Neuro PT I Midterm Studyguide
Neurologic rehabilitation models
NDT= more hands on
Contemporary Task Approach= Indep learn more from mistakes, modify, etc…
Motor Control Theory
Movement emerges from interaction of learner, task, environment
Movement= a combination of task, environment, individual
Motor Control
Feedback/Closed loop control
Use sensory information
Constantly adjust motor response as a result of environment
Early skill acquisition or complex movements requiring accuracy
Adam’s Closed Loop Theory (1970s)
Memory trace/ Perceptual trace
Feedforward/ Open Loop control:
Motor program (CPGs or GMP)
Generates movement without sensory inputs
Anticipate
Postural set
Well-learned, automatic, fast tasks
Use sensory input to adjust to unexpected changes
Skill Acquistion
Goal is to find a NEW movement strategy
New task or new strategy for previously learned task
Expect: high degree of attention to task
Variable performance
Heavy reliance on sensory information (FEEDBACK) to adjust motor response
Examples of the novice learner
Skill Retention
Goal is to LEARN the task
Permanent change in behavior
Develop skill
Increase efficiency
Increase consistency
More automatic
Decrease reliance on external feedback
Task Oriented Training
Manipulation of task and practice variables
Patient-Centered functional goals
Facilitate motor problem solving by patient
Consider patient’s stage of learning
Are they in skill acquisition or are they in skill learning?
Practice session
Amount of variation: blocked vs random practice
Motivation: challenge vs success
Define task: speed vs accuracy
Practice motor problem solving
Feedback…
Feedback (info you give the patient)
Feedback= ALL sensory information available
Intrinsic/Extrinsic
Manual guidance (hands on)
Type of external feedback or form of demonstration
Useful when introducing task or when patient unable to do task safely
Immediate/Continuous vs Terminal/ Summary
Being stingy with feedback helps with learning
Concurrent is detrimental to learning
Hold your tongue let them try and figure it out
Summary of Task Oriented Treatment
Skill acquisition strategies
Immediate feedback, use of manual guidance
Blocked practice with less variation
Motivation important
Skill retention strategies
Summary feedback
Random practice
High variation and challenge
Add components such as counting, talking, etc
Clinical decision making
Level of evidence:
Systematic Reviews, RCTs, Cohort Studies, Case Control studies, Case Series, Case
Reports, Ideas/Editorials/Opinions, Animal Research, In vitro research
Task oriented tx approach: critical component in making the connection with your patient to get
the participation component
Disability as Diversity
Disability reconsidered: The paradox of PT
Medical model vs Social Model
Disability is a form of diversity
Focus on improving access, change social policy,, improve social interactions, (vs fixing
impairments)
PTs perpetuate negative attitudes?
Helper/helpee relationship
Assume that individuals want to eliminate impairments
Rehab of patients with stroke
Stroke stats:
Leading cause of disability, 3rd leading cause of death (5% mortality rate)
Review Blood Circulation in the brain
MCA is most common site of CVA (expectations on presentation)
Other CVA presentations regarding ACA, PCA
MCA: derived from the internal carotid artery
Supplies a large area of the frontal, parietal, and temporal lobes
Occlusion causes dysfunction of the face and upper extremity, language, and speech
ACA: derived from internal carotid artery
Supplies the medial portion of the frontal and parietal lobes
Occlusion causes dysfunction of the cortical area supplying primarily the lower extremity
PCA: derived from basilar artery
Supplies the occipital lobe
Occlusion affects vision
Right VS Left Stroke
Right:
Left Hemiparesis
Visual-perceptual deficits
Poor judgement, cognitive, and behavioral issues
Left:
Right hemiparesis
Language deficits
Apraxia : (motor planning issues)
Processing delays, perseveration
Perserveration: repeating of tasks
Processing delays: don’t restate/repeat commands just adds to the delay, allow
time to process and respond to initial request
Pathophysiology
Ischemci Lesions
Ischemic Cascade
Ischemic Core- direct damage
Ischemic penumbra- possible damage
Thrombotic CVA
Thrombus: atherosclerotic plaques in first major branching of large cerebral arteries.
Progressively narrows
Uneven progression
Wake-rise fall
orthostatic hypotension that causes enough of a decrease in BP that adequate
blood to the brain is not maintained causing stroke
Thrombus in evolution
Thrombus in evolution: not stable yet, PT shouldn’t be seeing at this stage.
Affects of stroke still evolving
Common risk factors: HTN, DM, cardiac/vascular disease
Embolic CVA
Thrombus from outside brain (typically from plaque in carotid sinus, internal carotid, heart)
Risk factors as Previous PLUS
A-fib, DVT, Infection
Lodges in medium sized vessels (MCA, Vertebral, or Basilar branches)
Immediate impact: no collateral blood flow
Symptoms vary if clot moves
Hemorrhagic CVA
Abnormal bleeding in brain
Aneurysm
More global problems than ischemic CVA
Ischemic injury to area supplied by vessel
Mechanical injury from blood, edema to distant neurons
Transient Ischemic Attack
TIA or RIND (Reversible Ischemic Neurological Disorder )
Temporary interruption of brain blood flow, neuro symptoms last <24 hours
Evolving thrombus or small emboli
RED FLAG!
Use as motivation to encourage lifestyle changes
Emergency Room
Neuro exam on admissions to hospital
Performed by acute care physician, nursing staff, perhaps rehab consultants
PURPOSE:
Dx or r/o CVA
Determine etiology and pathology of CVA
Assess comorbities
Initial DX
History of events: timing important
PMH/Risk Factors
Dx Tests
Confirm CVA
Determine cause, location, extent
Evaluate complications
Assess risk of recurrent CVA
DX Tests
CT of brain shows bleed, doesn’t show ischemia
MRI doesn’t really affect course of treatment
Acute Care Priorities
Control life-threatening problems and prevent recurrent stroke
Initial bed-rest, monitor vitals
Prevent complications
DVT, aspiration, fall risk
Manage general health (e.g. DM)
Mobilize and resume self-care when “medically stable”
Hemorrhagic Lesions
Monitor/decrease ICP
Seizure prophylaxis
Surgery for large or progressing bleeds
Ischemic lesions
Important to rule out hemorrhage!
