuse, withdrawal)
 15+ days/month
 HA relieved by the Medication
 esp those w/caffeine
 NSAID, Tylenol, Excedrin, aspirin, coffee
 Rx drugs: sedative, codeine, narcotic, ITC Ergotamine, butalbital
 Regular overuse of 1+med for 3+ months
 Can’t attribute to another cause
o Chronic tension HA (each w/own Dx criteria)
 15+ days/mon for 3+ mos (180+ days)
 30 min – 7 days
 2+ of following
 Bilateral
 Pressing/tightening
 Mild-mod
 Not aggravated by routine physical activtiy
 NO NV
 NOT both Photo/Phonophobia (but 1 is ok)
 Can’t attribute to another cause
General Management of CDH
 Wean off/substitute medication
 Prevention: Use prophylactic/abortive Rx therapies
 Counseling
 CAM: adjust, herbs
 RX: change prescription
 By type:
o Migraines Prophylaxis
 Pharmacology, Behavior Mod, Diet, Avoid triggers
o Tension type Prophylaxis
 Behavior stress reduction, Medication
o Rebound
 Wean off, Botox
 WF 35 w/HA for years, mod, subocc achy, lasts hours to days, occasionally phonophobic =
tension
Giant Cell Arteritis
 50+ years (90% over 60 yo)
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New HA
Temporal artery abnormality (often visible)
ESR > 50+ mm/hour (can order, but not dx)
Biopsy = Definitive Dx
Prognosis
o Excellent if tx started early; possible permanent vision lost if not treated
Treatment
o High dose corticosteroids until no Sx & ESR is normal
Ex: 60 yo WF, R side HA, started days ago; pain constant, but severity fluctuates; complains of
malaise, loss of appetite, vague achiness, fatigue, temporal artery w/bruit & enlarged
Ocular Pain
Acute Angle Closure Glaucoma
 Repeated vomiting
 Globe is tender or hard
 Pupil is dilated
 Cornea steamy, corneal epithelial edema
 Mid-dilated nonreactive pupil
 Conjunctiva is injected (red) & eye pain
 ***EMERGENT referral
Iritis
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Decrease visual acuity
Unilateral small pupil
Eye floaters & photophobia
Conjunctiva infected (red) & eye pain
Referral
Rhinosinusitis (Sinus HA)
 Sinuses:
o Frontal
o Sphenoid
o Ethmoid
o Maxillary
 Sinusitis:
o Inflamed sinus lining
o Excess Mucous Sinus infection
 Pounding pressure
 Worse laying down/bending over
 Better w/rubbing
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Associated cough
Congestion
Toothache RU molar
+2 tenderness over frontal & maxillary sinuses
Neither frontal nor maxillary sinuses illuminated
Acute Bacterial vs. Viral Infection
- Signs/Symptoms last 10+ days
- Lacks evidence of clinical improvement
- Worsening signs/symptoms following initial improvement
o “Double sickening”
- Severe symptoms
o including fever 102°F
- Purulent nasal discharge 3-4+ consecutive days
- Chiro tx:
o Sinus stimulation,
o Heat therapies: Diathermy & Moist heat
o Adjustments,
o Acupuncture,
o Neti-Pot- saline wash
Hypertensive HA (G44.813)
Key Characteristics:
DANGER
- Females >50
- HA present @ awakening & decreases intensity as day progresses
- Pulsatile Pn behind eyes or V1 distribution
- Possibly:
o Dizzy, syncope, palpitations, dysrhythmia, SOB
- Severe HTN = 180/120
(180/120 = “hypertensive crisis”)
- **Clinical caveat to above: Proper instructions & documentation
 Diagnostic Criteria
- Causation Evidence by either or both of the following:
 HA developed in temporal (time) relation to onset of HTN
 HA worsens as BP goes up or gets better as BP comes down
- HTN Crisis:
o systolic BP 180+ & diastolic 120+
- Not better accounted for by another diagnosis
- Alternative DX Criteria
- HA 1+ of the following:
1. Bilateral,
2. Pulsating
3. Precipitated by physical activity
- HA develops during HTN Crisis, defined as…
o Paroxysmal (sudden) systolic rise 180+ and/or diastolic 120+ mmHg,
o No clinical features or HTN encephalopathy
- Resolves within 1 hour after BP normalizes
- Rule out: vasopressor toxins & medication as causative factors
HTN HA: Management
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HTN crisis is emergent
When BP comes down HA will dissipate
Stage 1 HTN & HA
o Evaluate for secondary causes of HTN
Stage 2
o If no 2ndary cause, initiate lifestyle modification (diet/exercise)
o Refer for possible drug therapy: ACEI, CCB, diuretics
Treat HA
o When BP is controlled /or in conjunction with BP tx
Tumor HA
- Never had it before “new HA”
- Worsening over time “worsening”
- Increased with bending over “worse bending over”
- Increased with exertion “worse w/exertion”
- Maybe Altered cranial nerve fxn? “Sx of CN”
o Depending on location
- Associated symptoms “sx like NV, vision, etc.”
o N/V, visual disturbances, ophthalmic exam findings possible
Aneurysm HA
- Never had it before “new HA”
- “Thunderclap” presentation
- Can lead to death
- Slow leak= severe HA over days-weeks
- Increased with bending over, exertion
- Maybe altered cranial nerves or vitals
- Associated symptoms:
o N/V, visual disturbances,
o Photophobia, aphasia (loss of ability to understand or express speech)
o nuchal rigidity, weakness
mTBI & CONCUSSION
mTBI and Concussion are used synonymously, yet concussion is only 1 type of mTBI
Mild TBI (mTBI or MTBI)
 Acute injury resulting from mechanical head injury from external forces
 May result in:
o Transient confusion
o Disorientation
o Change in consciousness
o Amnesia
o Observable neurologic dysfunction
o Intracranial lesion
 Concussion = Trauma induced alteration in mental status
o Acute brain injury
o +/- LOC
o No gross anatomic lesions
o Mechanically induced
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Epidemiology:
o Approximately 42 M worldwide/year
 1.74 M in US
 75-95% are mTBIs
 Annual sports mTBI in US = 1.6 - 3.8 M
 Contact sport mTBI likelihood is up to 20%/season
 Football rate = 10% in college, 20% in HS
 Females mTBI > Males
 Most common injury in College football & Female soccer
 Etiology
o Leading cause of TBI
 28% falls
 20-25% in MVA
 19% struck
 11% assaults
o Subpopulations predisposed
 Contact sport athletes
 Military personnel
 Domestic violence
o Linear vs. Rotational
 Rotational = more dysfunction
 Pathogenesis:
o CSF around brain acts as a cushion, protecting brain from excessive contact with skull
o Unexpected forces to head can cause exceed CSF ability to cushion brain.
 Brain impact with skull temporarily stops working normally
 No obvious signs of anatomic lesion
 Begins complex cascade of biomechanical dysfunction
 Disrupts brain delicate neuronal homeostasis
o Symptoms due to metabolic & physiologic abnormalities vs. structural pathology
 Coup Injury
o Under site of object impact
o When head encounters a Decelerative (moving) or Accelerative force (Stationary) head
 Contrecoup
o When the head is moving
 Coup-Contrecoup
o Head goes back & forth
 Coup & Contrecoup can happen individually or together**
DECELERATIVE FORCE:
o Bike example of head hitting into brick (he’s moving &
immediately stopped because brick wasn’t moving) =
 COUP INJURY
https://youtu.be/yhQAK8_bzpg
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o Football player example = catching ball into wall (he’s moving & immediately stopped
because wall wasn’t moving lol) = COUP INJURY
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ACCELERATIVE FORCE:
o Football example = player runs into other play & hits him in the head with his helmet =
COUP-CONTRECOUP
o Shovel Example LOOOL = dude beats the shit out of his friend with a shovel in the head =
COUP-CONTRECOUP
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Patient Presentation
o LOC only 10%
o CAB *always check***
 Circulation
 Airway
 Breathing
o HA (most common)
o Emotional disturbance
 Distraught
 Crying no reason
o Dizzy, vertigo, tinnitus
o Insomnia
o Photophobia
o Amnesia
 Retrograde – events preceding
 Anterograde – events after injury forgotten
o Confusion/ change in mental status
 Vacant stare (befuddled expression)
 Delayed verbal expression
 Inability to focus (easily distracted)
 Disoriented (time, date, location…walk in wrong direction)
 Slurred speech (disjointed, incoherent
 Incoordination (stumble, gait, can’t walk straight, etc.)
o Vomiting / nausea
o Symptoms compounded by stress
Example: https://youtu.be/rOoQar20uQE
o Note: if brain injury occurred = good chance that cervical spine injured
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On the field clinical examination SCAT 5
o Rule out emergent situation: CABFE
 circulation,
 airway,
 bleeding,
 fractures,
 etc.
o Level of consciousness = AVPU
 A = Alert
 V = Responds to Voice
 P = Responds to Pain
 U = Unresponsive
o Inspect the head & neck
 Battle’s Sign = Post auricular hematoma
 basilar fracture
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Otorrhea = Leakage of CSF from ears
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Racoon eyes = Periorbital ecchymosis (bruising) from leakage of blood
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Hemotympanum = Blood behind Tympanic membrane
o Palpate Head, Face, TMJ, Nose, Neck for tenderness/ potential fracture
o Use SCAT5 if person is responsive
Concussion (S06.0X0S no LOC; S06.0X9A w/LOC)
Traumatic Brain Injury (S06.2X9A w/LOC; S06.300A no LOC)
Definition:
World Health Organization (WHO) defines mild traumatic brain injury (mTBI) as “an acute brain injury
resulting from mechanical injury to head from external physical forces.” The terms “mTBI” &
“concussion” have become synonymous, although technically, “concussion” represents only one type of
mTBI.
Epidemiology
 Researchers estimate that mTBI affects ~42 million worldwide each year
o particularly common among teenagers & young adults.
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Estimated 1.74 million persons in US have TBI each year; 75-95% are mild
Annual incidence of sports-related concussion in US 1.6 to 3.8 million & likelihood of contact
sport athlete experiencing a concussion is as high as 20% per season.
o In football alone, 10% of US college & 20% US high school players have brain injuries/
season (Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury.
Neuropathol Exp Neurol. 2009;68(7):709.)
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Sports-related concussion
o more in girls vs. boys in similar sports
o 2nd most common injury in College football & Female Soccer
o HS-aged American football players have more concussions than college-aged players
Etiology:
Majority of injuries occur via falls & MVA
 mTBI present in ~25% of patients injured in MVA collision.
 Other subpopulations predisposed to mTBI:
o contact sport athletes (football, boxing, hockey, soccer, MMA, etc)
o military personnel
o domestic violence victims
Pathogenesis
Concussion injuries =
 result of physical force causing mechanically-induced brain trauma w/o obvious gross
anatomic lesion.
 Mechanical insult may provoke a complex cascade of biochemical dysfunction
o Begins w/mitochondrial dysfunction;
o disrupts brain’s delicate neuronal homeostasis.
o Concussion & related symptoms thought to result from functional metabolic &
physiologic abnormalities vs. structural pathology.
Clinical Presentation:
 Sx start immediately, or evolve over min-hours
 Headache = one of most common & identifiable symptoms
 Fatigue or low energy
 Dizziness/Tinnitus/Vertigo
 Insomnia
 Photophobia
 Amnesia
o Retrograde – events preceding the injury
o Antegrade – events following the injury
 Confusion/Mental Status Changes
o Vacant stare befuddled facial expression
o Delayed verbal expression slower to answer questions or follow instructions
o Inability to focus attention easily distracted & unable to follow through w/normal
activities
o Disorientation walking in the wrong direction, unaware of time, date, place
o Slurred or incoherent speech (making disjointed or incomprehensible statements)
o Gross incoordination observable (stumbling, inability to walk tandem/straight line)
 Emotions disproportionate to circumstances - distraught, crying for no apparent reason
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Loss of consciousness – occurs in about 10% of injuries
Patients often complain that symptoms are compounded by physical or emotional stress
Side note: if brain injury occurred, then high possibility of cervical spine too.
Clinical Evaluation on field:
 Rule out emergent situation; check Circulation, Airway, Bleeding, Fractures, etc
 Palpation of head, neck, face, nose, TMJ for tenderness indicating fracture
 Inspect head & neck for signs of serious injury:
i. Battle's sign = post auricular hematoma (indicates basilar fracture).
ii. Otorrhea = leakage of CSF from the ears.
iii. Raccoon eyes = periorbital ecchymosis secondary to leakage of blood from the
anterior fossa into the periorbital tissues.
iv. Hemotympanum = blood behind the tympanic membrane
 If conscious, ask patient to move fingers & toes, assess sensation
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Assess Level of Consciousness
 Glascow Coma Scale GCS
o part of the SCAT5
o used to assess LOC
o Not sensitive for defining MTBI or return to play
o Objective scale
 Scale based on score of 15 points:
o Assess eye movements, motor response, verbal response
o Anything < spontaneous eye opening, obeying verbal commands, participating in
oriented conversation represents an abnormal level of consciousness.
 Anything less than perfect is “bad”, athlete NOT cleared
 Use for: head injury acute medical & trauma patients
 Lowest score = 3 (unconscious or dead)
 Highest = 15 Concussion/Minor = 13-15, Moderate 9-12, Severe <8, LOC/dead <3
Emergency management is indicated for athletes who demonstrate;
 a Glasgow coma score less than 15
 progressive neurologic signs or symptoms
 deteriorating mental status
 persistent vomiting
 potential spinal injury
 suspected skull fracture
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seizures
coagulopathy
prior neurosurgery
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intoxication
multiple injuries.
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Indication for Neuroimaging (CT or MRI scan)
American College of Emergency Physicians (ACEP) clinical policy for adults ≥ 16 years old with
mild traumatic brain injury (GCS score 14 or 15)
if LOC or amnesia, non-contrast head CT
if NO LOC or amnesia, non-contrast head CT if
indicated only if 1+
 headache
 focal neurologic deficit
 vomiting
 severe headache
 age > 60 years old
 vomiting
 drug or alcohol intoxication
 age > 65 years old
 short-term memory deficit
 signs of basilar skull fracture – aka battle sign
 signs of trauma above clavicle
 GCS score < 15
 posttraumatic seizure
 coagulopathy
 GCS score < 15
 dangerous mechanism of injury, including
 focal neurologic deficit
o ejection from motor vehicle
 coagulopathy
o pedestrian struck by vehicle
o fall from > 3 feet (1 meter) or 5 stairs
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SEND TO HOSPITAL
o Documented or suspected LOC
o Unequal pupils
o Skull Fx
o Prior neurosurgery – scars of
o No reliable guardian
o Multiple injuries
o Progressive HA
o Cranial swelling
o Decreasing LOC
o Continued vomiting
o Mental status change
o Intoxicated
o Persistent neurologic defect/signs
o Suspected child/spouse abuse
Other methods of diagnosis
 Diagnosis of MTBI generally established by the presence of
o post-concussion type symptoms &
o absence of advanced imaging findings
 Diffusion tensor imaging (DTI) is an emerging imaging modality that measures water diffusion
rates to identify micro-bleeds & subclinical brain injuries that are not detectable by other
imaging means.
 New research suggests that measuring brain-derived neurotrophic factors (BDNF) may help in
the diagnosis of concussion.
o BDNF is secreted following brain injury to help “reconnect brain circuitry”.
o This protein can be easily measured & shows excellent ability to define & quantify brain
injury.
 N-acetylaspartate is a marker of neuronal metabolic wellness, & research suggests that
monitoring its level through proton magnetic resonance spectroscopy may be a useful indicator
of recovery. (10)
Evaluation:
 After ruling out medical emergency…
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Perform complete history
Perform a neurologic assessment
o CN screen (esp Pupillary light reflex & Ophthalmoscope)
o Motor / strength
o Sensation
o Balance Coordination Agility
Perform Exertional provocative tests – to see if Sx exacerbated:
o 40 yd sprint
o 5 push ups
o 5 sit ups
o 5 knee bends
Neuropsychologic testing
 Begins with Memory assessment: Mini Mental Status Exam
 Ask Questions involving recent & remote memory ***More sensitive
o Researchers validated “Maddocks questions” to assess concussed athletes.
1. Which ground/field/rink are we playing at?
2. Which team are we playing today?
3. Which half/quarter/period is it?
4. How far into the game is it?
5. Which side scored last?
6. Which team did we play last game?
7. Did we win last game?
Exhibit recall/memory problems or signs or symptoms of mTBI?
o Remove from field
o DO NOT allowed to return to play.
o If in doubt, pull them out
o If removed, cannot return until Medical Assessment finds reduced Sx
Sideline evaluation includes:
o Detailed neurologic evaluation:
 Motor, sensory, reflex tests, CN evaluation
 Test coordination & balance
 E.g. finger to nose test, standing/hopping on 1-leg w/eyes closed
o Use Standardized Concussion Assessment Tool (SCAT5)
 SCAT5 exists in two versions;
 Child SCAT3 for children age 5-12, Standard SCAT3 for athletes 13+.
o Remove Athletes suspected of having concussion post-Maddox & SCAT5
o Do not allow to return until medical assessment has determined resolution of symptoms.
o General policy should be “when in doubt, hold them out”
Allowing patient to return home:
 MONITOR 1ST 24 HOURS…
o Responsible person should stay with them for the first 24 hours.
 Observe every 4 hours to ensure patient is easily aroused & responds normally,
o pupils are equal, & does not develop deteriorating neurologic symptoms.
 Be alert for:
o worsening headache, irritability, persistent nausea/vomiting, difficulty speaking or
swallowing, tinnitus, shortness of breath, light headedness, numbness, confusion,
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memory loss, clear CSF discharge from nose or ears, unequal pupils, fever, visual
disturbances, seizures, LOC, etc.
Drink only clear fluids for 1st 8-12 hours following mTBI
o Avoid alcohol
Diet: Start light & progress to normal over the next 24 hours.
Avoid: Sedatives, sleeping pills, aspirin & ibuprofen (unless otherwise directed by a medical
physician.
Avoid unnecessary physical & mental activity for the first 24 hours, including:
o School, work, texting, video games, driving, operation of dangerous tools or heavy
equipment, etc.
Sleep with their head slightly elevated for the first 24 hours.
In-office follow up evaluation:
 I.D. subtle cognitive deficits involving: Attention, Memory, Information Processing
 DTI – Diffusion tensor imaging to identify microbleeds
 __________
 Neuropsychological testing may help define MTBI & recover
o Mode of testing more practical via computerized test platforms.
o Most tests take 15-30 minutes & are offered by a variety of companies;
 ANAM Sports Battery,
 CNS Vital Signs,
 Concussion Vital Signs, CogSport/ Axon, Concussion Resolution Index/
Headminder, ImPACT, etc.
Diagnosis
 Symptoms
o Corresponding history, examination & neurophysiological testing
o In office f/u evaluate:
 subtle cognitive deficiencies,
 attention/memory/info processing,
 neuropsychologic testing
Emerging Modalities
 Diffusion tensor imaging (DTI)
o Imaging measures water diffusion rates identifying microbleeds & subclinical brain
injuries, not detectable by other imaging means
 Lab testing
o BDNF Brain-derived neurotrophic factors:
 BDNF secreted post-injury to help “reconnect brain circuitry”.
 Protein easily measured w/excellent ability to define/quantify brain injury.
o N-acetylaspartate
 Neuronal metabolic wellness marker
 Research suggests monitoring via proton magnetic resonance spectroscopy is
useful indicator of recovery.
o Neuropsychologic testing via computer platforms
 Practical
 15-30 minutes to take
 ANAM sports battery, CNS vital signs, Concussion vital signs, CogSport/Axon,
Concussion Resolution Index/Headminder, ImPACT
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Management
 Co-management w/qualified professional
 Do through HX & Exam to r/o more sever neurologic damage (for permanent damage)
 Reassure patient that Sx improve over time in most cases
 Monitor Pt change in Health Status
 Don’t send Pt home alone
o Observe 24 hrs.
o Monitor signs of hemorrhage
 Adjust, CMT
 Vestibular training
 Cervical rehab
 Recovery Period
 Variable.
 Post-MVA study found median recovery time = 100 days;
o YET however, 23% of patients had not recovered after one year.
 Many report resolution of post-concussive symptoms within 1-2 weeks
 Most studies suggest that all symptoms, including cognitive deficits =resolved within 3 mos in
both children & adults
 10-15% of adults & up to 40% of children experience chronic symptoms
 Average revcovery = 3 months / 100 days
 Most feel better in one week (7-10 days)
 Most feel better w/in a week or 2
 10% of adults end up with chronic issues
 40% of children end up with chronic issues (development interrupted so treat neck
 Delayed Recovery when:
 Exhibit 4+ symptoms
 Headache lasts 60+ hours
 Pre-injury headache, particularly migraine
 Self-reported fatigue/fogginess
 Prior mTBI or concussion
 History of PTSD
 ADHD or learning disability, & advancing age psychologic component
 Feel tired (psychological Sx) need to reassure
 Grading
 Simple concussion: injury resolves over 7 -10 days and NO complication
 Complex concussion: persistent symptoms & specific sequelae
o i.e., convulsions,
o LOC > 1 min
o prolonged cognitive impairment after Sx subsider
 Grading can only occur after symptoms have subsided
Returning to Play RTP
 Complete clearing of all symptoms at rest, with no pain meds NO more Sx
 No symptoms after provocative testing (cycling, running or exercise that elevates HR
 Full return of cognitive ability, memory, & concentration
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“Zurich RTP Consensus Guideline 4th International (Zurich) Conference expert consensus (Nov 2012)
Athlete should proceed to next level only if asymptomatic at current level; levels include
 no activity, complete physical & cognitive rest
o in children, cognitive rest = refrain from texting, video games, school work
o may extend asymptomatic rest time or length of graded exertion in children or
adolescents
 light aerobic exercise
o walking, swimming, or stationary cycling;
o no resistance training
o training intensity below 70% max
 sport-specific exercise,
o no head impact activities
 noncontact training drills
o may begin progressive resistance training
 full-contact training
o following medical clearance
 resume game play
Each step usually about 1 day,
 Most athletes need ~1 week to proceed through total rehab protocol once asymptomatic @ rest
 If any post-concussion symptoms occur during the graduated stepwise program,
o Regress to prior asymptomatic level 24 hrs, rest 1 day, then progress again “rest a day”
Post-concussion syndrome (PCS) (F07.81)
Definition
Sequelae to mTBI, Complex that includes
 headache
 dizziness
 neuropsychiatric symptoms
 cognitive impairment
Epidemiology
 30-80% of patients with concussion/TBI will have it up to 80% of pts
 Sx occur within 7-10 days of injury
 Last up to 3 months
 Can persist for 1+ years
Clinical Presentation
 Headaches
 Dizzy
 Fatigue
 Irritability
KEY CHARACTERISTICS
 Irritable
 Noise & light sensitive….




Anxiety
Insomnia
Loss of concentration & memory
Noise & light insensitivity
Management
 Reassurance – most patients improve within 3 months
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
Symptom management: medications, cognitive behavioral retraining CBT
Chronic Traumatic Encephalopathy (F07.81)
CTE
Definition:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526170/
Progressive degenerative disease of brain
 found in athletes & others w/ history of repetitive brain trauma,
 includes symptomatic concussions & asymptomatic sub-concussive hits to the head
 TAU protein accumulation w/bx
 Sig risk of Neurodegenerative ds
 Multiple concussions/impacts increase risk
o Alzheimer’s disease
o Parkinson’s disease
o ALS
o Dementia, 3x risk
Clinical Presentation
 Progressive decline: Repetitive trauma found in athletes & service members
 Mood: depression, suicidality, apathy, anxiety
 Cognition: memory loss, executive dysfunction
 Behavior: short fuse, aggression
 Some cases motor disturbance: difficulty with balance & gait
 Definitive diagnosis is biopsy of brain postmortem
Treatment: None, prevention
Second Impact Syndrome (SIS)
Aka Malignant Cerebral Edema (S06.1)
Definition:
Occurs when a 2nd impact happens before full recovery from a
previous TBI. High risk of death.
 Syndrome develops when athlete sustains 2nd head injury
before symptoms of earlier head injury/concussion cleared.
 1st impact likely caused cerebral vasomotor paralysis
 2nd may not be as severe but effect is compounded.
o sets in motion the rapid development of cerebral
vascular congestion
o causes increased ICP
o results in brainstem herniation & death
(McCrory, 1998)
 A controversial syndrome, some of the literature states it doesn’t exist.
 Rare, but higher risk in kids & adolescents (shaken baby syndrome?
Epidemiology
 Higher risk in children & adolescents (possibly Shaken Baby Syndrome)
 More common in males, in contact sports, yet female in contact sport, more likely to get
concussion
Prevention:
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
American Academy of Neurology Prevention should be a policy:
o Don’t allow individuals to return to sports until post concussive symptoms are fully resolved.
o Neuropsychologic measures of speed of information processing & reaction times
 slowed in the early stages post injury.
o Therefore if an athlete returns to quickly they may not be able to respond appropriately to
dangers that arise in the course of play. (McCrory, 1998)
Management:
 Treatment: Avoidance is ONLY treatment
 Good exam & no sports participation until cleared
 If no signs post head trauma, then player can return in 15 minutes.*Rules differ by state & org.
 If signs, at least 1 week before RTP.
 Call 911 immediately if occurs
o Patient is intubated & hyperventilated (facilitate vasoconstriction by lowering CO2 levels.
o Place an IV with Osmotic diuretic & a Foley catheter to remove excess fluid.
 Mortality rate approaches 100%
Head Injury Patient Instructions (form for practice)
The examination that you have received today has been rendered on an emergency basis. It is not
intended to be a substitute for comprehensive medical attention.
 Should your condition worsen or any new symptoms develop, or should you not recover as
expected, contact your doctor or report to the nearest hospital at once.
You have suffered a head injury.
 Common symptoms include headache, nausea & slight dizziness. There may be some swelling &
pain at the site of impact.
 A head injury can cause slow bleeding or other problems inside the head that may not be
detected at this time.
 You may return home, but a relative or friend must stay with you. Have them read the following
instructions & check you every 4 hours for the next day or two.
Contact your doctor or report to the emergency department if any of the following occur:
 A stiff neck
 Unconsciousness or fainting
 Personality changes
 Areas of skin numbness
 Persistent nausea or vomiting
 Difficulty speaking or slurred speech
 Ringing or other unusual sounds in the ear
 Shortness of breath or difficulty breathing
 Dizziness, trouble walking or staggering gait
 Confusion, unusual drowsiness or loss of memory
 Bleeding or clear fluid drainage from the ears or nose
 Inability to wake up completely or excessive sleeping
 A severe headache or a headache that is worsening or persistent
 Pupils of unequal size (the pupil is the dark center portion of the eye)
 Fever (greater than 101F/38.3C by mouth) or if shaking chills begin
 Visual disturbances including blurring of vision, double vision or sensitivity to light
 Convulsions such as twitching movements of either the eyes, arms, legs or body
 Any other unusual or abnormal symptoms.
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Home Treatment
Do not take any sedatives or sleeping pills. Do not take aspirin or compounds containing aspirin. Do not
take products containing ibuprofen such as Motrin, Advil or Nuprin. If needed, the use of
acetaminophen (Tylenol, Panadol, Tempra or Liquiprin) is recommended.
 Do not drink alcoholic beverages
 Do not exert yourself (No school for children or work for adults)
 Do not eat or drink much for the next 24 hours. (Clear liquids are best if your stomach is upset).
 Do not lie flat. (Sleep or nap with head elevated on at least one or two pillows).
 Do not drive a car or operate tools which could harm you if you are not alert.
I have received a copy of the above instructions. I understand that I have received an emergency
evaluation only. I have been advised as to the occasionally slow insidious nature of head injuries & the
possible fatal consequences, & I clearly understand that although I have been permitted to return
home, that I am responsible for arranging follow-up care as instructed above.
Patient
Signature:______________________________ ____ Date:____________ Time:____________
TMJ Syndrome (M26.60)
Epidemiology
 ~10 million American's affected.
 75% of people may suffer from TMJ problems
 Affects women > men
Background
Muscles of Mastication
Open: Lateral pterygoid
Close
 Temporalis
 Massester
 Medial pterygoid
Protrusion
 Lateral & medial pterygoids, (masseter)
Retraction: Temporalis
Lateral Deviation
 Ipsilateral temporalis
 masseter
 contralateral medial & lateral pterygoids
Note capsule of tmj
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Ortho Lecture Notes Combined
Biomechanics of TMJ
Relaxed & inactive state called MANDIBULAR POSTURAL REST POSITION
 Teeth should not touch: 2 to 5 mm space
 Space is called intraocclusal space or freeway space
 Fully occluded is called the intercuspal position
Clenching or grinding of the teeth is called bruxism
 May result in growths to increase strength: torus manibulis
During OPENING:
 Rotation is primarily the first 1/3 of opening
 Causes first 12 to 15 mm of mandibular opening & closing
 Translation and rotation counts for 2/3 of movement
Biomechanics of disc:
Biconcave, fibrous tissue & divides joint
 Not vascular or pain sensitive
 Pain is from retrodiscal tissue
Stability of the DISC
 Med & lat collateral discal ligs: Limit forward movement
 Attached to the pterygoids
 Capsular ligament (b/c a synovial joint)
 TM ligament: Prevents compression of retrodiscal tissue behind condyle
Etiology
Clicking
 Happens w/reduction – disc moves fwd due to tight pterygoid or lack of stability
 Reduction means disc moves too soon
Opening
 condyle slipping over posterior border of disc
Closing (reciprocal) double click on open and then on close
 at end
 pull of sup lat pterygoid causes disc to slip anterior 1st click
 condyle moves over post border closing click
VIDEO: “YOUTUBE Temporomandibular Joint (TMJ) Anatomy and Disc Displacement”
PATIENT HISTORY
 Jaw pain, HA, ear ache, tooth ache
o Pn w/opening = capsule, muscle stretch
o Biting = synovitis/joint, increased pressure
o Clicking/pop/crepitus = disc, arthritis, aadhesions, lig laxity
 Describe the clicking (opening/closing)
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
o Fatigue w/chewing may indicate
o Inability to open fully? Locked closed
o Inability to
Parafunctional Habits that contribute
o Breathing patterns
 Apical
 Mouth
 Diaphragm
o Piercings
o Inspect hands
 Nail biter?
 Finger sucking?
o Pens chewed?
o Ice chewed?
o Inspect how they talk
EVALUATION (see slide)
 Inspection
 Palpation
 ROM Mand gait, APROM
 Ausc joint
 Provocative tests: distract, compress, _________
Clinical Presentation
 Disc Derangement
o Popping & clicking with opening & closing (from disc going forwards)
o From anterior disc…_____
o Clicks felt on palpation
o 4 click are worse than 2
o The later the POP the worse the condition
IF without reduction, DISC stays behind the whole time, so pain, but not POP
W/reduction disc moves, so will have a click
DDD/DJD
Joint stiffness in morning; increased motion in afternoon
Crepitus with auscultation
+ Compression testing
Capsulitis
Pain with
 protrusion or
 lateral movement;
 chewing on opposite side or
 opening widely
Overstretch of capsule
+ distraction test
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Synovitis
Ipsilateral pain with
 Full closure
 Chewing on same side
 From trauma, chronic malposition, loss of teeth high, anterior disc displacement, hypertonic
temporalis
+ Compression testing
Lateral deviation in rest position
Reduction of pain with biting on tongue blades because more open,
 but in general increased pain w/biting
Myofascial Pain Syndrome
“S Curve” when opening & closing …Usually reduced opening of mouth
Palpable trigger points
Increased ROM w/Counter + counter irritation test
Locking
Closed:
 Inability to fully open maout
o Pn and difficulty opening mouth
o Liited to 25 mm or less
o Mandible deviates to affected side
o Decreased contralater dv
 Due to dislocated dis
o Anterior or medial dislocation
 Operpressure is uncomfortable
OPEN
 Jaw locks when fully open
 Pn from reactive mm spasm
 Apprehensive
 Swollen inflamed retrodisc tussue
 Condyle dislocates ant to dis
o From traum, hypermobility of ris dislocates posteriorly
 R/O trauma
Management
 Gentle mobilization
o Compressive vs. distractive
 Myofascial work
 Diet changes
o Soft food, no gum, no straws
 Referral for splinting, meds, orthodontics
 Physical therapy
o Electrical stimulation
o Ultrasound
o Spray & stretch
o Ice
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Ortho Lecture Notes Combined

o Hypermobile/hypomobile exercises
o Can adjust w/proper training *use caution, refer out if you can’t treat
Surgical options
o Discoplasty
o Discectomy w/ or w/out implant
o High incidences of OA
Ortho 2 - Dizziness
Objectives:
1. Describe the equilibrium triad.
2. Identify the systems that can cause dizziness
3. Describe the categories of dizziness
4. Identify the etiology & pathogenesis of dizziness
5. Describe the clinical manifestations (symptoms & signs/exam findings) for the different conditions
6. Identify which diagnostic studies would be useful & the expected findings.
7. Describe the management options for the conditions.
Dizziness is defined as a feeling of uncertainty about one's physical orientation in space. It is a broad
term & is applied by the patient to a number of different sensory experiences - a feeling of
 rotation or whirling as well as non-rotary swaying, weakness, faintness, light-headedness, or
unsteadiness. Blurring of vision, feelings of unreality, syncope, & even petit mal or other seizure
phenomena may be called `dizzy spells’.
 Accounts for 5% of medical visits
Equilibrium Triad
o Visual Receptors – EYES
o Input from the retina & ability to recognize horizon. (CN II)
o Vestibular Receptors – INSIDE EAR
o inner ear, particular the labyrinths that identify changes in
 velocity, motion & body position
o Semicircular canals
 signals the brain about the direction & speed of rotation of the head.
o Utricle & saccule are called the otolithic organs
 & are responsible for detecting linear acceleration & gravity. (CN VIII)
 Two other organs that are part of the Vestibular system
o Somatic Receptors (proprioception)
o Information from the proprioceptive organs from the muscles & joints. Neck extremely
important.
All three components are needed for proper balance. A problem with anyone one of these systems can
lead to dizziness or balance issues.
When dealing with dizzy patients one should consider an evaluation of all three systems; additionally
problems with the cerebrovascular & cerebellar systems are also may need to be evaluated based on
the rest of the symptomatic picture.
Dizziness Categories
1) Vertigo (H81.399) - Spinning
 subjective & objective illusions of motion usually rotational/spinning or tilting.
 True vertigo is usually related to a vestibular dysfunction problem of the inner ear
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Ortho Lecture Notes Combined

o If severe it may be accompanied by nausea & vomiting.
o Vertigo occurs when there is conflict between the signals sent to the brain by various
balance- & position-sensing systems of the body.
You feel like your moving
Objective vertigo - environment moving/spinning around the person Environment moving
Subjective vertigo - the patient feels as though he or she is moving/spinning/tilting/rotating within the
environment. The patient may feel like they are being pulled towards the floor. Sensation may worsen
with motion or even when laying down. May feel like motion sickness (car or ferris wheel) Feel like
spinning within environment that is blurry around you
Vertigo is often seen in the conditions like:
 Inner ear: BPPV, Meniere Disease, Vestibular Neuritis & Acute Labyrinthitis.
 Head injuries
 Migraines
 Vertebrobasilar artery insufficiency
Peripheral Vertigo – due to prob of inner ear
 e.g. BPPV, Meniere, Labyrinthitis
 Unidirectional nystagmus, horizontal or rotational
 Usually peripheral, so if focus on a spot, spinning will stop
 Spinning slows w/eyes closed
 Positionally induced
 Accompanied by hearing loss
Central
 Nystagmus lasts longer – takes longer to go away (weeks to months)
 Nystagmus vertical and persists w/eyes open or closed
Periph
Central
Onset
Sudden
Gradual
Imbalance
Mild/mod
Severe
Nausea
Frequent
Infrequent
CNS signs
Absent
Present
Nystagmus
Torsion/horizontal
Vertical
Duration
Brief/sec-min
Weeks/months
Auditory symptoms
Common
Rare
2) Presyncope (Near-Faint Dizziness) (R55)
 Sudden feeling of impending loss of consciousness.
 FROM diminished amount of oxygen to the brain.
o Cardiac mechanisms, atherosclerosis
o Due to exercise (high CO2 causing acidity, drugs, acidity of blood)
 The patient may describe the following associated symptoms:
o Pallor, diaphoresis/sweating, a roaring sensation in their ears, sighing respirations (to
increase O2), restlessness, abdominal distress, yawning, weakness and/or dimming or
blurred vision.
 Often caused by medications
o Othostatic hypotension
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Ortho Lecture Notes Combined
o Vasovagal syncope
o Cardiac disease
3) Syncope (fainting)
 a transient loss of consciousness accompanied by the loss of postural tone that is due to
inadequate blood flow to the brain (a fall in systemic arterial pressure).
 Recovery is usually spontaneous; no need for resuscitation.
 A frequent cause is acute hypotension (vasovagal response).
3) Disequilibrium (R42)
 Feeling of being off-balanced when standing or walking (inability to maintain an upright
posture); sensation of being off balance & most often characterized by frequent falls in a specific
direction
 This may occur due to:
o cerebellar, motor, or posterior column problem.
 There is associated ataxia & it is considered a multi-sensory problem
 May be common in elderly
 Not associated with nausea or vomiting.
 It is an unsteadiness, imbalance or loss of equilibrium,
 Commonly seen with:
o Cervicogenic dizziness
o Multisensory disorder
o Parkinson’s disease
o Diabetic neuropathy
4) Visually-induced dizziness - an alteration in the vestibulo-ocular reflex system resulting in dizziness.
 Change in visual acuity such as ocular pathology or
 New prescription for one's glasses can cause such an alteration. E.g. adjusting to new glasses
5) Lightheadedness (giddiness) (R42) -all other vague & hard to describe sensations of uneasiness in the
head.
 May feel like they will faint or their head is weightless.
 patient may have subtle dysfunction within the orientation systems or psychological problems
 Often attributed to emotional causes
o Examples: Hyperventilation is a common cause of dizziness in anxious young people.
Panic attack is another example. (Baloh, 1998)
 Lightheadedness is a feeling that the patient is about to faint or "pass out."
 Although they may feel dizzy, they do not feel as though their surroundings are moving.
 Lightheadedness often goes away or improves when they lie down.
Lightheadedness usually is not caused by a serious problem.
 Often is caused by a momentary drop in blood pressure & blood flow to your head that occurs
when you get up too quickly from a seated or lying position (orthostatic hypotension).
 Many causes, including:
o allergies, illnesses such as the flu or colds, vomiting, diarrhea, fevers, & other illnesses that
cause dehydration, very deep or rapid breathing (hyperventilation), anxiety & stress, the use of
tobacco, alcohol, or illegal drugs.
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Ortho Lecture Notes Combined
o Many prescription & nonprescription medicines can cause lightheadedness.
 Knowing what medications your patients have can help diagnosis this condition.
o Lightheadedness can also be the result of depression, anxiety or hyperventilation syndromes.
o NOTE: More serious cause of lightheadedness is bleeding.
 Sometimes bleeding is not obvious (occult bleeding).
 Internal bleeding from major traumas or bleeding from the digestive tract can take
weeks to be noticed & the first signs might be lightheadedness & fainting.
 Usually 1st sign of slow bleed is lightheadedness
Basic Evaluation of the “Dizzy” Patient
 History
o Ask the patient to describe the symptoms without using the word dizzy.
o Have the patient differentiate vertigo from pre-syncope or near-syncope.
o Determine if the patient has a sense of being pushed down or pushed to 1 side (pulsion). A
peculiar sense of movement of objects viewed when the patient moves is termed oscillopsia
(object appears to be oscillating).
o Ascertain whether the symptoms are related to an anxiety episode; patients with
agoraphobia may describe their symptoms as dizziness.
o Determine if the sensation is continuous or episodic;
 if episodic, find out if the sensation is fleeting or prolonged.
o Ascertain whether the onset & progression of symptoms were slow & insidious or acute.
o Ask the patient about head trauma & other illnesses to determine the setting of the initial
symptoms.
 Trauma resulting in damage to an ear often manifests as unilateral hearing loss,
which may be the cause of episodic vertigo even years later (post-traumatic hydrops).
 Hearing loss can be associated w/peripheral vertigo
o Determine if the episodes are associated with turning the head, lying supine, or sitting
upright.
o Determine if symptoms of an upper respiratory infection or flu-like illness preceded the
onset of vertigo.
o Inquire about associated symptoms such as hearing loss or tinnitus (ringing in the ears), aural
fullness, diaphoresis, nausea, emesis, pallor, weakness, sighing, yawning, abdominal distress.
o Determine if the patient has an aura or warning before the symptoms start.
o If hearing loss is evident, find out if hearing fluctuates.
o Determine if the patient has headaches.
o Ask the patient about brainstem symptoms such as diplopia, dysarthria, facial paresthesia,
or extremity numbness or weakness.
o Ascertain the degree of impairment during an episode.
o Inquire about medications. Many medications can cause dizziness;
 most common culprit = antihypertensive agents. Ask if onset of patient's symptoms
was associated with starting a new medication or a change in dose/ frequency of a
medication.
 Physical examination VIPIRONNE
o Perform a complete examination of pertinent systems, such as the cardiovascular &
neurologic systems (especially cranial nerves), before proceeding to specific office tests of
the vestibular system.
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Ortho Lecture Notes Combined


Assess for nystagmus. Nystagmus of peripheral (ie, labyrinthine) origin typically is
unidirectional. Nystagmus of brainstem or cerebellar (ie, central) origin may be
bidirectional & have more than one direction,
 For example: torsional plus horizontal movement. Pure vertical nystagmus
almost always is a sign of brainstem disease & not a labyrinthine disorder.
 If a patient experiences pre-syncope
 perform auscultation of the heart & cervical vessels,
 determine orthostatic blood pressure & pulse.
 Orthostatic vital signs
 Carotid sinus reflex
o Examine the ears for retraction, bulging or perforated tympanic membrane or inflammation.
Assess hearing in both ears. (Global hearing, Weber’s, Rinne)
o Orthopedic
 Swivel test
 Nylen-Barany test (Dix-Hallpike)
 Barany chair records eye movements
 Romberg's
 Valsalva
 Head-shake test
 The examiner vigorously shakes the patient's head in the horizontal plane
from side to side for 10-15 seconds. After the shaking is stopped, the eyes are
observed for nystagmus.
 This test can reveal latent nystagmus & indicate which labyrinth is
malfunctioning.
o Office examination of the vestibular system
 Gait test: Determine whether the patient staggers or consistently leans to 1 side or
the other.
 Past Pointing: Ability for patient be able to touch an object with eyes open & closed
to test for vestibular nerve & cerebellar function.
https://www.youtube.com/watch?v=1NtDhHSGXEs
Diagnostic Studies
o Electronystagmography with caloric testing
o Electrocochleography:
 Although electrocochleography is not extremely sensitive, it is highly specific for
conditions related to inner ear fluid imbalance (most commonly Ménière's disease).
 Assess fluid imbalance (imbalance = Meniere’s)
 Classic Meniere’s = Vertical, Hearing loss, Tinnitus
 Common includes above + ear fullness
o Auditory brainstem response: Testing of the auditory brainstem response (ABR) can help in
the diagnosis of rare cases of microvascular compression of cranial nerve VIII in the
cerebellopontine angle or root-entry zone.
o Audiometry
o Electrocardiogram
o Echocardiogram
o Chest x-ray
o Lab: CBC, Glucose levels, Electrolytes, Cardiac Enzymes
Conditions that induce Vertigo
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Meniere’s Disease (H81.09)
 aka: Paroxysmal Labyrinthine Vertigo,
 Primary Endolymphatic Hydrops,
 Lermoyez Syndrome,
 Meniere’s Syndrome
Definition:
 disorder that affects the semicircular canals & cochlea of the inner ear, characterized by recurrent
vertigo with fluctuating hearing loss, roaring tinnitus & fullness in the ear.
Epidemiology:
 Age: 40s-50s, can occur any age but rare after 70
 Higher incidence in pregnancy
 40% have bilateral involvement
Etiology:
 Etiology is not known.
 It appears to be the result of the abnormal volume or composition of fluid in the inner ear
(endolymph). Because no single cause has been identified, it's likely that Meniere's disease is
caused by a combination of factors.
FYI: Meniere’s syndrome is the diagnosis if an identifiable cause of fluid build up is determined.
Pathogenesis:
 endolymphatic hydrops = accumulation of fluid in the endolympathic spaces.
 All patients with Meniere’s have endolympathic hydrops but not all patients with endolymphatic
hydrops has Meniere’s
Clinical presentation:
 Classic triad of symptoms
 Vertigo- Reoccurring severe vertigo, which peaks within minutes then slowly subsides over
hours.
o Attacks can last from 20 minutes to 24 hours.
o They can occur with the frequency of many attacks each week;
o can be separated by weeks, months, & even years.
 progressive, fluctuating low tone sensory hearing loss
o Loss of Low TONES 1st
 tinnitus
 Other common symptoms
o aural fullness - Sensation of fullness & pressure along ear w/decreased hearing &
tinnitus, usually unilateral
o pallor, nausea, diaphoresis may occur during a severe attack.
o vomiting/diarrhea
o anxiety
o depression
o drop attacks
o persistent disequilibrium for days after an episode.
Episodes vary in frequency & intensity – initially it starts with vertigo than progresses to fluctuating lowfrequency hearing loss.
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Following the attack, a period of extreme fatigue or exhaustion often occurs, prompting the need for
hours of sleep
Stages of Meniere’s
it is impossible to predict the timing or severity of each stage for each individual.
 Stage 1 – transient, short, sudden, nausea, vomiting, brief hearing loss, tinnitus
o Episodes 20 min – 24 hr.
o sudden & unpredictable attacks of vertigo;
o usually accompanied by nausea & vomiting.
o May lose some hearing during the attack which then may revert to normal, & there is often
tinnitus at the same time.
o Ear may also feel blocked & uncomfortable, with a sense of fullness.
 Stage 2 - "classical" – less severe vertigo / worsening hearing loss, tinnitus
o continuing attacks of vertigo, with the attacks becoming less severe.
 Vertigo starts to get better after a period of worsening (even temporary remission)
o Tinnitus & hearing loss often become worse.
 Stage 3 – Hearing loss & tinnitus getting worse & problematic, may no longer get vertigo
o Hearing loss worse & on both sides
o Vertigo episodes occur far less frequently & may stop altogether.
o May have balance problems.
o Hearing problems & tinnitus may become progressively worse during this stage.
Key Examination Findings:
 Caloric testing =
o will show a lack of response or abnormal response on the affected side.
o Put hot/cold water in the ear
 Barany chair = will be positive
 Nylen-Barany = (+,-)
 Low pitched hearing changes
Diagnostic Criteria:
American Academy of Otolaryngology-Head & Neck Surgery diagnostic criteria (all must be present)
 vertigo
o ≥ 2 spontaneous episodes
o lasting ≥ 20 minutes during single attack of Meniere's disease
 tinnitus with or without perception of aural fullness
 sensorineural hearing loss confirmed by audiometry on at least 1 occasion (may be difficult to
confirm in early stages of disease)
 other causes ruled out
Diagnostic Studies:
 Audiometry - basic hearing test
 Electrocochleography (ECOG) - measures the excess fluid accumulation in inner ear.
 Electronystagmography (ENG) - looks for signs of vestibular dysfunction or neurological
problems by measuring nystagmus.
 Rotary-chair testing (Barany chair) - Like a VNG, this measures inner ear function based on eye
movement.
 MRI - rule out an acoustic neuroma or other brain tumor as a possible source of symptoms.
Management
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Ortho Lecture Notes Combined

There is no evidence to support the use of manipulation although several case studies have
indicated some positive results. No evidence of CMT
 Patients may be advised to avoid:
o alcohol, caffeine, & tobacco
o all of which can aggravate symptoms of Ménière's.
 Low salt diet = 2-3 g/day or less; Lower salt intake to under 2-3 g/day
 Vestibular rehabilitation therapy (VRT)
o sometimes used to help with the imbalance that can plague people between attacks.
 Rest
 Meniett device (percussion)
 Medication: diuretics
Rehabilitation strategies most commonly used are:
 Gaze stability exercises - moving the head from side to side while fixated on a stationary object
(aimed to restore the Vestibulo-ocular reflex) An advanced progression of this exercise would be
walking in a straight line while looking side to side by turning the head.
 Habituation exercises - movements designed to provoke symptoms & subsequently reduce the
negative vestibular response upon repetition. Examples of these include Brandt-Daroff exercises.
 Functional retraining - including postural control, relaxation, & balance training. Avoid positions
that irritate
Medical Management:
 Medications can be used during an attack to reduce the vertigo, nausea/vomiting or both.
o Diuretic if lifestyle changes are not sufficient, evidence is not great supporting the use of
diuretics
o Intratympanic gentamicin – chemical labyrinthectomy (vestibular ablation)
 Meniett device – painless micropressure pulses into the ear that may reduce excess inner ear
fluid, tube is placed in middle ear
 In severe, unremitting cases = destruction of the labyrinth or vestibular nerve or shunting to
drain endolymph.
Prognosis:
It is difficult to predict how Ménière’s disease will affect a person’s future.
 Symptoms can disappear one day & never return.
 Or they might become so severe that they are disabling and result in hearing loss
BPPV - Benign Paroxysmal Positional Vertigo (H81.10)
aka: Canalolithiasis, Cupulolithiasis, vestibulolithiasis *named for where the stones are
Definition:
a disorder arising in the inner ear. Its symptoms are repeated episodes of positional vertigo, that is, of
a spinning sensation caused by changes in the position of the head.
Paroxysmal = sudden
Etiology:
 Idiopathic (over 50 yrs)
 Head trauma (under 50 yrs)
 Inner ear damage
 Migraines
Pathology
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Ortho Lecture Notes Combined
Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia.
 Canalithiasis = the otoconia are dislodged from their usual position
o Usually in utricle, but now move in the fluid of the canal.
o With this form after movement of the head it usually takes < 1 minute for the fluid to
stop moving
o so vertigo is usually < a minute
 Cupulolithiasis = the otoconia adhere to cupula (sensory fibers that detect fluid movement).
o This form is less common
o vertigo & nystagmus can last longer; due to attachment of sensory fiber
o until the head is moved out of the offending position.
Epidemiology:
 Age: middle age to elderly.
 2:1 Women to men
 Most common cause of vertigo = BPPV
Clinical Manifestations
 Vertigo induced by head motion (duration: if canalithiasis < 60sec, if cupulolithiasis – variable but
still shorter duration).
 Nausea
 Nystagmus
o Nystagmus associated with BPPV has several important characteristics that differentiate it
from other types of nystagmus.
 Positional: the nystagmus occurs only in certain positions
 Latent onset: there is a 5-10 second delay prior to onset of nystagmus
 Nystagmus lasts for 5–120 seconds, usually less than 30s.
 Visual fixation suppresses nystagmus due to BPPV focus makes it stop if BPPV
 Repeated stimulation cause the nystagmus to fatigue or disappear temporarily.
 Response fatigues w/repeat situation e.g. testing Nyalan Barany
 (+) Nylen-Barany &/or Dix-Hallpike = response fatigues after repeated testing
o Posterior semicircular canal involvement (most common)
 elicits a rotatory or vertical upbeat nystagmus.
 Rotatory nystagmus is clockwise if left ear involved & down; counterclockwise if
right ear involved & down
o Anterior semicircular canal involvement –
 Rotatory & downbeating nystagmus on Dix-Hallpike maneuver,
 Upbeating nystagmus on return to sitting
o Horizontal semicircular canal involvement –
 horizontal nystagmus on Dix-Hallpike maneuver,
 horizontal (opposite direction) nystagmus on return to sitting {Arch Otolaryngol Head Neck Surg
1996 Mar;122(3):281}
o
o
o
Posterior canal (Most common) =
 CW rotary if L involved & down (see slide)
 CCW is R ear involved & down
Anterior Canal:
 Rotary & downbeating nystagmus going dow
 Upbeating nystagmus returning to seated
Horizonal canal
 Horizontal nystagmus going up & down
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Ortho Lecture Notes Combined
See slide w/URL
 Bandt Darroff Tx
o For home tx of canalolithesis
 If R inner ear affected the Turn head L & lay on R while looking @ ceiling
 Stay until sx reside up to 30 seconds or more
 Sit up, look R and then do other side
 START on the side that is affect
o 2 wks, 3x /day
o 3 wks 2s/day
 Antivertigo drugs (refer)
 Surgery
 (-) Caloric reflex tests
 Emesis is uncommon but possible.
Diagnostic Criteria: American Academy of Otolaryngology-Head & Neck Surgery Foundation diagnostic
criteria for posterior canal BPPV
 history of repeated episodes of vertigo with changes in head position
 vertigo with nystagmus elicited by Dix-Hallpike maneuver
 latency period (typically 5-20 seconds) between completion of Dix-Hallpike test & onset of
nystagmus & vertigo
 nystagmus & vertigo increase & then resolve ≤ 60 seconds from onset of nystagmus
Management
o Canalith repositioning procedures
o Epley
 Held 45 to side, wait for nystagmus, then straight up, then Opposite side 90
degrees
o Semont – for cupulolithiasis aka livertory maneuver
 E.g. L posterior canal
 Sit on bed, lay quickly on L
 Then switch quickly to lying diagonally on R face for 1 M
 Then sit up on bed for 10 min
o Manual manipulation
o Medications - antivert
o Surgery - sectioning the nerve to the ampulla of the posterior semicircular canal, this
procedure may result in deafness.
Prognosis:
One third of patients remit at 3 weeks & the majority of patients at 6 months from onset. Surgery is
very rarely required (less than 1%). Reoccurrence is frequent.
 1/3 better in 3 weeks
 Most w/in 6 months if treat at home too
 Surgery is rarely req.
WF 61 yo, episodic dizziness. Occur @ anytime of day, but worse in am when turning in bed. Also when
turn head throughout day. Last 45 sec.
 Exam findings
o Latent nystagmus w/Nylen barany
o Visual fixation helps
o Decreased sx w/repeat testing
o
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Ortho Lecture Notes Combined
Labyrinthitis (H83.09)
Etiology:
 In addition to viral & bacterial infections, it may be due to head injuries, stress, allergic response
or adverse response to medication, & cholesteatoma.
 Usually result of viral or bacterial infection
o Infection affects both branches of the vestibulcochlear N
 Sometimes from trauma stress or allergies that put pressure on labyrinth
Clinical Manifestations:
 Vertigo may worsen with head movements
 Nystagmus may be present & worsen with head movements
 Possible hearing loss in the affected ear. Otoscope examination usually normal although higher
incidence of otitis media so signs of that maybe evident.
 Tinnitus is possible
 Symptoms usually peak within 24 hours then slowly resolve over the next several weeks.
 May have fever, chills, ear pain, +/- hearing loss, otitis media, tinnitus,
 Improved sx in 1st week and gone by 2-3 month
Diagnostic testing:
Usually not needed. Tests will be done to rule out other causes of your symptoms. These may include:
 EEG
 Electronystagmography
 Head CT scan
 Hearing tests (audiology/audiometry)
 MRI of the head
 Warming & cooling the inner ear with air or water (caloric stimulation) to test eye reflexes
Management
Vestibular rehabilitation therapy is a highly effective way to substantially reduce or eliminate residual
dizziness from labyrinthitis.
Medications that may reduce symptoms include:
 Antihistamines
 Medicines to control nausea & vomiting
 Medicines to relieve dizziness
 Sedative-hypnotics such as Valium
 Treat sx, as usually self-resolving
o Reduce inflammation
o Help w/sleep
 Vestibular rehabilitation & balance training
Prognosis:
Severe symptoms usually go away within a week. Most patients are completely better within 2 to 3
months. Continued dizziness is more likely to last in older patients. Hearing loss may be permanent.
 1 week resolves
 At most 2-3 weeks
34
Ortho Lecture Notes Combined

In older population may have residual effects, e.g. Hearing Loss
Vestibular Neuronitis (H81.2)
Etiology:
 Paroxysmal (sudden)
 Souza:
o Cause UNKNOWN
o 50% have had common cold
o Peak age 40-50 y
o Theory = reactivation of dormant herpes infection in Scarpa’s ganglion
o Initial severe vertigo, nausea, disequilibrium lasts a few days
o Provocation by rapid head movts lasts weeks
o DDX from Labyrinthitis b/c Labyrinthitis affects both Vestibular & Cochlear NN
 Labyrinthitis has hearing loss / Vestibular neuritis does NOT
 Labyrinthitis has signs of infection (fever, chills, ear pn) / Vest neur does NOT
o DDX from Inferior Cerebellar infarct/hemorrhage:
 25% pts have risk factor for stroke when present @ ER w/vertigo, nystagmus,
disequilibrium
 Vest Neuronitis is Peripheral NS, so nystagmus:
 worse looking in direction of unaffected side = Alexander’s Law
 improves when fixate on object
 HYPO or no findings w/Caloric testing
 Cerebellar stroke is Central NS, so nystagmus:
 Not improved w/fixation
 May change direction
 Accompanied by cerebellar signs: dysarthria, ataxia, dysdiadokinesis,
finger to nose, and disequilibrium is more CC than vertigo
o Management:
 Central compensation over time on own
 Perform vestibular training (focus on object w/head movt in all direction
 Perform eye-head coordination exercises
 Perform balance exercises
 Rx in ACUTE phase: *NOTE that it may delay central compensation healing
 Benzodiazepines (lorazepam, diazepam)
 Single attack of vertigo, series of attacks, or persistent condition that occurred suddenly
 SUDDEN ONSET, SEVERE for DAYS, IMPROVES OVER WEEKS
o Possible N/V
 NO HEARING LOSS B/C not cochlear N (only balance affected)
 Possibly acute localized ischemia
Additional Clinical Information:
Patient will state the vertigo:
o Gradually gets better over a span of a few days to weeks.
o After the first symptoms of vertigo go away, there may be a period lasting a month or more when
any sudden head movement can trigger dizziness & loss of balance.
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Ortho Lecture Notes Combined
o
o
o
o
Patient tends to fall toward his or her affected side when attempting ambulation or during Romberg
tests.
NOT Vestibular neuronitis if any of the following findings are present:
o Multidirectional, non-fatiguing nystagmus (this suggests vertigo of central origin)
o Hearing loss
o Other cranial nerve deficits
o Truncal ataxia (suggests cerebellar disease or another CNS process)
o Inflamed tympanic membrane
o Mastoid tenderness
o High fever
Treatment: self-limiting, hydrate, vestibular rehab,
o MAY need MRI to determine cause if not resolving
Diagnosis
o Perform Hallpike maneuver - Failure either to observe or to provoke unidirectional nystagmus
casts doubt on whether the process is localized to the peripheral vestibular system.
o Cerebral imaging may be necessary to assess causes. MRI over CT.
Prognosis:
 Most patients experience complete recovery within a few weeks.
 A minority have recurrent vertiginous episodes following rapid head movement for years after
onset
Disequilibrium or Vertigo
Cervicogenic Dizziness (Vertigo)
Definition:
It is a nonspecific sensation of altered orientation in space & dysequilibrium originating from abnormal
afferent activity from the neck.
 Cervicogenic dizziness does not result from vestibular dysfunction and,
o therefore, rarely results in true vertigo.
Etiology 3 mechanisms implicated
o Irritation of the cervical sympathetic nervous system
o Mechanical compression or stenosis of vertebral artery
o Involvement of the proprioceptors of the upper cervical spine (C0-C3) caused by
overstimulation or another disorder
Risk factors:
 Cervical trauma  whiplash (flexion/extension injury) (50% of cases)
o E.g. WAD, so check of concussion & head trauma too
 Degenerative joint disease - Less space for nn, so irritated
 Muscle spasm - Less space for nn, so irritated
Clinical presentation:
o History of neck trauma or injury. Neck pain. Likely due to proprioceptive change
o “Dizziness” for minutes -hours, or longer.
o Worse with neck movement or sustained postures
o Possible headache, possibly nystagmus
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Ortho Lecture Notes Combined
o Upper cervical muscular tenderness. Palpation may increase dizziness.
o Feels like falling & may feel off balance
o Upper cervical spine segmental dysfunction
o Cervical spine findings (palpatory & ROM), restrictions,
o (+) Swivel
Diagnostic Criteria:
o Temporal relationship between neck pain & symptoms of dizziness
o including time of onset & occurrence of episodes
o eg., decrease pain  decrease dizziness
o previous neck injury or pathology
o eliminate other causes of dizziness
Management:
o Upper cervical manipulation
o Positional cervical stabilization exercises
o Soft tissue modalities
o Vestibular rehabilitation
Prognosis:
Conservative/chiropractic treatment has very high success rate.
Treatment:
 Upper cervical manipulation
 Stabilization exercise, cervical
 Soft tisus
 Vestib rehab, balance
 Conservative chiro tx has high success rate***
Presyncope/Syncope Conditions
Vasovagal syncope (R55)
aka: Vasodepressor syncope, “Fainting”
Definition:
Temporary loss of consciousness resulting from an acute global reduction in cerebral blood flow.
Etiology: Usually a trigger, most often emotional or pain that affects blood pressure
o emotional stress common cause
o fear
o pain
o venipuncture, other painful or medical procedures
o prolonged standing or sitting (waiting at the alter)
o hot environments, overheat
o dehydration
o systemic illness
o alcohol
37
Ortho Lecture Notes Combined
Pathology:
 Vasovagal syncope trigger causes a sudden drop in your heart rate & blood pressure.
 That leads to reduced blood flow to your brain, which results in a brief loss of consciousness.
 Vasovagal syncope is usually harmless.
 Most risk is from hitting head when fall
Epidemiology:
 Adolescents & young adults b/c they stress out more easily
 F > M; elderly males
 Most common cause of syncope = VASOVAGAL SYNCOPE
Clinical Manifestations
Before a vasovagal response patient may experience:
o Skin paleness or clamminess
o Lightheadedness
o Tunnel or blurred vision
o Nausea
o Dilated pupils
o Weak pulse
o Abnormal movements of extremities.
 Recovery after a vasovagal episode generally in < 1 minute. Yet, risk of fainting remains with
standing within 15-30 minutes of fainting.
Diagnostic Studies
o Tilt table test - to determine blood pressure of patient at different positional levels. Dx study of
choice.
o Blood Volume determination - to evaluate intravascular pressure & blood flow.
o Autonomic reflex testing - series of different test to monitor blood pressure, blood flow, heart rate,
skin temperature & sweating in response to certain stimuli.
Management:
Patient usually revives in less than a few minutes
Treatment may not be needed however if occurrences become frequent the following maybe done.
o changes in medications or new medications.
o Wearing support garments or compression stockings to improve circulation
o Making certain dietary changes such as eating small, more frequent meals; increasing salt, fluid
& potassium (note: may need to consult with allopathic physician before making these
recommendations); & avoiding caffeine & alcohol.
o Education in taking certain precautions when changing positions from sitting to standing.
o Elevating the head of bed while sleeping.
o Avoiding or changing the situations or “triggers” that cause a syncope episode.
Carotid sinus syncope (G90.01)
aka: Carotid sinus hypersensitivity, “Tight-collar” syndrome
Definition:
A brief unconsciousness from impaired blood flow to the brain. Unlike the ordinary faint, this syncope is
not preceded by pallor, nausea, & sweating. It results in dizziness or syncope from transient diminished
cerebral perfusion.
38
Ortho Lecture Notes Combined




Recurrent dizziness
Nonaccidental unexplained falls
Sx produced by head turning, extension
Collared shirts
Essentially increased pressure on the carotid sinus makes the body think has high BP, so it drops BP
Two Categories of Carotid Sinus Syncope:
o Spontaneous carotid sinus syndrome refers to a clinical situation in which the symptoms can be
clearly attributed to a history of accidental mechanical manipulation of the carotid sinuses
(taking pulses in the neck, shaving) & is reproduced by carotid sinus massage. Spontaneous
carotid sinus syndrome is rare & accounts for about 1% of causes of syncope.
o Induced carotid sinus syndrome refers to a clinical situation in which a patient has no clear
history of accidental mechanical manipulation of the carotid sinuses & has a negative result from
workup for syncope, except for a hypersensitive response to carotid sinus massage, which can
be attributed to the patient's symptoms. Induced carotid sinus syndrome is more prevalent than
spontaneous carotid sinus syndrome & accounts for the bulk of patients with an abnormal
response to carotid sinus massage observed in the clinical setting.
o Etiology:
o Most common causes = coronary artery disease, hypertension, then Neck tumors.
o Other causes include orthostatic hypotension, Alzheimer's or Parkinson disease or
Concurrent medication with digitalis, beta-blockers, & methyldopa.
o It may be associated with an identified precipitating trigger such as
o turning of neck
o wearing a tight necktie
o shaving the neck
o neck malignancy
Pathology
Nucleus tractus solitarii in brainstem is directly / indirectly activated by triggering stimulus, resulting in
simultaneous enhancement of parasympathetic nervous system (vagal) tone & withdrawal of
sympathetic nervous system tone resulting in a spectrum of hemodynamic responses:
1. On one end of the spectrum is the cardioinhibitory response,
a. Drop in heart rate (negative chronotropic effect) & contractility (negative inotropic
effect)
b. Leads to decreased cardiac output, significant enough to cause loss of consciousness.
c. It is thought that response results primarily from enhancement in parasympathetic tone.
2. On the other end of the spectrum is the vasodepressor response,
a. Drop in blood pressure (to as low as 80/20) without much change in heart rate.
b. Occurs due to vasodilation, likely from withdrawal of sympathetic nervous system tone.
3. Majority of people with vasovagal syncope have a mixed response somewhere between these
two ends of the spectrum.
Epidemiology
Rare prior to 50 yrs
M>F
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Ortho Lecture Notes Combined
Clinical presentation:
o Recurrent “dizziness” (presyncope/lightheadedness)
o Recurrent syncope
o Non-accidental, unexplained falls
o Symptoms produced by head turning or wearing garments with tight-fitting collars.
o Possible prodrome or retrograde amnesia for the syncopal event
o Typical trigger factors are shaving, head turning, neck extension or tight collars. Even mild
stimulation to the neck may cause marked bradycardia & hypotension. The features of CSH may
occasionally occur without any stimulation.
o Auscultation for a carotid artery bruit is essential in the evaluation of carotid artery occlusion.
o Carotid sinus massage - considered positive if asystole longer than 3 seconds or a drop in
systolic BP by 50 or more (carotid sinus massage should not be done in chiropractic office)
Management
o Lifestyle modification:
o Avoid triggers that increase pressure on the carotid sinus
o Loose clothing with open collars may be helpful.
o Maintain adequate fluid intake.
o Learn to be aware of warning symptoms.
o There has not been shown to be any consistent benefit of medical therapies.
o Cardiac pacing with a permanent cardiac pacemaker, however again not shown to be highly
effective.
o Surgical denervation of the carotid sinus. Not commonly performed.
Prognosis:
o Untreated symptomatic patients
o have a syncope recurrence rate as high as 62% within 4 years.
o Patients treated with a pacemaker have fewer syncope attacks but may experience a
recurrence rate as high as 16% in 4 years.
Orthostatic hypotension (I95.1)
aka: Postural hypotension, Orthostasis
Definition:
 a drop in systolic pressure of at least 20mm Hg and/or diastolic pressure of at least 10 mm Hg
within two to five minutes of standing up.
 Symptom is sometimes caused by blood pooling in the lower extremities upon a change in body
position.
 Loss of blood flow to head problems w/sit to stand= get dizzy, blurry vision
Etiology:
Orthostatic hypotension can be caused by many different things, including:
o Medications are the most common cause.
o Hypovolemia ~ Dehydration another very common cause. Caused by Fever, vomiting, not drinking
enough fluids, severe diarrhea & strenuous exercise with excessive sweating.
o Heart problems. Some heart conditions that can lead to low blood pressure include extremely low
heart rate (bradycardia), heart valve problems, heart attack & heart failure.
o Diabetes. Untreated diabetes can cause dehydration by causing frequent urination.
40
Ortho Lecture Notes Combined
o
o
Nervous system disorders. Some diseases, such as Parkinson's disease, multiple system atrophy
(Shy-Drager peripheral neuropathies) & amyloidosis, can disrupt your body's normal blood pressure
regulation system.
Associated with Addison's disease.
Pathology
It is due to a lesion of the baroreflex loop, which senses a change in blood pressure & adjusts heart rate
& activates sympathetic nerve system fibers to cause the blood vessels to narrow & correct blood
pressure
Clinical presentation:
 Lightheadedness/presyncope is most common Sx when patient stands up
 Symptoms tend to resolve quickly (a few seconds)
 blurred vision
 weakness/leg buckling
 fatigue
 syncope – may occur & can be gradual or sudden
 chest pain, orthostatic dyspnea, neck pain, & headaches are less common Sx
Classification of Orthostatic Hypothension:
 initial orthostatic hypotension - lightheadedness/dizziness, visual disturbances a few seconds
after standing *may be dehydrated younger person
 classical orthostatic hypotension - dizziness, pre-syncope, fatigue, weakness, palpitations, visual
& hearing disturbances 30 seconds to 3 minutes after standing middle aged
 delayed (progressive) orthostatic hypotension - prolonged prodrome dizziness, fatigue,
weakness, palpitations, visual & hearing disturbances, hyperhidrosis, low back pain, neck, or
precordial pain followed by rapid syncope 3-30 minutes after standing *older person
Evaluation of Orthostatic Hypotension:
1. Review medications the patient is taking BP meds?
2. Review coexisting medical disorders
3. Determine the relationship of episodes to meals, exercise, straining, valsalva, standing up
4. Orthostatic (postural) vitals =
a. BP & Pulse in the supine position & repeat in standing positioning after 3 minutes (or
seated position if the patient appears to be unsteady)
i. Positive = decrease in systolic blood pressure ≥ 20 mm Hg or ≥ 10 mm Hg in
diastolic blood pressure within 3 minutes of standing compared to sitting or
supine
ii. Decrease in systolic by 10+ mmHg & increase in heart rate by 30+bpm
5. Neurological work-up - In patients with neurogenic causes of orthostatic hypotension, the heart
rate may not increase (Engstrom, 1997)
Diagnostic studies
o Cardiac work-up: ECG, Tilt table testing, Holder monitor, Stress test, Echocardiogram
o Blood work: anemia or diabetes
Management
o Review medications & possible referral for changes
o Increased water & electrolyte intake to help prevent dehydration.
o Review daily behaviors
o Avoid activities in the morning or after immediately after eating
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Ortho Lecture Notes Combined
Avoid extreme heat
Teach slow position changes to avoid episodes.
Sleep in a slight incline.
Avoid Alcohol
Increased frequency of meals (4-6 meals a day)
Coffee intake shown to help (2 cups).
Compression stockings may be considered to help prevent fluid from pooling in the legs
when a person is sitting or lying down.
o Teach patient to perform isometric exercises (such as squeezing a rubber ball or a towel
for a few minutes) before assuming an upright position. These exercises will raise blood
pressure & may prevent a significant drop in blood pressure when they stand up.
Upper cervical adjustments may help condition. Caution should be used to make sure your hand
placement is not contacting the carotid sinus.
Referral
o MD may prescribe a medication to treat the orthostatic hypotension, drugs that work by
increasing blood volume or by constricting (narrowing) blood vessels.
o
o
o
o
o
o
o
o
o
Cervical Spine & Brachial Plexus Conditions
Objectives:
1. Describe the etiology, pathogenesis, clinical presentation, risk factors, diagnostic studies, &
management for the cervical spine conditions reviewed in Orthopedics I.
2. Identify the etiology for the conditions presented.
3. Describe the pathogenesis for the conditions.
4. Explain the clinical presentation for each of the conditions.
5. Identify the most appropriate diagnostic studies to order for each condition & explain the
expected findings.
7. Describe the classification scheme for TOS.
8. Determine how to best manage the conditions.
Cervical disc disease with radiculopathy (M50.10)
aka Degenerative intervertebral cervical disc,
aka Cervical disc syndrome,
aka Intervertebral disc disorder


Definition:
o Impingement of a cervical nerve root secondary to:
 disc herniation &/or
 degenerative disc disease,
o characterized by:
 unilateral shooting,
 shock-like pain in the upper extremity, neck pain &
 possible sensory &/or motor deficits (even a VERY light touch will disrupt signal)
o Usually history of neck pain & or cervical trauma.
 A cervical disc tends to degenerate naturally over time becoming more ligamentous
than disc-like by age 50.
 70-75% of cases -caused by foraminal encroachment due to degeneration.
 Normal motion helps maintain function
Classification:
o Bulge - involves more than one quarter (25% of disc) of the circumference of a disc;
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Ortho Lecture Notes Combined



bulges are always gradual & broad
often involve the whole disc (circumferential bulge). It is responsible in part (along
with endplate bowing) for the disc height loss that is seen with aging.
 Nucleus propulsus pushes out on annulus
o Protrusion – less than 25% of the disc circumference
 focal or localized abnormalities of the disc margin.
o Extrusion – defect in annulus,
 Nucleus propulsus not contained
 allows displacement of the nucleus beyond the confines of the disc
o Sequestration – extruded material separates from the rest of the disc (floating fragment)
 Dislodged piece can resolve or be problematic
Epidemiology:
 Acute Disc
o M=F,
o age peaks in mid to late 30’s
o associated with trauma
 Degenerative Disc –
o F>M,
o Prevalence is:
 10% in 20s
 up to 90-100% in 70+ yrs
o Levels: C6-C7*, C5-C6*, C4-C5
*most common
 C7 root is found affected in 37%-75% of the patients. C6 is found affected in
15.8% to 48% of the patients. The other cervical levels are rarely involved.
(Borenstein, 1996)
Etiology:
 Acute cervical spine trauma (flexion/extension injury)
o disc function is to absorb shock, yet forces can overwhelm disc resilience
 Twisting action of the head/neck combined with compression
 Degenerative joint disease (etiology of degeneration sometimes unknown usually thought to be
secondary to old trauma)
 Theories:
o White & Panjabi propose that disk failure is due to tensile load
o Farfan feels disk injury is due to combined torsion & compression loads.
Risk Factors
 Driving vibrating equipment *constant repetitive stress
 Recurrent lifting of heavy objects (associated with job) *constant repetitive stress
 Smoking *weakens everything
Pathogenesis:
 Acute disc herniation causes radicular pain through chemical radiculitis
o in which proteoglycans & phospholipases released from the nucleus pulposus mediate
chemical inflammation and/or direct nerve root compression.
 The chemical radiculitis is a key element in the pain caused by HNP because nerve root
compression alone is not always painful unless the dorsal root ganglion is also involved.
Herniation may induce nerve demyelination with resulting neurologic symptoms.
Forms of Disc herniations:
 Acute disc herniation (soft disc)
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Ortho Lecture Notes Combined

o Manifest: acute neck pain & paraspinal muscle spasm, with radicular symptoms/signs.
o Patient usually doesn’t have a history of neck pain. Patients tend to be younger & there may
have been a traumatic etiology (high energy injury or awkward twisting or turning). Soft discs
resolve more frequently than hard discs. (Scherping, 2002)
o Chemical radiculitis is key component of acute herniations
o Younger patients – more imbibition, hydrated, so more nucleus propulsus
Degenerative disc disease (hard disc)
o Found in patients age 45+
degeneration & less imbibition
o Most common form of disc disease more people age than are injured
o Onset is more insidious severity increases w/time
o Radiculopathy more common
o Usually have episodic neck stiffness & pain. (Scherping, 2002).
o History of trauma noted only in about 15% of cases.
Clinical Presentation
 Posterior, Posterior-lateral neck pain,
 May or may not have persistent radicular symptoms -pain, paresthesia, weakness in arm
 Typically unilateral
 Neck pain is persistent even at rest due to chemical radiculitis
 Exacerbation with extension
 Flexion may push disc further out & cause pain
 Antalgia is possible - lean to one side
 Possible edema, erythema
 Tenderness
 Cervical muscle spasms of mm innervated by the inflamed NN
 A/hypotonicity, Myotomal weakness,
 A/hyporeflexia,
 Dermatomal changes in sensation
o of mm innervated by the inflamed NN
 Cervical distraction may relieve arm pain open IVFs
 Shoulder depression may reproduce complaint on the side of head deviation
 Cervical ROM decreased & often provoking
Diagnosis requires:
2 clinical signs + 2 clinical symptoms + imaging* required
Clinical Prediction Rule for Identifying Cervical Radiculopathy
(Wainner RS, Irrgang JJ, Boninger ML, Delitto A, Allison S. Reliability & diagnostic accuracy of the clinical
examination & patient self-report measures for cervical radiculopathy. Spine 2003;28(1):52-62.)
1. (+) Upper limb tension test (method I) with one of the following
 Symptom reproduction
 Side-to-side difference>10 degrees in elbow extension
 with regard to involved/painful side: ipsilateral neck lateral flexion decreases symptoms and/or
contralateral neck lateral flexion increases symptoms.
2. (+) Spurling (lateral flexion combined with extension & compression) test
 Symptom reproduction
3. (+) Distraction test
 Symptom reduction
4. Cervical rotation less than 60 degrees
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Ortho Lecture Notes Combined


3 positive tests: Sensitivity=.39, specificity=.94, +LR .88 (1.5, 2.5), posttest probability of 65%
4 positive tests: Sensitivity=.24, specificity=.99, +LR 30.3 (1.7, 38.2), posttest probability of 90%
Diagnostic Studies:
 Plain film radiographs may demonstrate spondylosis, curve reversal, vacuum phenomenon
 MRI ***diagnostic
 NCS – Nerve conduction test to confirm radiculopathy
o Electrodiagnostic studies to confirm nerve involvement
o help differentiate root from peripheral nerve
 Possible discography
Management:
Pain management
 Manipulation/mobilization – SMT is less effective with radiculopathy than without
 Ice, E-stim (Sensory level stimulus {SLS}), IFC, TENS
 Rest
 Possible brace (cervical collar) (30% improvement in pain at 6 weeks compared to control)
 NSAIDs, analgesics, homeopathic meds for pain/inflammation
 Anti-inflammatory diet, supplements (Vit C, E, Omega 3, Ca, Mg, D, etc)
 Traction (negative pressure & open IVF)
Functional restoration
 Exercise therapy *lose WT if applicable to relieve stress on body*
 ROM & stretching exercises
 Isometric/ isotonic exercises
 Cervical stabilization
 Nerve gliding
Medical Management
 Soft collar
 NSAIDs, analgesics, narcotics, muscle relaxants
 Steroid injection
 Surgical decompression
 Cycle of Rx to control pn, steroid shots & degeneration and a lack of healing the cause…
o Results in surgery
Prognosis:
75% of patients get conservative care
90% will respond to conservative care. 1/3 will continue to have symptoms after therapy.
Cervical Myelopathy (M47.12)
Definition:
Damage/irritation/inflammation of spinal cord that can manifest with:
 difficulty with manual dexterity, gait disturbance, upper motor neuron signs (Hoffman sign,
Babinski sign, hyperreflexia, & clonus), &
 Other long tract signs:
o alteration in: proprioception, touch, pain, temperature, balance, etc
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Ortho Lecture Notes Combined
Epidemiology:
 +45 years.
 Most common cause of spinal cord dysfunction in individuals older than 55 years of age.
Etiology
STIFD
 Spondylosis
 Tumor
 Ischemia
 Fractures/dislocations
 Disc herniation
Pathogenesis:
 Direct pressure &/or ischemia to the cord alters function of the tracts
 Decreased blood flow
Clinical Presentation
 Vary depending where on cord: Anterior=motor, Posterior = sensory
 Symptoms & signs vary depending on:
o Level of involvement (C1-C7)
o Part of cord that is involved (anterior vs posterior vs lateral aspect of the cord)
 Overlapping symptoms of posterior & anterior cord involvement are usually:
o Headaches, neck stiffness, shoulder pain,
o Paresthesias & other radicular signs.
 The timing of the appearance of symptoms & their progression is also highly variable from
person to person.
o Rate of progression of an individual’s symptoms may change over time, with periods of
relatively rapid change interspersed with periods of stability or minimal progression.
Clinical prediction rule –
 +Babinski sign
 +inverted supinator sign
 +Hoffmann sign
 +gait dysfunction
 >45 years old
3 out of 5 = 95%
Diagnostic Studies:
may or may not be symptomatic
 Plain film radiography bony elements = spondylosis, fx, dislocation
 MR/CT  visualization of the cord
 Electrodiagnostic studies
Treatment:
 Probable co-manage (get ortho/neuro consult for possible decompression)
• Mobilization &/or gentle manipulation (avoid extension)
• Traction & other modalities for pain control
 Surgery = decompression & possible fusion
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Ortho Lecture Notes Combined
Cervical Spine Instability (M53.2X2)
Definition:
 Painful excessive motion of the vertebral bodies within the cervical spine in relation to one another
Etiology:
 Degeneration &/or mechanical injury of the spinal stabilization components
 Associated with:
o repetitive trauma,
o poor posture,
o acute trauma,
o weak muscles,
o congenital anomalies,
o connective tissue disease
 Marfans,
 Sharp Pursor for C1 instability of transverse dens ligament
Epidemiology:
 Levels: C1-C2,
 Facet dislocations between C4-C7
Pathogenesis:
 Ligamentous and/or capsular sprain
 Muscle strain