Anticoagulants
IV heparin
Coumadin, (Warfarin Sodium)
Anitplatelets
Aspirins
Clopidogrel/Ticopidine
Persantine (dipyramidole)
Ischemic Lesions
Thrombolytic Agents
T-PA tissue plasminogen activator (3 hour window)
Prourokinase
via microcatheter (6 hour window)
Ischemic Lesions
May want HIGH BP to perfuse ischemic tissue (loss of autoregulation)
Goal to decrease BP if
BP>220 systolic, >120 diastolic
Other organ damage (e.g. pulmonary edema, retinal hemorrhage, renal failure)
Use of tPA
Acute Care Rehab
Early Mobilization
Prevent DVT, decubiti, contractures, pneumonia, atrophy
Start recovery process
Functional mobility assessment
Precautions
Coma/stupor
Progressing neuro signs
Unstable vitals
Sever orthostasis
PT screening for Rehab Services
Identify patients that may benefit
Identify problems that need treatment: IMPAIRMENTS/FUNCTIONAL LIMITATIONS
Determine appropriate setting for rehab after discharge from acute care
Inpatient Rehabilitation
Rehab Hospital
Rehab unit of hospital or rehab center
3-6 hours of therapy per day
Medically stable with functional disability and adequate endurance. Cognition intact
Sub-Acute Care
Skilled Nursing Facility
Variable amount of therapy
More serious disability, less endurance. Cognition intact
Long-Term Care
Nursing home
2-3 days/week
Need for long term 24 hour care because of cognition, comorbidities, lack of home
support
Inpatient Rehab
Physiatrist/Neurologist
PT, OT, SLP, Dietician, Social Worker, Neuropsychologist, Case Manager, Rec. Therapist
Home Care Rehabilitation
Provided by home health agencies
Patients who live at home but are functionally homebound
May be a simple “check out” for safety/function
Rehab services can be provided if necessary, typically 2-3 times per week for 30-45
minutes each session
Limited equipment, focus is on functional training in relevant setting
Outpatient Rehabilitation
Outpatient therapy office or outpatient dept of hospital
PT most common, OT/Speech also available
patients who live at home and are mobile in community
Typically 2-3 times per week for 30-45 minute sessions may include strength or
endurance training
“Community Ambulation”
Important for discharge planning
Distance 1000’
Speed: traffic lights, busy sidewalks
Ambient conditions: rain, temperature, light
Physical load: packages, manual doors
Terrain: stairs, curbs, slopes, obstacles
Attentional demands
Other promising Interventions
Bodyweight supported treadmill training
Constraint induced movement therapy
Robot assisted training
Mental imagery
Virtual Reality
EMG Biofeedback/electrical stimulation
Clinical Decision Making
Integrated Framework for CDM
Patient Centered
Integrates
Research
Guide to PT practice
Disablement/Enablement models
HOAC
HOAC II Model: Hypothesis-Oriented Algorithm for clinicians
HOAC II Part I
Initial presentation of patient
Patient identified problems
Exam strategy/collect data (tests/measures)
Add non-patient-identified problems
Generate hypothesis for why problem exists
Establish goals
Plan for intervention and re-evaluation
HOAC II Part 2
Re-assessment of problem
Have goals been met?
If NO:
Is hypothesis appropriate?
Improve implementation of treatment
Change Tx
Change strategy
Are goals viable?
Good Clinical Assessment Tools (Score of 4)
Body Structure/Function
Fugl-Meyer Assessment (LE only)
Orpington Prognostic Scale
STREAM (limb subscales)
Activity
6MinWT
10meter WT
Berg Balance
Dynamic Gait Index
FIM (in-pt rehab only)
Functional Reach
Participation
Stroke Impact Scale
SF-36
Traumatic Brain Injury
Protective Coverings of the brain
Scalp/Hair
Skull 2-6mm thick (except temporal fossa)
Dura mater-Inelastic membrane
Pia Mater-Many blood vessels
What defines TBI?
TBI is a sudden trauma that causes injury to the brain
Closed (non-missile; dura mater intact) vs Open (penetrating injury)
Focal vs Diffuse
Said to be a violent storm of noises with the inability to filter things out
Primary Damage post-TBI
Coup injury (at the site)
Forceful blow to resting, moveable head
Maximum injury is at the point of cranial impact
Contusion with/without skull fracture
Contracoup (opposite side)
Moving head
Injury is opposite of impact
Frontal and temporal lobes
Coup/Contracoup Injury
Whiplash injury
Car accidents, football player
Multiple areas of the brain injured
Temporal, frontal, occipital
Cerebral Spinal Fluid
Shock absorber, dissipates forces
Forces on the brain tissue
Compression: Diving, bleeding/swelling
Tensile: stretching
Shearing-axon snaps/tears
Diffuse Axonal Injury (Big cause of coma or vegetative state)
Brain Swelling
Craniotomy if swelling is severe
Cerebral edema
Increased ICP (12mmHg normal)
Seizure
Hypoxic Ischemic injury
Anoxia: no O2 for a period of time
Hypotension
Difficulty regulating pressure
HOB at 30˚ so pressure doesn’t increase
Hematoma
Epidural Hematoma: Skull and dura
Subdural Hematoma: between dura and arachnoid
Intracerebral Hematoma
Important Considerations
Balance vs Vision
Cognition vs Hearing loss/changes
Structures are vulnerable
Injuries to any of these regions/structures can be catastrophic
Need to be protected
Regeneration of tissue limited within specific structures
Recognizing what’s injured, its affect, and preventing secondary injury
Causes
MVC #1 cause
Violence (GSW) ~20%, 91% of firearm related brain injuries result in death (2/3 suicidal intent)
War
Falls, 11% of falls are fatal in elderly (75 and older)
Sports Injury (~3%) in 2003-2009
Concussion ~75% of TBI
Pedestrian cyclist accidents
Drug Overdose/Poisoning
Drowning
Carelessness
Types of Brain Injury
Concussion
Experience one of the following
Physical (headache, dizziness, nausea, sleep problems/fatigue
Cognitive (decreased attention span, concentration, and short term memory loss)
Behavioral (irritability, emotional labiality, depression/anxiety)
Grading Scale
Grade 1: (mild)
No loss of consciousness
Post-traumatic amnesia
Post-concussion
Signs or symptoms lasting less than 30 min
Grade 2: (moderate)
Loss of consciousness lasting less than 1 minute
Post-traumatic amnesia
Post-concussion
Signs or symptoms lasting longer than 30 min but less than 24hrs
Grade 3: (severe)
Loss of consciousness lasting more than 1 minute
Post-traumatic amnesia lasting longer than 24hrs
Post-concussion signs/symptoms lasting longer than 7 days
Grade1:
Most frequent, but most difficult to recognize and judge the severity
>50% of all concussions
Often described as “bell rung” or “dinged”
Tx: Remove player and observe for symptoms for 15-30 minutes
Return only if NO symptoms at rest or with exertion
Grade 2:
Remove from play, refer to neurologist for examination
Grade 3:
Remove from play and transport via ambulance to hospital
Consider possibility of C-spine injury during LOC
MUST consider intracranial hemorrhage
Leading cause of death due to head/neck injury
Hematoma
Epidural hematoma
Occurs with fracture/arterial insult
Rapid progression of negative symptoms
Subdural hematoma
Surgical emergency
Intracranial hematoma
Most common fatal athletic injury
Rapid progressing, torn artery
Subarachnoid Hematoma
Bruise
Second Impact Syndrome
Occurs due to loss of autoregulation of blood supply to the brain
Happens more easily after initial concussive event
Presents with rapid deterioration of status, collapse and can be fatal
Do not allow athletes to be returned to play too early and be placed at risk
Second Impact Syndrome Pathophysiology
Initial concussion impairs normal brain function
Brain vulnerable during this time
Second impact unleashes series of metabolic events
Loss of autoregulation of brain’s blood vessels
Congestion, vasodilation, and large increase in blood flow
Large increases in ICP
Long-Term Consequences
Neurodegenerative changes- due to loss of autoregulation of blood supply
Mild cognitive impairment
Alzheimer’s disease
Chronic Traumatic Encephalopathy (CTE)
Progressive degenerative brain disease, repetitive concussive injuries
Depression
Types of Brain injury
Moderate
Loss of consciousness (minutes to hours)
Day/weeks of confusion
Physical, congnitive, behavioral changes can be permanent or make a complete
recovery
Severe
Coma or prolonged unconsciousness
Can recover but deficits will remain
Brain Injury Recovery
Spontaneous functional recovery (first 3-6 months)
Dependent on extent of injury, and neural plasticity
Neurons in uninjured areas can take over (regenerative sprouts/collateral sprouts)
Brain is always reorganizing to store new information
Glasgow Coma
Eye opening: 4= Spontaneous 3=to voice 2= to pain 1= none
Verbal: 5=normal 4= Disoriented conversation 3=words; not coherent 2=no words; only sounds
Motor: 6=normal 5= localizes to pain= 4=withdraw to pain 3=decorticate 2=decerebrate 1=none
Levels of consciousness
Abnormal
Stupor=unresponsive; aroused by strong stimulus
Coma= unconscious; unaware, unarousable, absent sleep-wake cycle
Vegetative state=unconscious and unaware but have sleep-wake cycle
Persitent vegetative state= don’t recover w/in 30 days
Locked in syndrome= aware and awake but can’t move or communicate
Rancho Los Amigos Scale
PARKINSONS
Age of typical onset >65
Cardinal characteristics: 1)Resting tremor 2)Bradykinesia 3)Rigidity 4)Postural instability
(have to have 2 out of 4 cardinal characteristics to be diagnosed)
Other symptoms: micrographia (small writing), masked face, slow ADLs, stooped and
shuffling gait with decreased arm swing
Clinical exam is “gold standard”, can only have definitive diagnosis with autopsy ( to
analyze substantia nigra)
Parkinsonism
Corticobasal degeneration
Dementia with Lewy bodies (small microvascular strokes)
Multiple system atrophy
Progressive supranuclear paulsy: typically more global neurodegeneration in multiple
areas of brain, gliosis, accumulation of tau protein (progresses much faster than PD,
difficulty moving eyes vertically)
Consider response to L-Dopa to determine Parkinsonism vs Parkinson’s
Stages of PD
I/Early=unilateral tremor, rigidity
II/Early Middle=Bilateral symptoms, gait deviations
III/Late Middle=Balance problems, but still indep with ADLs (falls prevalent in this stage)
IV/Late=Severely disabled
*PTs tend to see pt’s that are in level III or IV (should be getting into an exercise
program by Level I or II)
Drugs
L-Dopa: replaces dopamine, does NOT change progressive loss, effective for <10 yrs
Amantadine: stimulates dopamine
These drugs prevent dopamine breakdown, but do NOT replace: COMT inhibitors,
MAO-B inhibitors, Anticholinergics
Cognitive Issues
11-29% of patients with PD have memory difficulties (may present like Alzheimers)
Psychosis: vivid dreams/nightmares, disorientation, hallucinations
May have to stop L-Dopa if it becomes too serious
Treatment
Want to bypass basal ganglia and activate SMA (pt can then respond to cues rather
than relying on a set motor program), can use tiles on floor, rhythmic auditory
stimulation, etc. Make sure to address freezing. Want to also reduce stress b/c this will
only exacerbate symptoms
Locomotor training in early stages: 1) Baseline data to evaluate progression 2) Teach
core strategies for large quick movements 3) Practice gait with variation (longer steps,
different cues, concurrent activities) 4) Fall prevention education 5) Lifestyle activities
(such as an exercise program, Tai Chi, etc)
Locomotor training after L-Dopa: 1)Monitor response to off/on meds 2) Focus on safety
(avoid secondary tasks if needed, address freezing, etc)
Locomotor training 5-8 years later: 1) Maintain functional movements 2) Optimize
postural alignment 3) Focus on postural stability (become very kyphotic, monitor fall
risk, footwear recommendations, make gradual turns, consider “on” and “off” cycles)
PT for advanced disease: may need assistive device, provide education and support to
caregiver, need to address gait dyskinesia, enhance participation in community
HUNTINGTON’S DISEASE
Inherited and progressive disorder, autosomal dominant
Excessive face and trunk movement
Symptoms appear at 30 years (death around 15 years from onset)
May have dementia, behavioral and emotional disorders
No specific treatment options
OTHER BASAL GANGLIA DISORDERS
Wilson’s disease: faulty copper metabolism, rare, autosomal recessive
Tardive dyskinesia: extraneous facial rhythmic motion, due to psychotropic meds
Dystonia: sustained end-range rotation contraction
MULTIPLE SCLEROSIS
Progressive disorder with periods of exacerbations and remissions (stress can trigger
exacerbations)
Typical pt presentation: 1) 15-45 years old 2) Women>men 3) Charcot’s Triad (intention
tremors, speech, nystagmus)
Demyelinating lesions of the CNS (axons spared), UMN disease
Etiology: Autoimmune, genetics, environment (more prevalent in northern states) may
all play a role (all still questionable)
Diagnosis: Clinical presentation + lab results (rules out other things); can test using MRI
(small and tend to not show up until function already disrupted), CT (can only see big
lesions), EMG (slowed nerve conduction velocity), blood tests and CSF (elevated T cell
count)
Prognosis: mean survival rate=20-25 years after diagnosis; + indicators= <35 and initial
onset with 1 symptom; - indicators= >35 and insidious onset with multiple symptoms