Fracture
Ligamentous laxity
Clinical Presentation
 Perception that neck & upper spine are moving more than what the bone, muscle & ligament can hold
~ unstable feeling excess motion
 The feeling that a patient must be careful with head motion or a sharp pain & “catch” will occur.
o Motion must be reproducible with same motion at most times to be considered instability.
 E.g. If it occurs only once a week = not be considered unstable but if it occurs 5-8 times
a day, instability considered as a diagnosis.
o Dysfunction often leads to issues with other tissues in the neck leading to a disruption of
normal everyday activities.
 Sharp neck pain with motion or position & possible upper back pain &/or headaches.
 Pain is provoked by sustained weight bearing positions & better when non-weight bearing
 Muscle spasms are common due to increase contraction to try a provide stability.
 Complaints of locking/catching in the neck
 Altered ROM – global motion may be normal or slightly increased
 Hypermobility - segmental motion
 Poor cervical muscle strength (multifidus, longus capitis, longus colli)
 +Rust Sign
 +Sharp-pursar…if C1 instability
Diagnostic Studies:
 Plain film radiography (flexion/extension films)
o demonstrate displacement/instability/ increased ADI
 MR/CT
Treatment:
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Ortho Lecture Notes Combined



Spinal stabilization exercises
Ergonomics to prevent putting the neck in position of instability
o typically a flexion & twisting motion
Chiropractic manipulation is not recommended as these segments move too much & manipulation
would increase the motion.
Torticollis (M43.6)
aka: Wry neck, Cervical Dystonia
Definition:
A contraction or contracture of neck muscles causing head to be tilted to one side *SCM
 Congenital torticollis *birth trauma
 Spasmodic torticollis *woke up wrong, can be neurologic in origin
 Pseudotorticollis
*
Clinical presentation:
 Head lateral & or rotation presentation
Refer to Souza:
 Several presentations based on age & cause
o Congenital: fixed asymmetry of head w/in hours to weeks of delivery
o Adult: Painful spasm of SCM
o Pseudo: Pain w/head movement in all directions *woke with condition, head neutral
 Cause
o Congenital: birth trauma, breech, damage to SCM becomes fibrous
o Adult: CNS infection, tumor, basal ganglion ds, psychiatric ds
o Pseudo: UNKNOWN
 Evaluation
o DDX –
 Meningitis: fever? Brudzinski or Kernig
 Masses: palpate anterior neck & SCM
 Pseudo: PROM erect vs. supine – marked ROM increase when supine
 Neuro: eval UMN & LMN function
o Imaging:
 X-ray not usually needed
 MRI/ CT if CNS ds suspected
Treatment:
 Congenital
o Parents shown stretching exercises to help lengthen SCM & muscles
o Tx must be consistent, can last a year…
o Very mild soft tissue work can be performed
 Spasmodic
*may self resolve
o Stretching SCM
o Soft tissue modalities
o Manual manipulation CMT
o Physical therapy
o Injections
o Biofeedback
o Pain control medications
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Ortho Lecture Notes Combined

Pseudotorticollis
o Manual manipulation ASAP to decrease global mm spasm *use caution
o Soft tissue work
o Soft tissue modalities
o Refer for medical eval if no resolution…
Thoracic Outlet Syndrome (TOS) (G54.0)
aka: Cervicobrachial Neurovascular Compression Syndrome (M53.1)
Definition:
 Nerves & vessels of Thoracic Outlet or Inlet get compressed
 A condition producing upper extremity symptoms thought to result from neurovascular
compression at the thoracic outlet.
 TOS is a number of syndromes in which the symptoms & signs are:
o Result of compression of the brachial plexus (C5-T1), its constituents, the subclavian or
axillary vessels in the thoracic outlet (or inlet).
Epidemiology
Female adult +
 F>M
 Rare in patients <20yrs
Etiology:
Physical trauma:
 Hyperflexion/hyperextension injury (inflammation)
 Repetitive injuries from job- or sports-related activities (overuse - inflammation)
 Clavicle fracture
Congenital anomalies:
 Cervical rib (approximately 1-2% of population have cervical ribs & out of those <10-20% have TOS
symptoms; however resection of cervical ribs may not alleviate the symptoms)
o Cervical rib (1-2% of population & only 10-20% of those have Sx)
 Elongated TP of C7
 Muscular anomalies (especially the scalene muscles) *Most Common
 Fibro-cartilaginous bands associated with incomplete cervical ribs
Other Causes:
 Pregnancy
 Ergonomics (posture)
SEE PICTURE ON PHONE
Sites of possible compression:
 Cervical rib & scalenus anticus syndrome: in which abnormal scalene muscle or the presence of a
cervical rib my cause compression.
o Symptoms often relieved with arm abduction.
 Costocompression syndrome: in which compression may occur under the clavicle.
o Physical depression of the shoulder will increase or exacerbate symptoms.
o Carrying heavy objects (not tight pecs?)
 Hyperabduction syndrome: in which compression may occur in the sub-coracoid area with
shortening of the pectoral minor muscles.
o Often associated w/ overhead work.
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Ortho Lecture Notes Combined
o Exacerbated w/ arm ABDUCTION
o Goes under the pec minor
Classification of TOS Sanders RJ, Dx of TOS. J Vasc Surg. 2007;46(3):601
True neurogenic TOS– rare (maybe 1% of the cases) sensory & motor
 Sensory changes
 Motor changes
Disputed {non-specific}) neurogenic TOS – 95% of cases are disputed numb & tingling
 Paresthesias
 No objective neurological findings
Venous TOS
3% of cases
 Symptoms/signs of venous insufficiency (refer to Ortho I vascular notes)
Arterial TOS – 1% of cases
 Symptoms/signs of arterial insufficiency (refer to Ortho I vascular notes)
 Hands blue, shiny skin
IF cervical rib – presentation more likely ulnar & median N distribution b/c of rib contact C8/T1
Otherwise, clavicle more likely to compress C 5/6
Historical Classification of TOS
Scalenus Anticus Syndrome
 Etiology/Pathology:
 Spasm or hypertrophy of anterior scalene muscle, a cervical rib, presence of fibrous bands, or
anomalous wide insertion of the scalene on the 1st rib, subluxation of the 1st rib at the costotransverse joint and/or any combination exert pressure on the neurovascular bundle. The C8/T1 roots
emerge in front of the first costo-transverse joint which could explain why the majority of the
symptoms of TOS are on the medial side (following the ulnar distribution).
 Symptoms:
o May be worse at night & increased by recumbence
o Turning head to unaffected side,
o Downward traction of the arm & shoulder. *carry suitcase
o Symptoms may be relieved by arm abduction
 + Adson’s or Halsteads
Cervical Rib Syndrome
 Etiological factors:
 Anomalous supernumerary rib(s) (cervical rib), fibrous bands from cervical rib to 1st rib
 Signs/symptoms:
 Similar to scalenusanticus syndrome
 + Adson’s or Halsteads
Costoclavicular Syndromes
 Etiology:
 A narrowed space between the clavicle & first rib that creates pressure on the neurovascular bundle
 Symptoms:
 Exacerbated by depression or retraction of the shoulder
 +Eden’s Test
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Ortho Lecture Notes Combined
Hyperabduction Syndrome / aka Subcorcoid-Pectoralis Minor Syndrome
 Etiology:
o Hyperabduction of the arm causes pressure on the stretched vascular structures as they pass
posterior to the shortened pectoralis minor muscle & under the subcoracoid process
 Symptoms:
o exacerbated by overhead work
 +Wrights Test
First Thoracic Rib Syndrome
 Etiology:
o May be associated with an anomalous rib or a normal rib with that has poor biomechanics
 Symptoms:
o Exacerbated by a drooping shoulder
Typical TOS Clinical presentation:
 Paresthesia (numbness & tingling) in the medial: arm, forearm and/or hand Numb/tingle medial
hand/forearm
 Aching pain in the arm, forearm and/or hand
 Subjective weakness
 Palpation:
o scalenes, first rib, clavicle, &/or pect
o may provoke pain &/or paresthesia
 Provocation &/or relief with motion of the neck &/or upper extremity (depending on site of
compression)
 + TOS tests
 Neuro signs (less likely/atypical presentation) – atrophy fleshy base of thumb (Gilliatt-Sumner
hand); sensory changes, weakening grip & intrinsic muscles of the hand (lower brachial plexus C8T1)
 Vascular findings:
if vascular TOS
o color change, temperature change, pitting edema, ischemic pain, pulses, bruit, sores
(Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome.. J Vasc Surg. 2007;46(3):601)
Factors That May Exacerbate Symptoms (Talmage D, Lemke C. Thoracic outlet syndrome: How has it changed over the
centuries? TICC. 1999;6(4):39-50.)









Overhead activities
hyperabduction
Overuse of the arm
Static neck and/or arm postures
Downward loading on the arm/shoulder costoclavicular
Lifting heavy objects or carrying heavy loads with arm by the side of the body (i.e., briefcase) or
off the shoulders (i.e., backpack).
Driving long distances shortening of mm
Sleeping on the affected side or with arm(s) overhead
o shorten of mm in position of sleep,
o scalenes
Trauma
Degenerative changes
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Ortho Lecture Notes Combined
Diagnostic Studies:
 Plain film radiography - Look for bony abnormalities, signs of trauma cervical rib
 Electrodiagnostics – may reveal true nerve compression for True Neurogenic TOS
 Vascular studies: dopplar, angiography to check for arterial/venous TOS
Treatment:
 Adjustments: Cervical, Thoracic spine, Shoulder, Ribs
 Soft tissue manipulation *must do these top 2 together b/c co-dependent
 Passive modalities (pain control, relaxation, tx atrophy)
 Exercise rehabilitation including strengthening & stretching: Scalenes, rhomboids, traps
 Postural retraining
 Ergonomics at work or activity: minimize overhead work, repetitive motions. Increased breaks.
 Sleeping habits
 Diet:
o Decreased sugar & caffeine.
o Increased vegetable intake.
 Supplementation: Vitamins A, C, D, E & B complex (esp B6 & Niacin) anti-inflammatory
Medical Management:
 Drug therapy = analgesics, anticoagulants, muscle relaxants, botulism toxin injection into scalenes
 Surgery: Resection of: cervical rib, supernumerary bony abnormalities (not a high success) or fibrous
bands
Other Brachial Plexopathies
Erb-Duchenne, Klumpke, Horner’s Syndrome
The brachial plexus consists of nerves that originate in the fifth, sixth, seventh & eighth cervical (C5-C8), &
first thoracic (T1) spinal nerves, & innervate the muscles & skin of the chest, shoulder, arm & hand.
Brachial plexus injuries, or lesions, are caused by damage to those nerves
Erb’s Palsy (P14.0)
aka: Erb-Duchenne Paralysis, Waiter’s tip deformity, Flail arm
Definition:
 Paralysis of the arm by injury to the upper group of the arm's main nerves, specifically the severing of
the upper trunk C5–C6 nerves. These form part of the brachial plexus, comprising the ventral rami of
spinal nerves C5–C8 & thoracic nerve T1. Although injuries can occur at any time, many brachial
plexus injuries happen when a baby's shoulders become impacted during delivery & the brachial
plexus nerves stretch or tear.
Epidemiology:
Most commonly seen during deliveries, however can be seen with trauma.
Etiology:
 Dystocia - an abnormal or difficult childbirth or labor
o infant's head & neck are pulled toward the side at the same time as the shoulders pass
through the birth canal
o Excessive pulling on the shoulders during a cephalic presentation (head first delivery), or by
pressure on the raised arms during a breech (feet first) delivery
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Ortho Lecture Notes Combined



Clavicle fracture
o Unrelated to dystocia in neonates
Trauma to the head & shoulder
o which cause the nerves of the plexus to violently stretch (any age)
Direct violence, including gunshot wounds & traction on the arm, or attempting to diminish shoulder
joint dislocation. The level of damage to the constituent nerves is related to the amount of paralysis.
Clinical presentation:
Arm straight & medial rotation & pronation “Waiter’s tip”
 loss of sensation
 paralysis & atrophy of the supraspinatus & infraspinatus are most commonly involved in severe
conditions the deltoid, biceps, subscapularis and/or brachialis muscles
 arm hangs by the side & is rotated medially; the forearm is extended & pronated
 arm cannot be raised from the side; all power of flexion of the elbow is lost, as is also supination of
the forearm. The resulting biceps damage is the main cause of this classic physical position commonly
called "waiter's tip."
Treatment:
 Acute injury - Referral
 Chronic - Rehabilitation.
o Some brachial plexus injuries may heal without treatment.
o Many children who are injured during birth improve or recover by 3 to 4 months of age.
o Treatment for brachial plexus injuries includes physical therapy and, possibly, surgery.
Klumpke Palsy (P14.1)
Bottom of brachial plexus
Definition:
 a paralysis of the arm caused by injury to the upper group of the arm's main nerves, specifically the
severing of the lower trunk C7-8 & T1 nerves. These form part of the brachial plexus, comprising the
ventral rami of spinal nerves C5–C8 & thoracic nerve T1.
Epidemiology:
 Most commonly seen during deliveries however can be seen with trauma, cervical ribs, or tumors.
Etiology:
 avulsion injuries caused by excessive abduction (person falling from height clutching on object to save
himself)
 cervical rib
 lung metastasis in lower deep cervical lymph nodes.
 Arm pulled in overhead position
Clinical presentation:
 Paresis/paralysis of all small hand muscles (ulnar & median nn), clinically presents “claw hand”
 Extension: Wrist because of the unopposed wrist extensors,
 Hyperextension: MCP & flexion of IP joints due to loss of intrinsic muscles.
Treatment:
 acute = referral to a neurologist
 chronic = rehabilitation
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Ortho Lecture Notes Combined
Horner’s Syndrome (G90.2)
Definition:
 avulsion of the T1 root resulting in interruption of the T1 sympathetic ganglion
 results in interruption of sympathetic nerve supply = Interrupts innervation to the eye
Etiology (partial list):
 Trauma to the brachial plexus
 Tumors (eg, Pancoast) or infection of the lung apex
 Dissecting carotid aneurysm
o In one study, 44% (65/146) of patients with internal extracranial carotid artery dissections had
painful Horner syndrome, which remained isolated in half the cases.
 Migraine
 Cervical rib
 Cervical spondylosis
Clinical presentation:
 Miosis results from loss of sympathetic pupillodilator activity
 Ptosis results from loss of sympathetic tone to the eyelids dropping eye lid
 Anhidrosis is variable & depends on the site of the injury to the sympathetic pathway
 Pseudo-enophthalmus
o (appearance of a sunken eyeball) but it doesn't truly occur, it is an illusion created by the
ptosis.
 Eye change color In early Horner's the pigmentation of the iris may be affected, the eye may
change color.
Diagnosis:
 Ciliospinal Reflex - the eye will be abnormal.
Treatment:
 Referral to Neurologist.
LECTURE EXAM 1 Material thru HORNERS XXXX
Start Exam 2 Material
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Ortho Lecture Notes Combined
Shoulder









Describe the etiologies/mechanism of injury for each condition.
Explain the pathogenesis for each condition.
Describe the clinical manifestations (symptoms, clinical signs, & examination findings) in order to diagnose the condition
Identify the epidemiological &/or risk factors associated with the conditions.
Select the most appropriate historical questions and/or examination procedures to be performed in regards to the
patient’s complaints.
Identify the diagnostic studies & describe the findings on those studies that would aid in the diagnosis of each condition
List the Diagnostic criteria/Guidelines for the conditions (if applicable).
Select the most appropriate management/treatment techniques for each condition including referral/co-management.
Explain the classification scheme/stages/types for such conditions as: Adhesive capsulitis, AC/SC sprains, GH
Instability/dislocations, SLAP lesions.
Rotator Cuff Tears (M75.100)
Definition:
Partial (micro tears) tears: Grade 1 – 2 strains
 Typically found In a young, active patient
o may include an avulsion fracture from greater tuberosity.
 Degenerative cuff failure, oft starts with partial thickness defect on
deep (under) surface near attachment of supraspinatus @ greater
tuberosity.
Full Tear:
Grade 3 strain – all the way torn
 Common also in older people
RCT commonly misdiagnosed as: tendonitis, bursitis, impingement synd.
 may actually be a rotator cuff tear/ failure of the deep surface fibers
of the rotator cuff.
 The degree that intact fibers hypertrophy, strengthen, or adapt to
stabilize the tear & take up function of damaged fibers is unknown.
Etiology: Possible mechanisms include:
 repetitive stress
 acute trauma
 normal wear & tear.
 degenerative changes – Impingement Syndrome Neer Stage 3
3 TYPES OF Partial TEARS:
 Bursal side tears – likely due to subacromial impingement
 Articular-sided tears – likely from trauma to a degenerated tendon. (More common)
 Intratendinous tears - result from differential shear stress within the supraspinatus tendon.
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Ortho Lecture Notes Combined
Epidemiology:
More common after 40 yrs (degenerative)
 after 40 years, ~ 30% of patients will have cuff tears
 after 60 yrs, up to 80% of patients
 asymptomatic full-thickness tears present in
o 13% of the population age 50-59
o in over 50% of people 80+ years old
Increased incident in sports (throwing athletes) & some occupations (construction)
Most common tendon: supraspinatus
RCT = most common cause of shoulder pain
RC pathologenesis
 Intrinsic
o Aging tendons lead to micro tears AGE & microtears
o Eccentric tensile overload (throwing) can lead to tearing OVERUSE
o Compromised vascular supply leads to a critical avascular zone AVASCULAR
 Extrinsic
o Compressive forces on cuff
 type III acromion,
 superior migration of humeral head,
 OA,
 thickening of coracoacromial ligament COMPRESSION
Clinical Presentation:
 May be asymptomatic in SIS Neer stage 3 patient *hooked acromium
 S - Minimal to severe pain
 Q - Dull, achy pain deep in the shoulder
 R - Refers to deltoid tubercle
*If pt comes in w/shoulder pain, ALWAYS PALPATE ROTATOR CUFF
 Prov –
o Movements above shoulder height. OVERHEAD USE = PAIN
o Sleeping, lying on affected shoulder
 CC - Weakness, instability, roughness or grinding.
Acute Tear
Chronic Tear
 Edema,
 Tenderness,
 Erythema,
 Atrophy
 Tenderness,
 Defect are possible;
 Heat,
 Probable decrease in inferior glide of GH joint
 Palpable defect
 Shoulder stiffness may present
 limited AROM w/pain @ end of motion.
 Most commonly seen in partial thickness tears- sensory components left intact,
 May also be seen w/ full thickness tears.
AROM
PROM
 Weak, loss of elevation past specific point
 motion improves,
 Shoulder hiking
 decrease in pain is possible,
 Altered scapulohumeral rhythm
 painful arc may decrease
 Painful arc sign
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Ortho Lecture Notes Combined

Shoulder muscle testing
o Weakness w/external rotation & abduction
o 60- 120 degrees (70 – 120 taught too)
 + Ortho tests:
o HIP60, SIE, HIE Abduction, ER, Impingement
o Lift off sign, Codman, Neer, Hawkins Kennedy,
Modified Lift off
Predictive of Tears… Supra, infra, impingement
Findings predictive of rotator cuff tear are:
Supraspinatus weakness, weakness in external rotation infraspinatus, & impingement
 positive all 3 tests, or 2 tests patients > 60, = 98% positive predictive value for RC TEAR
 absence of all 3 findings = rule out RTC
Diagnostic Studies:
X-ray limited value
Chronic tears, may show
superior humeral head
migration
May find calcification
Ultrasound
Accurate - full
thickness
Arthrography
Definitive Dx - full
thickness
97% specificity for
partial-thickness
NOT helpful for
partial or tendinitis
MRI
Excellent full-thickness
Limited for partialthickness
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Ortho Lecture Notes Combined
Management
 Initial phase – Pain/inflammation Control & mobility/ROM
o Rest & Modify– avoid
provoking activities & positions
 keep elbows close to
side of body when doing
activities to diminish
pain
o Passive modalities for pain,
effusion: EMS, INF, US, CL
o Stretch capsule (anterior &/or
posterior),
o Mobilize Joint prevent adhesive
capsulitis
 Shoulder ROM exercises
 Codman's, wall
crawl, stick,
towel, pulley
 Important to
introduce soon
o Isometric exercises for rotation
o Analgesics for pain & inflammation

ACUTE 4-6 or 1-2 wks if 40+
Intermediate phase – emphasize strength & endurance
SUBACUTE, pn less, now strengthen
o Isometrics exercises
MTK
o Isotonic strengthening
 primarily the external rotators, scapular
stabilizers, humeral head depressors
 same force thru a ROM
o Progress to Isokinetic exercises same speed through a
ROM
o Continue mobilization, stretching
o Continue modalities PRN *per required necessity…
"pro re nata" = "as needed”

Final phase – proprioception & sport/occupation specific
o Proprioception & coordination exercises such as gym
ball pushups, balancing a pole
o Progressively increase resistance exercises
o Muscle energy techniques
 Proprioceptive neuromuscular facilitation
o Plyometric exercises –
 advanced exercises involving horizontal &
vertical movements
 fast eccentric & concentric loading
CHRONIC
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Ortho Lecture Notes Combined
Medical Management:
 Surgery – definitely indicated in full-thickness acute tears,
o May be required with if conservative measures fail.
o No evidence between early or late surgery makes effect.
o NO significant differences between rehabilitation results & surgery results
 Cortisone injections, NSAIDs
 Conservative care – majority of patients, should be tried before surgery
GH Dislocation/Subluxation
humeral head out of fossa
Unspecified subluxation = Rt – S43.001A, Lf – S43.002A;
Ant dislocation = Lf - S43.015A, Rt –S43.014A
present arm ABDucted elbow bent
Post dislocation = Rt – S43.024A, Lf – S43.025A
Definition: Complete/partial separation or displacement of humeral head from glenoid surface.
Etiology:
First-Time Dislocations
 Indirect: E.g. from throwing hard
o arm forced into abduction, external rotation, & extension
o humeral head levered out front of glenoid,
o EXTREME PRESSURE on: Subscapularis tendon, middle & inferior glenohumeral ligaments, biceps
tendon
 Traumatic:
o Anterior dislocation –
 blow to an abducted, externally rotated, extended arm;
 blow to the posterior humerus;
 fall on an outstretched arm. *More common
o Posterior dislocation –
 blow to anterior humerus; FOOSH,
 axially load adducted, internally rotated arm; land on elbow while hugging ball
 violent muscle contractions during seizure or electrocution
o Inferior dislocation = not common
o ~25% shoulder dislocations have associated fracture**
Recurrent Anterior Dislocation
Fairly common
 Traumatic: anterior stabilizing structures are disrupted by mechanisms describe above.
 Minimal trauma in lax shoulder: AMBRI
o Recurrent anterior dislocation with minimal trauma in individuals with multidirectional
shoulder laxity (generalized ligamentous laxity).
o May result from collagen disorders or affected dynamic stabilizers of the shoulder (stroke).
o Often constant fear of instability & functional limitation (apprehensive shoulder).
o Often episodes of recurrent subluxations in addition to their dislocations.
o Usually requires surgical stabilization
o Seizures may also cause dislocations in those with laxity
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Ortho Lecture Notes Combined
Epidemiology AMBRI:
 Most common direction of dislocation is anterior & inferior
 Recurrence after first time dislocation is as high as 92%.
 Dislocations – bimodal (adolescents males} & 50-60 yrs females}
Clinical Presentation:
 Shoulder pain & muscle guarding especially if currently dislocated
 Difficulty moving arm
 Arm is held in either
o External rotation with anterior dislocation, ERAD
o internal rotation with posterior dislocation. IRPD
 Acromion may be more prominent & absence of the normal fullness beneath acromion.
 Visible signs of dislocation
o winging of scapula
o step deformity
 Check peripheral nerves & BLOOD SUPPLY
o Atrophy –
 deltoid (axillary nerve damage),
 rotator cuff (suprascapular or infrascapular nerve damage),
 coracobrachialis or biceps (musculocutaneous nerve damage).
 Tenderness & apprehension
 ROM –limited, provoking, weak
 Ortho test: load & shift, Dugas, Sulcus test
LOOK Posterior & anterior dislocation slides…NO PANOPTO IN lab, so ask teacher
Diagnostic Studies:
 Plain film – may be normal, demonstrate dislocation, reveal a
o Hill-Sach’s deformity (bankhart lesion – inferior glenoid fossa
o step deformity
o calcification
o degeneration
 Ultrasound –may reveal
o instability
o RCT
 MRA – may demonstrate:
o labral tears (Bankart’s Deformity, SLAP)
o RCT
 Arthroscopy
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Ortho Lecture Notes Combined
Management:
*NOTE – if a 1st time dislocation, then refer out*
*exception….If recurrent dislocation then you can fix in the office
If first time dislocation:
 Referral.
o Dislocation to be reduced & immobilized,
o Return for rehabilitation.
o Closed reduction/no surgery, is most common initial treatment.
o Medications may be required for sedation to help facilitate the reduction.
 Immobilization is important to decrease the risk of a repeat dislocation.
o 1st dislocations are immobilized in an external rotation position, esp in those <30 yrs.
If recurrent: possible to reduce in office& then REHAB to prevent recurrence.
 Recurrent dislocations may be immobilized in a regular sling.
 Stimson technique – lie prone on table, weight arm 1-15 and “hang out”
 Kocher – Traction. Flex elbow. ER. ABD, IR.
 Self-Correction - If common, show patient how to hold knee extend head and push knee:
o IPSI knee bent @ 90
o Clasp hands around knee
o Extend neck
o Lean backwards
Prognosis:
 normal function in 12-16 weeks = Uncomplicated rehabilitation & healing
 typically require surgery:
*less favorable outcome w/conservative
o Traumatic instability,
o Connective tissue disease
o Instability secondary to repetitive overuse
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Post-surgical Rehabilitation:
 Recovery post-surgery depends upon the type of procedure the surgeon
performs. Usually:
o ROM of: hand, wrist, elbow begin day after surgery.
o Write, Eat within 3-7 days after surgery.
o Initiate supervised PT program @ 1-4 weeks
o Full ROM usually returns after 6-8 weeks.
o Strength usually returns ~3 months.
o Driving = several weeks.
o Return to work or sporting activities
 depends on specific nature & demands of that activity,
 can take up to 1+ years for heavy laborers or high level
athletes.
 Focus of REHAB? Stabilize joint & rehab
GH Instability - (Glenohumeral)
(Unspecified Recurrent dislocation – M24.419)
Definition:
 Any condition that causes excess motion of the GH joint.
 joint instability = common disorder of shoulder.
 Instability can occur in all directions, including anteriorly, posteriorly, inferiorly, multi-directional
depending on injury (from most to least common).
Types of Glenohumeral Instability:
T.U.B.S.
 (Torn loose)
o Trauma
o Unidirectional
o Bankart
o Surgery

A.M.B.R.I.
(Born loose)
o Atruamatic
o Multidirection
o Bilat
o Rehab
o Inf capsule shift
Etiology:
 Acute traumatic instability (dislocation) TUBS
o Initially the instability may not be apparent & pain is only complaint.
 Repetitive microtrauma (Overuse) AMBRI
o Overhead activities
 Causes stretching of anterior stabilizing structures.
 Labrum fraying & avulsion,
 capsular laxity,
 glenoid & humeral articular erosions.
o Functional instability without excessive capsular/ligamentous laxity falls into this category.
 Congenital laxity AMBRI
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Ortho Lecture Notes Combined
Epidemiology:
Instability is more likely in:
 Younger active patients
o Age at the time of dislocation = biggest determinant of future recurrence.
 Recurrences rom anterior glenohumeral instability
 Most commonly in patients younger than 20 years.
 Before 20 Yrs = 70-100% more likely to recur
 Patients with concurrent RCT *once injure Rotator cuff, then more impact on GH
 Males > Females
 Higher in baseball pitchers
Direction of instability: Anterior>posterior>inferior/multidirectional
Clinical Presentation
 HX findings
o Previous acute injury/dislocation
o Repetitive activity the patient engages in
o Paresthesia when carrying heavy objects by side – possible inferior instability
o Provocation when pushing (e.g., pushing heavy door open) – possible posterior instability
o Repetitive Popping, clicking, crepitus – possible labral tear
o Dead arm syndrome – anterior subluxation
 Athlete = sharp pain on extreme external rotation or after a blow to the shoulder.
 Can cause of loss of muscular control over the extremity.
 Severe pain usually subsides quickly, but soreness & weakness persist for a time
o Palpation:
 Tenderness over all musculature & joints of the shoulder
 Possible inflammation
 Feeling of instability –
o “shoulder will pop out”; “slipping out” when throwing (possible anterior instability)
o Vague shoulder pain/discomfort/fatigue/weakness
 Possible findings:
o Atrophy
o Winging of the scapula
o Signs of dislocation
o DDX: observe joint motions of the GH, AC, SC joints
 ROM testing - look for abnormal motions & increased motion. Signs of "giving away"
 Muscle testing = signs of weakness
 (+) Orthopedic tests : Apprehension / Fulcrum + Relocation
 PERFORM Neurological tests. Results maybe negative.
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Ortho Lecture Notes Combined
Diagnostic studies:
 Plain film - looking for bony deformity (e.g. Hill-Sachs) or Glenohumeral malposition.
 US: signs of rotator cuff damage
 MR: evaluate…
o Labrum (Bankart)
o Cuff (strain, atrophy, tendinosis)
o Joint (effusion)
Treatment:
 Goal of therapy is to return joint to proper function & pain free ROM
 Increase strength of RC & surrounding shoulder muscles to prevent further instability and/or
dislocation.
Phase I – pain & inflammation control
 Rest (restrict overhead activity – pushing, pulling, lifting, reaching)
 Pain control (NSAIDs or homeopathic; ice & modalities for pain; possibly immobilize);
 AVOID mobilization/manipulation (esp distraction & ext rotation)
 Gentle ROM - especially light PROM if shoulder is in immobilizer
•
decrease mm guarding
•
Prevent capsular contractures DO IN SCAPULAR PLANE
 Immobilizer (unstable shoulder) in acute cases
•
<20 yrs = up to 3-4 wks
•
>30 yrs = 10 – 14 days
•
40 yrs = only a few days
Phase II – ROM & strengthening for RC & scapular stabilizers (serratus anterior, pectoralis, latissimus)
 ROM exercises = Codman’s, pendulum wall crawl),
• Perform initially in sagittal or scapular plane
 inferior capsule is not twisted during elevation
 stress minimized on anterior & posterior capsule & rotator cuff
 Scapulothoracic –
• start with protraction/retraction,
• proceed to elevation/ depression
 Isometric exercises followed by isotonic exercise.
• Start adducted, forward-flexed position
 reduces stress on glenohumeral joint
• Progress to abduction in scapular plane
 ROM performed in pain free manner
 Note:
• Apply ice pre & post exercise to minimize pain/edema
• Tape can help rehabilitation by reducing pain & edema.
Phase III - endurance program; goal =reach 90% strength in injured shoulder vs. uninjured shoulder
 Proprioception retraining (dribbling, ball toss, balance board)
 Mobilize other joints: AC, SC, Scapulothoracic articulation & possible one direction of the GH capsule
(posterior capsule maybe tight in anterior instability)
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
Muscle strengthening ***PAIN FREE
 Supraspinatus
• greatest activity occurs w/ patient prone & humerus
abducted 100 deg + ER 90 deg.
• So strengthen in this position
 Biceps - (anterior stabilizing function)
• best to train for endurance vs. hypertrophy.
 Latissimus dorsi – assists deceleration of throwing motion
• Strengthen with theraband or pulley system.
• Limit extension when working lats so anterior capsule is not stretched.
Phase IV – JOB/SPORT specific
 progressively increase activity level to sport- or job-specific level
 Push-up against a wall
• Then traditional push-up on floor
 Then push-up off a tilt board or medicine ball
 Then start Plyometric training
Prognosis:
 LESS FAVORABLE IF:
 Experience traumatic instability,
 have connective tissue disease,
 have instability secondary to repetitive overuse
 have a less favorable outcome with conservative care & typically require surgery.
 Despite a course of physical therapy in which full shoulder motion & strength are restored, shoulder
may still be loose or unstable.
 Treatment options then consist of
1) activity modification &
2) surgery.
 Activity modification is primarily an option for patients who experience instability only with certain
activities such as playing basketball or overhead racquet sports.
 In these patients, avoidance of the activity can completely eliminate episodes of subluxation or
dislocation.
 Surgical treatment is considered if:
• Not willing to give up the activities or sports that provoke their episodes,
• In patients w/instability during routine daily activities (dressing, sleeping, etc) or work.
Labral Tears
(Unspecified sprain – S43.409A; Sup Glenoid Labrum Lesion – S43.439A)
Definition: Injury to the fibrocartilaginous rim attached around the margin of the glenoid cavity.
Etiology:
Traumatic injury include:
 FOOSH: shoulder flexed & externally rotated compression injury
 A direct blow to the shoulder
 A sudden pull, such as when trying to lift a heavy object
 A violent overhead reach, such as when trying to stop a fall or slide
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Repetitive/overuse include:
 Throwers
 Weightlifters
 Repetitive motions
 Age related changes
Epidemiology:
 Incidence is unknown
 Type II & Type I = most common
Labral Tear Types:
 Superior - The most common aka SLAP lesion.
 Inferior e.g. Bankhart
Four types of SLAP Lesions: *types 2 & 4 = instability and can fix w/laparoscopic surgery
 Type 1: PARTIAL IN LABRUM “frayed”
o Partial tear & degeneration of superior labrum, where edges are fray along free margin, but
labrum is not completely detached.
 Type 2: FULL LABRAL TEAR = Most common type of SLAP tear.
o Superior labrum is completely detached from glenoid w/ injury (often shoulder dislocation).
o Leaves a gap between articular cartilage & the labral attachment to the bone.
o Further subdivide into anterior, posterior & combined AP lesions.
o Surgical
 Type 3: BUCKET HANDLE W/CLUNKING
o “bucket-handle” tear of the labrum, where torn labrum hangs into joint & causes symptoms of
“locking” & “popping” or “clunking”.
 Type 4: TEAR INTO BICEPS TENDON *
o Tear of the labrum extends into long
head of biceps tendon.
o Surgical
Types 2 & 4 can cause shoulder instability that is
only remedied by arthroscopic reattachment of the
labrum to the glenoid.
Types 1 & 3 do not cause instability but the patient
may need arthroscopic debridement.
Clinical Presentation
 Pain usually with overhead activities or cross-body movements
 Deep Pain hard to localize but in joint
 Catching, locking, popping, grinding Crank test
 Occasional night pain or pain with daily activities
 Sense of instability in the shoulder especially with arm raised
 Decreased range of motion (especially over 90 degrees of abduction)
 Weakness, Loss of strength
 Tenderness: superior anterior GH joint.
 Decreased ROM above shoulder height
 Weakness above shoulder height
 + Ortho tests: “CARLS” cluster
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Diagnostic Studies
 X-ray = May be normal
o show loose bodies, degenerative changes
o show an avulsion (Bankart's or Hill-Sach’s),
o diminish size of the subacromial arch
 MRI = May miss smaller tears
o cannot reliably make the diagnosis in larger tears of the labrum
 CT-arthrogram (with contrast) = 80-85% accurate.
 Arthroscopy – BEST
o The best way to make the diagnosis of labrum tearing.
o Unfortunately an operative procedure.
Treatment:
 Activity modification/rest
 PROM exercise
 Light exercises as those mentioned for instability rehab starting with arm by side of body
 Scap stabilization exercises
 Modalities for symptom control.
 Analgesics for pain control
If NO improvements in 2 to 4 weeks, surgical consult recommended.
 Surgery: Takes 3-4 months post-surgery for shoulder to be completely healed
Case: WF, 19,








collegiate volleyball player presents following laser assisted capsular shrinkage w/tingling in the 1st, 2nd & 5th
digits w/pain in ant shoulder upon blocking & overhand motions.
Prior to surgery she was complaining of ant. shoulder pn & was unable to play. Since the surgery she had 6 mos
of rehab. Rehab: ROM exercises, strength training w/elastic bands & hand weights, PNF patterning (exercise).
As an incidental finding, she reports a bilateral dislocated patellae last year.
Do you think the pt was managed appropriately post-operatively?
o For the most part yes, although sport specific rehab & monitoring return to sport was not done.
List the examination procedures that should be performed on this patient.
Exam findings:
o +2 tenderness @ biceps tendon & insertion pect major
o Trigg.Ps @ scalenes, infrasp, pect major & teres minor that repro the tingling.
o AROM C/S full, pnless, TS
o AROM GH - 90% of normal = twitching in upper shoulder when descending from abd.; 2:1 rhythm
o Neer’s sign (+); EAST, Adson’s & Phalen’s (-); 4 out 5 Gen lig laxity signs
o MM tests = 5/5
What is the working diagnosis at this time? Myofascitis/MFPS & post-surgical instability
What treatment is indicated for this pt?
o Adjust manipulable lesions (not GH)
o MRT to mm containing Trigg.Ps
o Immediately following MRT perform active sport specific movements
o Scapular stabilization exercises
o W/improvement: following MRT, progress to AROM to using a weightless ball (soft toss) to using 1-2 kg
medicine ball while performing specific movements
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AC Sprain
(aka. Separated shoulder) (Unspecified S43.50XA)
Definition: Injury to the ligaments of the acromioclavicular joint
Epidemiology:
 Account for approximately 12% of shoulder girdle dislocations.
 AC joint is involved in 9-12% shoulder injuries
 M >F (5:1) (most common in those who play contact sports, hit on acromion/shoulder w/fall)
 Age: 20s
Etiology:
 Falling directly on shoulder with humerus in an adducted position
 Indirect trauma with arm/elbow/hand in adducted position causing humerus to migrate up
 Indirect trauma - fall on the outstretched arm/elbow which drives humerus up FOOSH
 Direct blow to the acromion/scapula driving it down
Clinical Presentation:
History of either a distinctive, traumatic mechanism of injury or a more insidious type of onset that began
with pain & dysfunction.
 Shoulder pain – superior
 Possible guarding
 Point tenderness
 Edema?
 Separation/step deformity (grades 3-6)
 Instability?
 Provoked by:
o horizontal adduction (Forced cross flexion),
o probable provocation with abduction
 R/O RC involvement or involvement of the other 3 articulations of the shoulder, DJD of the AC
and/or clavicular fx/osteolysis
Classification Scheme Rockwood Classification acromioclavicular, coracoclavicular
 Grade 1 – stable, mild AC ligament sprain,
o local P/T, restore full ROM,
o may sling up to 1-3 days,
o but do ROM ASAP,
o RTP quickly
 Grade 2 - unstable full AC lig rupture, coracoclavicular in tact,
o pain , edema, instability, decreased ROM,
o TX 6: splint 1-2 wees, tape & treat pain, US for collagen formation, ROM ASAP, Functional
exercises,
o AVOID AC MOBILIZATION,
o 6 weeks to heal
 Grade 3 – unstable with migration both AC & CC lig rupture
o step deformity,
o tearing of deltoid and trap from distal clavicle,
o PN, TENDER, loss ROM, edema;
o Brace if conservative or surgery, NO manipulation
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From this point onwards the scale & grade of injury depends on the degree of displacement of the clavicle.
PSI = “pounds /square inch”
o Grade 4 - Complete dislocation with posterior displacement of distal clavicle into/through trapezius
muscle
o Whenever clavicle is displaced, then surgery required
o *Grade 5 - Superior dislocation of the joint of one to three times the normal spacing, increasing the
CC ligament distance two to three times normal;
o disruption of the deltotrapezial fascia
o Whenever clavicle is displaced, then surgery required (*)
o *Grade 6 - Complete dislocation with inferior displacement of distal clavicle into a subacromial or
subcoracoid position
o Whenever clavicle is displaced, then surgery required (*)
May look like a dislocation *DO NOT confuse because you can further hurt if AC separation
Diagnostic Studies:
Radiographic findings by type
 I - normal
 II- lateral end of clavicle may be slightly elevated; x-ray usually normal but may demonstrate slight
widening of AC joint
 III - obvious separation of AC joint; 25-100% increase in coracoclavicular distance compared to normal
side; clavicle appears high on stress views, but in actuality, acromion & remainder of upper extremity
displaced inferior to horizontal plane of lateral clavicle
 IV - posteriorly displaced clavicle on axillary x-ray; evaluate SC jt for possible anterior dislocation of SC
joint & post dislocation of AC joint
 V - 100-300% greater clavicle-to-acromion distance
VI - distal clavicle may be either: subacromial or subcoracoid
Treatment:
Grades 4-6 (possibly 3) typically require surgery
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
Refer to Souza
GRADE





Presentation
Sprain of the AC ligament
Local tenderness on palpation
Full range of motion (Painful arc)
No loss of structural strength
Normal stress x-ray film






2nd or 3rd degree sprain AC lig
1st or 2nd degree sprain CC lig
Pain, edema, instability
ROM, Painful arc
Tight deltoid & trapezius
No significant increase in the CC
interspace on stress film
 Slight widening of the AC joint on
stress film
 Grade 3: AC & CC
 Torn deltoid & trapezius from
distal clavicle
 Step Deformity
 Significant pain, tenderness, ROM
loss & edema
 Increased CC interspace on stress
film
 Widening of AC joint on stress film
Treatment
 Re-establish full ROM & strength
 Ice, electrotherapy
 NSAIDs
 Possible sling 1-3 days, ROM ASAP.
 Most people return to full activities
between 3 days - 2 wks
 Requires 6 weeks to heal
 1-2 wks AC splint or shoulder
immobilizer