Most common problems: 1) Fatigue (might need to break up PT session, heat exposure
increases fatigue) 2) Visual disturbances 3) Cognitive dysfunction (denial and poor
safety awareness) 4) Bowel/bladder dysfunction
Manifests within sensory (n/t) and motor systems (spasticity, ataxia, paresis), may also
cause problems with dizziness and speech/swallowing
Types
Benign: mild, little or no disability
Exacerbating/remitting: almost full recovery from exacerbations
Remitting/progressive: incomplete recovery from exacerbations
Progressive: very little recovery (steady downward decline)
***not mutually exclusive (patients can go back and forth)
Medical management
Corticosteroids decrease inflammation during periods of exacerbation
Interferon injections: prevent exacerbation by 30% (make sure women not using this
when trying to get pregnant)
Anti-spasticity meds
Avoid heat exposure
Do NOT push pt too hard during an exacerbation
Ask pt what they have been told and if they would like more information (figure out what
they know about their disease)
ALS
Progressive and fatal neuromuscular disease (50% die within 3 years of diagnosis>muscles of breathing and swallowing eventually are affected)
Upper AND lower motor neuron disease, voluntary muscle action affected (cognition
and sensation not affected)
Typical pt presentation: 1) 40-70 years old 2) Men>women
Again, ask pt what they have been told and if they would like more information (figure
out what they know about their disease)
TUMORS
Benign vs malignant (benign can still interfere with function)
Most common signs: 1)Headaches 2) Nausea/vomiting 3) Papilledema (pressure in the
pupil)
Primary brain tumors: Gliomas (most common, men>women, invasive, rarely
metastasizes)
Types of gliomas: 1) Astrocytoma (occurs in frontal lobe in adults and cerebellum in
children, Grades I-IV) 2) Medulloblastoma (children)
Meningiomas: affects women>men, encapsulated and slow growing
Neuilemomas: Schwann cells, acoustic neuroma (CN VIII) typically one sided)
Pituitary Adenomas
***Adjust expectations as disease progresses
CEREBELLAR DISORDERS
Cerebellum compares planned movement to actual movement
Ipsilateral symptoms
Inherited/Idiopathic cerebellar degeneration: group of disorders (progressive
degeneration)
Friederich’s Ataxia: adolescent disorder with children going through growth spurt (onset
8-15 years)
Acute Alcoholism
Chronic Alcoholism: Nutritional deficiency of vitamin B1, Wernicke-Korsakoff syndrome
(all characteristics of cerebellar problem along with a cognitive component)
Cerebellar CVA (unilateral symptoms) or tumor (unilateral or bilateral symptoms)
OTHER NEUROMUSCULAR DISORDERS
POLIO: virus infected alpha motor neuron cell body, remaining motor neurons reinnervated
POST-POLIO SYNDROME: surviving motor neurons work extra hard and eventually
give out, avoid exercise (energy conservation is essential)
PERIPHERAL NERVE DISORDERS: 1) Axonal neuropathy (DM, toxins, drugs)
2)Demyelinating neuropathy (Guillian Barre and CIDP); CIDP continues to progress
which is unlike AIDP/Guillian Barre; Guillian Barre is ascending motor neuropathy which
may be triggered following virus
MYASTHENIA GRAVIS: affects neuromuscular junction
LAMBERT EATON MYASTHENIC SYNDROME: affects neuromuscular junction,
associated with cancer malignancy
MYOPATHIES: 1) Muscular dystrophies (inherited and idiopathic, Duchenne’s-lacks
dystrophin protein) 2) Metabolic muscle disease (inherited) 3) Inflammatory myopathies
(acquired)
CNS INFECTIONS
Types: 1) Brain abscess: (cavity filled with purulent exudate) 2) Meningitis (bacterial
infection of CSF in subarachnoid space 3) Encephalitis (viral/HIV)
TRANSVERSE MYELITIS: inflammation of spinal cord (white and gray matter), acute
onset of paraplegia, sensory loss, and bladder incontinence, stable->not progressive
(1/3 with minimal deficits, 1/3 ambulatory with difficulty, 1/3 complete paralysis)
OTHER DISORDERS
CONVERSION DISORDER: present with specific symptoms based on their mental
state
WEST NILE VIRUS: due to mosquitoes, damage to anterior horn of the spinal cord,
currently no tx available
LYMES DISEASE: caused by ticks
Stage 1: Rash around tick bite 8-9 days later
Flu symptoms
Stage 2: Cardiac and neurologic complications several months later
Headache, neck stiffness, cranial nerve palsies
Stage 3: Chronic arthritis 1 year later in large joints of the body
May have memory, cognitive dysfunction
***Nervous system complications in 10-15%
SPINAL CORD INJURY
Mechanism of injury: Traumatic (MVA, fall, sports injury, etc) vs atraumatic (infection,
MS, AV malformation, etc)
**The cord does not need to sever to have complete injury (even bruising can result in
complete paralysis)
Higher risk for SCI if: 1) African American 2) Male 3) age 16-30
Quadriplegic=tetra
Critical information to obtain during PT eval: method of injury, co-morbidities, PMH,
precautions (pre and post surgical), level of injury, ASIA level
Stabilization
ORIF=open reduction internal fixation->can be combined with bracing:
1) Halo traction (more for high cervical injuries and those with no signs of neurological
damage->may be more of ligamentous injury)
2) Cervical collar (Aspen, Miami J, Philadelphia->most uncomfortable and least form
fitting )
3) CTLSO (can’t separate cervical from thoracic-may be seen with injury at C7 or T1)
4) TLSO
**Bracing is physician dependent
Spine Precautions (Based on KU Hospital-precautions will vary by facility)
Cervical: If spine is unstable-> pt is on bed rest, If spine is pending clearance but has no
fx/dislocation is identified->pt can move with use of a collar, If pt is post fixation->may
be up with use of a collar (collar is typical but physician dependent)
Thoracic/Lumbar: Do NOT elevate head of bed, bed rest, limit extremity movement to
avoid spine movement, place pt in reverse trendelenberg to prevent aspiration, log roll
with assist x2
Determining Level of Injury
Level of injury is determined by last intact muscle group of at least 3/5 rather than by
level of spinal fracture
For thoracic injuries, it is determined by sensory level
C1-C4=diaphragm and sensory
C5=Biceps
C6=Wrist extension
C7=Triceps
C8=Finger Flexors
T1=Small finger abductors
T2-L1=Sensory level
L2=Hip flexors
L3=Knee extensors
L4=Ankle dorsiflexors
S1=Ankle plantarflexors
S2-S5=Sensory level and sphincter tone
ASIA Levels
A: Complete: no motor or sensory function is preserved in the sacral segments S4-S5
B: Incomplete: sensory but not motor function is preserved below the neurological level.
Sacral segments S4-5 are intact
C: Incomplete: motor function is preserved below the neurological level and more than
have of key muscles have a muscle grade less than 3
D: Incomplete: motor function is preserved below the neurological level and at least half
of key muscles have a muscle grade of 3 or more
E: Motor and sensory function is normal
**May be typical for ASIA C to go to D as they recover and ASIA A to go to B
**Incomplete tetraplegia is most common
Types of Incomplete Lesions
Anterior cord syndrome (sparing of dorsal columns): preservation of light touch,
proprioception, and deep pressure; absences of pain and motor function
Central cord syndrome (sacral sensory sparing): UE weakness >LE; due in part to
corticospinal and spinothalamic tracts of LE being spared bc of lateral positioning in
spinal cord (typically seen with hyperextension injury->generally favorable prognosis)
Brown sequard syndrome: hemi-section of cord, ipsilateral paralysis and loss of
proprioception; contralateral loss of pain and temperatures (not common with trauma,
more likely to see due to tumor)
Posterior cord syndrome: preservation of temperature, pain, and touch with varying
degrees of motor preservation
Cauda Equina: LMN injury resulting in flaccidity (tend to have bowel/bladder problems)
**The most important prognostic variable relating to neurologic recovery is
completeness of the lesion
Treatment
The pt with complete injury will not be able to strengthen or influence recovery of lost
motor function; will need to focus on compensations in order to carry out certain
functional activities
Transfers: head moves opposite of bottom; need to lead with bottom rather than head;
make sure pt has shoes on; do NOT stretch finger flexors when in wrist extension (they
may need this for compensatory movements)
Balance: long sit achieved more easily than short sit due to larger base of support (may
have difficulty if pt has tight hamstrings)
Primary focus in initial stages=prevention of secondary complications, gain tolerance to
upright positioning in order to begin rehab, positioning, prevention of DVTs and
pneumonia, promotion of GI function
Pressure relief
Dependent: reclining (more supine positioning) or tilt in space (seat to back angle stays
the same) wheelchair ->In reference to ischial tuberosity: 65 degree backward tilt for
actual pressure relief, 35 degrees for minimal drop in pressure
Pressure ulcer: redness that does not fade within 20 minutes
Physiologic changes to skin include thinning of the epithelial layer, changes to collagen
and hyperhidrosis for T8 and above
Might be a candidate for ambulation if lower level and incomplete (may need
KAFOs/AFOs)
Teach pt how to fall bc this WILL happen
Wound Assessment
Grade 1: Skin area with erythema of in duration overlying a bony prominence
Grade 2: A superficial ulceration that extends into the dermis
Grade 3: An ulcer that extends into the subcutaneous tissue but not into muscle
Grade 4: Deep ulceration that extends through muscle tissue down to the underlying
bony prominence
Grade 5: An extensive ulcer with widespread extension along bursa and into joints or
body cavities
Wheelchairs
Consider: patient’s functional level, ability to perform pressure relief indep, type of
terrain, amount of time pt will be in wheelchair, transfer technique, weight of wheelchair,
position desired, number of caregivers, accessibility at home and other destinations,
patient preference
Power vs manual (C6 and above-power; C7-T1 MAY be able to propel wheelchair, but
must weigh energy expenditure costs) Power controls may be head control, sip and puff
or joy stick. Paraplegia should be able to manage manual w/c.
If new w/c user, rigid frame is more efficient than folding
Pros of using a back: better posture and shoulder positioning, Cons: hassle loading into
car
Expected Outcome vs Variability
Knowing the expected outcome and reasons for variability will help with goal setting and
treatment planning
CARDIOVASCULAR: Higher level of injury will have more difficult time maintaining
blood pressure (may require use of ace bandages and abdominal binder for maintaining
vascular support)
Dysreflexia: If someone has tolerated upright positioning and then has a problem with it
all of a sudden, may be a signal of infection
RESPIRATORY: C6-C7 have intact diaphragm, but may have limited intercostal
musculature (the lower the level of injury, the better the respiratory function)
ROM: May have limitations with ROM due to HO (develops over time), premorbid
contractures, arthritis and spasticity; **have to have 90 degrees of hip flexion in order to
balance without any abdominals
STRENGTH: Muscles may be be flaccid initially and become spastic once shock has
passed; if LEs stronger than UEs (suspect central cord); if unilateral differences
(suspect Brown-sequared); if there is progressing weakness proximal to the spinal cord
lesion (big red flag, especially at C level)
SENSATION: may have phantom pain below the level of the lesion with absent
localization/sensation
BOWEL and BLADDER: neurogenic bladder/bowel-bladder/bowel will not empty with
voluntary control, hypo reflexive-does not empty (more prone to infection), hyper
reflexive-empties too often
SEXUAL FUNCTION: some may achieve psychogenic or reflex erections (may be due
to vagus nerve); infertility common with males due to problems with temperature
regulation, women still have potential to get pregnant (should continue birth control if on
it previously)
Complications
AUTONOMIC DYSREFLEXIA; Single most common cause is a blocked urinary catheter
(risk for patients at T6 and higher); get assistance, check catheter, elevate head, look
for other sources if catheter is not the culprit. Symptoms: headache, sweating, nasal
congestion, sustained penile erection, hyperhydrosis above level of lesion, paresthesias
(If the face is red raise the head, if the face is pale raise the tail)
POSTURAL HYPOTENSION: lightheadedness, low BP, may yawn or pass out; ace
wrap LEs, binder, TED hose, reclining wheelchair, meds
HETEROTROPHIC OSSIFICATION: sudden limitation of ROM, may be warm over joint;
early detection is important so meds can be started, no aggressive ROM
DVT: swollen calf or LE, warm to the touch and may be painful; use SCDs, IVC filter,
movement, and may use meds such as heparin, coumadin
HYPOTHERMIA/HYPERTHERMIA: body is unable to regulate temperature, very
susceptible to external conditions; should provide education on proper clothing and
avoiding extreme temperatures
BURNS: may occur from touching hot products such as coffee or or plate due to loss of
sensation; be cautious with modalities!!
PAIN: often in shoulders along with area of injury; may use modalities for pain
SPASTICITY: hypertonicity of extremities denervated distal to the lesion; can manage
with medications such as baclofen and valium
SYRINGOMYELIA: progression of weakness proximal to the level of injury, especially
problematic for cervical injuries; requires surgical management (be alert to change in
level of function->decrease in motor function is a sign of new pathology)
CONTRACTURES: fixed limitation of ROM over a joint or multiple joints; managed by
prevention, ROM, and proper positioning (surgical release is also an option)
OSTEOPOROSIS: lack of bone density due to lack of weight bearing over time;
managed by weight bearing in a standing frame, be cautious with PROM
SPINAL DEFORMITIES: scoliosis, pelvic obliquities, kyphosis; due to poor wheelchair
positioning over time (only correction of a fixed deformity is a surgical correction)
SHOULDER INJURIES/CARPAL TUNNEL SYNDROME: overuse injuries from
wheelchair use which cause pain/weakness in shoulders and wrists; manage by proper
positioning in wheelchair and may need power chair vs manual
ADAPTATION SUGGESTIONS
Ramps: one foot of run for one inch of rise
Replace carpet with hardwood floors and remove throw rugs
Pedestal sink or cut out cabinet in the bathroom
Flat surfaces for bathroom sink for easier access
Place frequently used items on lower shelves
The clapper or other remote control ideas
Loops on the cabinet for easier opening
Lever door handles
Raise the floor of the kitchen (eliminate the toe box
Stackable washer and dryer
Safety Suggestions
Cordless/cell phone
Smoke detectors
Encourage pt to call fire depart and inform them there is a person with a disability in the
home
Adjust hot water heater to lower temperature
Weakness:
Muscle Performance
Peripheral factors
Length-tension properties
Viscoelasticity
Central factors
Motor units
Firing rate
Sequencing
Postural stabilization
Muscle Performance with CNS Pathology
Decreased force production: inadequate input to alpha motor neuron
Secondary factors
Incoordination
Spasticity / synergy patterns
Sensory loss
Disuse
Atrophy from disuse or LMN disease (Fasciculations)
Endurance / fatigue
Muscle spindle performance= Alpha-gamma coactivation
Muscle Spindle
Connective tissue capsule
Intrafusal muscle fibers
Gamma motor axons
Innervate intrafusal fibers
Cell bodies in ventral horn of spinal cord (with alpha mn)
Not involved in stretch reflex pathway
Alpha Gamma Coactivation
Sensory axons= endings in central region of intrafusal fiber
Types
Ia / primary sensory ending
Sensitive to low amplitude, high velocity stretch inputs
result of activation:
autogenic facilitation
reciprocal inhibition
II / secondary sensory ending
sensitive to slow, sustained stretch
activation results less clear:
complex polysynaptic response
Stretch sensitive channels
Examination of Weakness
AROM/MMT (is it Reliable?)