Tape
Pain relief
US for collagen enhancement
Start ROM exercises ASAT, tolerated
Functional exercises
No AC mobilization/manipulation.
Surgical or conservative
Conserve: deformity, function ok,
slight discomfort/ instability at loads
 Ice, electrotherapy
 Analgesics
 Kenny-Howard splint 2-4 wks




ROM & strengthening ASAT, tolerable
Return activity btw 6-12 wks
Ortho consult if pain persists***.
No manipulation
SC Sprain
(Unspecified – S43.60XA)
Definition: Injury to the ligaments of the sternoclavicular joint.
Epidemiology:
 Young males
 Anterior SC dislocation is the most common form
 Posterior dislocation can be life threatening: tracheal compression,
laceration of great vessels, pneumothorax, or recurrent laryngeal nerve
damage
Etiology:
 Direct or indirect force to shoulder
 Anterior dislocation –
o blow rotating anterior shoulder back transmits forces to SC
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
Posterior dislocation –
o force drives shoulder forward
o direct impact to superior sternum or medial clavicle
Clinical Presentation:
 Pain & stiffness are the main symptoms.
 Clicking, popping, grating sensation might be felt w/a sprain.
 Dislocation – severe pain, especially w/movement of arm.
 Displacement/Instability
 Posterior dislocation = Possible dyspnea, paresthesias, dysphagia &/or hoarseness
 SC joint is tender, edematous, palpable defect
 Medial clavicle displaced
Classification
 First degree injury:
o simple & most common,
o incomplete tear or stretching of the sternoclavicular & costoclavicular ligaments.
o Grade 1
o Mild pain & edema
o Tx w: Ice, NSAIDs, compression, ROM exercises
 Second degree injury:
o Clavicle subluxes either anteriorly or posteriorly
o complete tear of the sternoclavicular ligament & a partial costoclavicular ligament tear.
o Mod pain & edema
o Tx – Reduce & Immobilize, ice, NSAIDs, compression, ROM exercises
 Third degree injury:
o complete tear of the sternoclavicular & costoclavicular ligaments 
o dislocation of clavicle from sternum.
o Significant, edema, deformity
o Visceral signs if posterior
o Tx: referral for open or closed reduction
Management:
 Posterior displacement - ER/ Urgent referral (may require open or closed reduction)
 Anterior displacement = closed or possible open reduction
o Ice, NSAIDs;
o Figure-8-brace 4-6 wks,
o Resume overhead activities @ 6 wks
o Restrict contact sports or activities for 6-8 wks
 No displacement = figure-of-eight strap or sling & swathe for 4-6 wks
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Adhesive Capsulitis
(aka: Frozen shoulder) (M75.00)
Definition: American Academy of Orthopedic Surgeons:
“A condition of varying severity characterized by gradual
development of global limitation of active & passive shoulder
motion where radiographic findings other than osteopenia are
absent.”
Epidemiology:
 Affects approximately 2-5% of population.
 Age: between 4th& 7th decades
 Gender: females > males
 Extremity: usually the non-dominate arm
o although bilateral involvement in 6-50% of cases
o simultaneous involvement in about 14% of cases
Etiology:
 Primary (Idiopathic)
 Secondary
o Intrinsic
 Acromioclavicular joint arthritis AC arthritis
 Rotator cuff tendinosis/tear
 Bicipital tendinosis
o Extrinsic
 Cardiac disease & cardiac surgery surgery
 Neurologic disorders with impaired consciousness or hemiplegia neuro
 Pulmonary disease (tuberculosis, antituberculosus drugs, carcinoma)
 Shoulder trauma or humerus fracture trauma
o Systemic
 Autoimmune response AI
 Diabetes mellitus (4.3%)
 Thyroid disease (hyper- & hypothyroidism)
Pathogenesis:
 Initially inflammation develops in & around the axillary fold & anterior joint capsule,
 followed by adhesions & fibrosis of the synovial lining,
 then thickening & contraction of capsule,
 followed by decrease in joint volume
Stages/Presentation:
 Painful stage
 Frozen (adhesive) stage
 Thawing (resolution) stage

Painful stage:
o Severe pain & stiffness occurs with any movement of shoulder
o Rest pain & worse at night
o Onset is insidious
o NSAIDs no help
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o Motion (AROM & PROM) aggravates & slowly starting to lose motion (capsular pattern of
limitation).
o Possible joint glide restrictions
o Findings not clear so may be difficult to diagnose in this stage
o Lasts 10-36 wks
o Gradual diminution of articular volume (as assessed on arthrography);
 Frozen (adhesive) stage:
o Pain may begin to diminish during this stage, yet shoulder is stiffer & ROM decreases notably.
o Lasts 4-12 months
o Stiffness & severe loss of motion
o ADLS are impaired
o Pain is less pronounced, but is severe at extremes of motion
o External rotation/abduction are most affected (both AROM & PROM) w/ same pain
o Isometric muscle tests are not as provoking & strong when tested by the side of the body
o Atrophy of deltoid & rotator cuff (supraspinatus) may be present
o Dysfunction of the AC, SC, & scapulothoracic articulations may be present
o Trigger points & muscle spasms are common
 Thawing (resolution) stage:
o Range of motion in shoulder begins to improve – possibility of full recovery (40% have slight
persistent limitation in motion; 10% have gross limitation in motion)
o Pain continues to decrease
o Lasts 12-42 mos
o Spontaneous improvement in ROM
Diagnostic Studies:
 X-rays to make sure there is no other problem such as arthritis, may see superior migration of
humerus.
 MR may show thickening of the capsule, synovium, coracohumeral &/or inferior glenohumeral
ligament
 Arthroscopy has been described in 4 stages
o stage 1 - pre-adhesive stage, mild erythematous fibrinous synovitis over entire joint especially
in axillary fold, no limited motion, could be confused with rotator cuff tendonitis
o stage 2 - acute adhesive synovitis, erythematous thickened synovium spreading across axillary
fold to humeral head
o stage 3 - synovium less erythematous & less reactive, adhesions matured
o stage 4 - synovitis abates, joint capsule severely contracted, chronic adhesive phase, severely
restricted glenohumeral motion
Management:
Phase 1
 Modalities
 Analgesics/NSAIDs
 Avoid mobilization & adjustive techniques to GH joint, may work on the other joints
 Exercise therapies such as Codman’s & isometric exercises to tolerance to help with mobility
 Sleep on unaffected side
 Oral corticosteroids – can reduce pain & slightly increase motion but duration is only a few weeks
 Corticosteroid injections – may have more benefit in the initial freezing stage
Phase 2
 Continue pain management
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Ortho Lecture Notes Combined




Ultrasound helpful prior to stretching
Proprioceptive training with passive stretching
Light mobilization & manipulation can be performed per patient tolerance
Possible Manipulation under anesthesia – rupture the fibrotic buildup. The patient may require
intensive pain control & physical therapy afterward. The technique has also been reported to cause
humerus fracture & vascular & neurologic injury; another major concern is articular cartilage injury.
The incidence of complications is low.
 Possible Capsular distention (Hydroplasty)–injecting saline & steroid into the capsule to increase joint
volume – it provides a short term decrease in pain & increase in motion.
Phase 3
 Continue stretching & other activities (mobilization/manipulation) to improve ROM
 Increase strengthening exercises for prevention
Surgical capsular release. This procedure is done arthroscopically or via incision. Contracted tissues are
directly visualized & released. Reports indicate that patients are 90% pain free & have normal to near
normal motion within 3 months after surgery.
Little League Shoulder
Additional Information
Epidemiology:
Pitchers who throw curve ball or sliders are at increased risk.
Treatment:
Due to the nature of the injury rest is the best therapy (usually 3 months recommended, although full
force throwing may take up to 12 months), then strength training for the arm & back can help to help
restore balance to muscles. When return to sport occurs, proper training in throwing technique will help
prevent injury.
Following the proper guidelines for young pitchers can help prevent injury.
Age of Athlete
Pitch limit per day.
17-18
105
13-16
95
11-12
85
10-Under
75
Number of Pitches Thrown
1-20
21-40
41-60
61+
Days of Rest
O
1
2
3
Prognosis:
Low risk of permanent injury; small chance of early growth plate closure, which may result in a shorter
arm. Little league shoulder will often heal completely with rest, & the athlete will not lose any functional
ability.
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Ortho Lecture Notes Combined
Elbow
1. Describe the etiologies/mechanism of injury for each condition.
2. Explain the pathogenesis for each condition.
3. Describe the clinical manifestations (symptoms, clinical signs & examination findings) in order to diagnose the condition
4. Identify the epidemiological &/or risk factors associated with the conditions.
5. Identify the diagnostic studies & describe the findings on those studies that would aid in diagnosis of each condition
7. List the Diagnostic criteria/Guidelines for the conditions.
8. Select the most appropriate management/treatment techniques for each condition including referral/co-management.
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Ortho Lecture Notes Combined
Ortho 1 Conditions to KNOW:
MCL sprain
Epicondylopathy
Cubital tunnel syndrome
Olecranon bursitis
Tendinosis
Distal biceps tendon rupture
Anterior Interosseous Nerve Syndrome
aka Kiloh-Nevin Syndrome
Etiology: COMPRESSION @
1. anomalous musculo-tendinous bands of deep or superficial
pronator teres mm heads
2. tendinous origin of flexor digitorum superficialis mm to middle
finger
3. accessory head of flexor pollicus longus
Epidemiology: fairly rare…more likely something else
 Isolated injury to the anterior interosseous nerve is distinctly rare
o <1% of upper extremity neuropathies), although may occur
with significant trauma to the forearm.
 More commonly, AINS develops in patients who present with
neuralgic amyotrophy.
Risk Factors those who do repetitive pronation
 Repetitive, strenuous movements (pronation) of forearm & wrist
o e.g., rowing, racquet sports, carpentry, weight lifting
 Poor strength & flexibility
 Diabetes, hypothyroidism
 Compression sites: Pronator teres, flexor dig superficialis, flex poll
longus
Clinical Presentation
 Constant or intermittent PN
 vague pain in the proximal forearm (not nerve pain)
 Feeling of tightness in the proximal forearm
 Dropping things
 Unable to do “ok” sign (e.g. touching pads instead of tips of finger to thumb) + Pinch grip
 Possible atrophy, pinch deformity
 ROM – inability/difficulty with flexing DIP of 2nd & 3rd digits, difficulty with thumb flexion & pronation.
Elbow flexion/extension may have no effect on the patient. Pronation could be provoking.
 + Pinch grip test
 SENSORY = No changes
 Motor – test pronator quadratus – weakness when patient attempts to pronate arm with elbow
flexed against resistance +pronator teres test =weak ness
Diagnostic studies:
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Ortho Lecture Notes Combined


EMG – demonstrates a deficit in nerve function
US &/or MRI – determine the cause
Treatment:
Spontaneous recovery may occur between 3 & 18 mos.
 Activity modification change activity, esp if overuse
 NSAIDs/Analgesics & modalities (Cryotherapy) to decrease pain/inflammation in forearm if
present – this may decompress the nerve reduce inflammation
 ROM activities of the fingers to prevent contractures stretch
 Myofascial release reduce adhesions
 STM, CMT mobilization
 Heat prior to strengthening exercises/modalities for muscle contraction
 Nutritional support (vitamins B3 B6 B12)
 Possible splinting – elbow 90, forearm neutral, wrist slight extension (8-12 weeks)
 Joint mobilization splint if not obeying instructions to reduce exacerbating activity
 Surgical decompression – if no improvement by 8 wks
Pronator syndrome
Etiology:
Entrapment usually were the nerve passes through pronator teres mm
 Trauma to forearm
 Compression Localized anatomic nerve entrapment
 Overuse (using screwdriver, hammering, biking)
Possible compression sites: Similar to AINS, but WITH SENSORY, r/o
Carpal tunnel syndrome
 @ pronator teres: between superficial & deep heads (most common)
 @ ligament of Struthers
 @ Lacertus fibrosus
 @biceps aponeurosis
 @ under flexor digitorum superficialis arch
Epidemiology:
Rare disorder most often seen in the dominant arm
<1% of UE entrapment neuropathies, yet more common than AINS
F >M by 4x
Risk Factors:
Same as those for AINS
Clinical Presentation weakness, sensory, weak grip, pain w/pronation
Can mimic CTS or AINS
 Forearm discomfort & fatigue
 Insidious onset
 Complaint of vague numbness &/or
weakness/clumsiness in the hand (gripping)
 r/o Carpal tunnel syndrome
(has NIGHT pain, but PTS doesn’t usually)
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Ortho Lecture Notes Combined




PTS
aggravated by elbow flexion
symptoms in forearm as well as hand.
Night pain uncommon
Prolonged wrist flexion aggravates






o Less likely to have night time symptoms (CTS common to have nocturnal symptoms)
Tenderness & enlargement of the pronator teres (characteristic finding)
Possible atrophy in hand
Tinel's sign may be positive
+ Test for Pronator Teres Syndrome / provocation with resisted pronation
Sensory changes in median nerve distribution
Weakness in the median nerve distribution




CTS
aggravated by wrist motions.
Very little forearm pain
Night pain common
No affect by prolonged wrist flexion
Diagnostic studies:
 NCV & EMG studies may confirm nerve deficit
 X-rays to rule out bony abnormalities causing compression
Treatment:
Recommendation is rest & splinting for 3-6 mos.
 Rest & modify activities
o Avoid pronation type activities
o Cryotherapy/NSAIDs to decrease pain/inflammation
 Bracing (especially helpful at night) to enforce rest
o Immobilization of the elbow in 90° of flexion & forearm neutral position
 Strengthen - if weaknesses noted strengthen grip strength
 Stretch the forearm musculature (pronator & flexors) - critical
 Myofascial release
 Acupuncture to relax mm
 Joint mobilization
 Nutrition: B6, niacin, B12, anti-inflammatory
 Refer if symptoms continue 2-3 months with conservative care.
o Nerve block or corticosteroid injection
o If severe nerve pain – Rx for anticonvulsants
o Decompression
 Median N GLIDING (see picture)
Prognosis:
50% of patients have resolution of symptoms within 4 mos with conservative care.
90& of patients who have decompression surgery have complete resolution of symptoms
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Ortho Lecture Notes Combined
PT
Pronator Teres
CTS
AINS
ant interosseous n synd
Aggravated
Sx
Night Pn
Aggravated
Motor
Sensory
Elbow flexion
Forearem + hand
No
Prolonged wrist flexion
Weak no “OK”
Yes
Wrist motion
Hand
Yes
Not so much
Weak
Yes
No
no “OK”
NO loss
Radial Nerve Syndrome
aka: Saturday Night Palsy
Etiology:
 Nerve entrapment @ spiral groove (radial sulcus) along shaft of humerus
 Prolonged compression
o Leaning arm over back of chair (usually while inebriated & then
falling asleep)
o Poor positioning/fitting of crutches causing compression
 Humeral fracture
Clinical presentation:
 Arm Pain
 Paresthesia in radial nerve distribution
 Weakness in radial nerve distribution (usually spares triceps)
o Sparing of triceps
o Isolated sensory loss to dorsum of hand
o DDX: Both helpful in determining:
 Radial neuropathy vs. NR or cord lesion
Treatment:
 Remove compression
 Pain management
 Wrist splinting to maintain function
 Stretching (ROM) & strengthening
Prognosis:
 If “Saturday night palsy” = good prognosis, short time frame & recovery is full
 If due to another source = POOR PROGNOSIS
Posterior Interosseous Nerve Syndrome (PINS)
Etiology:
 Severe trauma (Monteggia fx, Radial head fx)
 Extrinsic/intrinsic compression - Bone, inflammation
o ex. RA or other inflammatory issues, ganglion, lipoma
 Possible overuse – repetitive pronation/supination
 MOTOR ONLY
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Ortho Lecture Notes Combined
Compression Sites:
 Arcade of Froshe, fibrotend @proximal supinator = MC nn entrap site
 Btw heads of supinator mm
 Fibrous tissue anterior to radiocapitellar jt - btw brachialis &
brachioradialis
 Medial proximal side of ECRB
Epidemiology: M >F
Risk Factors
 Manual laborers, Body builders (repetitive grip +supination)
Clinical presentation
 Insidious onset of vague, proximal posterior/lateral forearm pain
 Weakness of hand (extensors)
 Atrophy, wrist/finger drop
 Tenderness @
o lateral epicondyle
o more distally over the arcade of Froshe (4 fingers width distal from elbow)
 Probable provocation w/resisted supination of forearm & frequently w/resisted pronation
 Paresis/paralysis of finger/thumb extensors
 Paresis of the wrist extension (ECRL receives innervation from Radial N not
PIN)
o Possible medial deviation of the wrist during extension because
ECRL is spared
 Forearm supination is also weak & may also provoke the pain
3 main signs: Wk finger & wrist extensory, prox post forearm pain
Diagnostic studies:
 EMG – help to determine level of compression
 MRI – not needed for dx but may be helpful in determining cause of compression &/or if surgery is
a consideration
Treatment:
Treatment depends on etiology
 Rest & modification of activities
 Splinting to limit
o elbow extension &
o forearm pronation/supination,
o keep wrist in neutral
 ROM exercises (passive/active assisted stretching) to prevent contractures
 Strengthening exercises
 STM
 Nerve gliding exercises
 NSAIDs
 Joint mobilizations
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Ortho Lecture Notes Combined




Modalities
Nutrition: B6, niacin, B12, anti-inflammatory
SURGERY: If no evidence of improvement in approx. 3-6 mos surgical decompression
Lidocaine or steroid injections (pain & inflammation)
Radial tunnel syndrome
aka: Resistant Tennis Elbow (G56.3) DDX FOR LATERAL EPICONDYLITIS
Etiology:
 Tunnel is too small, it can squeeze the nerve & cause pain.
 Repetitive, forceful pushing & pulling, bending of the wrist,
gripping, & pinching can also stretch & irritate the nerve.
 Sometimes direct blow to outside elbow injures radial nerve.
 Constant twisting arm movements- common in assembly work,
pinches radial nerve leading to radial tunnel syndrome.
 It can also be caused by tumors
 Where NN passes under supinator mm
 To distinguish from lateral epicondylitis: RTS is a few centimeters
distal from lateral epicondyle
Clinical Presentation
 Stabbing, cutting, piercing &/or achy/fatigue pain at the proximal lateral forearm that may radiate
down the arm
 Pain a few centimeters distal from lateral epicondyle where nn goes under the supinator muscle
 Paresthesia & weakness rare…If complaint, usually secondary to pain
 Tenderness to palpation
 Provoke pain with resisted 3rd finger extension (with elbow in extension) while patient extends their
wrist & fingers
 Pain & symptoms may be relieved by passive flexion of wrist.
Diagnostic studies:
 Electrodiagnostic studies: usually negative
 MD’s may inject lidocaine into the radial tunnel to see if that alleviate the symptoms, if so, than RTS
was diagnosis, if not maybe it was tennis elbow.
Treatment:
Should be improved within 3-6 wks with rest & conservative care
 Rest & activity modification
o Avoid repetitive activities that require wrist to be repeatedly bent backwards.
 Recommend brace while sleeping w/elbow in flexion, forearm in supination & the wrist in extension.
 Forearm stretches & strengthening esp extensors.
 Modalities – Cryotherapy, heat, IFC
 NSAIDs
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Ortho Lecture Notes Combined



Nerve gliding exercises
Joint mobilization
Nutrition: B6, niacin, B12, anti-inflammatory
 Lidocane &/or steroid injections if conservative care fails.
 Surgery as last resort
 Rest, brace stretch Ice, anti inflammatory & diet,
Critical diff between RTS & PINS?
a. Post prox elbow pain NO
b. Pain distal to elbow not enough to distinguish
c. Pain w/ Rsupination and resisted pronation
d. Weakness in fingers or wrist extensors PINS has weakness, RTS (aka resistant tennis elbow) does
NOT
Lateral Antebrachial Neuropathy *SENSORY ONLY*
Etiology:
 Trauma
o biceps insertion
o betw biceps & brachialis m
 Biceps Compression e.g. due to over throwing
 Acute twisting injury of the forearm “MERCY”
 Traction injury – hyperextension of the wrist
 Venipuncture injury
Epidemiology:
 an uncommon, but easily overlooked, cause of elbow pain in the
throwing athletes
Clinical Presentation
 onset usually insidious unless acute trauma
 dorsoradial/lateral forearm/wrist to base of thumb
o electric, shock-like, shooting, burning pain &/or paresthesia in the same distribution
 worse with forearm/hand motions (keyboard use, piano; forced pronation during throw)
 point tenderness just lateral to biceps insertion
 Tinel’s @ Olson’s point - intersection of lateral border of biceps tendon & elbow crease
 Full elbow motions, provocation with resisted flexion & or supination biceps fxn = pain
 Testing sensation with elbow extended - may add motion of pronation or supination while testing
Diagnostic studies
 NCV – can rule in the diagnosis
 Lidocaine injection can also be used to diagnose
Treatment:
 Rest & activity modification
 Possible splinting: avoid full flexion
 NSAIDs
 Soft tissue modalities
 Joint mobilization
 Nutrition: B6, niacin, B12, anti-inflammatory
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

Case:













PT
Patient should respond in 1-2 weeks
Possible injection &/or surgery if sx not resolving
Pt has R wrst/hand numbness & pain
Anterior wrist, forearm, fingers
NO MOI, prior Hx
Off/on for last month
Provoked: typing / relieved w/rest, massage of wrist & forearm
Waking at night (don’t do anchoring BIAS)
DDX: carpal tunnel, AINS, Pronator teres, maybe lateral antebrachial neuropathy
Pn was mild, now moderate
EXAM: vital normal
Grade 2 tenderness @forearm; provoke CC w/wrist palp, thenar hypotonicity
AP wrist flexion/pronation PROVOKES, but no limit ROM
2 pt discrim 8mm distal 1st 3 digits
4/5 pronator quad, flexor carpi rad, flex dig superfic, opponens pollicis
Pronator Teres
CTS
AINS
TOS
ant interosseous n synd
Aggravated
Sx
Night Pn
Aggravated
Motor
Sensory
Tender w/palp
Hypotonicity
Provoked ROM
Elbow flexion
Forearem + hand
No
Provoked wrist flexion
Weak no “OK”
Yes +2pt
Wrist motion
Hand
Yes
Not so much
Weak
Yes
Thenar?
Yes
thenar
Yes
No
Night pain
no “OK”
NO loss motor only
Yes Thenar
yes
Yes
yes
DDX:
 pronator syndrome – both motor & sensory & forearm tenderness = CLOSEST
 carpal tunnel – would present in hand more
 TOS - double crush: 1 @ cervical NN root, 1 @ CTS
*could have started as PTS, but developed into CTS
*consider that may have 2 diagnoses
*consider double crush… Nerve trapped in 2 places: scalenes & wrist = present w/CTS (for example)
NOT:
 AINS – b/c motor & sensory (AINS is not sensory)
 lat. Antebrachial neuropathy
 Not tunnel of Guyon (first 3 digits vs. ulnar is 4 & 5)
 radial tunnel synd. (relieved w/flexion)
 cubital tunnel – ulnar distrib, so no
Significance of 2-point discrimination?
Indicates neuropathy, can be posterior column ds.
Posterior tennis elbow aka: Triceps tendinosis, Boxer’s elbow Souza
Etiology:
Rapid extension leads to straining of the tendon RARE condition: tendonitis @ olecranon
 tender where touches olecranon
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Ortho Lecture Notes Combined

Rapid extension will irritate: boxing tennis testing & Resisted elbow extension
Risk Factors:
Activities that require rapid or repetitive elbow extension
 Throwing
 Punching
 Serving motions
Weightlifting
Clinical Presentation
Refer to Souza this is supplemental
 Key test: Resisted elbow extension with elbow in flexion & the forearm fully supinated
 Joint play movements should be full and painless.
 Tenderness may be palpated over the insertion of the triceps tendon into the olecranon.
 Visual inspection is usually normal
Treatment:
Refer to Souza
 Counterforce bracing & taping might be useful
 Soft tissue
 Rest
 US, IFC
 Strengthening concentrating on total arm strength & balance; consider eccentric focus
 Visually appears normal
 REST
Posterior Impingement Syndrome
Refer to Souza – this is supplemental
Repetitive forced extension: Boxers, Javelin thrower, trauma, contact sports, MMA
Etiology:
 Caused by repetitive forced elbow extension OVERUSE
o deceleration/follow through phase of throw may hyperextend elbow
o repetitive punching, forcing the elbow into hyperextension.
 Trauma - in contact sports
o collision to the back of the elbow,
o forcing the elbow to bend in the wrong direction.
Risk Factors
 Throwing athlete (pitchers, javelin throwers, cricketers)
 Boxers &/or other martial arts
Clinical Presentation
 gradual increase in posterior elbow pain
 swelling & stiffness.
 Palpatory tenderness will be noted in the posterior portion of the elbow.
 Crepitus noted with active & passive ROM may be fragments of bone from trauma
 3 phases of development
o Pain after activity
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Ortho Lecture Notes Combined


o Pain w/activity
o Pain all the time
ROM changes – loss of extension & provocation
o Crepitus, locking, catching ?
o Crepitus may be noted with active and passive ROM
Valgus extension overload test: may reveal valgus instability or medial and posteromedial pain
Diagnostic Studies:
 X-rays may not adequately diagnosis the condition unless there are spurs or loose bodies in the
back of the elbow. Can only see if spur or fragment
 Ultrasound or MRI better diagnostic tools.
Treatment
 Rest, Rehab
 Work on Shoulder & Wrist always w/elbow injury
 Tape, brace, Adjust
Nursemaid’s Elbow
Refer to Souza – this is supplemental
Etiology:
Axial traction & falls are most common causes.
Epidemiology
 2-4 years old most common can occur from infancy to about 7 years old
 females > males
 tends toward non-dominant arm but can be either
Clinical Presentation
 Anxious child, overly protective of elbow
 The forearm is usually flexed 15-20 degrees at the elbow, & the forearm is partially pronated.
 Often, the weight of the affected arm is supported with the other hand
 Tenderness or malposition at the head of the radius may be present.
 The patient resists supination/pronation as well as flexion/extension of the forearm
 Dislocates from annular ligament
Diagnostic studies:
 Ultrasonography has been used as a noninvasive modality to assess for annular ligamentous injury
& displacement of the radial head from the capitellum. It has also been used to assess progress of
treatment for patients with recurrent subluxations.
 Circulation normal
 MM strength normal
 ROM restricted by pain
Treatment:
1. Put pressure on head of radius
2. Grab wrist & supinate while flexing the elbow and putting pressure on the radial head
3. Should pop right in
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Ortho Lecture Notes Combined
Little League Elbow
Refer to Souza – this is supplemental
Epidemiology:
Overhead throwers under 16 years of age.
May have hx of other issues, injury, change in patter
Clinical Presentation
 Pain is most commonly localized to the medial epicondyle, although patients may also present with
lateral or posterior elbow pain.
 Medial elbow pain
o During palpation
o During cocking and/or acceleration phases of throwing is typical.
 Pain during the deceleration phase is more likely to be associated with posterior elbow
injuries.
 Past history of injuries such as shoulder, back, or knee injuries that can easily alter the biomechanics
of throwing may place the elbow at increased risk for overuse injuries.
Treatment
 Rest
 Tape
Panner’s disease
*rare, essentially osteochondritis dessicans of the elbow
Refer to Souza
Epidemiology:
 Athletic overhead throwers age 5-10.
 Male>Female
 Bone appears flattened out at the trochlea of the elbow
Treatment: Rest, ice, anti-inflammatory
 Prognosis good if they rest and treat well
Case: 14 yo BM presents to office complaining of posterior elbow pain
DDX & why not
 Post impingement – ROM would be limited in extension, would have crepitus, swelling
 Olecranon bursitis – not b/c there’s no swelling and full ROM
 Post tennis elbow – Best Dx
 Little league elbow - wrong phase of throwing, not pain in stress test
 Panners – too old
Exam:
Palpate
RROM
Findings: Visual normal
ROM normal
RROM extension hurt in supination
No locking or creptiis
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Ortho Lecture Notes Combined
Wrist & Hands
Learning Objectives:
1.
Identify the MOI for carpal instability & TFCC tear.
2.
Discuss the pathogenesis of the conditions presented.
3.
Determine who is at greatest risk for the conditions.
4.
Describe the clinical manifestations of the conditions
5.
Describe the stages of CRPS
6.
Identify the most appropriate diagnostic studies & the expected outcomes.
7.
Determine the most appropriate management for the conditions.
8.
Explain the clinical findings associated with carpal instability
Scapholunate sprain/dissociation S63.519A
Ingari JV. Wrist & hand. In: DeLee JC, Drez D Jr., Miller MD, eds. DeLee & Drez's Orthopaedic Sports
Medicine. 3rd ed. Philadelphia, Pa: Saunders Elsevier;2009:chap 20
Etiology:
 FOOSH (most common) onto the hand with wrist positioned in extension, ulnar deviation &
carpal supination; which forces the capitate between the scaphoid & lunate.
o If severe hyperextension injury of the wrist, there is tear of scapholunate interosseous
ligament & radioscaphoid. These injuries may result in DISI (dorsal intercalated segmental
instability) – scaphoid goes into flexion & lunate in extension
 Degenerative tears
o in >50% of people over 80 yrs
 Severe twisting
 Blunt force trauma
Risk Factors
Common injury in athletes:
 Bikers, Skaters, Skiers, Skateboarders, Gymnastics, Divers,
 Contact sports: Basketball, Football, Soccer, Baseball
Clinical Presentation
 Dorsal & radial-sided wrist pain (anatomical snuff box)
 Pain increases with loading (e.g., pushup position)
 Weakness/instability (difficulty grasping)
 Clicking or catching
 Wrist stiffness
 Edema, swelling
 tenderness over the scapholunate junction
 decrease grip strength
 provocation w/motion
 (+) Watson’s Test or Shuck Test.
 hypermobility of the carpals: after swelling subsides.
Diagnostic Studies:
 Plain film: Altered positioning of the carpals on the various views.
o “Terry Thomas” sign = scapholunate distance of greater than 2mm (3mm abnormal)
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

o Signet Ring sign
o If standard views are negative it may require stress views to visualize the instability
MR or MR arthrogram – due ligament size, possibly miss the tear
Arthroscopy – is only way to confirm the diagnosis of other imaging has failed
Treatment: Kuo CE, Wolfe SW. Scapholunate instability: current concepts in diagnosis & management. J Hand Surg 2008;33A:998-1013
 Acute
o Grade 1 or 2 sprains - treat as you would any other sprain injury.
 Activity modification – avoid tight gripping or pushing activities
 Cyrotherapy
 Bracing - depending on severity
 Joint mobilization depending on grade of injury
 Nutrition to support soft tissue healing
 NSAIDs
 Rehabilitation to strengthen dynamic stabilizers
 Proprioception exercises
o Grade 3
 Immobilization for 6-8 wks may work if caught before disassociation
 if fails= surgery to stabilize wrist
 Surgery if dissociation is present –
 may take up to 6 mos pos-surgery for full RTP depending on sport
 Chronic injuries
o may require stabilization surgery (ligament repair, reconstruction or fusion)
 Post-surgical
o Physiotherapy for pain control & improve ROM
 Passive ROM to active assisted ROM to active ROM to resisted ROM.
Complication:
 Surgical repair or reconstruction of the scapholunate interosseous ligament
 normally required to prevent long-term complications in grade 3 injuries.
 Capitate moves into gap
o Scapholunate Advanced Collapse (SLAC wrist) proximal migration of the capitate between the
scaphoid & lunate with resultant degenerative disease. With progression the degenerative
changes will effect the capitolunate & scaphoid-trapezium joints. Capitate than migrates
proximally into the gap betw the scapholunate of this will eventually result in collapse of the
midcarpals  DISI
Nutrition – see picture to update:
 Protein:
1-2 g/ kg per day to 0.8 g/kg/d
 Zinc: prevent delayed healing
o 20X RDA =300 mg/d RDA = 15 mg/d
o Increased many immune markers
 Manganese for cartilage healing RDA: 2.5 – 5 mg/day
…Safe up to 11 mg
 Copper: w/zinc to prevent Cu++ deficiency when treating w/zinc; RDA = 1mg/day
 Vitamin C: needed for heathy CT; 2000 mg/day to bowel tolerance
Treatment: Dart thrower motion
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Ganglion cysts M67.439
Pathology:
Soft tissue tumors that arise in tendon sheaths or capsules; they are typically round/oval & are filled with
a jelly-like fluid – possible mucoid degeneration of periarticular structures. In Tendon Sheath
Etiology:
Unknown, possible:
 Direct injury.
 Overuse or repetitive motions, such as those you do at work.
 Can be on foot
Epidemiology:
 F>M
 20-40s, can occur at any age however
 Most common soft tissue tumor of the hand & wrist
 Most common occurs on the dorsum (lateral) of wrist (50-70%)
 Volar of wrist is the next most common site (18-20%)
 Often seen in Gymnasts who repetitively apply stress to wrist.
Clinical Presentation
 Usually develop over a period of months although occasional will be sudden.
 Usually solitary, firm, smooth, round & fluctuant
 Typically asymptomatic
o Possible achiness &/or paresthesia from mass effect or compression
o maybe present (ex. median nerve or radial nerve)
 Mass that fluctuate in size (from 1-3cm)
 Usually soft but larger ones may be firm, may be moveable
 ROM may provoke
 Possible muscle weakness- if the cyst is connected to a tendon (b/c on mm tendons)
 Can be transilluminated – help differentiate from solid masses used do see if fluid filled
Diagnostic Studies: Typically not required unless diagnosis is in question use to r/o bone lesion
 X-ray - used to rule out other bone or joint abnormalities
 Ultrasound - Helpful to demonstrate smooth cystic walls that may be separated
 MRI - not often done, used to differentiate malignant bone lesion from cystic structures
 Needle Biopsy
Treatment
 Assess biomechanics to guide treatment
o Observation if asymptomatic although may want to assess biomechanics of wrist/forearm
& do work to optimize
 Activity modification if you believe cause is due to a repetitive motion
 Aspiration followed by steroid injection
o ~50% recur within yr
 Surgical removal (85-95% success rate)
 Bible therapy
o Rupture cyst by sharp blow with a book or compression –
o "bible therapy" – low success rate & high rate of recurrence
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Triangular Fibrocartilage Tears (S63.599A)


Type 1: TRAUMA
Type 2: Degenerative, Repetitive use, likely Positive ulnar variance
3 parts to TFCC:
Etiology: Most common = wrist hyperextension & pronation o
Type I – Traumatic Tears
 Fall on extended wrist, esp when wrist is pronated
 Sudden excessive pronation or supination
o e.g. Power drill injuries can also cause triangular fibrocartilage complex rupture when the
drill binds & the wrist rotates instead of the drill bit) may lead to TFCC disruption or
peripheral tears (DRUJ instability)
 Distraction forces applied to the volar forearm & wrist
 Radial fractures
Type II – Degenerative (Chronic) Tears
 A degenerative tear may occur as a result of ‘ulnocarpal impaction syndrome’ when the end of the
ulnar chronically ‘impacts’ on the TFC & triquetrum & lunate. A + ulnar variance increases the risk.
 Repetitive loading with heaving lifting & ulnar deviation or ulnar loading (racquet sports
Epidemiology:
 Gymnasts, skateboarders
 Workers who do a lot of pulling or twisting with hands (lifting heavy tools)
 Participate in racquet/bat/club sports
 Degeneration starts in 3rd decade & by 5th decade it is rare to have normal TFCC )
Clinical Presentation
 Dull aching sensation on ulnar side of wrist radiating to dorsal wrist
 Grip weakness with possible associated clicking esp w/pronation & supination activities (turning
doorknob, key, can opener)
 Pain increases with ulnar deviation
 A feeling of instability, like the wrist is going to give out on them.
 Tenderness @ dorsal depression distal to ulnar head, localized around the
ulnar styloid or between the triquetrum & the ulnar styloid May have sag
 ROM may be full or limited – possible clicking with active / passive ROM
 Pain with forced forearm pronation & supination or pain with gripping &
ulnar deviation;
 Ulnar carpal sag may be visualized
 (+) Triangular fibrocartilage compression test
 Extensor carpi ulnaris tendon may be subluxated (ECU tendon sheath
floor connects broadly to the TFCC) – may be felt during extension
 Piano key sign - a prominent & ballottable distal ulna with full pronation of the forearm
 Diminished grip strength
 DRUJ Compression (Grind) test should be performed to help r/o concurrent injury – compress radius
& ulnar together & then pronate/supinate; + test increase in pain
 DRUJ Ballottement test – hold both the distal radius & ulna & apply a shear (A-P, P-A)first to the one &
then the other; + increase translation
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
Squeeze Ulnar & Radius hurts when twist
Diagnostic Studies:
 X-ray - may illustrate the presence of a fracture, + ulnar variance, possible DJD

MRI with contrast is best - demonstrates a 0.8 sensitivity & 0.7 specificity (Iordache SD, Rowan R, Garvin GJ,
Osman S, Grewal R, Faber KJ. Prevalence of triangular fibrocartilage complex abnormalities on MRI scans of asymptomatic wrists. J Hand Surg Am.
2012 Jan. 37(1):98-103.)


Arthrogram – diagnostic utility is in question
Arthroscopy – diagnostic standard
Treatment:
Conservative management tends to be ineffective for chronic (>6 mo.) & symptomatic injuries.
 If chronic, tends to be ineffective
 Immobilization
o Degenerative tears immobilize in short arm cast in slight flexion
& ulnar deviation for 3-6 wks;
o Traumatic tears immobilize in a long arm cast for 4-6 wks
 NSAIDs during immobilization
 Possible steroid injections
 Removable wrist splint & rehabilitation after initial immobilization
o AROM & Assisted AROM exercises – wrist (flexion / extension, ulnar / radial deviation),
fingers/thumb (flexion / extension), forearm (pronation / supination), elbow
(flexion/extension).
 Note: initially may need to avoid ulnar deviation &
compression for a period of time after splinting.
o Tendon Glide exercises – differentiate wrist from finger
tendons, increase their movement
o Functional exercises – fist formation, opposition & grip
o Massage – reduce swelling & scarring/adhesion formation
o Passive Accessory Movement Glides – particularly wrist (AP,
PA & Med/Lat)

Surgery –
o Depending on size & location of tear (if tear is in center of
cartilage which is the avascular zone) surgery may be the
treatment of choice
o If pt has + ulnar variance surgery is better option
o Pt not responding to immobilization
Dupuytren’s Contracture M72.0
Etiology: Unknown
 Pronounced genetic predisposition
 Possible trauma
Pathology
 Fibroblastic proliferation, disorderly collagen type II, fascial thickening.
 Nodule(s) = pathognomonic in early proliferative stage
o due to proliferation of fibroblasts in superficial palmar fascia
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Epidemiology:
 50+ yrs
 Male > Female
 Genetic component: Northern European descent (white males)
Risk factors:
 Workers exposed to repetitive handling tasks or vibration
 Diabetes
 Family history
 History of seizures
 Alcohol & smoking
 Increasing age
Clinical Presentation
 Possibly asymptomatic with mild cases
 CC: Painless thickening or nodule in the palm
o painful if concurrent tenosynovitis
 CC: loss of motion of affected finger(s) usually 4th & 5th, possibly 3rd
 Earliest sign = triangular puckering of skin over flexor tendon (MCP jt) just proximal to flexor crease
of finger.
o Passive extension of fingers demonstrate puckering of skin over MCPs
 Discrete visual or palpable nodules along course of tendon distal to palmar crease
 Limited extension of MCP & PIP, deformity
 Possible tenderness of nodule
 (+) table top test = can’t push hand flat when volar side down
 Progression is variable – some patients have minimal involvement & therefore
minimal function loss others have gross involvement causing deformity & severe
functional impairment
Grading
 grade 1: thickened nodule & band in palmar aponeurosis
o may include skin tethering, puckering, or pitting
 grade 2: peritendinous band
o Limited finger extension (limited ROM)
 grade 3: flexion contracture
Treatment:
 Conservative: Stretch, treat fibrosis, splinting, educate on
repetitive use
o Little efficacy with conservative care
o Stretching exercises performed in warm water – no data to support efficacy
o Ultrasound to prevent the fibrosis.
o Splinting of the fingers
o Manipulation/mobilization of the wrist & hand
o Avoid having to use a tight grip on tools – pad tool handles or wear thick/heavy gloves
especially during heavy grasping tasks
Medical Management:
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


Collagenase injections {3 injections} (newest treatment) - cords are weakened by injection of small
amounts of the enzyme collagenase, which breaks peptide bonds in collagen. Injecting a type of
enzyme into the taut cord in the palm can soften & weaken it —
o allowing the doctor to later manipulate the hand in an attempt to break the cord & straighten
fingers. Fairly high rate of re-occurrence but procedure can be repeated.
Needling to break cords – This technique uses a needle, inserted through your skin, to puncture &
"break" the cord of tissue that's contracting a finger.
o Contractures often recur but the procedure can be repeated.
o Main advantages of the needling technique are that there is no incision, it can be done on
several fingers at the same time, & usually very little physical therapy is needed afterward.
o Main disadvantage is that it cannot be used in some locations in the finger, because it could
damage a nerve or tendon.
Surgery – various forms of fasciectomy or fasciotomy (Because it is a genetic disorder – the
contractures may return post-surgery) –
o Main advantage to surgery is that it results in a more complete joint release than that
provided by the needle or enzyme methods.
o Main disadvantages = physical therapy is usually needed after surgery, & the recovery time
can be longer.
Complex Regional Pain Syndrome (CRPS) G90.50
Definition:
 Painful array of conditions; continuing (spontaneous or evoked) regional pain disproportionate to
usual course of any known trauma or other lesion.
 Pain is regional (not in a specific nerve territory or dermatome)
o usually distal predominance of abnormal sensory, motor, sudomotor, vasomotor, trophic
findings. The syndrome shows variable progression over time
 Major involvement of SYMPATHETIC NERVOUS SYTEM
Synonyms: Have been & may still be used on boards
 Reflex Sympathetic Dystrophy (RSD)
 Shoulder-Hand Syndrome
 Causalgia
 Sudeck’s atrophy
Pathology:
Both etiology & pathogenesis are unknown. Proposed theories: *GROSSLY SWOLLEN HAND*
 Direct nerve injury release of inflammatory mediators & pain-producing peptides by peripheral
nerves
 Central sensitization - increased nociceptive afferent activity due to:
o peripheral noxious stimuli,
o tissue damage, or nerve injury
o increases synaptic transmission at somatosensory neurons in dorsal horn of spinal cord
 Sympathetic overactivity due to catecholamine hypersensitivity & may involve reflex arc formation
after inciting incident
 Genetic factor - significantly increased HLA-DQ1 among patients affected by CRPS type I
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Type I – aka RSD –
 no evidence injury/peripheral nerve injury
 90% of the pts have this form= MC
Type II – aka causalgia – secondary peripheral N injury
 “Warm” CRPS – increased skin temp @ onset of Sx
– suggests inflammatory type
 “Cold” CRPS – decreased skin temperature at onset
of symptoms
Epidemiology:
 F >M (highest postmenopausal women)
 55-75 yrs
Risk Factors:
 Trauma – fractures, crush injuries, sprains, surgery
 Immobilization following trauma
 ACEI use
 Stroke
Clinical Presentation STAMP –
 Symptoms beyond initial site of trauma
 Trophic changes
 Autonomic changes
 Motor
 Pain
 Sensory – hyper, distal
Main symptoms: pain, sensory changes, motor impairments, autonomic symptoms, trophic limb change
 ONSET: approx. 4-6 wks after inciting event
 Symptoms go beyond the initial site of trauma & may actually spread to other limbs
 Pain - Most debilitating symptom
o Out of proportion to the injury
o Burning, stinging, tearing sensation deep in limb (may be superficial)
o Usually continuous but may be paroxysmal
o Exacerbated by movement, contact, stress, temperature change
 Sensory - Hyperalgesia, Allodynia, Hypesthesia
o Usually distal – possibly follows glove/stocking distribution
 Motor - Limited by pain, edema, contracture
o May develop: tremors, myoclonus &/or dystonic postures
 Autonomic differences
o Skin temp
o Skin color
o Sweat
o Edema
 Trophic changes
o Hair growth
o Increased/decreased nail growth, yet skin atrophy
o Contracture/fibrosis of joints & fascia
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Stages:
 In most cases, CRPS has three stages.
o However, CRPS does not always follow this pattern.
o Some people develop severe symptoms almost right away.
o Others stay in the first stage or can skip phases.
Early identification has best prognosis (within 1st 6 months, but IDEALLY w/in 1st 3 months)
 Stage 1 (lasts 1 - 3 months): The first 2-stages are considered reversible, can go into remission.
o Severe burning, throbbing, aching pain which doesn’t follow a known nerve distribution
o Sensitivity to touch or cold
o Localized edema
o Altered skin color - slowly becomes blotchy, purple, pale, or red; thin & shiny
o Sweating
o Faster growth of nails & hair
o Muscle spasms & joint pain
o Radiographs are typically negative although possible to have isolated demineralization
 Stage 2 (lasts 3 - 6 months): “Dystrophic Stage”
o Progression of soft tissue edema
o Thickening of skin, ligaments, capsules (stiffness)
o Muscle wasting, atrophy, stiffness
o Brawny skin development
o Worsening Pain
o Slower hair growth
o Osteopenia
 Stage 3 (irreversible changes can be seen): Atrophic stage unlimited amount of time
Permanent changes start to persist
o Limited movement in limb because of tightened muscles & tendons (contractures)
o Marked atrophy
o Entire limb pain
o Waxy, trophic skin changes
o Brittle, ridged nails
o Condition may spread to other limbs at this stage
o Severe Osteopenia
Budapest consensus criteria for the clinical diagnosis of CRPS
A: Pt has continuing pain; disproportionate to MOI
B: Pt has at least one sign in two or more categories categories
C: Pt reports at least one symptom in three or more categories
D: No other diagnosis can better explains signs and symptoms
Categories- STAMP Signs – see or feel a problem Symptoms – patient reports a problem
(Hardin, Bruehl. (2007) Proposed New Diagnostic Criteria for Complex Regional. Pain Syndrome, PAIN MEDICINE, 8(4):1-6)
1. Continuing pain, which is disproportionate to any inciting event
2. Must report at least one symptom in three of the four following categories:
 Sensory: Reports hyperesthesia and/or allodynia
 Vasomotor: Reports skin temperature or color change or asymmetry
 Sudomotor/Edema: Reports of edema and/or sweating changes or asymmetry
 Motor/Trophic: Reports decreased range of motion, motor dysfunction (weakness, tremor,
dystonia) and/or trophic changes (hair, nail, skin)
3. Must display at least one sign at time of evaluation in two or more of the following categories:
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
Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or
temperature sensation and/or deep somatic pressure and/or joint movement)

Vasomotor: Evidence of temperature asymmetry (>1°C) and/or skin color changes and/or
asymmetry

Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating asymmetry

Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness,
tremor, dystonia) and/or trophic changes (hair, nail, skin)
4. There is no other diagnosis that better explains the signs & symptoms
Diagnostic Studies: Not very effective in Dx
 Infrared Thermography — to detect changes in body temperature that are common in CRPS. A colorcoded "thermogram" of a person in pain often shows an altered blood supply to the painful area,
appearing as a different shade (abnormally pale or violet) than the surrounding areas of the
corresponding part on the other side of the body. An abnormal thermogram in a patient who
complains of pain may lead to a diagnosis of CRPS.
 Radiography – may show spotty or localized demineralization – not diagnostic
 MRI - not very useful in diagnosis of CRPS
 Bone Scan – there is active reabsorption of bone so increase uptake- may be helpful in the diagnosis
in 1st 5 mos; negative scan may help r/o CRPS but doesn’t rule out.
 Autonomic Testing – helpful but not practical as routine tests
o Resting sweat output (RSO) = good predictor of CRPS
o Resting skin temperature (RST) – useful in the diagnosis but not practical to perform it requires
serial skin temperature readings at 1 minutes intervals for 5-8 hrs
o Quantitative Sudomotor Axon Reflex Test (QSART) – measures heat output in response to
iontophoresis cholinergic challenge (such as acetylcholine)
Treatment:
 Occupational/Physical Therapy - Main form of therapy for condition. Most common
o Increasing exercise program to help preserve or restore mobility & function to the affected limb.
o Aerobic conditioning is very important to improve coping ability, sleep, & pain control.
o Pool therapy may be used to help patients with trouble weight bearing.
o Graded motor imagery (esp preceding mirror visual feedback) – patient imagines moving painful
limb into a position seen in a photograph of a limb, then followed by moving both limbs into the
position while watching unaffected limb in a mirror that obscures the affected limb
o Mirror Visual Feedback – so see a well limb
o Postural control & gait retraining
o Vocational support
o Desensitization program –
 rubbing affected limb gently,
 increasing weight bearing,
 stretching,
 hot or cold baths –
 progress to isometric exercise when patient can tolerate touch stimulus,
 progress to isotonic & ADLs activities next
 Psychotherapy - depression, anxiety, or post-traumatic stress disorder.
o A psychologist or psychiatrist may be able to improve coping ability & motivation as well as detect
& address any substance dependency issues.
o Imagine moving the limb
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
Refer to Pain management
 Nerve Blocks - Many patients experience significant relief from nerve blocks,. By relieving pain,
blocks can enable more effective therapy, improve mood, & improve level of activity.
 Medications - may include: NSAIDs, topical analgesics (lidocaine or capsaicin), anti-seizure drugs
(decrease neuropathic pain), antidepressants (for depression & neuropathic pain), corticosteroids,
muscle relaxants, Bisphosphonates/Calcitonin, opioids, & sleeping medications.
 Spinal cord stimulators
 Pain pumps
 Epidurals - clonidine
 Trigger/tender point injections
 Surgery - If the CRPS is from a compressed nerve, such as with carpal tunnel syndrome, then surgery
to release pressure on the nerve may be needed (e.g., carpal tunnel release). Rarely, an operation
known as sympathectomy is used to divide the sympathetic nerves in patients who are helped by
nerve blocks, & its use is controversial.
Prognosis:
 Favorable prognosis if treatment is begun early, ideally within 3 months of the first symptoms.
 Poor to Guarded - if treatment is delayed the disorder can quickly spread to the entire limb &
changes in bone & muscle may become irreversible.
o In 50% of cases, pain persists longer than 6 months & sometimes for years or indefinitely
 25-30% = have full recovery
 Younger the patient the higher chance of complete recovery (NIH)
Prevention:
 Taking Vit C after trauma - Studies have shown that people who take daily vitamin C supplements
after injury have a lower risk of CRPS compared with those who don't.
 Early movement after a stroke - Some research suggests that people who get out of bed & walk
around soon after a stroke lower their risk
 Early mobilization after limb injury
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Cherialgia paresthetica Radial N
Aka: Wartenberg Syndrome
Aka Superfical radial neuropathy
Aka Handcuff neuropathy G56.30
Etiology:
 Compression of the sensory branch in wrist or distal
forearm (handcuffs, watch, casts).
o Direct trauma to the nerve
o Fractures or lacerations frequently completely
disrupt the nerve
o Damaged via surgical of De Quervain's
tenosynovitis
Clinical Presentation - Rare condition
 Paresthesia/pain/dysethesia in superficial radial nerve distribution
 Possible sensory changes in that distribution
 Provocation w/ulnar deviation (e.g., similar to Finkelstein’s)
 Tinel’s over the SRN may also provoke
 NO MOTOR involvement
 Inspection: may see tight watch
 Palpation: possibly tender N
 ROM – better w/extension & radial deviation, worse w/ flexion & ulnar deviation
Treatment:
 usually settles w/ conservative therapy;
may take up to 2 months
o NSAIDs
o Avoidance of external compression.
o Soft tissue modalities
o CMT
o Splint the wrist in extension &
radial deviation if indicated –
Decompress N
Medical Management:
 Possible steroid injection or surgical
decompression
 Complete anaesthesia suggests complete
severance of the radial nerve & should
prompt urgent surgical referral
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Intersection syndrome
-Aka-
Peritendinitis crepitans
Oarsmen's wrist
Subcutaneous perimyositis
Squeaker's wrist
Adventitial bursitis
Crossover syndrome
Supplemental to Souza
Etiology:
 overuse
 direct trauma to the second extensor compartment
Epidemiology:
 Weightlifters, rowers, & other athletes are particularly prone to this condition
 Wait staff
 Extensors
Clinical Presentation
 dorsoradial wrist or forearm pain
 Pain can spread down to the thumb or up edge of the forearm.
 Active or passive wrist motion produces a characteristic "wet leather"
crepitus w/ROM
 Tenderness, redness & swelling 4-6cm proximal to Lister’s tubercle
 Swelling
Imaging
 X-ray-little value
 MRI - Peritendinous edema, Centered near crossover, May extend to radiocarpal joint
 US - Peritendinous edema, Interrupt hyperechoic plane b/w groups, subcutaneous edema
Treatment
 Immobilization
 Cock-up splint (20deg wrist ext)
 Thumb spica splint (APL and EPB involvement)
 Activity modification - avoid repetitive flex & extend
 Activity modification –
 CMT/STM
 Modalities
 Stretching
 Strengthening
 NSAIDs, Steroid injection
 If conservative fails, surgical consult
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Dorsal impaction syndrome
aka scaphoid impaction syndrome M24.839
Etiology:
 occurs usually as result of repetitive hyperextension stresses
o floor exercises of gymnasts
o when weight lifters rest the weight bar on their palms
o excessive push-ups
o manipulation
 occasionally single forceful injury will suffice
Epidemiology
 More than 50% of young beginning to midlevel gymnasts has it. Furthermore, the pain is
persistent with 89% of competitive gymnasts.
 Second most common group is Chiropractors
Clinical Presentation
 Pain @ dorsoradial aspect of wrist usually aggravated by extension & loading of the wrist
 Possible weakness
 point tenderness over dorsal scaphoid rim is elicited w/ wrist in modest flexion & ulnar deviation
Diagnostic Studies:
 x-rays - occasionally show small ossicle contiguous w/ scaphoid rim on lateral views in slight
flexion
Treatment:
 modification of training programs;
 wrist strengthening exercises;
 the use of wrist guards or a brace to prevent excessive dorsiflexion;
 for more severe pain, complete rest & immobilization
PIP, DIP, MCP & Thumb injuries (see Souza)
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Kienbocks Disease
 AVN of lunate
 Stress or compression FX
 Repetitive minor trauma
 Xray, MRI, CT for dx
 Cast immobilization
 Allow for revascularization
 Decompression surgery if casting fails
 Before lunate collapse
 Lunate replacement
Mallet Finger
 Ext digitorum tendon avulsion; Rupture of the Extensor Tendon
 MOI: Ball to end of extended finger
 Forced flexion causes finger to drop into flexion
 AKA
 Baseball finger
 Drop finger
 No active extension
 Splinting DIP 6 weeks
 DO NOT include PIP
 DIP must remain in ext
Jersey Finger aka Football Finger
 Forceful extension while grabbing moving object
 Opponent’s jersey
 Rupture of FDP (flexor digitorum profundus) tendon
 No active flexion at DIP = Immediate surgical referral
 Better prognosis first 4 days
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Boutonniere Deformity
AKA Central Slip Tear
 Pain @ PIP after forced flexion
 Tear of central slip of extensor digitorum tendon
 Lateral band drops
 No active extension
 DIP stays extended
 Immediate immobilization of PIP in extension- 6 weeks
 Discontinued after 45 deg of flexion and full ext are achieved
Gamekeeper’s Thumb
 Pain @ base of thumb
 Forceful abd or hyperext
 Tearing of UCL @ MCP
 Fall
 Ski pole
 Tender & swollen
 Complete tear if pinch grip strength is lost
 First & Second Degree
 Immobilize with tape; possible thumb spica
 Third Degree = Surgery; possible avulsion
 Ulnar collateral ligament injury at MCP and resulting in instability that was accompanied by pain and
weakness of the pinch grasp
 X-ray to rule out Avulsion Fx.
 abduction
>35 degrees
 Ortho test?
Thumb Ulnar Collateral ligament laxity test
Bowler’s Thumb Compressed ulnar digital N (br. median) may cause perineural fibrosis w/nodule
 Pain/numbness/tingling at the end of the thumb, prox phalanx &
webspace; palmar surface
 Bowler- irritation of ulnar digital nerve, Leads to perineural
fibrosis
 Thumb hole or tools
 Passive extension may hurt
 Tx: Give ergonomic advice- enlarge thumb hole; rest, thumb
guard, change grip
 Tapping causes symptoms distal Tenderness @ MCP
 Activity modification
Bennet Fx
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Severe pain due to axial blow to thumb
Base of first MCP
Deformity and rapid swelling
Bone fragment with shaft dislocation
 Held out by APL
Refer for open reduction and pinning
Bennett’s – First metacarpal base
Boxer Fx
 Pain and swelling over area
 Direct, axial blow to unprotected hand
 Hitting a wall or a face
 Rotational deformity evidenced by nail position
 Refer for reduction and possible fixation
 Boxer’s/Bar room – fifth metacarpal
TEST 3 start w/thoracic
Thorax
Objectives
 Describe the etiology, pathogenesis, risk factors, clinical presentation & treatment for the
conditions discussed in Orthopedics I.
 Differentiate between visceral causes of chest wall pain & musculoskeletal causes
 Describe the etiologies & pathogenesis for the conditions
 Describe the clinical presentations for each condition
 Identify risk factors for the conditions
 Identify the most appropriate diagnostic measures for each condition & the expected findings
 Determine the most appropriate treatment measures.
Long Thoracic Neuropathy/Palsy
(G54.0 – brachial plexus)
Long thoracic nerve (LNT) C5-C7 nerve roots & innervates serratus anterior. Vulnerable b/c long & thin
Etiology:
 Neuralgic amyotrophy – brachial plexus inflammatory disorder
o onset severe pain
o followed by patchy weakness in distribution of involved trunk or cord of plexus;
o in this case scapular winging muscle atrophy b/c nerve isn’t working
 Trauma* Worst prognosis & may not heal
o direct blow to shoulder or lateral chest wall or from
o invasive procedures (mastectomy w/axillary node dissection, chest tube placement, first rib
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
resection, etc) or
o post-op from traction of upper arm while under anesthesia
Compression – carrying heavy objects (backpacks) across shoulders ok prognosis
Stretch or traction - repetitive activities (sports, overhead work, etc)
Possible sites: Nerve length & small diameter = susceptibile to injury. TOS like symptoms
 Supraclavicular region in the middle scalene interface
 Between the clavicle & second rib.
Clinical Manifestations
 Winging scapula weak serratus anterior
 Burning pain around scapula
 Weakness
o Provoked by overhead activities (feeling of instability) –
o Difficulty in pushing arm forward (throwing a punch) or overhead activities
 Altered arm ROM & scapulohumeral rhythm
 TEST: + Wall push-up… Weakness of serratus anterior
Diagnostic studies:
 EMG - differentiates a long thoracic neuropathy from a tear of the serratus.
 Whether or not nerve is firing/working
Treatment:
 Heat modality
 Galvanic stimulation
 Activity modification – avoid precipitating motions/activities
 Taping
 Exercise = strengthening exercises for the rhomboids, pectoralis, & trapezius muscles.
o Tape scapulae while performing exercises & scapular setting exercises
http://www.mtbj.net/pdf/Shoulder.pdf

Surgery – Repair nerve direct or grafts. One of the widely employed surgical procedures is
scapulothoracic fusion (fuse scap to underlying ribs). This procedure is generally not warranted
because the nerve only innervates one muscle.
Prognosis:
 If neuralgic amyotrophy - slowly resolve over 1-3 yrs.
 If it is due to carrying heavy load or repetitive activity - resolves 6-24 mos.
 If it is due to trauma - recovery is incomplete or doesn’t occur
Scheuermann’s Disease aka: Adolescent kyphosis
(M42.04 thoracic osteochondrosis; M42.05 T/L osteochondrosis)
Definition:
 A structural deformity
 anterior wedging of >5 degrees @ least 3 adjacent vertebral bodies/segments
 Usually taller adolescent
Etiology:
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Unknown – most think damage to growth plate leading to abnormal growth
 possible genetic component (higher incidence in monozygotic twins)
 possible transient osteoporosis associated with prolonged bedrest compression fx
 possible association between repetitive heavy lifting in a taller individual with a shortened sternum
Epidemiology:
 Prevalence: 4-8% of population in US
 M >F (Taller boys > shorter boys)… More common in dancers & gymnasts
 Radiographic changes are first noticed between 10-11, so subclinical onset of disease is earlier; typical
age of onset is 13-17 yrs)
 Site: mid-lower T/S, sometimes in L/S
Types
 Typical = Apex: typically between T7-9
 Atypical = acute angle in 1-2 bodies between T10- L4
Clinical Manifestations
 Poor posture with increased kyphosis (usually noticed by parents) – progression is slow
 Possible fatigue & mild to moderate midback pain (dull & achy) might be initial manifestation in an
adolescent
 Pain/fatigue tend to decrease once skeletal maturity is reached although as the patient ages greater
likelihood of pain/fatigue returning due to posture & associated degenerative changes
 Rigid kyphosis (>40 degrees) which helps to differentiate it from a postural kyphosis
 Possible tenderness above & below apex & paraspinal taut bands
 Curve/symptoms worsens with flexion & partially corrects with extension
 Possible compensatory increase in lumbar lordosis & tightening the hamstrings usually hyperlordotic
 Possible scoliosis *common concomitant sx
 May cause pulmonary compromise if angle reaches or exceeds 100 degrees (unable to expand lungs)
& eventually cardiac compromise breathing problems
 Extension feels better
 Flexion feels worse… will be visibly obvious
 In rare instance the pt may have symptoms/signs of myelopathy
o
{Jagtap SA, Manuel D, Kesavdas C, Nair MD (2012) . Scheuermann disease presenting as compressive myelopathy. Neurology.;78(16)}
Possible Presentations:
1. Gradual posture changes w/mit to lowere T/S pain
2. ___ppt
3. ___ ppt
Diagnostic Studies x-ray should be enough, but Bradford criteria definitive
Plain film: Radiographic criteria of Bradford
1) Irregular vertebral end-plates
2) Narrowing of the intervertebral disk space
3) 3+ adjacent vertebrae wedged >5 degrees
4) Abnormal kyphosis beyond 40 degrees
Possible spondylosis as the patient’s age increases
Management:
 Rest
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Modify activities
o especially those requiring excessive flexion – avoid being on phone/slouching
o Cessation of gymnastics in atypical type (if applicable)
Bracing (Milwaukee) typically reserved for adolescents.
o Especially while still growing
o Bracing = curves less than 75 degrees.
o If consistently worn there is a chance for correction of the deformity within 2 years.
o Brace is worn 16 hrs or around the clock for 1 year & than @ night for 2 years.
 Milwaulkee brace
 Dupont brace
Exercises –
o use of exercises, specifically extension or postural exercises (for flexibility),
 Not proven to improve or halt progression.
 Exercises is kyphosis less than 60 degrees.
o Postural exercises
o Hamstring stretching
o Taping for proprioceptive awareness
o Stretching anterior muscles
o Spinal extension exercises
CMT – contraindicated w/active disease
Analgesics – may be helpful in diminishing the pain that may be associated with this condition.
Surgery – typical form > 80 degree curve &/or smaller curve with complications, with atypical >70
degree
Thoracic Disc Disease
(M51.24 w/o myelopathy; M51.04 w/myelopathy, M51.14 w/radiculopathy; M51.9 unspecified)
Etiology
 Trauma is a factor in 25% of the cases. (Ridenour, et al).
 Biomechanical studies have shown that thoracic disc are at risk for injury with combined:
 Torsional & bending loads
 Due angulation of the facets forward bending is limited = why incidence is low
 Degenerative changes
 Rare – less than 1% in thoracic spine, and usually due to trauma or degeneration
Epidemiology
 0.25% to 1% of all disc herniation <1% of disc herniations
 3rd-5th decade
 Majority are central or centrolateral, minority is lateral
 Below T7
 T11-T12 is most common level T/L Junction
 followed by T10-T11. Predilection lower thoracic maybe due to greater mobility & subjected to
greater torsional movements.
Clinical Presentation
The presentation is variable. Mean duration of symptoms is 23 months (Ridenour, et al)
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3 presentations
1. Radicular pain – most likely into abdomen
2. Myelopathy – 2nd most common presentation (may not have pain)
 Bladder dysfunction – urgency
 Sensory impairment – paresthesia, dysesthesia, sensory loss
 Motor deficits – most likely to be paraparesis than monoparesis
 “long tract signs: Babinski, gait, etc.
3. Thoracolumbar pain, Localized – most common presenting symptom***
Exam findings
 Possible antalgia, gait/station changes
 Tenderness
 ROM is provoking & probably limited
 Sensory changes? YES
 Motor weakness? YES
 Long track signs? YES
Diagnostic studies
 Plain film = Degenerative changes (majority of discs are calcified at time of presentation)
 MR/CT = herniation
 Electrodiagnostic studies for nerves
Natural History / Time:
 7-12 weeks conservative care= usually sufficient improvement in symptoms & function seen.
 Surgery: only about 0.2% to 1.8% of the patients go to surgery.
Management:
Medical: Epidural or Surgical decompression and/or discectomy especially in patients who are showing
signs of myelopathy or unremitting pain.
Conservative:
 Rest/activity modification
 Mobilization/CMT to patient tolerance
o instrument assisted, drop piece, flexion-decompression/distraction
 Walking
 Analgesics/anti-inflammatories (medication or homeopathic/supplements/diet)
 Modalities
 Possible bracing
 McKenzie protocol
 Extension & Postural exercises
Surgery: more likely if presenting w/myelopathy and/or unrelenting pain
Case study
DDX
 Sprain, strain,
 Intercostal neuroitis
 Rib fracture
 Osteochondritis – usually one level
 Tie Tze – like osteochondritis, but w/inflammation, swelling & multiple levels
IMAGING
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Shepelmans: strain sprain vs. intercostal neurits
EXAM:
 R 16, shallow, BP 136/78, P80, T 98.0
 Mild distress w/breating
 Many more and didn’t get to see
Most probable diagnosis: COSTOCHONDRITIS
T4 Syndrome aka: Upper Thoracic Syndrome
(M99.02 – segmental dysfunction)
Etiology:
Hypothesized that sustained or extreme postures can lead to relative ischemia within multiple tissues
contributing to symptoms of sympathetic origin
(Evans P. The T4: syndrome some basic science aspects. Physiotherapy 1997;83(4):186-189).
Epidemiology:
 30-50 yrs
people in their 30’s
 F >M
 May originate from T2-T7
 Usually person in prolonged postures, leads to ischemia then sympathetic responses
 Upper cross is posture (vs. clinical presentation is sx)
Clinical Presentation
 Unilateral or Bilateral
 Upper extremity paraesthesia & pain with or without neck and/or head pain
 Paraesthesias in all five digits, or whole hand, or forearm-hand (glove-like distribution)
 Hands feel hot or cold
 Heaviness in upper extremities
 Hands feel & may objectively be swollen
 Non-dermatomal aches/pains in arm and/or forearm
o Hand, arm, head
 Pain often described as crushing or like a tight band Pressure
Less common symptoms
 Pain and/or stiffness radiating around chest wall
 Interscapular pain and/or stiffness
 Worse pain at night often waking from sleep
 Creepy-crawly feelings or sensations of gushing water in arm
Exam
 Hypomobility in upper thoracic spine, palpation may provoke or decrease Sx
 Palpation of rib angles may elicit distal symptoms ***
 Forward head posture and/or possible flat thoracic spine
 Cervical & trunk AROM may be pain free normal ROM, pain free
 Hands may appear discolored (red or purple) & feel hot or cold to touch YET, neuro is normal
 Negative neurological exam
 Posture changes
 Forward head carriage
 Thoracic fixation tenderness
 Muscle spasm
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Normal ROM
Normal sensory & motor
+ DURAL TESTs
Hypomobility of THORACIC spine
Treatment
 CMT/ SMT – thoracic spine, ribcage & possibly cervical spine
 STM to hypertonic musculature in cervicothoracic region
 Self-mobilization techniques to the upper thoracic spine
 Ergonomic - frequent breaks for stretching, work-station modification
 Tape
 Puppy dog pose
 Strengthening of the scapulothoracic musculature (esp. scap stabilizers)
 Stretching tight pectoral & other upper quarter musculature upper cross
 Exercise
 McKenzie exercises for the cervicothoracic spine
o Example: Chin retractions or Retraction with slight extension & rotation
 Postural correction exercise
o Pt is supine- the back & neck is repetitively pressed towards the floor, held for a few
seconds & the relaxed. Can also be performed standing while leaning against a wall.
 Klapp’s Crawling or Praying Position = pt kneel w/ knees flexed to 90 degrees (thighs vertical), the
thorax is lowered as far as possible (arms outstretched above the head on the floor), held for a
few seconds & then relaxed.
Maigne’s Syndrome
aka: Dorsal Ramus Syndrome, Posterior Ramus Syndrome, Thoracolumbar junction syndrome
(M99.02 – segmental dysfunction) *correlate w/ortho
Definition:
A facet syndrome
 @ thoracolumbar junction,
 Results in inflammation of posterior rami & subsequently cluneal nerves (cutaneous innervation
to buttock/pelvic region)
When you see a patient w/low back pain ALWAYS check to mid back***
Etiology:
 Rotary movements of the trunk
 Prolonged strenuous postures
 Lifting
 Unknown
 Up to 40% of LBP cases
Epidemiology T/L Junction
 May be responsible for up to 40% of low back pain cases
 T11-T12
 T12-L1 levels
 possibly T10-T11
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Image of cluneal NN radiation:
 Testicular shooting pain, unilateral *if recreate in certain motions, likely an oblique m strain
 SI joint
 Great trochanter
 IF PAIN IN ALL 3 areas, the very likely Maigne’s syndrome
Clinical Presentation
 Pain in 1+ of the following areas (pain in all 3 is virtually diagnostic):
o SI/buttock/Iliac crest,
o groin
o anterolateral thigh pain
 Typically unilateral
 Provocation w/palpation at T/L junction motion units
 Iliac crest point sign –
o Pain, deep tenderness @ location
o @ level of iliac crest at a point which is consistently
o located 7 cm from the midline
 T/L ROM provocation (esp w/rotation & contralateral side bending)
 Skin rolling (Pinch-roll test)– hypersensitivity/hyperalgesia on involved side
 +/- Trophic changes of skin in prolonged condition
o Cellulalgia consisting of thickening or nodularity
o Skin & hair loss
o Swollen puffy appearance where cutaneous nerve ends
Treatment:
 SMT &/or mobilization is the main treatment
 Pelvic stabilization exercises (i.e., learning to perform activities in pelvic neutral)
 Cat–camel exercises increase motion
 Strengthening quadratus lumborum (Side bridge)
 Psoas muscle stretches Pulls lumbar spine anteriorly
 Curl-ups & Plank to strengthen abdominal musculature
 Facet injections may be warranted if patient doesn’t respond to conservative care
 Vitamins B, C, D, E
Musculoskeletal Causes of Chest Wall Pain
differentiate:
Mechanical (NMSK) – if can reproduce it w/movement:
Pain w/coughing, sneezing, trauma, Rib fracture, PN @costosternal junction:
Tietze (swelling & multi-level or constochondritis (no swelling, @ 1 level) Visceral
Sternal Fractures
(S22.20XA {closed fx}, S22.20XB {open fx})
Etiology: Someone or something hit them
 High impact injury (i.e. sternum hitting steering wheel) however this is not a very common injury
Clinical Manifestations:
 Pain over the sternum exacerbated by inspiration
 Possible visual sternal defect
 Exquisite point tenderness
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Diagnosis: X-rays of the sternum will reveal fracture.
Complication:
 As a consequence to that type of injury (force to the sternum)
 patient may also experience a myocardial contusion
o pericardial sac fills up with fluid not allowing the heart to beat
Management: REFER OUT
 Rest. Observe & monitor the patient for cardiac a/dysrhythmias.
 Chiro should probably refer the patient
Herpes Zoster (Shingles)
(B02.9 zoster without complications)
Etiology:
 Patient has a localized reactivation of Varicella-Zoster virus (virus that causes chickenpox)
 Infection in the ganglia & nerve trunk
Epidemiology:
 32% US experience Zoster during lifetime
 1 million cases annually
 Incidence rates increase with age
Risk Factors:
Those who have impaired cellular immunity:
a. Pregnancy
b. Malignancies
c. Organ transplant patient
d. Chemotherapy patients
e. Patients with HIV
f. Patients on steroids
g. Pts with autoimmune diseases
Clinical Characteristics:
 Preherpetic neuralgia
 Radicular pain, pruritis, paresthesias appear 1 week before appearance of 1st skin lesions
 Can last 100+ days (described by Cluff & Rowbotham, 1998)
 Vesicular or bullous eruption Worse skin eruption = the worse pain & longer duration
 Limited to a dermatomal distribution.
 Prior to eruption may have a pre-eruptive tenderness or hyperesthesia throughout the involved
dermatome.
 Differentiating this condition may be difficult, especially if the rash is not present. The pain may
simulate pleurisy, myocardial infarction, disc disease, abdominal disease.
 Prodrome: Some patients experience symptoms: fever, malaise, headache.
 Localized lymphadenopathy
Course: typically lasts 3-6 weeks
 In elderly or debilitated it may last longer.
 Subsequent outbreaks are common *commonly recur
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Diagnosis:
 Definitive Dx is made via isolation of the Varcella-Zoster Virus (VZV) in blood or CSF
 Clinical diagnosis is via history & presence of rash
Treatment:
 Manipulation/adjusting
 Mostly nutritional:
 Lysine supplementation
 Vitamins to help immune system
 Analgesics – may help for patients whose pain severity is mild to moderate
 Suppression of inflammation & infection (Burow’s solution or Betadine)
 Acyclovir, famcyclovir or valacyclovir = anti-viral agents
 Dosage = 800 mg, 5 times/day for 7-10 days
 Shown to decrease duration of rash & severity of pain
 Must be given within 72 hours of onset of the rash to be effective
 Corticosteroids – in conjunction with anti-virals may help pain
 Calamine lotions – control pain & reduce pruritus
 Capsaicin cream – pain control once rash has crusted over
 Prevention of post-herpetic neuralgia = use of steroids (questionable efficacy), Capsaicin cream,
tricyclic antidepressants & anti-convulsants (gabapentin)
 Don’t scratch & wash hands frequently – the patient is contagious (spread chicken pox not shingles)
Prevention
 Zoster vaccine should be considered for all immune compromised individuals (it is a live attenuated
virus so in some patients it may actually be considered contraindicated ) & individuals who are 60+ yrs
of age.
Snapping Scapula Syndrome aka Scapulothoracic Syndrome
(M75.80 – other shoulder lesion, unspecified)
Definition: Snapping scapula syndrome = rare cause of shoulder/posterior chest wall pain. Scap hits ribs
Pathology:
 Convex chest wall normally is congruent & allows smooth gliding motion to the concave, deep surface
of the scapula & interposed serratus anterior & subscapularis muscles.
 Inferior, medial, & superior borders are not well cushioned & may rub against the chest wall causing
grating or snapping noises. Causes can be divided into bony & soft tissue problems.
Bony
Soft tissue
Abnormal curvature
Subscapular bursitis
Omovertebral bone (bone from shoulder to vertebra)
Interstitial myofibrosis
Tubercle of luschka
Atrophy of subscapularis
Osteosarcoma
Chondrosarcoma
Clinical Presentations
 Grating, grinding, popping, snapping sensation as the scapula glides over the ribs
 Pain is possible over the area & in shoulder especially with overhead activities
 Possible scapular malposition
 Possible atrophy of subscapularis
 Tenderness w/a bursitis
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Sound heard/felt during ROM will hear or feel
Altered scapulohumeral rhythm – this may contribute to shoulder dysfunction/pain
Treatment:
 Exercise to strengthen subscapularis & other muscles as indicated (scapular stabilizers)
 Anti-inflammatory medication &/or diet/supplements/homeopathics if subscapular bursitis is present
(if bursitis especially)
 Possible cortisone injections
 Surgery:
o bony anomalies/tumors or not responding to conservative care –
o remove anomalie/etc
o resection of a small piece of the top medial border of the scapula.
VISCERAL CAUSES OF CHEST WALL SYNDROME
Organs that cause left-sided chest wall pain = Heart, lung, pancreas, kidney, spleen, diaphragm
Organs that cause right-sided chest wall pain = Lung, liver, kidney, diaphragm, gall bladder*
*GB refers to inferior angle of the right scapula
Pneumothorax
(J93.9 – unspecified)
Definition: An accumulation of air or gas in the pleural cavity causing the lung to collapse
Types:
 Traumatic - wound to chest cavity leads to lung collapse (most common is rib fracture)
 Spontaneous - etiology unknown may be secondary to some other systemic condition. A spontaneous
pneumothorax occurs without chest trauma & is usually due to the rupture of a small cyst on the lung
surface. Such cysts may occur without any associated lung disease, or they can develop due to a
variety of underlying lung disorders, emphysema being the most common.
*Either can result in a collapsed lung
Epidemiology:
 Spontaneous pneumothorax occurs in tall, thin males between the ages of 20 & 40.
 Men > Females 6:1
 Usually occurs at rest or sleep.
 There is a higher incidence in smokers.
o Male smokers have 22 times the likelihood of spontaneous pneumothorax compared to nonsmoking males.
 Spontaneous pneumothorax are more likely to occur in the fall or winter months.
o and in tall, thin, smoking males
Clinical Presentations
 Dypsnea (SOB)
 Chest wall/shoulder pain
 Dizziness
 Asymmetrical excursion due to atelactasis
 Tracheal or mediastinal shift away from collapsed lung, due to air filling lungs
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 Decrease in fremitus, hyper-resonance, & diminished or no breath sounds.
Diagnostic studies: Plain films no lung markings (opacity) will be seen in the lung field, it will be black.
Treatment:
 Emergent referral
 If left untreated, HIGH recurrence rates of a spontaneous pneumothorax.
o Same side recurrence rates are as high as:
 30% at six months
 up to 50% @ two years.
 The objective of treatment is to remove the air from the pleural space,
o allow lung to re-expand.
 Small pneumothoraces may resolve on their own.
Gastroesophageal Reflux Disease (GERD)
(K21.0 GERD w/esophagitis, K21.9 GERD w/o esophagitis )
Definition:
Inflammation of esophagus
 Sphincter not working & acid burns esophagus
 usually resulting from reflux of low pH gastric juices
 Contents (acidic) that irritates the wall of the distal esophagus
Epidemiology
 33% to 40% of adults at some point in their lives
 10% of United States population experiences GERD symptoms daily
 50% of pregnant women will experience GERD
Risk Factors
 Obesity & family history may be risk factors for GERD.
 Ingesting large quantities of caffeinated beverages
 Foods
Pathogenesis
 Sphincter tone = transient relaxation of the lower esophageal sphincter (LES) - dietary factors, which
diminish the tone are: fat, whole milk, orange juice, tomatoes, anti-flatulent drugs, chocolate, & high
doses of ethanol. Factors that increase tone: protein, carbohydrates, nonfat milk, & low doses of
ethanol
 Prolonged exposure to
o gastric contents (acidic in nature) –
o Acidic foods are citrus juices, tomatoes, & coffee.
o Agents that diminish acidity: oral antacids, bicarbonate in saliva & anticholinergic agents.
 Large hiatal hernia
 Esophageal motility disorders
 Delayed gastric emptying
Clinical Presentation
 Heartburn lower retrosternal region, spreads up into chest, back, interscapular region, throat, jaw.
 Usually postprandial pain *after a meal
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Provoked w/ingesting cold fluids, or when the patient bends over or when lying down
Regurgitation may or may not occur
Exam is typically negative, possible epigastric tenderness
Symptom scale for diagnosing GERD:
Calculate points: daily (3) at least once weekly (2) at least once monthly (1) never (0)
 heartburn
 regurgitation
points: yes (1) no (0)
 dysphagia
 dysphonia
 asthma
points: permanent (2) occasional (1) never (0)
 chest pain
 nocturnal cough
cut-off of 3 points correlates with GERD
Diagnostic Studies:
Endoscopy – study of choice
 EGD - Esophagogastroduodenoscopy
 Manometry – measure strength of motility in the gut
Management - Includes life style modifications
 Stop smoking
 Lose excess weight
 Eat small meals
 Reduce caffeine, chocolate, fatty foods, alcohol, onions, peppermint & spearmint
 Elevate head of bed 6”- 9”
 Avoid tight fitting garments
 Do not eat 2-3 hrs prior to going to bed
 Antacids, H2 receptor antagonists (for example: Tagamet), PPI
 CMT
 Anti-reflux surgery (hernia reduction, etc)
HIATAL HERNIA (K44.9)
Definition:
Herniation of a portion of stomach into the thoracic cavity through diaphragmatic esophageal hiatus
Pathology
Thought from imbalance between normal pulling forces of the esophagus through the diaphragmatic
hiatus during swallowing & supporting structures maintaining normal esophagogastric junction position
w/repetitive stretching that results in rupture or stretching of the phrenoesophageal membrane
Epidemiology
 Most commonly (50%) found in 50+ years
 Women > Men 4:1
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Types:
 Sliding (90% of cases) – widening of the esophageal hiatus MOST COMMON
 Paraesophageal – tearing of phrenoesophageal membrane
Clinical Manifestations
 Asymptomatic
 Reflux
 Respiratory symptoms
 Heartburn
 Coughing/hiccups increase abdominal pressure, so increase risk of GERD
 Abdominal exam is negative
Diagnostic studies
 Plain film
 Endoscopy
Management:
 No treatment may be required
 Manual reduction of the hernia
 SMT
 dietary changes
 antacids/H2 blockers/PPIs, possible surgery
 Teach self-massage
Complication:
 Incarceration & strangulation
o If pressure, may choke out a part of stomach
ANGINA
(I20.9 - unspecified)
Mechanism: Ischemia to the cardiac muscle
Clinical Manifestations
 Stable angina – provoked with excitement/exertion, relieved by rest. Usually caused by a fixed
coronary artery obstruction secondary to atherosclerosis.
 Unstable angina (Prinzmetal) – can occur at any time, rest doesn’t change it,
 Usually caused by coronary artery spasms with or without superimposed coronary artery disease.
 Chest pain: short duration from 30 seconds to around 30 minutes
 pain = substernal heaviness, pressure or squeezing sensation sometimes described more as
discomfort that can radiate. Often explained as similar pain as intestinal gas or dysphasia.
 Dyspnea, diaphoresis are possible
 irregular heart beat or bradycardia, hypotension (shock) or hypertension (+/-)
 vitals may be normal
 Heart exam may not be helpful
Management
 If undiagnosed – emergent ER
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
If diagnosed –
o encourage patient to take their medication (nitro) –
 if patient doesn’t respond after the first dose call 911;
 the patient can take 1 table at 5 minute intervals up to 3 tablets
Low Back Pain
Objectives








Describe the etiology, pathogenesis, risk factors, signs/symptoms, diagnostic studies associated with the
conditions discussed in Orthopedics I.
Describe the etiology & pathogenesis of the conditions presented.
Identify the risk factors associated with the conditions
Cite the types of spondylolisthesis
Describe the clinical manifestations of the conditions
Determine the best diagnostic study to order & the expected outcomes.
Describe the guidelines/criteria associated with the conditions
Determine the best course of management.
Lumbar Canal Stenosis
(Central stenosis M48.06, Lateral Canal M99.63)
Definitions:
 Stenosis = narrowing of a tube or canal
o central canal, lateral recess or neural foramen. Central & sometimes lateral canal stenosis
leads to neurogenic claudication. Lateral recess or foraminal zone stenosis leads to
radiculopathy.
 Neurogenic claudication = direct compression of the cord and/or cauda equina which produces vague
symptoms/signs of pain (cramping, aching), radicular pain, paresthesias, heaviness, sensory changes,
paresis, paralysis, &/or etc. direct cord compression
 Arterial claudication = claudication symptoms that are due to inadequate blood supply to an area
Lateral canal stenosis = radicular sx
Central conal stenosis = neurogenic signs
Zones of lateral canal stenosis “compression”
o Lateral Recess - It is a groove that is bordered laterally by the pedicles, posterior by the superior
articular facet & anterior by the posterior lateral surface of the vertebral body & the disc.
 Each exiting nerve root traverses through this part of the canal. This is the most
common site of lateral canal stenosis.
 SUPRA-Articular Facet
o Foraminal Zone - this zone is bordered by the
 lateral margin of the pedicle.
o Extraforaminal Zone - This is entrapment of a root outside IVF.
o It most commonly occurs only at the L5/S1 level.
o Entrapment
o Lumbarization or sacralization
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Epidemiology: AGE
 Neurogenic claudication typical onset >60 yrs “Shopping Cart Sign”
 Incidence & prevalence of symptomatic lumbar spinal stenosis unknown
 Estimated prevalence of radiographic lumbar stenosis in asymptomatic adults > 55 years old
o 21%-30% for moderate stenosis already have
o 6%-7% for severe stenosis
 About 30% of adults may have radiographic spinal stenosis
 L4-L5 most common level
Etiology:
The most common cause of lumbar spinal stenosis is age-related changes of the spine (90-95%). These
changes include thickening of soft tissues & a gradual deterioration of spinal discs & joints that connect
the spine's vertebrae. Any of these conditions can narrow the spinal canal.
 Acquired *compression, direct or indirect -or- ischemia are main causes
o Most common (90-95%) degenerative changes (osteoarthritis/spondylosis) in the facets & discs.
 Hypertrophy/osteophytes of the superior articular facet in an anterior direction may narrow
the lateral canal
 hypertrophy /osteophytes of the inferior articular facet on a medial direction may narrow the
central canal
 hypertrophy of the ligamentum flavum
 or anything compressing into the area
o Disc herniation
o Instability – arthritic changes to the facets & disc may lead to vertebral subluxation
o Skeletal diseases
 Paget's disease, ankylosing spondylitis, rheumatoid arthritis, & diffuse idiopathic skeletal
hyperostosis, may soften the spinal bones or cause too much bone to grow.
 Tumors
o Traumatic or post-operative
 Spinal fracture
 Fibrosis-which is in excess, ropy tissue much like scar tissue-from having spine surgery in
the past.