Position modifications / substitutions
Hand-held dynamometer
Reliability (ICC) ranged from 0.85 to 0.98 for both hemiparetic and non-paretic Isokinetic
dynamometer
Interventions for impairments in muscle performance
No active movement
0 or 1 on MMT scale
Insufficient alpha motor neuron input
Facilitation techniques:
Utilize stretch reflex pathway for autogenic facilitation
Tapping, vibration, also light touch
But activating only alpha motor neuron
Modify functional task / environment
Trying to activate alpha and gamma mn
Some Active Movement
Lack anti-gravity muscle power (2 or 3 on MMT scale)
Possibly only activating alpha mn
Use gravity-eliminated positions; can begin PREs
Functional task training / NDT
Modify task requirements to make it easier
Manual guidance may be required for safety
help learn new task
Goal to maximize patient-initiated activity as soon as possible
NDT
Hierarchical model of motor control
First goal of treatment is to normalize tone
Use of dev’t sequence to challenge trunk muscles, proximal mm stability
Use of resistance not advocated secondary to hypertonicity
Functional relevance
Manual guidance:
Mvmt should be effortless, if patient compensates then provide assistance
Goal to provide pt with experience of correct mvmt pattern
FES and Biofeedback
Appropriate when “some” active movement
Augmented feedback
Important to withdraw for learning
Bilateral Training
Weak “intact” upper extremity
Involve both motor cortexes
Stronger arm models weaker arm
Active Movement but Weak
Weakness as a primary or secondary impairment
Lack full muscle power (4 on MMT scale)
Resistance:
PREs with weights
Manual resistance in PNF diagonals
Consider body position
Trunk and extremity muscle power
Endurance
Overload principle
Rationale for strengthening in neuro population
Alpha-gamma coactivation
Use neuro pathways
Peripheral strength gains
Functional Task Training
“Repetition without Repetition” as an exercise
LE strength difference is a significant individual predictor for gait speed, gait endurance, and
functional balance. Cognition significantly predicted only gait speed
Resistance Exercise Training
Intensity and number of reps
Sets and frequency
Duration and Speed
Mode of exercise such as static, eccentric , of concentric
Range of movement e.g short arc vs. long arc
Position of the patient
Ottawa Panel Guidelines
Clinical practice guidelines for therapeutic exercises
Adult patients (>18 years of age) presenting with hemiplegia or hemiparesis following a
single clinically identifiable ischemic or hemorrhagic CVA
Use of progressive resistance training in lower extremity has clinically important
benefit in patients with post-acute stroke.
Proprioceptive Neuromuscular Facilitation
Definition: methods of promoting the response of the neuromuscular mechanism through
stimulation of the proprioceptor
Methods are most useful for: Stretching and Strengthening
PNF Diagonals
Upper extremity, Lower extremity, Trunk diagonal patterns
Move from passive, active assistive, resisted
D1 upper extremity
Wrist and finger flexion, Elbow flexion and supination, shoulder ER and flexion
TO: wrist and finger extension, elbow ext and pronation, Shoulder IR and extension
D2 upper extremity
Wrist and finger flexion, elbow flexion and pronation, shoulder IR and extension
TO: Wrist and finger extension, elbow ext and supination, shoulder ER and flexion
D1 lower extremity
Hip ext and IR, knee ext, PF and pronation
TO: Hip flexion and ER, knee flexion, DF and supination
D2 flexion lower extremity
Hip flex and IR, knee flex, DF and pronation
TO: Hip ext and ER, Knee ext, PF and supination
D2 extension lower extremity
Hip ext and ER, Knee ext, PF and supination
Good for working on standing
Trunk Patterns
Isolate one component of the pattern, Scapula or Pelvis
Perform in sidelying
PNF Techniques (Review)= Facilitation / Strengthening; Stretching
Rhythmic Initiation: Opposite patterns (D1 flex/ext & D2 flex/ext)
Start with passive movement
Encourage gradual patient participation
Incorporate resistance if goal is for strengthening
Hold Relax (Mostly for Ortho pts)
Stretching technique:
Take muscle to point of limitation
End-range isometric contraction (10 seconds) into direction of stretch
Contraction of antagonist muscles
Relax and passively move limb to new range
Repeat if indicated
Useful if tight muscle (agonist) is painful to contract
Contract Relax (Mostly for Ortho pts)
Stretching technique:
Take muscle to point of limitation
End-range contraction with rotation (10 sec) into opposite direction of stretch
Contraction of agonist (tight) muscles
Relax and passively move limb to new range
Repeat if indicated
PNF Techniques (New)= Developmental Sequence; Facilitation / Strengthening Stretching
Developmental Sequence
Sidelying Sitting Modified plantigrade Standing / walking
Quadriped
Bridging
Kneeling / half kneeling
Repeated Contractions
Induce contractions with quick stretch
Distal muscle groups
3-4 stretches applied, then apply resistance when contraction is strongest
Use with pattern or functional activities
Used as a strengthening technique when little active movement present
Agonist Reversals
Resisted concentric then eccentric of same muscle group
Use with pattern or during position changes (rolling)
Strengthening technique when poor eccentric control
Alternating Isometrics
Patient holds position with isometric resistance of agonists followed by antagonists
Use to hold positions, less useful to use with patterns
Strengthening exercise when poor trunk control
Rhythmic Stabilization
Isometric resistance in rotational mvmt (similar to AI)
Use to hold positions, less useful to use with patterns
Strengthening exercise when poor trunk control
Resisted Progression
Resistance applied during gait
Should not disrupt patient’s momentum or coordination
Manual resistance or with elastic band/tube
Abnormalities in Voluntary Movement:
Coordination:
 Involves the ability to carry out any motor task precisely and quickly.
 Dependent upon the environment and proprioceptive input (whereas strength does not).
 Multiple joints and mm’s activated at appropriate times to work together.
 Common to have frontal plane instabilities with incoordination issues.
Role of cerebellum:
 Input/Output to M1
 Corrects mistakes.
 Cerebellar pathology leads to unique coordination problems without motor weakness
-e.g. Friedrich’s ataxia, acute/chronic alcoholism, stroke/TBI, MS
 The primary problem w/cerebellar issues = balance/coordination whereas
balance/coordination will be a secondary issue with stroke and others.