Congenital/developmental
o Dwarfism (Achondroplasia)
o Spinal dysraphism (spina bifida, etc)
o Shortened pedicles – trefoil canal
o Variations in facet joint orientation/development
Pathogenesis:
Mechanical compression &/or ischemia are the main pathological processes involved with stenosis
 Direct compression
 Indirect compression – increased intrathecal pressure - venous congestion & reduced arterial blood
flow
See claudication slides
Clinical Presentation of Stenosis
 Intermittent to constant symptoms usually developing over several years
 Neurogenic claudication - leg, buttock or back pain precipitated by walking & relieved by sitting
(primarily with central canal stenosis, although maybe lateral)
o Typically bilateral
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o
o
o
o
o


Back, buttock, lower extremity pain (burning, achy), discomfort
Possible incontinence
Intermittent priapism with walking
Achy, cramping, heaviness in the lower extremities
Worse with extension position, exercise (especially in upright postures – eg. Walking,
standing, running) & better with flexion position, sitting, squatting, rest close lateral canal
o Complaints of paresthesia &/or weakness
o Possible saddle paresthesias w/cauda equine syndrome
o Simian posture/antalgia (forward flexed)
o Possible gait changes – widened base width
o + Romberg
o Possible atrophy, tenderness, spasms, hypotonia, step deformity, pulses should be strong &
present
o ROM: provoked by extension & better w/flexion, possible limitation in motion
o Ortho: SLR + in 10% of cases; Stoop, Valsalva – no change or negative
o Neuro: vague sensory/motor/reflex changes w/Central; Saddle anesthesia w/cauda equina,
Note: If the patient's neurological examination is normal have the patient exercise until their
symptoms begin & then immediately perform the neurological examination again.
Pt Hx SEE PPT
o Simian sign
o Shopping cart sign
Radicular pain – primarily with lateral canal stenosis
o Symptoms & signs of radiculopathy
o Lateral – worse with flex/ext and/or rotation
o Usually unilateral presentation
Clinical Prediction Rule based on history & presentation
 Factors identified & points assigned to develop prediction rule
o 1 point for age 60-70 years, 2 points for > 70 years
o 1 point for absence of diabetes
o 3 points for intermittent claudication
o 2 points for exacerbation of symptoms when standing
o 3 points for symptom improvement when standing
o -1 point for symptoms induced when bending forward
o 1 point for symptoms induced when bending backward
o 3 points for good peripheral artery circulation
o 1 point for abnormal Achilles tendon reflex
o -2 points for straight leg raising positive for pain
 prevalence of lumbar spinal stenosis
o 6.3% for score -2 to 5
o 99% for score 12-16
 positive score (≥ 7 points) associated with
o 93% sensitivity
o 72% specificity
o positive likelihood ratio (LR) 3.3
o negative LR 0.1
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Differential diagnosis of claudication by symptoms & signs
Findings
Neurogenic claudication
Type of pain
Location
Radiation
Exacerbation
Improvement
Time to Relief
Walking Uphill
Walking
downhill
Limitation of
Spinal Motion
Neurological
Examination
Dural tension
tests
Pulses
Skin
Bicycle test
(bicycle test of
van Gelderen)
Arterial claudication
Vague cramping, aches, sharp, burning in
legs
Back, butt, legs
Common proximal to distal
Standing (particularly w/trunk extended),
Walking, Bicycling w/trunk extended
Sitting, flexing, squatting (early stages)
Slow
No pain
Pain (lumbar extension)
Tightness, cramping (usually in calf)
Common
Uncommon
occasional findings, usually asymmetric
Rare Findings
Negative, Rarely Positive
Negative
Present or symmetrically diminished
Diminished or absent, often
asymmetric
Hair loss
Positive
Normal
Negative/positive with lumbar extension
Leg muscles
Localized in legs
Walking, Bicycling (lower extremity
activities)
Standing, cessation of mm activity
Quick
Pain
Pain
Types of Lateral Canal Stenosis
 Dynamic Lateral Canal Stenosis (DLCS) - In the presence of degeneration & instability (Kirkaldy-Willis
Phase II), the capsule of the posterior facets is lax & permits an anterosuperior subluxation of the
superior articular facet on the inferior articular facet. Therefore certain movements (flex/ext &
rotation) of the body may result in an intermittent narrowing of the lateral canal & symptoms/signs.
Pt may respond to manipulation immediately but then they need stabilization.
o If instability, facet may move not space
o IF adjusted, may get better really fast
o Next stabilize the joint
 Fixed Lateral Canal Stenosis (FLCS) - Osteophytic & hypertrophic changes of the facets have occurred
in order to stabilize the segment therefore the stenosis is permanent & symptoms/signs are constant.
o Permanent changes
Diagnostic Studies:
 Plain film - decrease disc height, osteophytes, sclerosis, decrease IVF height, hypertrophy facets,
transitional vertebra
o “Eisenstein's Lines” Measurement: Verbiest & Eisenstein have determined that the normal
distance of the central spinal canal is between 15-23 mm. The canal is measured from a
perpendicular line drawn through the posterior border of the vertebral body to the
perpendicular line drawn through the anterior aspect of the superior facet.
 Minimum normal sagittal diameter is approximately 15 mm.
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 Absolute stenosis - the diameter is <10 mm
 Relative stenosis - the diameter is between 10-12 mm
 Measurement between 12-13mm is considered below normal.
 MRI shows the soft parts of the spine better than the bones.
 With spinal stenosis, the position of the spinal nerves & evaluation of the space available for them
is easier to see on an MRI.
 Disc problems show up better on MRIs than on CT scans.
 MRI may also show tumors, infections, & other disorders. (Sensitivity 80-90%; Specificity 95%)
o recess < 3mm = stenosis lateral canal
o recess between 3-5mm highly suggestive of stenosis
o recess > 5mm = normal
 ON Lateral canal (above dx)
 CTScan - Similar to MRI slightly better at seeing bones than soft tissue. (Sensitivity 75-85%; Specificity
80%)
 Myelography - Look for narrowing of the canal, not commonly ordered due to utilization of the
MRI/CT technology & because it is an invasive technique. (Sensitivity 77%; Specificity 72%)
 Electrodiagnostics – overall utility is limited , sometimes done to see if you might have problems other
than or in addition to lumbar spinal stenosis
o NCV/SSEP - Look for signs of diminished nerve conduction
o EMG - Will show diminished muscle activity. (good instrument to determine which root
level is involved.)
Criteria for Referral:
 Unremitting pain/disability
 Progressive neurological deficit (LMNL, UMNL, Cauda equina)
Management:
Following based on the treatment recommendations of the APTA (2012) for spinal stenosis only.
 Flexion exercises:
o Combined with other interventions
 manual therapy, strengthening exercises, nerve mobilization procedures, progressive
walking),
 flexion exercises can be used to reduce pain & disability in older patients (weak
evidence)
 Manual therapy: For back-related lower extremity pain (which can be the case in spinal stenosis)
manipulative procedures reduces pain & disability, while improving spine (and hip) mobility (strong
evidence)
 Found physiotherapy had really limited evidence but suggest minimal benefits for passive
physiotherapy. The effects of active physiotherapy remain unknown (Duong et al. 2010).
 Manipulation/Mobilization: 50% positive response to adjustments (other 50% do surgery)
o Lateral canal stenosis = 50% of the patients respond favorably to chiropractic care, 50% go to
surgery.
o Cassidy & Mior did a study on 70 patients with lateral canal stenosis over a 5-year period & it
showed 50% of the patients had good results with manipulation. Manipulation is effective with
dynamic lateral canal stenosis, but it has minimal benefits with fixed.
The purpose of manipulation is to:
 reduce minor subluxations that occur due to capsular laxity,
 alleviate capsular pain by inhibition to the cells,
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




 Increase circulation & increase stability to the area of involvement.
o Lumbar Spinal Stenosis (Central) = Study by Whitman demonstrated that manipulation
combined with exercise have a promising effect in pts w/mild to moderate central stenosis.
Flexion/Distraction; Pelvic blocking, Instrument assisted
Exercise therapy:
o Core stabilization
o McKenzie
o Williams Flexion
o Flexibility (Stretching hamstrings & extensors)
o Strengthening (abdominals, gluteals),
o Cardiovascular (Prevent deconditioning, help weight loss)
o Ergonomic training
o Aquatic exercises
Modalities:
o Interferential
o Soft tissue techniques
o Lumbar Traction
o Acupuncture
o Lumbar bracing/support/corset (try to avoid their use)
Nutrition
o Promote healing - Vitamins. C, E, B, bioflavinoids, Arnica (homeopathic remedy for pain)
o Anti-inflammatory diet
o Possible weight loss diet (Staying at a healthy body weight, which may relieve symptoms &
slow the progression of the stenosis.)
Medications
o NSAIDs
o Epidural steroid injections - used to reduce inflammation & pain in the legs.
o Opioids - Used to relieve severe back pain.
Surgery
o surgical decompression (removal of hypertrophied ligaments)
o fusion
o Facetectomy
o Laminectomy
o Discectomy
Guidelines for recommending surgery:
1. Persistent leg pain that interferes with quality of life.
2. Failure of non-operative care to relieve symptoms over a period of at least two or three months.
3. Documented spinal stenosis confirmed on either myelogram/CT and/or MRI.
4. The patient's health allows surgery. *must be healthy enough
5. Hard neurological signs (progressive motor deficits, neurogenic bladder/bowel)
Prognosis:
o ~ 20% of patients w/ surgery require repeat surgery within 10 yrs. Nearly 1/3 continue to experience
pain.
o Dynamic lateral canal - if left untreated it will eventually progress to fixed. If treated there may be
some resolution.
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o Degenerative stenosis has a relatively slow benign course in most patients, although it can interfere
w/ADLs. Slow, benigh arthritis
o North American Spine Society (2010) reported that: in patients with mild or moderate degenerative
lumbar stenosis, rapid or catastrophic neurologic decline is rare. The natural history of pts w/clinically
mild to moderate degenerative stenosis can be favorable in 1/3 to ½ of pts.
o Patients with stenosis may require supportive care for an extended period of time if not life long.
Spondylolisthesis
(Congenital spondylolisthesis Q76.2, lumbar spondylolisthesis M43.16, unspecified site M43.10,
Definition:
An anterior displacement of a vertebral body in relation to the segment immediately below
 Upper segment slides anterior
Etiology & Pathogeneses:
o Type 1: Congenital (dysplastic) spondylolisthesis 9-15 yrs
characterized by the presence of dysplastic sacral facet joints allowing anterior translation of one
vertebra relative to another. Strong association with spina bifida
o F>M
o This form accounts for 14%-21% of all spondylolisthesis
o Strong genetic component: 1 in 3 relatives affected
o If slippage occurs it is usually between the ages of 9 & 15 years.
 Doesn’t usually exceed 25% but if it does it may result in cauda equina syndrome
o Most common level – L5/S1
o 25-35% are symptomatic
o Type 2: Isthmic spondylolisthesis (Spondylolysis): “Scotty dog”
A defect of the pars interarticularis
o Grade 1 most commonly seen of this type.
o M>F, although females are 4x more likely to have high-grade slippages
o Further slippage is unusual after skeletal maturation is reached
o Most common form of spondylolisthesis in pts < 50 yrs
o Inuits have highest incidence; W>B
o Most common level – L5/S1
Isthmic Subtypes:
o Subtype A (spondylolysis): fatigue fracture of the pars. It develops as a response to cyclic
flexion & extension and/or rotational loading.
o Subtype B: elongation of the pars but it remains intact (no separation)
o Subtype C (spondylolysis): acute pars fracture. This subtype is uncommon
o Type 3: Degenerative spondylolisthesis, arthritis, Female L4, 40/50’s yrs slippage 25-30%
Associated with intersegmental instability from facet arthrosis
o Most common form in patients >50 yrs.
o Associated with increased BMI, age & angle of lordosis in women
o F>M
o L4/5 most common level
o 4x more common in patients w/sacralization
o Slippage is generally no greater than 25-30%
o The Three F's of Degenerative Spondylolisthesis = Female, Four (L4), Forty (40+)
o Type 4: Traumatic spondylolisthesis, trauma to neural arch (vs. pars which is subtype C)
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Acute trauma to the neural arch with the exception of the Pars; this type is extremely rare in the
lumbar spine
o Type 5: Pathologic spondylolisthesis,
Results from damage to the posterior elements from metastasis or metabolic bone disease.
o Iatrogenic: caused by doctor or medical treatment
Another proposed type – post-surgical
Risk Factors: SPORTS, Lineman, gymnastics
Activities that require repetitive flexion & extension or hyperextension (e.g., gymnasts, football players
{linemen}, weight lifting, dance, diving, figure skating)
o Young 9-15
o Ligamentous laxity
Clinical Presentation
o May be asymptomatic
o Pain, if present (~ 10% of patients with spondylolisthesis),
o usually associated with a particular activity,
o upright posture or hyperextension
o described as a localized deep-seated, dull, achy pain
o patient may have nerve root involvement manifesting with radicular pain; leg pain may be
greater in patients who have a higher degree of slippage.
o Sx often due to secondary Sx such as facet syndrom
 Nachemson, Junghan's & Schmorl - say pain is not related directly to the
spondylolisthesis/ spondylolysis. It has been suggested that the fibrous union involving
the spondylolytic defect may separate with repetitive motion, creating strain. The
defect as well as the supraspinous ligament sprain may create localized pain. It is also
thought that the symptoms may be due to a facet syndrome or sacroiliac joint
syndrome. There is no definite clinical correlation between the degree of anterior
displacement & the severity of symptoms.
o Guarded gait or other gait disturbances (pelvic waddle due to tight hamstrings & lumbosacral
kyphosis)
o Phalen-Dickson sign (i.e., a knee-flexed, hip-flexed gait) may be demonstrated in cases of
spondylolysis especially with spondylolisthesis. “Pimp walk”
o Step defect (deformity) = If the spondylolisthesis is unstable a step defect may be positional induced
o Possible hyperlordosis with lumbosacral kyphosis
o Paraspinal muscle spasms/myofascitis
o Tenderness
o Hamstring tightness/spasm.
o due to a postural reflex to try to stabilize the segment. With slippage the hamstrings readjust
the anterior displace center of gravity by extending the pelvis.
o ROM: possible decrease especially with degenerative;
o extension may provoke the CC, complaint of stiffness
o Ortho tests = +Stork test; possible +instability tests, possible +neurodynamic tests
o Neuro - root signs or cauda equina syndrome w/25% slippage of L5 over the dome of the sacrum;
increase in neurological involvement with degenerative spondylolisthesis
Diagnosis studies:
Plain film x-rays
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o Forward slippage in reference to the one below – lateral view
Meyerding's Classification
o Grade I:
0-25% slippage
o Grade II:
26-50% slippage
o Grade III:
51-75% slippage
o Grade IV:
76-100% slippage
o Grade V:
Complete slippage of vertebral body in relation to the segment below
o Napolean hat sign – P-A view
o Spondylolysis Spondylolisthesis: lucent defect of pars with forward slippage
o Appears as “Scotty Dog” collar: anteroposterior spot film gives better view of L5-S1 disk space.
OBLIQUE view
o Flexion/extension views will help rule out instability. If more than 25% migration or progressive
neurological involvement, refer for surgical consult.
o Compression/distraction views can be used if flexion/extension views do not demonstrate instability.
Natural History:
The following are clinical risk factors for progression of slippage:
o adolescent age
o presence of symptoms
o presence of generalized ligamentous laxity
Progression: only 2%-3% of spondylolisthesis cases show progressive displacement. Progression of
spondylolisthesis is rare for those with less than 30% slippage & rarely occurs after adolescence
Management:
o Rest/activity modification
o Modalities for pain control (heat)
o Topical analgesics (capsaicin cream)
o Manipulation: Manipulate the sacroiliac joints if needed. Specific high-velocity, low-amplitude
manipulations to the dysfunctional joints in side posture are the technique of choice.
o A study by Mierau et al. showed that specific manipulation to the dysfunctional joints above
and/or below the defect can reduce the pain & disability in chronic low back pain patients
with spondylolisthesis. Prone lumbar manipulations man be harmful.
o Exercise therapy:
o Abdominal strengthening exercises
o Lumbar stabilization exercises
o Possible Williams flexion exercises although there is conflicting data (some studies suggest
extension exercises)
o Hamstring stretches
o Weight loss (if applicable)
o Bracing – controversial due to compliance, segmental motion may not be limited in a brace &
deconditioning issues it isn’t warranted or effective, others say it might be beneficial with isthmic
spondylo (Boston brace). Another controversy is in the type: anti-lordotic vs lordotic bracing. Antilordotic puts lumbar spine in a kyphotic position decreasing the stress on the pars; lordotic bracing
loads the posterior elements which promotes healing. Only if acute
o RX: NSAIDs, muscle relaxants, epidural/intrathecal injections
o Surgery indications
o Failure of conservative care
o Progressive neurological deficit
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o
o
o
o
o
Cauda equine syndrome
Radiographic instability with neuro signs/sx
Progression of slippage
Symptomatic grade 2 or higher
Unremitting pain affecting ADLS
Children/Adolescents Treatment:
o If asymptomatic no treatment is required but risks for progression should be explained &
recommend periodic follow-ups
o Skeletally immature patient with slippage greater than 30%-50% is @ increased risk for
progression & should undergo spinal fusion (i.e., conservative treatment has no role in their
management). (Smith & Hu, 1999)
o Vit D & Calcium supplementation have been suggested in children with spondylolysis
o NO walker/saucer until can stand on own
o If have spondy for 10+ years, then may want to limit activites, especially gymnastics
Return to Play Guidelines
Most athletes RTP after an appropriate period of rest (usually 90 days) & the patient is asymptomatic
Step 1 (approximately one month in duration; typically begins during the period of relative rest)
o To participate, the patient must demonstrate that they can perform an abdominal crunch without
pain, & that they can walk without pain or limp. If so, the patient begins performing core
strengthening exercises (eg, planks, bridges) daily. Low intensity aerobic activity is performed for
30 to 45 minutes daily (eg, walking or biking). Running & swimming are not permitted.
o Must be able to walk w/out limp & no pain
o Must be able to crunch w/out pain
Step 2 (approximately one month in duration following completion of step 1; may overlap with final
stages of relative rest period)
o To advance to step 2, the patient must demonstrate that they no longer experience pain with
hopping, normal back motions, & when performing a one leg hyperextension test.
o Continue core strengthening exercises. Add weight lifting with back supported to prevent any
lumbar extension beyond neutral. Include deadlifts with light weight to begin rehabilitation of hip
& back extensors. Continue aerobic activity; okay to perform any such activities that do not cause
pain. Patient can begin performing sport-specific drills that are low risk (eg, ground strokes in
tennis, shooting drills in basketball, forward tumbling in gymnastics).
o Must be able to Hop w/no discomfort
Step 3 (approximately one month in duration following completion of step 2)
o To advance to step 3, the patient must demonstrate pain-free running & jumping, as well as painfree back extension.
o Continue core strengthening exercises. Advance weight exercises as needed for sport. Gradually &
cautiously, increase the weight used for weight-lifting exercises.
o Begin normal sport activities, but avoid any involving full contact. If the patient remains pain-free,
the level of activity is increased weekly & more intense sport-specific drills are performed. At the
end of this stage, full participation, including full contact for contact sports, is permitted to
determine whether the patient can perform without pain. If not, step 3 of the recovery is
extended for two weeks using exercises just short of full participation that do not cause pain, &
then the athlete is reassessed.
o Must be able to run & jump pain free
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Chronic low back pain LBP 3 mos+
(Low back pain M54.5)
Definition:
Low back pain is considered to be chronic if it has been present for longer than three months. Chronic low
back pain may originate from an injury, disease or stresses on different structures of the body.
Leading cause of disability worldwide
Etiology:
Some cases of chronic pain can be traced to a specific injury that has long since healed -- for example, an
injury, a serious infection, or even a surgical incision. Other cases have no apparent cause -- no prior
injury & an absence of underlying tissue damage.)
There are psychological, physiological, & monetary reasons for the development of chronic pain.
(Weintraub, 1996; Markenson, 1996)
Examples are:
o Hysterical conversion reaction = a subconscious, neurotic behavior that alters sensory & voluntary
motor systems producing bodily dysfunction. Symptoms arise because the patient wishes to obtain
some gain. (Financial or interpersonal)
o Neurotic
o Malingering = the false & fraudulent imitation or exaggeration of physical disease or mental
symptoms in order to obtain financial reward.
o Peripheral mechanisms (pathological causes) = include stimulation of nociceptors through injury or
inflammation with liberation of serotonin, histamine, bradykinin, & prostaglandins.
o Facet syndrome, sprain/strain, cancer, infection, abscess, fractures, arthritis, scoliosis, disc
disease, stenosis, SI joint syndrome, Failed back surgery, visceral causes, etc
o Psychophysiology = stress can produce muscle spasm, local vasoconstriction, visceral dysfunction, &
liberation of endogenous pain-producing substances.
o Stress
o Decompensation = due to some sort of injury or illness, the musculature is not used & becomes
unable to meet the functional demands imposed on them. Decompensation is a functional not an
organic term; it cannot be seen in roentgenograms, myelograms, or in results of other laboratory
studies.
o Secondary to something else
Epidemiology:
Prevalence is increasing
o F >M
o 45-65 yrs has highest range
Risk Factors:
o overweight/obesity
o pregnant
o lack of exercise
o stressed or depressed
o Have a job in which require lifting, bending & twisting, or that involves whole body vibration (such
as truck driving or using a sandblaster)
o Smoker
o Poor job satisfaction depressed
o Patients with compensation issues (monetary)
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o Medications = taking prescription analgesics for a long period of time, possible addiction issues
o Poor sleeping habits
Ex of conditions that may result in LBP chronic pain (see photo)
Clinical Presentation:
Low back pain can differ from person to person. The pain may be mild, or it can be so severe that patients
are unable to move.
o Dull aching
o Sharp pain
o Tingling or burning sensation
o Weakness in legs or feet
o Symptoms must last >3 months
o Other symptoms are possible depends on the original cause of the pain
o Possible Minor’s sign & other guarded movements (ex: disrobing)
o Generalized tenderness
o Tightness &/or loss of ROM & flexibility tests (asymmetrical muscle firing with respect to flexion &
extension (Janda)
o Dural tension signs may or may not be positive and/or provoking
o Neurological signs may or may not be present
o Waddell’s non-organic signs (credible tool for screening for psychological distress, however the
presence of these signs does not imply a causal relationship & should be conceptualized as one
component of a biopsychosocial model of chronic pain – meaning there may be psychological
factors related to functional status & response to treatment)
Diagnosis studies:
Used to r/o non-mechanical causes of the LBP
o
Blood tests, especially a complete blood count & erythrocyte sedimentation rate
o
Plain film radiography
o
CT scan of the lower spine
o
MRI scan of the lower spine
o
Myelogram
Management
o Cognitive behavioral therapy CBT to help w/constant pain
o Fear-avoidance therapy
o Cold & heat therapy
o Spinal manipulation – CMT Manipulation is slightly better than pain clinics (Wilkey,2008)
o Acupuncture/acupressure
o Foot orthotics
o Soft tissue techniques - shown to have some benefit in subacute & chronic non specific LBP
o Traction
o Exercise therapy - core stabilization, stretching, strengthening, endurance training, proprioception
retraining & cardiovascular exercises – has a positive effect on chronic LBP & was better than
medical treatment, bed rest & patient instructional information (Aure, 2003; Amato, 2004)
o NSAIDs, topical analgesics
o Dietary intervention – possible weight loss, anti-inflammatory diet, use of glucosamine sulfate
(bony & cartilaginous repair) LOSE WEIGHT almost always helps
o Advise to be active (normal ADLs) – as effective as PT (Frost,2007)
o Medium-firm mattress (Kovacs, 2003)
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o Occupational therapy - Work hardening programs - objective is to increase the injured person’s
functional capacity & productivity through individually prescribed, graded work tasks. Program
length is 4-6 weeks.
o Vocational rehabilitation Work Hardening 8 hr training
o RX: NSAIDs, Anti-convulsants, Opioids, Muscle relaxants, Non-opioid analgesics
o Epidural/intrathecal Injections &/or pain pumps
o Spinal cord stimulator
o Prolotherapy – is effective (Dagenais, 2008)
o Spinal Surgery
Lumbar Instability (M53.2X6)
Definition:
An abnormal response to applied loads & is characterized by movement of spinal segments beyond the
normal constrains”
Types:
"Functional Lumbar Instability (FLI)"
 clinical instability = lack of neuromuscular control of the joint during activities
o Altered motion during sagittal motions
o Loss of NM control during mid-range motion = lack of stability in neutral zone
o Motion may be increased or just aberrant
"Mechanical Lumbar Instability (MLI)" - radiographic instability structural – disruption of the passive
 stabilizers & decreased structural integrity. Several causes are but not limited to: degenerative
disease, trauma, postop, or cancer. This decreased stability can produced pain during normal
activities.
o Radiological signs (e.g., spondylolisthesis, spondylolysis)
o P-A mobility assessment
o TX = Surgery or Rehab
Clinical Presentation
o Lower back pain, which +/- sciatica.
o Painful locking, catching, arc with movements in the spine (e.g. returning from forward bending)
o Sudden pain during normal activities “sudden catching”
o Problems in unsupported sitting & increasing pain in sustained positions
o Pain in the morning &/or with weather changes
o Rest may help, depending on the position
Examination Findings:
o Observation - while entering & moving about the treatment area. Moving into the seated position
may be difficult for them, as well as moving from a seated to standing position (Magee, 2006). An
‘instability jog’ or twitching also may be seen in the muscles during an active movement (Magee,
2006).
o Step defect??
o P-A Glide = This test assesses glide of each segment from posterior to anterior.
o Kappa = .71 for the least mobile segment
o Kappa = .29 for the most mobile segment
o Which means it’s not a reliable method of identifying the most mobile segment but it is for
identifying a segment that is stiff or resistant to motion.
o AROM - to identify which movements are the most painful or difficult (Beazell et al. 2010).
o Aberrant Motion = Although this is a qualitative test there is a moderate rating for interrater agreement. Kappa = .60.
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o The patient is standing & asked to forward flex. Observe if there is an:
•
Instability catch
•
Painful arc of motion on flexion
•
Painful arc of motion on return from flexion
•
Thigh climbing
•
Reversal of lumbopelvic rhythm
o Ortho tests
o SLR = SLR ≥91° passive may indicate lumbar instability.
•
excellent inter-examiner reliability ICC=.94-.96.
•
other reasons besides lumbar instability possible so it must be interpreted
cautiously & correlated with the other tests & history.
o Double SLR Test
o Prone Instability Test = This test has a high Kappa rating = .87.
Case – a secreatery presents w/ intermit LBP, 1st thin in moring, and occasionally locks up. Sometimes
feels unstable…
Diagnosis studies:
MRI look for soft tissue causes, but could still be functional if negativeo The use of MRI in diagnosing lumbar spine dysfunction has increased in the past two decades. The
degree of disc degeneration, using standard MRI, is not thought to correlate with the amount of
angulation (> 15°) or segmental instability (> 3 mm translation) (Beazell et al. 2010).
o An MRI can be used to measure the current status of the intervertebral discs, facet joints, &
ligamentum flavum, which should be taken into consideration when evaluating stability within the
lumbar spine (Kong et al. 2009).
o Functional instability can exist without any radiological evidence (Alqarni et al. 2011).
X-Ray - indirect signs associated with spinal instability: e.g. osteophytes
o Moderate disc degeneration with mild space narrowing, osteosclerosis & osteophytosis of the
vertebral end plates (Kirkaldy-Willis 1985[6])
o Presence of traction spur, which is a particular type of osteophyte that is located 2-3 mm from the
end plate & has a horizontal orientation. (Remy et al 2001[7])
o Intervertebral vacuum phenomenon is due to rupture of the insertion of Sharpey’s fibres & may
be the result of vertebral instability (Alam 2002[8])
Management:
Treatment for lumbar instability may depend on whether the instability is MLI or FLI.
 # 1 = Exercise Strength training of trunk extensor muscles can be considered as part of functional
treatment (Davarian et al. 2012). *note that functional issues can become mechanical
o Patients can use core training exercises to maintain strength in the lumbar area using
techniques such as Pilates or McKenzie. In the case of a MLI, the underlying cause of the
instability must be treated.
o Exercise Therapy - active care, stabilizing the spine through low load exercises & eventually
strength training.
o The body does it on its own stabilization through the degenerative cascade – Kirkaldy-Willis
model.
o Surgery also will stabilize the spine but there are significant risks with surgery.
Prognosis:
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The natural course of FLI is that it may continue to degenerate morphing into MLI eventually. Even with
treatment this may occur.
Ankylosing Spondylitis
aka: Marie-Strumpell disease or Bechterew’s disease (M45.9)
Definition:
Chronic inflammatory condition involving the sacroiliac joints & axial skeleton, which is characterized by
ankylosis & inflammation at the tendon insertions (enthesitis).
Etiology:
Exact cause of AS is unknown,
 genetics play a key role in AS.
o Over 95% w/AS also "genetic marker" - a protein - called HLA-B27.
 This marker is found in over 95% of people in the Caucasian population with AS.
 Scientists suspect that other genes, along with a triggering environmental factor,
such as a bacterial infection, are needed to trigger AS in susceptible people. HLAB27 probably accounts for about 40% of the overall risk, but then there are other
genes working in concert with B27.
Epidemiology:
 Males >F 10:1
 Usually starts from 15 to 35 years old (<45 yrs)
Risk Factors:
 Testing positive for the HLA-B27 marker
 A family history of AS
 Frequent gastrointestinal infections
Clinical Presentation:
Almost all cases of AS are characterized by acute, painful episodes (also known as "flares") followed by
temporary periods of remission where symptoms subside.
o Back pain & stiffness (usually buttock region initially) _3+ months
 Pain worse with rest
 Pain increase with walking
 Fatigue
 Weight loss, anorexia
 Bilateral SI joint tenderness/pain
 Increased thoracic kyphosis, painful gait & posture. Stooped “question mark” posture.
 Limited Lumbar ROM
 Loss of chest expansion measured at the nipple line <2.5cm, reflecting rib cage involvement.
 Occasional, peripheral joint involvement (large joints are more commonly affected)
 Extraskeletal manifestations affecting the cardiovascular system *MC cause of death
o aortic insufficiency
o heart block
o cardiomegaly
o lungs (pulmonary fibrosis)
o eye (uveitis)
 + Schober's test is a useful clinical measure of flexion of the lumbar spine performed during
examination. (Silman 1998)
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


+ Amoss
+ Forester Bowstring
AS may have a relationship to intestinal dysfunction. Screen for increased intestinal permeability
(“leaky gut syndrome”) & intestinal dysbiosis
Clinical Diagnosis = Rome Criteria:
 LBP & stiff >3 months duration that is not relieved by rest
 thoracic region Pain & stiffness
 Limited ROM: lumbar spine in sagittal & frontal planes
 Decreased chest expansion
 History of uveitis
Diagnosis studies:
 X-ray - bilateral sacroiliitis (initial widening due to inflammation
 fusion), verebral bodies may become demineralized & a typical "squaring off" occurs,
Calcification of annulus fibrosus & paravertebral ligaments
 bamboo spine.
 Drawback of X-ray = signs & symptoms established as long as 8–10 years prior to X-ray-evident
changes occurring on a plain film X-ray.
 Elevated ESR & CRP
 Absence of rheumatoid factor
 Presence of HLA/B27 antigen 90% of patients
Management
 Manipulation contraindicated in inflammatory stage.
o May be tolerated after acute phase with no excessive force.
o Gentle manipulation of costovertebral joints may be beneficial to normal respiratory movt.
o Beware of osteopenia, aortic aneurysm, dens erosion
 Postural training - avoid stooping
 Sleeping training - supine on firm mattress, no pillows under head, knees.
 Swimming, stretching, hyperflexion/hyperextension exercises may prevent flexion deformities
 Modalities may benefit pain relief.
 Avoid moderate to high impact exercises like jogging
 Diet: Low-saturated-fat, fresh (whole) food is recommended.
o Limit/eliminate: Coffee, tea, alcohol, fried foods, simple carbohydrates
 Home Care Protocols
o Perform ROM, posture, & breathing exercises.
o Sleep supine on a firm mattress without a pillow.
o Take daily warm baths for stiffness.
o Avoid heavy lifting.
o Practice standing & sitting up straight.
 NSAIDs, Opioid analgesics
 Surgery - option in the form of joint replacements, particularly in knees & hips
Prognosis:
 Mortality is increased in patients with AS & circulatory disease is most frequent cause of death
(Bakland et al. 2011)
Coccydynia (M53.3)
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Definition:
Pain in the coccyx. Despite its small size, the coccyx has several important functions.
 insertion site for multiple muscles, ligaments, & tendons,
 serves as one leg of the tripod-along with the ischial tuberosities-that provides weight-bearing
support to a person in the seated position.
Etiology:
o Often idiopathic
o Fall on coccyx
o Repetitive minor trauma
o Childbirth
o Degenerative joint disease
o Somatization (depression, litigation)
o Bicycling, horseback riding
o Uncommon causes – tumors, AVN, arachnoiditis, cysts
Epidemiology:
o Rare to have cases that present with intractable pain
o Incidence is unknown although thought to be rare (~1% of all back pain cases)
o Females >M 5:1 (trauma of vaginal deliveries; coccyx may also be more posterior in women)
Risk Factor:
o Obesity – changes the way the patient sits
o Frequent &/or prolonged sitting on hard surfaces
o Bicycling, horseback riding
o A study found that the pattern of lesions was different depending on the obesity of the patients:
obese patients were most likely to have posterior luxation of the coccyx, while thin patients were
most likely to have coccygeal spicules. (Maigne, J., Doursounian, L., & Chatellier, G. (2000). Causes
& mechanisms of common coccydynia: role of body mass index & coccygeal trauma. SPINE,
25(23), 3072-3079)
Pathogenesis:
o Fracture/dislocation
o Inflammation
o Spasm of levator ani & coccygeus muscles
Clinical Presentation *in most all people
o Buttock pain*, especially when in the seated position & arising from the seated position
o Dyspareunia*
o Tenesmus* – feeling like the need to defecate
o Pain during bowel movements*
o Pain during sex*
o Headache
o Backache
o Pelvic pain
o Possible swelling, redness, contusion
o tenderness to palpation only, point tenderness at tip of coccyx, sacrococcygeal joint & along
coccygeal ligaments *Sure sign of problem
o decreased range of motion in sacrococcygeal joint, hypermobile distal coccygeal segments
o sharp pain on distraction & compression of coccyx, passive flexion or extension
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o painful excessive mobility if fracture of coccyx
Diagnosis studies:
Plain film: r/o fracture &/or dislocation/displacement
Management
o Manipulation = Internal or external* depending on restriction or displacement.
o patient may gain some relief when the doctor places cephalad pressure to the sacrotuberous ligament
(pain is prone with trunk slightly flexed {on a pillow}).
o point of contact =midway between ischial tuberosity & apex of sacrum.
o Hold contact usually several minutes.
o Padded seat better than donut cushion
o Diet high in fiber
o Stretching – Manual therapy
o Abductor Magnus or/and piriformis. Reduces pressure on the coccyx
o Pelvic floor rehabilitation
o Avoid sitting on hard surfaces
o Sit Leaning forward
o Ultrasound/ Ice/Heat/Sitz bath – may have some benefit
o Acupuncture
o With chronic pain observe for signs of depression
o Analgesics/NSAIDs/TCAs/Anti-epileptics
o May require referral for pain management
o Surgical excision of coccyx (Coccygyectomy)
Prognosis:
 90% of patients conservative care is successful.
Osteitis Pubis (M85.30)
Definition:
Idiopathic, inflammatory disease of pubic symphysis & surrounding tissues
Epidemiology:
 Most common in athletes = 0.5 to 6.2% (soccer, football, ice hockey, rugby players)
 Repetitive shearing of pubic symphysis
Risks:
o Rheumatologic disorders
o Pregnancy/childbirth
o Pelvic trauma (major or repeated minor)
o Pelvic surgery
o Athletic activities (running, football, soccer, ice hockey, tennis)
o Training errors
 Running on hard surface or uneven ground
 Starting intense program after long lay off
 Ill-fitting shoes
o Biomechanical Inefficiencies
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


Poor gait mechanics
Tight muscles in the hips, groin & buttocks
Leg length differences
Pathogenesis:
o Repetitive activities causing shear forces & inflammation.
Clinical Presentation
o Gradual or acute onset of:
o pelvic, lower abdominal, hip, thigh, testicular, or perineum pain
o Pain worse with activity _ better with rest
o Pain may be midline, unilateral or bilateral
o Dull, aching pain;
o may be sharp stabbing pain when running, kicking, changing directions, or even during routine
activities such as standing up or getting out of a car.
o Possible limp or wide-based gait.
o Tenderness @ pubic symphysis & sometimes an audible click or snap
o Hip motions provoke (decreased flexibility {abduction})
o Pain w/resisted adduction esp w/hips flexed to 90 degrees
o Patrick’s test may provoke CC.
o Trendelenberg may appear positive due to the groin pain
Diagnosis studies:
o Plain film: +/- show widening of the pubic symphysis or signs of degeneration. One-legged, standing
“flamingo or stork" view may show pelvic widening under strain.
o Bone scan – an increase uptake
o MRI – edema in joint & subchondral sclerosis. Modality of choice for evaluation, diagnosis, &
treatment planning ((2008). "Athletic pubalgia & the "sports hernia)
o US – r/o hernia & may see widen joint
Management
o REST -Avoid athletic activities until patient has been pain free for a week.
o CMT - pelvic ring
o Heat
o NSAIDs
o Aquatic therapy – emphasizing flexibility & strengthening of the low back, adductors, quadriceps,
hamstrings, & hip extensors. The patient should continue the aquatic rehab for several months. In
patients who have unremitting pain, a steroid injection may be tried or the patient may need surgery.
o Alternative to aquatic therapy - riding a bike, light jogging & exercises to stretch & strengthen the
thigh muscles may be substituted.
o Prolotherapy - For patients that fail conservative care. 1-6 injections. 82% recovered in 3 months
Prognosis:
Complete resolution of symptoms may take 2-3 months or in some patients it doesn’t resolve
Cauda Equina Syndrome (G83.4)
Definition:
A rare but serious condition that describes extreme pressure & swelling of cauda equina
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Etiology:
 Any spinal condition that compress lower back NN,
o Most common =lumbar herniated disc or lumbar spinal stenosis
 Inflammatory spine conditions eg. ankylosing spondylitis
 Spinal canal infections, such as a spinal epidural abscess in the spinal canal
 Spinal tumors that can put pressure on the nerves in the lower spine, such as neoplasms
 Injury penetrates lower back, e.g. gunshot or knife wound
 Lumbar spine Trauma, such as a car accident, fall, or surgery.
Clinical Presentation
Symptoms are variable in intensity & onset, & may include one or more of the following:
 Altered sensation, or severe or progressive weakness or numbness in lower extremities, legs and/or
feet, possibly difficult to walk
 Loss of sensation or a strange sensation in the "saddle" area (the area of the body that would sit on a
saddle: inner thighs/between the legs, buttocks, back of legs, sacral region)
 Urinary or bowel incontinence, including any dysfunction that causes retention of urine, inability to
hold urine in, or loss of rectal control
 Lower back pain, which may be described as an aching pain in a localized area
 Sharp stabbing pain in the leg.
o Saddle & perineum anesthesia
o Sensory changes in the extremities
o Motor weakness, which can progress to paraplegia
o Neuro deficits may become permanent after 48 hours (death of the neuron)
o Note in the initial stages findings may be subtle
Diagnosis studies:
o Plain film radiography may show signs of trauma (fracture/dislocation) or other condition
(stenosis/bone pathology/tumor) that has affected the cauda equina
o MRI/CT may show the compression
Management
Emergency surgical decompression to reduce or eliminate pressure on the nerve. Although there is no
prospective randomized trial to confirm without a doubt, it is generally thought that surgery within 24 to
48 hours gives the maximum potential for improvement of sensory & motor deficits as well as bladder &
bowel functioning, & most surgeons recommend surgery to decompress the nerves as soon as possible,
within about 8 hours of onset of symptom ( Ahn et al 2000). Manipulation is considered an absolute
contraindication in a CES
HIP
Learning Objectives:
1.
Describe the etiologies/mechanism of injury for each condition.
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2.
3.
4.
5.
6.
7.
8.
9.
Explain the pathogenesis for each condition.
Identify & describe the symptoms, clinical signs & examination findings of each condition.
Select the most appropriate historical questions & examination procedures to be performed in regards to the patient’s
complaints.
Identify the diagnostic studies that would aid in the diagnosis of each condition & describe the findings associated with
those conditions.
Select the most appropriate management techniques for each condition.
Identify when a referral may be warranted & to whom that referral should go.
Describe the Council on Chiropractic Guidelines & Practice Parameters (CCGPP) guidelines for treatment of applicable
conditions.
Differentiate between a peripheral neuropathy & a radiculopathy
Note: much of the information on the topics is out of Souza.
HIP Fracture
(Full & Stress Fractures of the Hip) M84.359
Stress fracture, hip, unspecified, M84.459A Pathological fracture, hip
Etiology:
Hip fractures most commonly occur from a fall or from a direct blow to the side of the hip. Some medical
conditions such as osteoporosis, cancer, or stress injuries can weaken the bone & make the hip more
susceptible to breaking. In severe cases, it is possible for the hip to break with the patient merely standing
on the leg & twisting
Stress fractures of the hip once most commonly affected military personnel who marched & ran day after
day. Today, stress fractures of the hip are more common in athletes, especially distance runners.
Pathogenesis:
There are two types of stress fractures.
 Insufficiency fractures are breaks in abnormal bone under normal force.
 Fatigue fractures are usually caused by new, strenuous, very repetitive activities, such as
marching or distance running. Fatigue fractures are breaks in normal bone that has been put
under extreme force. Most stress fractures of the hip are fatigue fractures.
There are three different types of hip fractures. The type of fracture depends on what area of the upper
femur is involved.
 Intracapsular Fracture: These fractures occur at the level of the neck & the head of the femur, &
are generally within the capsule. The capsule is the soft-tissue envelope that contains the
lubricating & nourishing fluid of the hip joint itself. Twice as common as other hip fractures & are
more likely to result in serious complications such as osteonecrosis, nonunion, thromboembolic
disease & osteomyelitis.
 Intertrochanteric Fracture: This fracture occurs between the neck of the femur & a lower bony
prominence called the lesser trochanter. The lesser trochanter is an attachment point for one of
the major muscles of the hip. Intertrochanteric fractures generally cross in the area between the
lesser trochanter & the greater trochanter. The greater trochanter is the bump you can feel under
the skin on the outside of the hip. It acts as another muscle attachment point.
 Subtrochanteric Fracture: This fracture occurs below the lesser trochanter, in a region that is
between the lesser trochanter & an area approximately 2 1/2 inches below.
When a stress fracture occurs in the hip, it usually involves the femoral neck.
 Compression fractures occur on the underside of the femoral neck.
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
Tension fractures occur on the upper side of the bone & can cause more problems than fractures
on the underside of the femoral neck.
 Displaced fractures, the bone cracks all the way through, & the two bones no longer line up
correctly
o A displaced stress fracture is a very serious problem in a young adult because it may lead
to damage to the blood vessels going into the upper end of the hip bone. This can cause a
very serious complication known as avascular necrosis (AVN) of the hip.
Stress fractures can also happen in the shaft of the femur bone, the greater trochanter, & the pelvis bone.
Epidemiology:
 Lifetime risk factor in woman for fracture is ~16%
 F>M 3:1
 90% of hip fractures are over age 60.
Risk Factors:
 Age. The rate of hip fractures increases substantially with age.. Most hip fractures occur in people
older than 60, with the risk increasing most rapidly after age 80.
 F>M. Women lose bone density at a faster rate than men do. The drop in estrogen levels that
occurs with menopause accelerates bone loss, increasing the risk of hip fractures.
 Chronic medical conditions. Osteoporosis is the most powerful risk factor for hip fracture, but
other medical conditions may lead to fragile bones. These include endocrine disorders, such as an
overactive thyroid, & intestinal disorders, which may reduce absorption of vitamin D & calcium.
 Certain medications. Cortisone medications, such as prednisone, can weaken bone if you take
them long term. In some cases, certain drugs or the combination of medications can make patient
dizzy & more prone to falling.
 Nutritional problems. Lack of calcium & vitamin D in your diet when young lowers peak bone
mass & increases risk of fracture later in life. Serious eating disorders, such as anorexia nervosa &
bulimia, can damage skeleton by depriving body of essential nutrients needed for bone building.
 Physical inactivity. Weight-bearing exercises, such as walking, help strengthen bones & muscles,
making falls & fractures less likely.
 Tobacco & alcohol use. Smoking & drinking alcohol can interfere with the normal processes of
bone building & remodeling, resulting in bone loss.
FRAMO Index consists of 4 independent risk factors
Albertsson DM, et al. Validation of a 4-item score predicting hip fracture & mortality risk among elderly
women. Ann Fam Med. 2007 Jan-Feb;5(1):48-56.
 age > 80 years
 weight < 60 kg (132 lbs)
 history of fragility fracture (hip, lower arm, upper arm or vertebra) after age 40 years
 need to use arms to rise from sitting position (asked as "Can you rise 5 times from a chair without
using your arms? (Try if you want)")
2-year cumulative incidence of hip fracture or death
 if 0 risk factors - 2.4% mortality, 0.8% hip fracture
 if 1 risk factor - 3.8% mortality, 0.7% hip fracture
 if 2 risk factors - 15.4% mortality, 5.7% hip fracture
 if 3 risk factors - 33.3% mortality, 4.1% hip fracture
 if 4 risk factors - 51.5% mortality, 9.1% hip fracture
Patient History: Full fractures
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 Inability to move immediately after a fall
 Severe pain in hip or groin
 Inability to put weight on leg on the side of injured hip
 Stiffness, bruising & swelling in & around hip area
 Shorter leg on the side of injured hip
 Turning outward of leg on the side of injured hip
Diagnosis studies:
 X-ray may help rule out other problems, but it probably will not show the stress fracture.
 A bone scan may be suggested to look for early signs of a stress fracture.
 MRI is especially useful in telling fatigue fractures from other types of injuries with similar
symptoms. The MRI is being used increasingly in cases where doctors suspect a stress fracture.
Treatment:
 Fractures: Referral
 Stress Fractures: Non-weight bearing recommended for 4-6 weeks, x-rays taken every two weeks
to confirm healing.
Medical Management: If the tension fracture is in danger of displacing, however, most surgeons will
operate. This is because the complication of AVN can cause the femoral head to actually lose its blood
supply & collapse
Pediatric Conditions – Refer to Souza; see supplemental below
Blaszko Helming, MA. (2015). Update on Selected Pediatric Hip Disorders. JNP; 11(10): 979-986
Legg-Calve-Perthes Disease (AVN) M91.10
Epidemiology
Male >F
Unilateral>bilateral (bilateral in only 20%)
Average age of occurrence btw 4 - 8 yrs
Risk Factors
 Genitourinary anomalies
 Inguinal hernia
 Low birth weight
 Lower socioeconomic status
Pathology
Epiphysis of the femoral head infarcts (medial femoral circumflex artery) AVNrevascularization &
new bone within 18-24 mos; bone is weak during this period & may fxpain
If > 50% of head affected by necrosis the potential for normal regrowth without deformity is lower
Stages:
 Initial – necrosis & inflammation painful limp; lasts months
 Fragmentation – body removes necrotic bone & replaces with softer woven bone (more easily fx);
can last 1-2 yrs
 Reossification – stronger bone forms in head; can last several yrs
 Healed – bone regrowth complete; shape of head is dependent on age of onset & amt of
fragmentation
Clinical Presentation
 Possible precipitation by trauma (jumping)
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 Abducter lurch (limp) – tends to be intermittent after exertion & can cause anterior thigh pain
 Pain may refer to medial knee or prox lateral thigh
 Pain better with rest
 Possible Trendelenburg gait
 Provocation with internal rotation
 Atrophy quads
 Adduction flexion contracture??
Management
 See Souza
 Conservative
o Activity limitation for high impact maneuvers
o NSAIDs
o Possible crutches/walker
o Physical therapy (parents should assist by taking limb to end range)
 Hip adduction exercises (clam shell while lying on back)
 Internal rotation exercises (legs extended out straight; fully internally rotate hip)
Transient Synovitis M67.359
Most common cause of non-traumatic limp in pediatric population
Definition:
Postinfectious reactive arthritis that usually develops 1-2 wks after a respiratory or GI infection (arthritis
may develop in ankles or knees instead of hip)
Epidemiology
3-10 yrs with mean age of 6 yrs
M>F
Clinical Presentation
 Low to no fever
 Limp
 Unilateral hip pain on passive ROM
 Little better in external rotation & abduction; worse with internal rotation
Diagnostic Studies
Differentiate Synovitis from septic arthritis
 WBC – may be normal in Synovitis & elevated in septic arthritis (may also be normal
 ESR – elevated in septic arthritis & in about 50% of Synovitis patients
 CRP – elevated in most septic pts but minimal or no pts with Synovitis
 MRI with contrast may help delineate the two
Management
NSAIDs may be helpful
Developmental Dysplasia of the Hips (DDH) Q65.89
Formally known as congenital dysplasia but it has been determined that the condition may develop after
birth, in infancy & childhood.
Definition:
Range of abnormalities (dysplasia, subluxation, dislocatable & fully dislocated hips) involving improper
alignment or growth of the femoral head & acetabulum.
Epidemiology
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 4x more common in females
 family hx
 If full dislocation more common to be in left hip
 20% of case are bilateral
Clinical Presentation
 Most common sign of DDH in lateral childhood is limited hip abduction.
 Missed DDH (not diagnosed) does not normally cause pain until the 4th or 5th decade of life when
osteoarthritis starts.
 DDH patients may have associated torticollis, metatarsus adductus, clubfoot & dislocated knee
 Asymmetrical gluteal folds???
 +Barlow’s, Ortolani, Galeazzi
 +Trendelenburg
 More sensitive test- hip adduction which is limited to <60 degrees while knees are in 90 of flexion
Four F’s of DDH
 First born
 Female
 Foot first (breech birth)
 Family Hx
Diagnostic Studies
 Ultrasound at approx. 4-6 wks of age
Management
 Pavlik harness for 6-12 wks (infants up to 6 mos of age) – keeps hip in flexion & abduction
Indications:
o Subluxation
o Dislocation
o Shallow acetabulum
 Closed hip reduction in surgery, if harness not successful, followed by spica cast for 3 mos
 Open reduction (femoral osteotomy), if above not successful, followed by full body spica cast for
6-12 wks
Femoroacetabular Impingement FAI
Definition:
a condition where the bones of the hip are abnormally shaped. Because they do not fit together
perfectly, the hip bones rub against each other & cause damage to the joint.
Pathogenesis:
FAI, bone spurs develop around the femoral head and/or along the acetabulum. The bone overgrowth
causes the hip bones to hit against each other, rather than to move smoothly. Over time, this can result in
the tearing of the labrum & breakdown of articular cartilage (osteoarthritis)
Types of FAI:
There are three types of FAI: pincer, cam, & combined impingement..
Etiology:
FAI occurs because the hips do not form normally during the childhood growing years. It is the deformity
of a cam bone spur, pincer bone spur, or both, that leads to joint damage & pain. When the hip are
shaped abnormally, there is little that can be done to prevent FAI.
Because athletically active people may work the hip joint more vigorously, they may begin to experience
pain earlier than those who are less active. However, exercise does not cause FAI.
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Clinical Presentation
 Pain in the groin area, although the pain sometimes may be more toward the outside of the hip.
 Sharp stabbing pain may occur with turning, twisting, & squatting
 Sometimes just a dull ache.
 +Anterior or Posterior Impingement tests
Diagnosis studies:
 X-rays. These provide good images of bone, & will show whether your hip has abnormally shaped
bones of FAI. X-rays can also show signs of arthritis.
 Computed tomography (CT) scans. More detailed than a plain x-ray, CT scans help doctors see the
exact abnormal shape of hip.
 Magnetic resonance imaging (MRI) scans. For soft tissue damage
Management
 Activity changes. Avoiding activities that cause symptoms.
 Non-steroidal anti-inflammatory medications.
 Exercise therapy. Specific exercises can improve the range of motion in hip & strengthen the
muscles that support the joint. This can relieve some stress on the injured labrum or cartilage.
 Surgery
Hip Labral Tears S73.191A (rt hip), S73.192A (lf hip)
Etiology:
 Trauma. Injury to or dislocation of the hip joint — which can occur during car accidents or from
playing contact sports such as football or hockey — can cause a hip labral tear.
 Structural abnormalities. Some people are born with hip problems that can accelerate wear & tear
of the joint & eventually cause a hip labral tear. Example FAI
 Repetitive motions. Sports-related & other physical activities — including the sudden twisting or
pivoting motions common in golf or hockey — can lead to joint wear & tear that ultimately results
in a hip labral tear.
Epidemiology:
Active adults between the ages of 20 -40 are affected most often.
Athletes who participate in such sports as
 ice hockey, soccer, football, golf & ballet are at higher risk of developing a hip labral tear.
Structural abnormalities of the hip also can lead to a hip labral tear. Most studies report
that symptomatic labral tears occur more frequently in women than in men.
Clinical Presentation
 Pain anterior hip (most often in the groin area) accompanied by clicking, locking, or catching of
the hip are the main symptoms reported with hip acetabular labral tears.
 Joint stiffness & a feeling of instability where the hip & leg seem to give away are also common.
 The pain may radiate (travel) to the buttocks, along the side of the hip, or even down to the knee.
 Symptoms get worse with long periods of standing, sitting, or walking.
 Pivoting on the involved leg is avoided for the same reason (causes pain).
 Some patients walk with a limp or have a positive
 +Trendelenburg sign (hip drops down on the right side when standing on the left leg & vice versa).
 The pain can be constant & severe enough to limit all recreational activities & sports participation.
 Burnett & colleagues studied 66 patients found to have labral tears by arthroscopy & reported
92% had predominant localized groin pain, 52% had associated anterior thigh pain, 59% described
lateral hip pain, & 38% reported associated buttock pain, while no patient presented with isolated
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buttock pain. (Hunt D, Clohisy J, Prather H. Acetabular tears of the hip in women. Phys Med
Rehabil Clin N Am. 2007;18(3):497–520.)
 + FADIR Impingement Test
Diagnosis studies:
 X-rays. X-rays are excellent at visualizing bone. However, X-rays don't produce images of soft
tissue, so these images can't be used to diagnose a labral tear, only to rule out fractures or
structural abnormalities.
 Magnetic resonance imaging (MRI). MRI alone is inadequate for visualizing the acetabular labrum.
Standard MRI produces both false-positive results & an underestimation of labral pathology & has
only 30% sensitivity & 36% accuracy
 Magnetic resonance angiogram (MRA). MRA produces better results, as the intraarticular or
systemic infusion of gadolinium is required to obtain the detail necessary to study the labrum.
The sensitivity & accuracy increased to 90% & 91%, respectively.
Management
 Rest
 Anti-inflammatories
 Physical therapy - with the goal of optimizing the alignment of the hip joint & the precision of joint
motion by reducing anteriorly directed forces on the hip & addressing abnormal patterns of
recruitment of muscles that control the hip
 Arthroscopic Surgery – When conservative treatment fails.
Sports Hernia
aka: athletic pubalgia, hockey groin, sportsman’s hernia
Definition:
 Persistent unilateral groin pain, often in an athlete, in which there is no demonstrable hernia;
therefore it is a clinical diagnosis. However, during surgery a small number of occult hernias was
identified. There is a strain or tear of any soft tissue (muscle, tendon, ligament) in the groin.
Etiology:
 Chronic, repetitive trauma/stress to the tissue (high speed twisting, bending, torqueing the groin
Pathology:
 Most probable is tear of the external oblique aponeurosis with subsequent injury to the
ilioinguinal nerve as it passes through area
 May be Osteitis pubis or musculotendinous strain to adductor
Epidemiology:
 M>F
 Sports: hockey, rugby, soccer, football, wrestling
Clinical Presentation:
 Severe pain in groin area
 Better with rest, but once return to sport pain returns
 May be exacerbated by sudden increase in intra-abdominal pressure (coughing, sneezing)
 May be provoked by performing sit-up or crunches
 Palpation of the adductor may produce tenderness
 Forced adduction against resistance (supine, knees bent, heels together) is typically provoking
Diagnostic Studies:
 Ultrasound is best to determine abnormalities in inguinal canal
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 MRI may reveal muscular abnormalities
 Bone scan might be helpful if trying to r/o or r/i Osteitis Pubis
Treatment:
Non-surgical
 Rest – first 7-10 days after initial injury
 Cryotherapy = 3-4x/day for 10min
 Physical Therapy – 2 weeks after injury strength & flexibility exercises
 NSAIDs – Ibuprofen or Naproxen
 Cortisone steroid injections
Conservative care doesn’t usually provide long-term relief in an athlete
Surgery is the most common treatment for Sports hernias
 Laparoscopic mesh repair - > 90% success rate – Return to play within 6-12 wks post-surgically
Lateral Femoral Cutaneous Nerve Compression (L2-L3)
Meralgia paresthetica, unspecified lower limb G57.10 Right lower limb G57.11 Left Lower Limb
G57.12 SENSORY
Definition:
The lateral femoral cutaneous nerve, a pure sensory nerve, is susceptible to compression as it courses
from the lumbosacral plexus, through the abdominal cavity, under the inguinal ligament, & into the
subcutaneous tissue of the thigh. Most often under the inguinal ligament.
Epidemiology:
 More prevalent in diabetics
 Age: 50 +
 Gender: M=F
Etiology/Risk Factors:
 increase intraabdominal pressure (pregnancy)
 obesity
 trauma
 tight clothes
 prolonged hip flexion (i.e. lying in a fetal position),
 diabetes
 masses (eg, neoplasms, contained iliopsoas hemorrhages) in the retroperitoneal space before it
reaches the inguinal ligament & toxins.
Patient Symptoms:
 Dull ache, itching, numbness, tingling, or burning sensation over the lateral & anterolateral thigh.
 Aggravated by standing or hip extension (i.e., walking)
 Relieved by sitting.
 Unilateral
Examination Findings
 Provocation w/deep palpation over inguinal lig & anterolat thigh
 Hypoesthesia/anesthesia – anterolateral thigh
 Negative neuro in leg ***THIGH ONLY
Treatment:
 Benign course, spontaneous remission common
 Eliminate or reduce the cause of the compression (avoid tight garments). Avoid using belts.
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 Cross friction massage followed by ice over the ligament.
 Interferential.
 Stretching the hip flexors
 SMT
Medical Management:
 Steroid injections,
 use of neurogenic pain medications (e.g. gabapentin) and/or
 surgical removal of masses if they are present or sensory release surgery.
FYI – Click on link below for more information regarding sensory release surgery
https://www.youtube.com/watch?v=-PTarMHeZQ0
Femoral Neuropathy (L2-L4) G57.21
Lesion of femoral nerve, right lower limb G57.22 Left Limb
MOTOR & SENSORY
Etiology:
 tumor, psoas abscess, fracture (pelvis/hip),
 aneurysm,
 Trauma,
 Diabetic mononeuropathy,
 iatrogenic following abdominal, pelvic, inguinal or hip surgery
Symptoms:
 Pain: if present, iliac fossa, inguinal region, groin, anterior thigh, or medial calf.
 Paresthesias/dysesthesias
 Weakness
Exam findings
 Gait: stiff-legged (no knee flexion). Patient cannot use the involved leg to step up when climbing
stairs & they must lead with the involved leg when descending stairs. SWINGING GAIT
 Tender inguinal mass may be found on some patients with a retroperitoneal hematoma
(ecchymosis is a sign of a retroperitoneal hematoma) or abcess formation.
 Motor:
o Loss of leg extension
o Partial loss of hip flexion
o Loss of patellar reflex & atrophy
 Sensory: changes may be noted in * Sensory symptoms may be mild or absent
o anteromed thigh or the
o medial calf
o OPPOSITE SIDE MERALGIA PARESTHETICA
Management:
 Brace knee (prevent buckling)
 Avoidance excess hip abduction & external rotation.
 SMT
 Modalities control pain & prevent atrophy
 Cross-friction massage followed by ice massage
 Exercises to prevent atrophy
 Possible steroid injection and/or surgical release
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

Femoral N flossing
Physical Therapy
Common Fibular Neuropathy (L4-L5): G57.30
The common fibular nerve winds around the neck of the fibula;
 Nerve superficial, covered only by skin & subcutaneous tissue & is predisposed to direct
compression.
 Nerve then dives into the fibularis longus muscle, where tethering can occur, making it
susceptible to stretch injury at this level. The nerve then divides into the superficial & deep
branches. *more commonly injured than tibial of Sciatic N
Etiology:
 vulnerable to injury where it winds around the fibular head (varus stress injuries &/or fibular
fractures) this may occur in people who habitually cross their legs.
 Baker’s cyst may entrap the nerve.
 Cast or elastic stockings may compress the nerve. Prolonged immobilization (comatose patients,
sitting on a plane, postsurgical) or the peroneal nerve, if tethered where it dives into the peroneus
longus muscle, also may be damaged by stretch injury.
 Prolonged squatting or a sudden stretch.
 Diabetes.
 Inversion Sprain
Clinical Manifestations:
 Steppage (equine) gait. It is usually an acute onset. It may be complete
 can’t dorsiflex the foot or toes or partial
 DROP FOOT
 Numbness in distribution of nerve.
 Night cramps in the calf in the chronic patient *due to stuck in plantar flexion
 Pain may occur at the site of compression.
 Tinel’s sign may be elicited when percussion of the nerve around the fibular neck.
Management
Usually recovery foot drop is spontaneous (in 2-3 months) but a brace would be beneficial to assist with
ambulation. The recovery may not be complete. Adjust the back, hip, & knee as indicated. Avoid crossing
the legs, squatting for long periods of time. Protective kneepads placed over the fibular head & neck,
especially if the patient underwent a recent weight loss.
Tibial Neuropathy (L4-S2{3}) S84.00XA
MOTOR & SENSORY
Epidemiology:
Rare, nerve is too deep in the thigh. Possible with femoral fracture or w/deep posterior compartment
syndrome in the leg
Clinical Manifestation
 Paralysis/paresis of: plantarflexion, inversion; toe flexion, adduction & abduction
 Motor to hamstrings & foot flexors
 Sensory to medial side of foot
 Hypo/Anesthesia over plantar, lateral foot, heel, posterolateral leg & ankle.
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


Trophic changes & causalgia(Constant burning knee pain)
Absent Achilles reflex
Can’t plantar flex foot…OPPOSITE OF DROPFOOT
Management
Based on etiology.
Follow neuropathy protocols
Surgery is usually required
Obturator Neuropathy (L2-L4) G57.80
Etiology:
Unknown, but it appears to occur
 at level of the obturator foramen & proximal thigh where the fascia entraps the anterior branch as
it passes over the adductor brevis.
May be associated with a chronic adductor tendinopathy/tendonosis
Epidemiology
 Rare
 Male>female
 Associated w/osteoitis pubis
Clinical Manifestations:
 3+ months duration
 Groin pain (deep ache centered on the adductor origin at the pubic bone) that may radiate to medial
thigh/knee
 Insidious onset
 Exacerbated by exercise
 Exercise related weakness (especially when jumping),
 Paresthesias down the medial thigh inner thigh may be present following exercise, & resisted external
rotation may provoke it Weak adductors
 Weak hip adductors & medial thigh atrophy
 Weak esp w/jump
Management:
Electrical stimulation, stretching & MRT of the adductors & flexors have little effect. Surgical release is the
treatment of choice.
 Conservative 1st before consider surgery
 Conservative not often effective
Knee & Leg
Learning Objectives:
1.
Describe the etiologies/mechanism of injury for each condition.
2.
Explain the pathogenesis for each condition.
3.
Describe the epidemiological & risk factors
4.
Identify & describe the symptoms, clinical signs & examination findings of each condition.
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5.
6.
7.
Identify the diagnostic studies that would aid in the diagnosis of each condition & describe the
findings associated with those conditions.
Select the most appropriate management techniques for each condition.
Identify the contents of each compartment in the leg.
Iliotibial Band Friction Syndrome (ITBS) M76.30
Description:
One of MOST common cause of lateral knee pain knee in runners & cyclists;
 pain develops where the ITB runs over the lateral epicondyle, less commonly it can create lateral
thigh pain where band runs over greater trochanter
 Fat pad under IT band gets inflamed & compresses blood supply
Etiology:
 combination of repetitive stress & biomechanical factors
 IT band attaches to Tibia & patella
Risk Factors:
 tightness of ITB
 weakness of hip abductor, esp G. medius *increases valgus forces
 low hamstring strength compared to quadriceps strength on same side
 femoral external rotation
o or internal knee rotation
 angle of knee flexion –
o bike seat too low
 ITB most likely to rub against or compress underlying structures at position of 20-30
degrees
 Foot on pedal should be parallel to ground
 leg length discrepancy (injury to longer leg Right leg on roads, Left leg on track)
o Running on banked road
 abnormal foot & ankle mechanics (rear foot pronation, internal tibial rotation)
 abnormal knee mechanics (valgum, varum
 shoe breakdown, esp on the lateral heel
 training intensity errors – increase mileage or intensity to fast
 Incorrect saddle height (to low) or position (to far back) in bikers
 Running on slanted surfaces
o Run with the traffic tend to have ITB troubles in their right thigh because that leg must
travel a greater distance each time it hits the ground)
o Run track (ITBS in the left thigh because the ITB must control a greater deceleration of
adduction in the left hip.
Epidemiology:
 F>M (slight difference)
 15-50 yrs
 Prevalence varies between 2 & 25% in physically active
Pathology:
o Most commonly thought pathophysiological cause of IT band syndrome is by excessive friction
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o distal iliotibial band as it slides over the lateral femoral epicondyle during repetitive flexion &
extension of the knee resulting in friction & inflammation of the band & underlying soft
tissues.
o Other research suggests that the highly vascular fat pad that is located beneath the IT band at this
location is the source of pain.
o When the knee is flexed (bent) the tibia rotates internally (inward) if there is no compensating
external rotation of the femur (hip bone) the IT band increases compressive forces on the lateral
aspect of the knee.
o The increased compressive forces prevent blood flow from passing through the fat pad. With the
decreased blood flow inflammation occurs within the fat pad causing pain. The pain is usually at its
highest intensity when the knee is flexed at 30 degrees.
Clinical Presentation:
 Lateral knee pain (possible lateral hip pain) initially during activity, then persists after the activity
with progression
 Achy, burning pain that can progress to sharp pain around lateral epicondyle
 Pain may radiate down to the tibia, occasionally radiates up the lateral thigh
 Pain worsens at heel strike or as knee extends during biking
 Pain that is worse when running down hills or stairs, on banked tracks, or next to the curb on the
street
 Possible snapping hip or snapping at knee
 Possible stiff-legged gait
 Tenderness 2-3cm prox to lateral joint line @ IT band
 Possible “wet leather” crepitus (spongy)
 Possible localized swelling
 Possible TrPs in the vastus lateralis, g. medius, biceps
 IT band Groove over lateral thigh “visible tightness”
 AROM – greatest provocation at @ 30 degrees, PROM – not as provoking greatest force on
protuberance of lateral epicondyle
 Strength of the lower extremity should be assessed with particular emphasis on examining the
knee extensors, knee flexors, & hip abductors.
o Weakness in these muscle groups has been associated with the development of iliotibial
band syndrome (Fredrickson et al. Clinical journal of sports medicine oct 2000)
 Assess for underlying risk factors
 (+) Noble’s compression & Renne’s test, (+) Ober’s , Thomas & Mod. Thomas
 DDX: lateral meniscus, LCL
Diagnostic Studies:
Studies are usually not warranted nor are they diagnostic
o Plain film – radiography is typically negative, possibly see a prominent lateral epicondyle
o US – may show thickening of ITB at lat epicondyle or edema at around lat epicondyle although this is
not a specific finding
o MRI – may show thickening
Management *INFLAMMATORY, so treat as such
Like shoulder, when something is wrong in the hip, you have to address it all….
 Areas to treat must include:
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o not only the ITB, but
o TFL, gluteus medius, gluteus minimus, piriformis, vastus lateralis, biceps femoris, soleus &
plantar surface of the foot.
 ICE
 Chopart brace
 Acute Phase – pain relief
o Activity modification/rest
o Cryotherapy (utilize an ice massage not pack to avoid thermal injuries)
o Ultrasound
o Analgesics/NSAIDs
 Intermediate & long term – correct strength & mobility problems
o Heat prior to Stretching (ITB, g. medius, lateral fascia {manual therapies}) & ice after
o Soft tissue techniques (graston, active release, myofascial release)
o Manipulation
o Strengthening hip abductors
o Possible orthotics
o Correct other biomechanical faults (e.g., LLI), changes in training & equipment
 Criteria for resuming athletic activity RTP return to running
o ≥ 2 weeks pain-free
o pain-free ROM hip adduction
o negative Noble Compression Test
Gradual increase in mileage & frequency
 cross train
 proper warm ups
 proper progressions
Medical Management:
 Possible cortisone injections (MAX 3)
 Surgical debridement if patient doesn’t respond to conservative measures (over 9 months of
symptoms & at least 3 months of conservative therapy before surgery is considered for the
condition)
Prognosis: Most can return to activities within 6-8 Weeks of conservative therapy.
Baker's Cyst
Aka Popliteal Synovial Cyst
M71.20
Definition:
 swelling in popliteal fossa due to enlargement of:
o gastrocnemius-semimembranosus bursa, (between these 2 muscles on medial side of
fossa slightly distal to the center crease in the back of the knee)
o Sometimes a connection between the bursa & the joint space especially in older adults so
cyst may contain synovial fluid
o Like ganglion cyst but in the knee
Types
 Primary – distension of bursa
 Secondary – communication between bursa & joint…may appear to spread into calf
Etiology:
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


Mostly in children
o secondary to trauma & irritation of knee.
Older populations:
o secondary to intra-articular mechanical & degenerative problems
o secondary to inflammatory disease
Possibly related to repeated trauma of bursa related to muscle contraction
Risk Factors:
 OA
 RA
 Meniscal injuries
 Fracture
 Patellofemoral chondromalacia
 Gout
 Pseudogout
 Infection (tuberculosis)
 Infectious arthritis
 Synovitis
 Osteochondritis dissecans
Pathogenesis:
 fluid distension of popliteal bursa, commonly involving gastrocnemio-semimembranosus bursa,
which may or may not be in communication with joint space
 effusion causes increased intra-articular pressure which forces joint fluid through weakened
posteromedial joint capsule into potential space of gastrocnemio-semimembranosus bursa
 possible joint capsule herniation into the fossa
Epidemiology
 incidence peaks @ 4-7 yrs & 35-70 yrs,
 primary cysts in children <15 yrs
 Prevalence: 5-40% & it increases with age
Clinical Presentation:
 Most common – asymptomatic
 Symptoms of stiffness, discomfort, posterior knee pain & swelling may have a greater association
with arthritis (RA, OA) or internal derangement than the actual cyst
 Symptoms worse with prolonged standing, hyperflexion, & activities
 Locking of the knee, Stiffness, may have numbness if compressing neurology
 Knee swelling - Palpable non-tender to slightly tender soft mass; If warm & tender think infectious
 ROM =
o Foucher's Sign - Cyst softens with 45 degrees knee flexion;
o if large enough it may restrict motion
 DDX
o Auscultate = If pulsating & bruit heard – think aneurysm
o Should transilluminate
o
Complications:
o Enlargement – simulates DVT
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o into calf (dissecting) = erythema, distal edema, + Homan (similar to DVT)
o into crease (space) compress adjacent vein = distal swelling associated w/obstruction
o Rupture –– simulates thrombosis
o Severe pain simulates thrombosis or mm rupture (erythema, edema, tenderness, warmth,
ecchymosis; Ecchymosis below medial malleolus (Crescent sign), ecchymosis may also go up
into thigh
o Rare – posterior tibial nerve entrapment; anterior compartment syndrome; posterior
compartment syndrome; popliteal artery occlusion
Diagnostic Studies:
 Ultrasound - Easy cost effective, excludes other causes of popliteal fossa pathology
 Arthrography
 MR - identifies coexisting joint pathology (OA, Meniscus)
 Aspiration
Management
 No treatment required if asymptomatic incidental finding
 Avoid strenuous activity *compressive
 Treat underlying joint disease – arthrocentesis & intra-articular injections (steroid)
 Manipulation – optimize biomechanics of the knee CMT ok to optimize knee movement
 Possible use of cane, crutch, walker
 Possible use of elastic wrap
 Analgesics/NSAIDs – tx underlying pain not the actual cyst
 Aspiration followed by steroid injection – if bothersome *1st line of treatment
o If the condition keeps recurring than removal of the cyst is indicated.
 Cysts in kids tend to resolve on own
Osgood-Schlatter's Disease
M92.40
Etiology:
 repetitive strain (Overuse)
 Common
Pathology:
 Traction apophysitis with possible avulsion or micro-avulsion leading to fragmentation
Epidemiology:
o Boys (12-15 yrs)
o Girls (8-12 yrs)
o M>F although incidence is increasing in females
o Occurs in 20% of youths who participate in sports
o Only 5% of youths who don’t participate
Risk Factors
 Involved in:
•
Running sports
•
Jumping sports
•
Dancing
•
Gymnastics
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
Activities that require repetitive eccentric rectus femoris contraction
Clinical Presentation:
 Low-grade anterior knee (apophysis) pain that gradually increases over time.
o May lead to limp & activity impairment.)
 Pain is aggravated by activity especially stair climbing, running, jumping, kneeling, squatting
 Pain improves with rest
 Unilateral or bilateral involvement
 Tenderness, swelling & enlargement @ the apophysis, more proximal tenderness think patellar
tendinosis
 If erythema & warmth present think inflammatory process (rule out: osteomyelitis)
 Possible quad atrophy
 ROM: provoking, especially active & resisted extension
 + Peripheral joint clearance test – knee pain
 Decreased flexibility of hams, gastro/soleus & quads
 DDX: osteomyelitis , Jumper’s knee, patella tendinosis
Diagnostic Studies:
Not typically indicated unless: patient has acute onset, night pain, pain unrelated to activity, atypical
pain.
 Palpation
 Plain film: Enlarged, irregularly shaped and/or fragmented apophysis in the later stages, negative in
the early stages
 US: may demonstrate thickening of the patellar tendon
Management:
Benign & self-limiting condition; symptoms resolve once growth plate ossifies
 Ice - especially after activity
 NSAIDs for 3-4 days only; analgesics
 Protective pad over the apophysis
 Bracing (knee brace or Chopat’s {jumper’s knee} brace)
 Decrease but do not restrict activities
o Running/jumping (it really depends on the patient’s pain tolerance).
o Squatting activities may need to be limited.
o Swimming is usually a good option for this condition.
 Exercise to promote strength
 Promote flexibility of the quads, hamstrings, ITB, gastroc
 Manipulation
 Pain control is main focus
Patellar Dislocation
S83.006A
Etiology:
 Lateral dislocations are the most common with disruption of the medial patellofemoral ligament &
medial retinaculum; may possibly result in osteochondral fractures from lateral femoral condyle or
patella
o Most common MOI = foot is planted with internal rotatory twisting force
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o Knee flexed knee in valgus (eg, spinning or twirling maneuver in dance or gymnastics,
swinging a baseball or softball bat, or quick lateral change of direction while running or
ice skating)
o Less common = direct trauma to medial knee
Risk Factors:
 Sports = soccer, gymnastics, hockey, dance, ball players
 external tibial torsion
 deficient vastus medialis oblique
 tightness of vastus lateralis &/or iliotibial band
 increased Q-angle
 femoral anteversion
 excessive foot pronation
 pes planus
 patella alta
 genu valgum
 below knee amputation
Epidemiology: 13-20 y athletes, females, tall heavy males
 2nd – 3rd decades
 Adolescent F >M
 Taller, overweight males
Clinical Presentation:
 "Giving way", "buckling" sensation followed by extreme anterior knee pain (lateral, medial or
both sides of patella) until the dislocation is reduced
 Patient may report a dislocation & subsequent reduction
 Patient may report a “pop”
 Difficulty in moving knee especially in extension
 If still dislocated knee held @ 20-30 degrees flexion
 Rapid acute swelling, warmth
 Hemarthrosis
 Atrophy &/or weakness of the vastus medialis
 Possible palpable bony or soft tissue defects
 ROM = If dislocated limited motion, esp extension b/c leverage reduced
 + Apprehension test
Diagnostic Studies: always get x-ray because more often associated w/fracture
 Plain film:
o rule/out fracture.
 Osteochondral fracture may not be easily visualized on film, so if the patient
experiences recurrent swelling, locking, or palpable fragments it usually requires
arthroscopic exploration & surgical removal
o Patalla alta/baja/displacement
 CT
 MRI: hemarthrosis, bone edema, osteochondral lesion
Management
 Refer if patella cannot be reduced
o Manually reduce – press on patella & straighten leg
 Immobilize for 2-3 wks, advise to weight bear as soon as pain is tolerable
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o Brace/tape/compression wrap after period of immobility to assist with tracking especially
during exercise
 Modalities for pain (Cryotherapy)
 Prevent of muscle atrophy (electrical stimulation) during the immobilization period.
 Analgesics/NSAIDs
 Isometrics during immobilization period (quad setting)
 Early mobilization of knee & of patellofemoral joint is begun
 ROM/flexibility exercises 5-7 days post injury (lateral retinaculum, ITB, hamstrings, quads, gastroc)
 Progress to more active resistive exercises in the following weeks.
 Closed kinetic chain squats & leg lifts limiting the terminal 20 degrees of flexion were begun 4 weeks
post.
 Possible surgical stabilization
Prognosis:
 full recovery can be expected within 3-6 weeks
Recurrent Patellar Subluxation
M22.00
Definition:
 Recurrent instability of the patella causing anterior knee pain
Etiology:
o most common cause recurrent dislocation is indirect trauma with:
o internal rotation of femur,
o leg in valgus with foot firmly planted
o recurrent episodes caused by pivoting & twisting in patients with prior ligamentous injury
Epidemiology:
 Young – recurrence rate higher if initially subluxated @ < 15 yrs
 Athletes
 Gender: F>M