Definitions:
 Ataxia: general term for incoordination. Gait ataxia = uncoordinated gait.
 Dysmetria: overshoot/undershoot phenomenon. E.g. finger to nose test or putting their toe on
the ‘X’ on the floor.
 Dydiadochokinesia: rapid alternating mvmts. E.g. supination/pronation or toe tapping.
 Tremors:
o Resting - Parkinson’s or some people might have neopathic tremors.
o Voluntary: Extra mvmts when completing tasks and resulting in incoordination.
Types of coordination Problems:
 Abnormal synergies means the inability to move a single joint w/o simultaneous mvmt in other
joints. Brunnstrom stages show abnormal synergies. With stroke, UE has higher
incidence of flexor synergy over extensor synergy whereas the LE has extensor synergy
(more common) > flexor synergy.
 Other sequencing problems include:
1) Coactivation across joint. Ex’s = toe walking where DF’s are coming on strongly but
the PF’s are over-powering them OR when someone has genu recurvatum when
there is coactivation of the hams/quads simultaneously.
2) Interjoint/trunk coordination – a stable/solid trunk is very important
 Reaction time (delayed)
 Slowed mvmt time
 Difficulty stopping mvmt
 Inaccurate force estimation – Happens when you go to pick something up, you need to have
the ability to grade their grip strength appropriately for the activity you are performing.
If there is a deficit in this, they will be unable to pick up varying cups due to they will be
unable to grade their grip strength appropriately.
Brunnstrom Synergy Patterns:
Stage 1: no mvmt
Stage 2: involuntary mvmt (like when they cough/sneeze)
Stage 3: abnormal synergy only (locked in that synergy pattern no matter what they do; they are
just stuck)
Stage 4: isolate one joint (they can have mvmt at one joint or body part only)
Stage 5: isolate two joints (ex: elbow ext with wrist flex or ext)
Stage 6: isolate all joints (still not coordinated and can still have slow mvmts or some ataxia)
Stage 7: normal mvmt
-These are developed for stroke only.
-Is useful to progress them through these stages.
-Stages 4 through 7 = where you move out of that locked in pattern.
Examination of Coordination:
 Brunnstrom stages
 Outcome measures
o Wolf Motor Function Test: for UE’s, has functional components (reaching, grasping),
used primarily for research.
o Gait: 10MWT for velocity, 6MWT for endurance
o Nine hole peg test: (more for OT) very standardized
 Special Tests (if there is active mvmt):
o Finger to nose (can time it and compare R and L) – tests for dysmetria.
o Knee to ankle (supine or sitting; can they hit the target or compare side to side; have to
make sure they have adequate strength/ROM for this)
o Rapid alternating mvmts – sup/pro; DF/tapping of feet; how long does it take to do 10
taps or how many can they do in 10 seconds – tests for dysdiadochokinesia.
Interventions for Coordination:
 Functional task training: Modify the task to make it easier or harder. Modify target constraints.
Reaching for various cups with different heights/weights or varying amounts of water.
 Practice w/varied timing or force demands.
 LE/Gait: Challenge them in different ways (accuracy vs speed). Can do LE target practice.
 Important to find out things that motivate them
 Make a big target and then make it smaller.
 Can start in sitting and progress to standing then walking, etc.
 PNF patterns: have both strength and coordination component.
 Frenkels Exercises “coordination ex’s”: Reciprocal mvmts of hands/feet or tracing
shapes/numbers. These are ways to exercise/practice outside of functional mvmts.
 The use of weights and the role of strengthening ex’s for coordination is unknown.
o The use of weights can be used to decrease voluntary tremors or decrease
incoordination. The weights are used to give proximal (trunk) feedback to
decrease tremors or decrease UE/LE (distal) symptoms.
o With strengthening ex’s you want to cover both strengthening and coordination. You
need to add a speed + accuracy component into treatment sessions in order to
improve coordination.
UE Intervention for Coordination:

Manipulation and dexterity:
o Examples include: 1) Finger tapping, 2) Picking up various objects (very small ones,
different weights, modifying cups), 3) Drawing/writing, 4) Turning pages, 5)
Using phone/keyboard
Motor Control Impairments: Tone/Spasticity
Muscle tone:
 Definition: resistance offered by mm’s when passively lengthened.
 Can be either hyper- or hypo- tonic.
 Range of mm tone is as follows from hypo to hyper tone: Flaccidity, hypotonia, normal,
spasticity, rigidity.
Hypotonicity:
 Can be an UMN or LMN problem.
 Examples include: Peripheral nerve damage, Down’s syndrome, cerebellar damage, UE after
CVA (b/c there is no alpha motor neuron or gamma motor neuron activation; no spindle
response to high velocity mvmts; the spindle is lax and isn’t taut like spasticity).
 Loss of normal alpha-gamma coactivation – slack spindle, no input.
 Upon examination, the pt will have a relaxed hand posture rather than the normal slighltly
flexed finger/wrist posture (in normal folks).
Spasticity:
 Encompasses many motor control issues clinically, not useful.
 Definition: Velocity-dependent hypertonia AND hyperreflexia.
o Examine this by passive motion for hypertone and reflex hammer for hyperreflexia
(Need to have both!)
 Rigidity: Severe, constant hypertonia
Hypertonicity:
 Diagnostic indicator of UMN problem
 Examples include CVA, PD.
 Causes can include neural mechanisms, non-neural mechanisms, or both.
o Neural: Alpha motor neurons are more sensitive to input (a small trigger can cause a
high motor response). When the neurons are depolarized, they are closer to the firing
threshold. This happens b/c there is a net increase in excitatory synaptic inputs and/or
net decrease in inhibitory synaptic inputs. This may develop over time as new synapses
form. The alpha motor neuron gets extra sensitive. A quick small stretch stretches the
spindle and gets facilitation/motor response. The alpha motor neuron is right at that
threshold so it doesn’t take much to depolarize. Is velocity-dependent.
o Non-Neural Cause: Immobilization has an effect of changing viscoelastic properties
(tendons, ligaments, joint capsule, and contractures). There is an actual change in mm
fiber structure (fibrosis, atrophy, or free calcium in motor fibers). Are NOT velocitydependent.
 Treatment
o Selective dorsal rhizotomy procedure: revealed weakness after neurosurgery to reduce
spasticity.
o Intrathecal baclofen studies.
Examination:

Passive mvmt of limbs at varying speeds
o Min, mod, severe tone on Modified Ashworth
Scale
Clasp-knife, cog wheel (release and catch), lead pipe (trying to bend that pipe to get rid
of tone)
o Describe specific mm groups and part of range resistance encountered
o No scale for hyptonia
o Reflexes
 DTR’s/Clonus
 H-Reflex: indicates sensitivity of alpha motor neuron system. This is a good way
to look at the sensitivity of an alpha motor neuron directly (good for research).
This will give an exact/precise measurement of hypertonicity. This is the only
way to physiologically measure this. It looks at the amount of depolarization of
the alpha motor neuron.
o Self report scale
o Functional performance
o Brunnstrom Synergy Patterns
Other related definitions for tone:
 Dystonia: Specific motor control disorder (Parkinson’s, Huntington’s)
 Spasm: Sustained involuntary mm contraction.
 Decerebrate rigidity: Extension of trunk, all extremities. Is seen in advanced brain cancer or very
bad hemorrhagic stroke. -There is limited clinical relevance
 Decorticate rigidity: UE flexion, trunk and LE’s in extension. -There is limited clinical relevance
with this.
Outcome Measures used for motor recovery in stroke:
 Fugl Meyer: Test of Motor Control
o Gold Standard
o Takes 20-30 minutes to administer
o Has sensation, UE, and LE component.
o Highly valid/reliable/standardized.
o 124 points total (0-35 is severe; 36-55 moderately severe; 56-79 moderate; >80mild)
 STREAM (Stroke Rehabilitation Assessment of Movement):
o Looks at UE mvmt, LE mvmt, and functional mobility.
o 15 minutes to administer
o Complicated scoring.
 Simplified STREAM
Treating abnormal tone:
 Need to consider:
o
o
Neural mechanisms: high velocity stretch puts a stretch on the spindle that sends signal
to the alpha motor neuron via Ia afferent fiber. The alpha motor neuron is the cause of
the tone NOT the spindle. The alpha motor neuron is hypersensitive to a quick stretch
b/c it’s at a lower threshold.
o Non-neural mechanisms: Tissue becomes fibrotic. Mm’s/tendons conform to being in
that same place = why you feel resistance/stiffness throughout the ROM
o Influence of other systems: Stress, effort, body position, bright lights, and loud noises
are all stimulating inputs which increase tone. Relaxing noises or slow rhythmic mvmts
will decrease tone.
o Functional relevance.
o Need to think: why are we treating tone? How does it relate functionally? You wouldn’t
treat JUST tone.
o Tone is in “Body Function/Structure” category of the ICF model.
 Surgical tx:
o Nerve cut or block (common in ped’s, not so much in adults)
 Pharmacological tx:
o Baclofen (oral or intrathecal)
o Valium
o Bo Tox injection
Treating Hypertonicity:
 Prolonged Stretch – affects neural and non-neural structures to decrease that sensitivity of the
alpha motor neuron and decrease the tightness of the soft tissues around that joint.
o NDT: reflex inhibiting positions (RIP)
o Serial casts – series of casts to increase stretch. These are really effective but has side
effects of not being able to weightbear. Disadv is that it will limit other motions and will
have the other effects of immobilization
o Air splints – temporary
 Rhythmical Rotation – stretching with a rotation component to decrease tone (hand/elbow).
 Weightbearing after you get it extended.
Rationale for treating hypertonicity (GTO/mm spindle explanation):
 The prolonged stretch activates the GTO’s autogenic inhibition and reciprocal facilitation.
 Is temporary but may allow functional task practice.
 Autogenic inhibition:
o GTOspinal cord via dorsal columnaction potentialIb inhibitory
interneuronsactivates inhibitory interneuron and causes inhibition of alpha motor
neuron
 Reciprocal facilitation
o Facilatory synapses
o Example: Prolonged stretch on the biceps leads to autogenic inhibition (relaxation) of
biceps and reciprocal facilitation of the antagonist (triceps)
 Basically with a prolonged stretch, there is autogenic inhibition of agonists mm’s which causes
them to relax and reciprocal facilitation of the antagonist mm’s(contraction of antagonist).
 GTO has stretch sensitive endings at the musculotendinous junction (Ib afferent fibers; no motor
component)
 GTO acts as a balance to the mm spindle where the mm spindle is facilatory and GTO is
inhibitory.
 Function of GTO:
o
o
1) Protective response
2) Fatigue
 Is very sensitive
 Has low threshold
 Even a very small threshold will activate the Ib afferent fibers.
 Is always active whereas mm spindle is not always active.
 2 ways to activate the GTO:
o 1) Manual prolonged stretch
o 2) Mm contraction which stretches the GTO and causes inhibition.
 Another way to inhibit GTO (besides prolonged stretch (is manual pressure on the tendon).
NDT Approach:
 Requirements for Normal Movement
o First you want to normal tone then move on to automatic reactions then to isolated
mvmts.
o 1) Normalize Tone
 With hypertone pt’s, perform rhythmic rotation, hands on stretching, RIP’s,
using GTO as inhibitory input, etc.
 With hypotone pt’s, you would want to do things to increase tone which may
include fast mvmts, bouncing, bright lights, activate excitatory ANS
 Inhibit other primitive reflexes (Abnormal synergy patterns, ATNR, ATLR, STNR,
STLR).
o 2) Automatic Reactions
 A.k.a. balance, trunk, head control
 Goal is to keep trunk upright and maintain good postural control.
 Righting reactions = head control
 Equilibrium reactions = trunk control
 Protective extension = After you lose your balance, you extend your extremities
as protection. This is why people with hemiparesis tend to fall to their weak
side b/c they might lack this automatic reaction.
o 3) Isolated Movement
 Individualized
 Key points of control
 Manual guidance – very hands on approach as compared to the traditional
approach which is very hands off.
 NDT is focused on doing the task correctly without a synergy pattern; if they
start to exhibit a synergy pattern then you would make the task easier.
 Advantages of NDT
o The therapist uses a hands on approach and are skilled at providing contact in certain
places to increase their function.
o Works on functional tasks; normal mvmts w/o a synergy pattern
 Disadv’s of NDT:
o Evidence is against NDT vs motor control (functional task practice) in terms of function.
Interventions for Limited PROM/Contractures:
 Stretching
o Stretching in healthy people can increase PROM (30second hold x15 mins)
o





Stretching can prevent a contracture in people with stroke w/minimal motor function
(daily positioning x30minutes static stretch)
o Stretching does not reduce a contracture if they have already obtained a contracture.
Splinting
o Static hand splints have no benefit in preventing contracture following stroke
o Dynamic hand orthosis only has case studies to support it and they ‘look promising’
o Other dynamic splints – Research is variable
Serial casting
o Effective at improving ROM in people with CP and TBI
o Disadvantages: Higher risk of adverse events, difficult technique/skill requirements,
impaired function due to being in cast.
Joint mobilization
o Small uncontrolled studies have shown increased PROM but no functional change w/use
of ankle joint mobilization in people w/stroke.
Heat modalities
o US effective at increasing Rom in healthy subjects.
o Limited research on hot packs (increased wrist Rom in subjects w/stroke)
o Take precaution with pt’s that have sensory/communication/cognition deficits.
Surgical release
o Tendon lengthening used in children w/CP (Achilles or hamstring)
o Achilles tendon lengthening in people w/diabetic neuropathy to prevent pressure ulcer
formation
o Resection of HO (heterotrophic ossification)
o Recurrence rates are common