Pathogenesis
 Patella subluxes out of its normal track laterally
 Tearing of the medial retinaculum & medial patellofemoral ligament, if they heal it is typically
inadequate with increased length allowing for recurrent subluxations
Risk Factors
 Increase sulcus angle *groove where patella tracks
 excessive femoral anteversion
 genu valgum
 external tibial torsion
 pes planus
 hypoplastic lateral trochlear ridge
 patella alta
 weak or hypotrophic vastus medialis obliquus
 hypertrophic vastus lateralis
 ligamentous laxity
 Q angle
o > 15 degrees for men,
o > 20 degrees for women
 Hx of acute dislocation
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Clinical Presentation:
 Recurring episodes of vague anterior knee pain or no pain
o Anterior knee pn = tracking prob, Osgood Schlatter, jumpers knee
 Sense of instability
 Crepitus, popping, catching
 Stiffness
 Signs of bony mal-alignment (miserable mal-alignment syndrome)
 Tenderness on either side of the patella
 ROM may be altered
 Assess for hypermobility syndrome (generalized laxity)
 (+) Fairbank’s, Waldron’s, Anterior apprehension
 Quad tightness,
 weakened VMO (atrophy = perform circumferential mensuration)
Management
 If acute manage like Patellar dislocation otherwise start rehabilitation
 strengthen quads, vmo, abductors
 increase flexibility of adductors
 neoprene brace with lateral buttress may support lateral displacement when initially exercising
 as therapy progresses add sport specific knee loading exercises
 strategies to prevent recurrence of instability
o activity modification
o maintenance of quadriceps strength (wall sits, straight leg raises)
o stretching
 Recurrent subluxators may need surgery (i.e. lateral retinaculum release & medial tibial tubercle
transfer)
Plica Syndrome
M67.50
Definition:
 an intraarticular band of thick, fibrotic tissue (fetal synovial remnant),
 may cause pain & popping sensation by rubbing across:
o medial femoral condyle or
o undersurface of the patella
Types:
 Suprapatellar plica lies between the suprapatellar bursa & the joint.
o Incidence: 87 to 91%.
o Similar symptoms to suprapatellar bursitis or chondromalacia patella (DDX).
o Most commonly symptomatic
 Mediopatellar plica arises from medial wall of joint, passes down & around the medial femoral
epicondyle, & inserts into the synovium surrounding the infrapatellar fat pad.
o Incidence: 55 to 92%.
o This type is most commonly symptomatic
 Infrapatellar plica arises from the intercondylar notch & inserts into the synovium surrounding
infrapatellar fat pad.
o Incidence: 86%
o This type is rarely symptomatic.
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
Lateral plica occurs rarely;
o Incidence less than 1%.
Etiology:
 Repetitive microtrauma causes plica to become fibrotic, thickened, avascular- leads to synovitis
Epidemiology:
 20% incidence of persistent plica in adults
 8-45% of knee pain patients may be due to plica syndrome
Clinical Presentation
 Anterior to anteromedial knee pain
 Worse with
o activity (running, walking, squatting) &
o prolonged sitting (cinema sign)
 May have popping, clicking, catching, pseudo-locking, giving way
 Typically unilateral
 Possible palpation of a fibrotic fold when knee is in flexion (not specific)
 Vague tenderness (esp on medial side)
 Swelling esp in adults (rare in kids) medial to patellar border
 Possible, not probable, reproduction of clicking/crepitus with active & passive motion
 Quad atrophy
 Tight hamstrings, quads, gastroc
 + mediopatellar plica test
 (+) Stutter test – pt seated & asked to extend knee while examiner palpates the patella.
 Positive: irregular patellar motion &/or clicking with pain
Diagnostic Studies:
 Not usually indicated
 Plain film – to rule out other differentials
 Arthroscopy is diagnostic
 US & MR will demonstrate plica but not if pathological *not useful
Management / treatment *RTP at full level = 4-6 weeks
 Activity modification – decrease repetitive flexion/extension activities (decrease mileage in
runners; switch to upright bike, swim, upper body cycle, water running)
o Maintain fitness
 Cryotherapy = TID or QID
 NSAIDs - up to 3 days than switch to another analgesic prn
In recovery phase:
 Increase knee extensor strength & flexibility of the gastroc/soleus, quads, hamstrings, hip
adductors
 Possible orthotic to control pronation & heel valgus
Medical Management:
 cortisone injection into the plica
 Surgical removal of the plica
Prognosis: nonsurgical return to normal activity within four to six weeks.
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Lateral Collateral Ligament Sprain
S83.429A
Etiology:
 Contact or non-contact: varus or twisting injury. *Varus Stress*
 Sudden varus movement while knee is hyperextending
 Note:
o Isolated injuries to the LCL is relatively uncommon,
o usually posterolateral (popliteus-arcuate) complex, PCL or ACL involvement.
o With MOI common fibular nerve and/or the ITB may also be damaged.
Epidemiology:
 Approximately 8% of all knee injuries is the LCL (e.g., 2nd least commonly injured ligament of the
knee) *PCL is least commonly injured
General Risk Factors for knee injuries:
o Female athletes
o Competition vs practice
o Playing in a sport that requires a lot of pivoting, jumping, contact
Clinical Presentation
 Pain over lateral knee, especially with walking/running on uneven surface
o DDX: IT band
 Effusion, limp (foot drop with nerve injury), ecchymosis
o Swelling over the site of the injury.
o Instability — the feeling that your knee is giving way.
o Paresthesias if common fibular nerve injured…foot drop
 Tenderness or ligamentous defect (easier to palpate if knee is in a figure 4 position or pt supine
with knee flexed to 90 & foot on flat on table)
 If knee is dislocated perform ABI; if result is <0.9 get arteriogram & vascular consult
 Patient maintains a flexed knee position during gait
 ROM slightly limited
 (+) Adduction stress (need to check other structures too)
 Possible motor/sensory changes with fibular nerve damage
Classification of LCL injury *KNOW GRADES
o Grade 1 – Mild sprain = result in localized tenderness. Laxity & mechanical symptoms are not present
o Grade 2 – Partial tear = tenderness may be localized or diffuse along the lateral & posterolateral knee.
Some swelling may be present. Mild to moderate laxity can be demonstrated (5 to 10 mm) but has a
solid endpoint.
o Grade 3 – Complete tear = varying degrees of pain; laxity without a solid endpoint & the patient
experiences one or more mechanical symptoms. These injuries are often associated with
posterolateral corner (PLC) pathology.
Diagnostic Studies:
 Plain film =, Ottawa rules stipulate that tenderness of fibular head is grounds for imaging
o Possible “Arcuate” sign = avulsion of fibular head styloid which is pathognomonic for
Posterolateral corner (PCL) injury & possible distal LCL avulsion
o Segond Fx (avulsion fracture of lateral tibial plateau)
 ACL tear may also indicate a LCL tear
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

o Varus stress views
MR - is diagnostic
US – is also diagnostic
Management
 Grade I-II (isolated LCL tears) can be managed non-operatively with:
o a protective hinged knee brace initially locked in extension but the patient should be able to
do full weight bearing
o Cryotherapy
o Perform full ROM in the prone position
o Strengthening the dynamic stabilizers
o Should be able to return to sport-specific therapy in 4-6 wks if strength & ROM is comparable
to uninjured side
 Grade III tears = best managed w/surgery operatively because they usually involve the arcuate
ligament complex & popliteus muscle.
Posterior Cruciate Ligament Sprains S83.529A
Etiology:
High-energy mechanism – MVA (not likely to be isolated injury)
o Posteriorly directed shear force to a flexed knee “dashboard injury”; if varus stress included
there is also a lateral or Posterolateral corner injury
o Knee flexed & hit tibia hard
Low-energy mechanism
o Fall on flexed knee with ankle in plantar flexion
o Direct blow to anterior knee
o Hyperflexion or hyperextension +/- posteriorly directed force
o Valgus or varus force (will not result in an isolated injury)
Epidemiology:
 Isolated PCL injury is rare < 7.5% of trauma related injuries, most likely to also involve the
Posterolateral corner, ACL &/or MCL
 Least common ligament to be injured
 Many who obtained isolated PCL can still function at a high level so do not present to a clinician
 45% of injuries associated with MVA, 40% were athletic injuries
Grades of Injury
o Grade 1 – Anterior border of the medial tibial plateau can be displaced posteriorly but remains
anterior to medial femoral condyle (0-5 mm posterior displacement). Tib still anterior
o Grade 2 – Anterior border of medial tibia plateau can be displaced posteriorly until it is flush with
medial femoral condyle (posterior displacement of 5-10 mm). Tib flush w/condyles
o Grade 3 – The anterior border of medial tibial plateau can be displaced posteriorly beyond anterior
border of the medial femoral condyle (posterior displacement >10 mm). Tib post of condyles
Risk Factors
o football, soccer, skiing, baseball
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Clinical presentation:
 Asymptomatic or minimal symptoms *likely still functional
 Pain & stiffness (not usually due to the ligamentous damage more likely associated with bony
contusion in the area) in the acute injury
 Heard/felt a pop, although this less likely in an isolated PCL tear
 Possible feeling of instability, others are unaware of the sprain (no instability)
 Chronic injury may lead so symptoms associated with osteoarthritis
 Possible increase in symptoms in chronic tears while using stairs, walking on inclines or
decelerating
Nothing overt on exam or:
 Effusion, erythema, ecchymosis?
 possible atrophy, signs of mal-alignment
 Chronic pcl deficient knee may demonstrate tibia vara & genu recurvatum
 “varus thrust” gait
 Tenderness
 ROM full or limited flexion if effusion is present, possibly provoking
 (+) Drawer, (+,-) Hughston’s Drawer, (+) Posterior sag (chronic injury),
 (+) Quadriceps active test – quad contracts & pulls tibia forward
Diagnostic Studies:
 Plain film rule/out avulsion (use Ottawa rules in decision making process) - can provide
information about a PCL injury. They can detect pieces of bone that may have broken loose from
the injury
 MR can find the exact location of a tear.
 US has limited use
 Arthroscopy in some instances
Treatment:
Referral is indicated if:
 Grade 3 tear,
 associated fracture,
 associated soft tissue injuries,
 &/or avulsion of the ligament from the tibia
 PRICE
 Mobilization - passive ROM
 Bracing if instability –
o hinged brace locked in full extension for 2 wks to reduce posterior lag;
o after 2 wks unlock brace to allow progressive ROM exercises (Chronic PCL deficient knee
doesn’t require bracing unless patient is reporting a high degree of instability)
 Weight bearing or non-weight bearing? *avoid OKC hamstring flexion
 Modalities = neuromuscular electrical stimulation to the quads
 Exercise therapy. As the swelling goes down, a careful rehabilitation program is started. Specific
exercises will restore function to knee & strengthen the leg muscles that support it.
o Strengthening the muscles in the quadriceps has been shown to be a key factor in a
successful recovery; start with open chain (quad setting exercises & ankle pumps)
o Avoid open chain hamstring exercises initially (e.g. sliding heel on table &/or resisted knee
flexion to prevent unopposed activation of the hamstrings leading to an increase in sag)
o Aquatherapy
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o Possible taping during the exercises
o Stationary bike
Prognosis:
Rehab for PCL tears takes longer than ACL tears.
 Post-surgical rehab protocols may take between 26-52 wks.
 If left untreated, patients reported occasional episodes of pain & had altered activity levels.
o 90% of patients had progressive degenerative changes.
Compartment Syndromes
T79.A0XA
*4 compartments in leg
Definition:
 A painful condition
 occurs when pressure 1 of 4 leg compartments builds to dangerous levels,
 pressure can decrease blood flow, preventing nourishment & oxygen from reaching nerve & muscle
cells.
 4 compartments = anterior, deep posterior, peroneal, superficial posterior.
Etiology:
 Acute Compartment Syndrome
o Acute compartment syndrome usually develops after a severe injury, such as a car accident or
a broken bone. Rarely, it develops after a relatively minor injury.
o Conditions that may bring on acute compartment syndrome include:
 A fracture.
 A badly bruised muscle.
 Reestablished blood flow after blocked circulation.
 Crush injuries.
 Anabolic steroid use.
 Constricting bandages.
 Chronic (Exertional) Compartment Syndrome RUN, BIKE, SWIM
o The pain & swelling of chronic compartment syndrome is caused by exercise. Athletes who
participate in activities with repetitive motions, such as running, biking, or swimming, are
more likely to develop chronic compartment syndrome. This is usually relieved by
discontinuing the exercise, & is usually not dangerous.
Epidemiology:
o <35 yrs is most common age
o M >F
Compartments of the lower leg:
 45% Anterior Compartment - Consists of the tibialis anterior, extensor hallucis longus, extensor
digitorum longus, fibularis tertius, deep fibular nerve & the anterior tibial artery foot drop, top of foot
numb
 40% Deep Posterior - Consists of: tibialis posterior, flexor hallucis longus, flexor digitorum, tibial nerve,
peroneal artery, & the posterior tibial artery numbness inside of foot & foot drop
 10% Lateral Compartment - Consists of: fibularis longus & brevis & the superficial fibular nerve
 5% Superficial Posterior -Consists of: gastrocnemius, soleus, plantaris, & the sural nerve
Clinical Presentation
Based on the involved compartment(s)
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Example:
o Anterior Compartment Syndrome: Transient or persistent footdrop with possible paresthesia.
Paresthesia is often felt over dorsum of the foot.
o Deep Posterior Compartment: Paresthesias of the instep of the foot
Acute vs Chronic Compartment Syndrome
Acute
Sx’s
onset during or after activity, pain
starts as ache, increases to piercing,
cramp like, or burning pain; pain is
worse than what would be expected
with the injury;
accompanied by hypoesthesia &
paresthesias (depending on
compartment)?
Feeling of tightness or fullness
Signs turgid extremity, erythema, edema,
increase temp in leg, pulse changes,
temp changes in foot?, pain w/passive
stretch, decrease sensation &
paresis/paralysis are signs assoc
w/permanent tissue damage
Dx
Hx, Px & compartment pressure
Chronic Exertional Compartment Syndrome
Asymptomatic at rest, w/activity pain, tightness,
aching, cramping, transient weakness & paresthesia.
Pts can give state precise area of pain & type of
activity that induces pain. Symptoms typically start
each time at either a given distance or intensity of
running/exercise. Relief of symptoms comes when
activity ceases (Wilder, 2004)
dependent upon which compartment is involved:
edema, tenderness, erythema, weakness,
hypoesthesia, ischemia
Mm bulging
S/Sx resolve within 20 min of cessation of activity
S/Sx only w/exercise; compartment pressures are
increased w/exercise
5 P’s of acute: Pallor, paresthesias, paresis, pain, pulselessness
5 Ps of Acute conditions
1. Pallor
2. Pain
3. Paresthesisa
4. Paresis
5. Pulselessness
Management:
Acute compartment syndrome a surgical emergency. Compartment syndrome can develop 2 hours to 7 days after injury. Monitor for
swelling. An ischemic event of 6 hours is sufficient to produce permanent muscle & nerve damage. Be
prepared to refer for fasciotomy.
Chronic compartment syndrome –
o Surgery may be necessary if compartment pressures > 30 to 35 mm Hg.
o If ischemia in soft tissues > 6 hours than permanent damage possible
o Orthotics may be helpful.
o Elevated pressures on a transient basis & influenced by activity, conservative management is felt
to be effective
o Rest is the only conservative measure that brings relief, although when activity is
resumed the pain & compression returns.
o Manipulation (joint & soft tissue) – flexibility & strength
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o Anti-inflammatories & anti-inflammatory diet
o Possible orthotics
o May try running on softer surfaces
o Cross train instead of focusing just on running
o Ice following training
surgery is required
 In cases where symptoms persist despite 6-12 weeks of conservative care, & pressure still high
 in cases with extreme pressure elevations. (Wilder, 2004)

Chronic compartment syndrome
asymptomatic @ rest
o 80% both legs
o With activity: pain, achy, cramp, tightness, muscle bulge
o See PPT for others
Treatment
 Rest
 Change routine: soft surfaces, decrease activity
Tibial Stress Fracture






Repetitive stress injury
Runner
o Middel to distal 1/3
o Ballet, middle 1/3 risk of full Fx
o Miliatary - prox tibia
Biomech
o High arches
o Forefoot varus
o ___
Onset
o Insidious pain
 Local specialized pain
 Possible growth on xray
Tx: rest, crutches, vitamin D & calcioum
o Aerobic condition
Change routine: soft surfaces, decrease activity
Foot & Ankle
Learning Objectives:
10. Describe the etio, epid, risk, patho, clinical manifestations & management for the conditions
presented in Ortho I.
11. Describe the etiologies/mechanism of injury for each condition.
12. Explain the pathogenesis for each condition.
13. Identify & describe the symptoms, clinical signs & examination findings of each condition.
14. Identify the diagnostic studies that would aid in the diagnosis of each condition & describe the
findings associated with those conditions.
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15. Select the most appropriate management techniques for each condition.
16. Identify when a referral may be warranted & to whom that referral should go.
Sesamoiditis *inflammation of tendons &/or bone
Flexor hallucis brevis
(Boike A, Schnirring-Judge M, McMillin S. Sesamoid disorders of the first metatarsophalangeal joint. Clin Podiatr Med Surg. 2011 Apr;28(2):269-85) (Cohen BE.
Hallux sesamoid disorders. Foot Ankle Clin. 2009 Mar;14(1):91-104)
Definition:
A well-localized inflammation of the sesamoids & flexor tendons involved with the sesamoids, probably
more of a tendinitis than inflammation of the bone The medial (tibial) sesamoid is usually more involved
than the lateral fibular) sesamoid.
Epidemiology:
 active teens & young adults
Etiology:
 Repetitive stress to the forefoot (athletic activities) high or low impact
Pathogenesis:
Possible
 Inflammatory changes to the tendon (flexor hallucis brevis) & surrounding structures
 Chondromalacia of the sesamoids
Risk Factors
 High or low impact activities (running, dancing, gymnastics)
 Pes cavus
 Plantarflexed 1st ray
 Ankle equinus
 Structural anomalies to the sesamoids
 Mechanical overload
Clinical Presentation
 Pain at base of 1st toe (typically more medial)
 Pain may be constant or intermittent (just w/activities)
 Provoked by weight bearing activities, esp heel to toe off
o The pain usually begins as a mild ache & increases gradually as the aggravating activity is
continued. It may build to an intense throbbing.
 Typically unilateral
 Exam may reveal one of the risk factors listed above
 Little to no ecchymosis or erythema
 Tenderness esp when toe is dorsiflexed
 Dorsiflexion of the 1st MTP provokes & maybe limited ROM
 Possible crepitus
 Dx is typically made by exclusion of other causes
Diagnostic Studies:
 Plain film: usually unremarkable, possible bifed sesamoid
 MRI or plain film may show: osteochondritis or Fx
Management:
 Cryotherapy
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








Activity modification avoid running (use non weight bearing aerobic activities)
Orthotic or stiff soled shoe, avoid wearing high heels
Donut support - a shoe pad to reduce pressure on the affected area. This may be accomplished by
placing a metatarsal pad away from the joint so that it redistributes the pressure of weight bearing
to other parts of the forefoot.
Possible immobilization in cast/walking boot
Taping the toe - big toe may be bound with tape or athletic strapping to immobilize the joint as
much as possible & allow for healing to occur. (Tape the great toe so that it remains bent slightly
downward (plantar flexion))
Adjust the foot
NSAID's
Proprioceptive retraining
In severe or unremitting cases: steroid injections or sesamoidectomy
Freiberg Disease aka Freiberg’s Infarction
Definition:
Osteonecrosis most often seen in 2nd second metatarsal head (the third & fourth may also be affected). It
can be bilateral in up to 10 % of cases
Etiology:
The cause of Freiberg infraction is controversial & is probably multifactorial.
 Acute trauma or repetitive = altered kinematics of the foot may predispose to repetitive or single
traumatic event causing abnormal loading & collapse of the MTH
 Vascular Compromise
Pathophysiology:
 Degenerative process involving the epiphyses resulting in osteochondrosis of the subchondral
cancellous bone
Epidemiology:
 Adolescent girls most common but can occur at any age range
Risk Factor
 Longer 2nd digit (Index minus)
Clinical presentation
 Forefoot pain localized to head of the second MT
 Worse with weight bearing activities, better w/rest
 Possible stiffness
 Limp?
 Tenderness on the plantar surface
 Swelling & limitation of motion in 2nd MTP joint
 Later = crepitus or deformity may develop
Diagnostic studies
 Plain film of foot xrays r/o osteochondritis & Fx
 Findings (see Smillie classification)
o sclerosis in early disease
o flattening of involved MT head
o joint destruction in late disease
o defect is usually located in the upper half of the articular surface of the MT head
can show patchy edema in metatarsal head
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Management
 Decrease/modify activity – rest
 Analgesics = possible NSAID for short duration (small studies indicate that they slow fx healing)
o Cryotherapy
o Shoe inserts
o Tape toe downward
 If severe pain non-weightbearing cast, others may be able to utilize walking cast &/or hard-soled
shoes
If chronic may use
 Donut/metatarsal bar/pad in shoe
 Rocker bottom shoes
 Surgery if the necrosis is severe
Friebergs
Osteonecrosis of 2nd MT head…
 Can be 3rd or 4th but less common
Greek foot & then Roman (same length
 Degenerative process
 Younger girls 11-17
 Greek food
Presentation:
 Forefoot pain R/O sesamoiditis
 Swelling, pain, crepitus
 Exacerbate w/high heels
 SMILLIE Classifiction
o Fissure
o Bone collapse
o Regular appearance
o Loose bodies
o Flattening
 Management
o Rest
o Non-weigth bearing
o Rocker bottom shoes
o Donut
o Surgery possibly
o Analgesics – NSAIDS, but can slow FX healing, so CAUTION
 Resolution
o Spontaneous
o Weeks to months
Tarsal Tunnel Syndrome (TTS)
Sensory* NT ON bottom of foot MOTOR 1/5th of cases = weakness of toe flexion
(Persich, Gianni, & S. Touliopolous. "Tarsal Tunnel Syndrome." eMedicine. Eds. John S. Early, et al. 6 Sep. 2007. Medscape. 3 Apr. 2009
Hollis, Minoo Hadjari, & David E. Lemay. "Nerve Entrapment Syndromes of the Lower Extremity." eMedicine. Eds. John S. Early, et al. 17 Mar.
2008. Medscape. 3 Apr. 2009
Definition:
A rare entrapment neuropathy that develops as a result of compression of the posterior tibial nerve in the
tunnel formed by the flexor retinaculum behind the medial malleolus of the ankle. Inside the tunnel, the
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Ortho Lecture Notes Combined
nerve splits into three different segments. One nerve (calcaneal) continues to the heel, the other two
(medial & lateral plantar nerves) continue on to the bottom of the foot.
Epidemiology:
 Rare (<200, 000 people in US) disease (office of Rare Disease of NIH)
o Most common in active adults, but it can also occur in children
 F=M
 People with severely flat feet are at increased risk of developing tarsal tunnel syndrome
Etiology:
 nerve compression may be caused by space-occupying lesions & other factors reducing area within
canal, including:
 fracture/dislocation of the talus, calcaneus, malleoli (most common cause)
 ganglia
 lipoma
 neurilemmoma
 neurofibroma
 traction neuritis
 posttraumatic peri-neural fibrosis
 tenosynovitis of adjacent flexor
 varicose vein or venous congestion
 osseous prominence (including after trauma)
 accessory muscle
 foreign bodies
 complication of total ankle arthroplasty
 hypertrophic flexor retinaculum
 generalized lower extremity edema
 abnormal pronation
 "double crush" syndrome
Types:
 Distal tarsal tunnel syndrome is caused by compression/irritation of the distal tibial nerve
branches (med or lat plantar, med calcaneal) & presents with heel pain, postmed aspect of heel,
ankle arch pain/paresthesia
 Classic tarsal tunnel syndrome compression of the posterior tibial nerve behind med malleolus &
under flexor retinaculum
Risk Factors
 Running, jumping activities
 Arthritides
 Diabetes
 Varicosities
 Obesity
 Rearfoot varus/valgus
 Ill-fitting shoes
Clinical Presentation
 Unilateral
 Aching, burning, cramping numbness, &/or tingling on the plantar surface of the foot (longitudinal
arch) possible radiating into medial ankle
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Possibly worse at night
Provoked by prolonged standing or walking, normally worsens as the day progresses & can usually be
relieved by rest, elevation or massage
 Rest may help but it is a gradual decline in symptoms
 May experience proximal radiation of symptoms to the calf & leg
 Tenderness behind or distal to malleolus
 Edema over tarsal tunnel
 Possible mass in tunnel area
 +Tinel's foot sign
 ROM = dorsiflexion & eversion provoke sx’s, inversion may help
 Sensory changes (2 point, pallesthesia) – symptoms along the course of the posterior tibial nerve in
the sole & heel.
 Atrophy of the intrinsic muscles of the foot is a rare finding & is only found in advanced cases.
 Weakness of toe flexion is the only reliable muscle finding, but it is only seen in approximately 19% of
the cases.
Differential Diagnosis: SEE PPT
 Medial Plantar Neuropathy (Jogger’s foot): Etiology, signs & symptoms are similar to TTS, except
they are present only on the medial sole of the foot. ONLY MEDIAL SIDE
 Lateral Plantar Neuropathy: Etiology, signs & symptoms are similar to TTS, except they are
present only on the lateral sole of the foot. ONLY LATERAL SIDE
Diagnostic studies: CT or MRI to confirm
 Plain film – to help r/o
 Electrodiagnostic: EMG & NCVs may show abnormalities. (often inconclusive)
 CT/MRI can be utilized to confirm the diagnosis.
Management:
Treatment is dependent on the etiology.
*Patients with space occupying lesion will not likely respond to conservative therapy.
 modalities
 adjustments
 STM & stretching
 orthotics (semi-rigid arch support w/
o medial heel wedge for medial plantar nerve or
o lateral wedge for lateral plantar nerve)
 shoe modification
 NSAID's
 Immobilization
 TIBIAL N flossing = Laseques w/dorsiflexion
 Local Steroid injections into tunnel
 TCA &/or anti-convulsants for neuropathic pain
 Surgical release
 If surgery is not successful the following may be why:
o insufficient release of the retinaculum
o compression occurring somewhere other than beneath the retinaculum (e.g., abductor
hallucis hypertrophy)
o misdiagnosis
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Prognosis
 Variable depending on extent of the damage to the posterior tibial nerve
Haglund’s Syndrome
aka: pump bumps *tendon growth puts pressure on bursa = bursitis
Definition:
Triad of:
 insertional achilles tendinopathy
 retrocalcaneal bursitis
 retro tendo-achilles bursitis
This results in pain at the back of the heel.
It is associated with calcaneal spurs, & the wearing of high heels (thus the colloquial term "pumpbump") or stiff-backed shoes in general.
Etiology:
 Friction
Pathogenesis:
 Bony growth (exostosis) that appears at the back of the heel at the insertion point for the Achilles
tendon  repetitive impingement of the bursa between the tendon & exostosis will create
retrocalcaneal bursitis.
Epidemiology
 W >M
 Athletes all ages
 Possible higher incidence in middle aged & older
Risk Factors
 Pes cavus
 Tight Achilles tendon
 Rearfoot varus
 Shoewear – stiffbacked shoes
Clinical Presentation
 a very noticeable bump on the back of the heel
 severe pain in the area where the Achilles tendon attaches to the heel
 worse with shoe wear & with heel & toe off
o Look @ shoes
 Tenderness at the insertion to the Achilles tendon
 Possible erythema & edema
 Provocation w/dorsi/plantarflexion
 Pes Cavus – increases tension on achilles & plantar tendon
Diagnostic studies:
 Plain film: exostosis at the insertion point of the achilles
 MRI – show swelling of the bursitis & help to r/in or out tendinopathy
Management:
 Backless shoes or sandals
 Adjust to correct improper biomechanics
 Ice
 NSAIDs
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Heel lift in pt’s w/pes cavus to decrease pressure on heel
Heel pads
US
Iontophoresis
Possible orthotics
Stretch Achilles
Soft tissue work
Athletes should rest
o avoid training on hills & hard surfaces, & run shorter distances.
Cortisone injection
Calcaneoplasty
Achilles Tendinosis *microtears of tendon
Tendonopathy is either tendonosis (microtears) or tendonitis (inflammation of tendon)
Carcia CR, Martin RL, Houck J, Wukich DK, Orthopaedic Section of the American Physical Therapy Association. Achilles pain, stiffness, &
muscle power deficits: achilles tendinitis. J Orthop Sports Phys Ther. 2010 Sep;40(9):A1-26
Definition:
This refers to tiny tears (microtears) in the tissue in & around the tendon.
 Some experts now use the term tendinopathy to include both inflammation & microtears. But
many doctors may still use the term tendinitis to describe a tendon injury.
 Seen as thickening of tendon
Epidemiology:
 Athletes – lifetime incidence is 24%
 Annual incidence in runners is 7%-9%
 Mean age: 30-50
 M slightly > F
Etiology
 Overuse, usually an athlete who is suddenly increasing their activity
 Poor running mechanics
 Improper footwear
Pathogenesis
 Inflammation, fibrotic changes & calcification of the tendon & peritendon structures
Risk Factors
Holmes GB, Lin J. Etiologic factors associated with symptomatic achilles tendinopathy. Foot Ankle Int. 2006;27(11):952
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Stop-and-go sports (eg, basketball, soccer, tennis)
Previous Achilles tendon problems
Sudden increase in duration or intensity of running
Male gender
Obesity
Increasing age
Poor running mechanics
Over or under pronation
Flat foot (pes planus)
High foot arch (pes cavus)
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 Leg length discrepancy
 Foot malalignment
 Fluoroquinolone (antibiotics) or glucocorticoid use
Clinical Presentation
 Pain –
o initially intermittent & related to exercise (worse at the beginning of activity keeps a little
better as activity continues but then worsens again with continued activity) then it progresses
to continuous pain.
o When exercise: feels pain, then better, then worse
 Swelling?
 Stiffness from inactivity & swelling
 Possible feeling of weakness with progression
 Assess for risk factors
 Palpable tenderness (2-6 cm prox to insertion), possible erythema & edema
 Crepitus
 Provocation w/AROM & RROM – plantarflexion &/or PROM – Dorsiflexion
 Possible weakness
Diagnostic Studies:
 Ultrasound
 MRI – changes in the tendon
Management:
 Rest/activity modification
 Ice
 Stretching
 NSAIDs avoid prolonged use
 Low-energy shockwave therapy
 Adjustments
 Eccentric exercise
 Proprioception
 Taping the Achilles in plantarflexion, heel cup &/or orthosis
 Transdermal patch of nitric oxide
 Injections (steroid or prolotherapy)
 Surgical debridement
If a 3-6 months trial of conservative measures fail for the tendinitis/tendinosis than surgery may be
recommended
Achilles Tendon Rupture
(Weatherall JM, Mroczek K, Tejwani N. Acute achilles tendon ruptures. Orthopedics. 2010 Oct;33(10):758-64)
Definition:
Partial or complete rupture of the tendon (traumatic or nontraumatic); rupture is 2-6 cm proximal to
insertion
Epidemiology
 Incidence of rupture is 7/100,000
 80% occur during recreational sports
*weekend warriors
Age: 20-50 yrs (mean age 40 in males, 44 in females) who are intermittently active
Etiology (multifactorial) & Risk factors
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Tendon rupture occurs when sudden forces are exerted upon the Achilles tendon during strenuous
physical activities that involve sudden pivoting on a foot or rapid acceleration (eg, stop & go sports such
as tennis, basketball, or softball)
 Overuse
 biomechanical malalignment
 hyperpronation & cavus foot
 marked forefoot varus
 medications that weaken Connective tissues
 inappropriate footwear
 overuse is most common cause in recreational athletes with acute rupture
 prolonged tendon degeneration or sudden severe stress can result in partial tearing or
complete rupture
Clinical Presentation
 Acute heel pain following running, jumping activity
 Pt may relate that it feels like they have been “kicked from behind”
 Pop w/hyper dorsiflexion
 Inability/difficulty with ambulation (some ruptures are missed because the patient can walk)
 Eccyhmosis, edema, visuable defect
 Tenderness
 Limitation or complete loss of active plantarflexion; weakness on resisted plantarflexion
 Difficulty to inability to do repetitive heel raises or toe walking
 + Thompson
Diagnostic Studies
 US or MR to confirm dx
Management
Surgery – full thickness tears, get patient weight bearing in approximately 2 wks
Non-surgical (partial)
 Ice, rest, NSAIDs with either:
 Serial casting progressing from plantarflexion to neutral to full dorsiflexion
 Solid removable boot with heel insert w/early mobilization
Medial Ankle Sprains
Definition:
involves the ankle being forced into eversion & external rotation. Sprains to the medial ankle complex are
less common because biomechanics of the ankle joint allow for less eversion than inversion. Also the
deltoid ligaments (ant & post tibiotalar, tibiocalcaneal, tibionavicular) are strong & often an avulsion
fracture at the medial malleolus occurs before a deltoid ligament sprain.
Etiology
 Eversion stress, especially when landing on an uneven surface, cutting or stepping down a stair wrong
 In almost 60% of the eversion injuries avulsion of the tip of the medial malleolus occurs instead of a
deltoid ligament sprain *60% of medial ankle sprains result in avulsion
Epidemiology
 10-18% of all ankle sprains are medial
Risk Factors
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male gender
higher competition levels
young populations
intercollegiate rugby
gymnastics
soccer
Clinical Manifestations
Ankle sprains grades based on severity of damage to ligament complex.
 Grade 1: Partial tear/stretching of a ligament
o Mild point tenderness
o Minimal edema
o Minimal to no loss of function; Patient should be able to tolerate weight bearing & perform
daily activity without complaint of severe pain.
o No mechanical instability; negative clinical stress tests.
 Grade 2: Incomplete tear of a ligament
o Moderate pain & edema
o Point tenderness over medial ankle complex
o Mild to moderate ecchymosis
o Loss of range of motion
o Loss of function; Patient will complain of pain with weight bearing & ambulation.
o Mild to moderate mechanical instability; Patient will have mild positive findings on the clinical
stress tests.
o + Medial stability test
o + External rotation stress test
 Grade 3: Complete tear of a ligament
o Severe edema
o Severe ecchymosis
o Severe loss of function; Patient will be unable to bear weight & ambulate.
o Mechanical instability; Patient will have moderate to severe positive findings on clinical stress
tests.
Diagnostic studies
 Plain film – a space greater than 4mm between the talus & medial malleolus on the mortise view
suggests a tear of the deltoid ligament.
 MRI - MRI must be used to determine partial & complete deltoid ligament tears to decide whether
surgical fixation is necessary. Patients with partial tears are treated nonoperatively & can respond
well to treatment
Management
 PRICE
o Protection-protect the ankle from further injury by resting & avoiding activities that cause
pain.
o Rest- the use of crutches will allow the ankle to rest until one can walk without pain.
o Ice-apply ice to the ankle for 15-20 minutes as often as once per hour.
o Compression- compression wraps are used to decrease swelling.
o Elevation- elevate the ankle above the level of the heart to decrease swelling.
 Treatment is similar to lateral sprains although it takes longer.
 ROM exercises: It is important to begin range of motion exercises within pain free range as soon as
possible. Active & passive range of motion exercises should be used to maintain range of motion for
optimal function. Range of motion should be restored before beginning training in stabilization,
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strength, proprioception & function. To improve or maintain ROM, stretching & joint mobs are
commonly used:
Stretching: Ankle Stretches (dorsiflexion, inversion): hold for 15 -30 seconds, 5 reps, every day. It is
important to begin ankle dorsiflexion stretches early due to the Achilles tendon’s tendency to contract
following injury.
Alphabet exercises: Instruct the patient to draw the alphabet, one letter at a time A-Z. This exercise
encourages movement of the ankle in all planes.
Joint mobilizations: Anterior-posterior joint mobs: mobilizing the ankle into restricted planes can help
to regain lost range of motion.
Joint Stabilization: Stabilization is achieved through muscle strengthening exercises, balance, &
proprioception exercises.
Isometric Exercises: Resistance can be provided by an immovable object (wall or floor), elastic bands,
or manual resistance. Exercises should be held for at least 6 seconds for maximal contraction, 10
repetitions & 3 sets daily. Exercise can be performed in dorsiflexion, plantarflexion, eversion,
inversion, & eventually diagonals.
Isotonic Exercises: Resistance can be provided by weights, theraband, or gravity. Exercises should be
performed for 10-20 reps, 2-3 sets & up to 2 times a day depending on intensity. Each repetition
should include concentric component & slow eccentric component. Exercises include plantarflexion
push downward, dorsiflexion push upward, eversion & inversion.
Balance & Proprioception training: Once balance is established, proprioceptive exercises can be
progressed by:
o
Balance on even surface
o
Balance with eyes closed
o
Balance on balance board
o
High surface balance
o
High surface with eyes closed
o
High surface on balance board
o
Walking
o
Jumping
Complete Ruptures – Referral for surgical stabilization.
High Ankle Sprain
aka: Tibiofibular Ligament or Syndesmosis Sprains
Etiology
 External rotation force applied to dorsiflexed ankle (e.g., leg is rotated forcefully against a planted
foot/toe) – most common
 Athlete is prone on the ground & another athlete steps or lands on their posterior leg while the foot is
externally rotated
 Eversion of the ankle
 Hyper-dorsiflexion
 Severe inversion
Epidemiology
 Approximately 10-20% of ankle sprains
Risk Factors (Ivins D. Acute ankle sprain: an update. Am Fam Physician. 2006 Nov 15;74(10):1714-20)
 History of ankle sprains
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 Wearing shoes with air cells
 Inadequate stretching/limited dorsiflexion
 Plays: basketball, soccer, ice skating
Clinical Manifestation
 Pt relates MOI
 Possible Pop
 Pain just above the ankle
 Inability or difficulty bearing weight
 Tenderness – over distal tib/fib
 Less edema & ecchymosis w/this type of sprain – distal tib/fib & into ankle & foot
 + Squeeze test
 + External rotation stress test
 (+,-) Medial/Lateral stability, Drawer’s Foot sign, Talar tilt (depends on the MOI)
Diagnostic studies
 Plain film – possible separation (diastasis) of the distal tib/fib
 MRI - Diagnosis
Syndesmosis Injury Classification
 Syndesmotic injury without diastasis or instability (stable) – conservative care
 Syndesmotic injury with diastasis or instability
 Syndesmotic injury with fracture
Management
 PRICE
 Conservative management is similar to lateral ankle sprains.
 Athlete may be out for 6+ wks with this type of sprain
 Surgery – internal fixation
Return to Play:
 One indicator that the patient is ready to RTP is the ability to hop on that foot 15 times without
symptoms
Prognosis
 Not as good as other sprains they usually take much longer to heal (i.e., double or triple the
amount of time it will take them to heel). Greater risk for further ankle injuries following a high
ankle sprain
 With internal fixation pts can return to full activity as early as 6 wks. (Taylor, 2007)
Koelhers disease – navicular bone AVN
Fat Pad syndrome
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