Clinical Considerations of the
Nervous System
Neurologic Examination
• The Neurological exam should consist
of the following six subdivision:
– Mental status
– Cranial nerves
– Motor exam
– Reflexes
– Coordination and gait
– Sensory exam
Mental Status
• Are the patients oriented to
– Person
– Place
– Time
• Ask specific questions that challenge:
– Memory
• Both long term and short term
• Ability to perform calculations and
judgment.
Cranial Nerves Review
I.
II.
III.
Olfactory: identify familiar smells
Optic: Seeing
Oculomotor: Eye movement, opening of eyelid, constriction of pupil,
focusing
IV. Trochlear Nerve: Eye movement
V.
Trigeminal Nerve: Sensory to face (touch, pain and temperature) and
muscles of mastication
VI. Abducens Nerve: lateral eye movement
VII. Facial : Motor - facial expressions; salivary glands and tear, nasal and
palatine glands Sensory - taste on anterior 2/3’s of tongue
VIII. Vestibulocochlear Nerve: Provides hearing and sense of balance
IX. Glossopharyngeal Nerve: Swallowing, salivation, gagging, control of BP
and respiration
X.
Vagus: Swallowing, speech, regulation of viscera
XI. Accessory Nerve: Swallowing, head, neck and shoulder movement
XII. Hypoglossal Nerve: Tongue movements for speech, food manipulation
and swallowing.
Reflex Test
• Looks at the integrity of the monosynaptic
loop. An abnormal response may indicate
lesions within the central or peripheral
nervous system.
– Achilles tendon: Sciatic nerve S1-2
– Patella: Femoral L3-4
– Biceps : Musculocutaneous Nerve C5-6
– Triceps :Radial C7-8
– Brachioradialis : Radial C5-6
Reflexes
• Scale
– 0: No evidence of contraction
– 1+ Decrease(hypo-reflexic)
– 2+ Normal
– 3+ above normal (hyper-reflexic)
– 4+ Clonus: Repetitive shortening of the
muscle after a single stimulation
Coordination Test
• Finger to nose testing:
• Rapid alternating finger ,hand and feet
movements:
– dysdiadokinesia may be indicative of
cerebellar disease.
• Gait assessment:
– Quality of movement :look for symmetry
– Antalgic Gait : looks for muscle weakness and
pain.
• Single leg stance and walking on heels and
toes.
Sensory examination
• Notice how the dermatomes correlate with the peripheral
nerves.
• Reflex test: test the monosynaptic reflex of a specific nerve
root level.
– Exaggerated reflex may suggest upper motor neuron lesion.
– Diminished reflexes is suggestive of nerve root or peripheral
nerve lesion
• Proprioception and vibration:
– large myelinated fiber and
– dorsal column medial
• Light touch and temperature
• small unmyelinated nerve fibers
• Anterior lateral tract (spinothalamic)
Cutaneous Innervation and
Dermatomes
• Each spinal nerve receive sensory input from a specific
area of skin called dermatome
Peripheral Nerve Distribution
Myotomal Weakness
• Look at # of motor units.
• If you use all of them you
go into neural fatigue in a
few seconds.
• Normally only use 25 %
of motor units.
• If you have 75-80% loss
in motor units it will
present as weakness.
– A protrusion or osteophyte
on nerve root.
• Test with slow build up of
pressure to allow max
recruitment.
UMN Associated Conditions
•
•
•
•
•
•
Multiple Sclerosis
Cerebral Vascular Accident ( Stroke)
Traumatic Brain Injury
Spinal Cord Injury
Cerebral Palsy
Amyotrophic Lateral Sclerosis (ALS)
Upper Motor Neuron Lesion (UMN)
• A motor dysfunction associated with
lesions of cortical, subcortical, or
spinal cord structures:
1.
2.
3.
4.
Muscle weakness to paralysis
Hyperreflexia, (spasticity and clonus)
(+) Babinski sign in LE
(+) Hoffman's sign in UE
Spasticity
• Spasticity occurs when upper motor neurons of
the primary motor cortex are damaged.
– The result is a loss of inhibitory input from upper
cortical areas to inhibitory interneurons in the spinal
cords.
– Inhibitory interneurons prevent muscle spindles from
responding to all quick movements.
– Spastic muscle contractions are in response to length
change and not volitional thought.
Case Study 1
• Your treating a patient who has a pmhx of
middle cerebral artery CVA . Predict the types
of deficits you might expect to find.
Cerebral Vascular Accidents( Stroke)
• Progressive arteriosclerosis can eventually lead
to damage and occlusion of the arteries that
supply the brain.
• This may lead to complete occlusion or vascular
rupture that will deprive the brain of O2 and
nutrients.
• Intracranial lesions will become a space
occupying lesion that further compromises
circulation and damages brain matter.
• Looking at what area of the brain was damaged
can explain what deficits patient may present
with.
Cerebral Circulatory System
Blood Supply to the Brain
• Anterior cerebral
artery
• Middle Cerebral
Artery
• Posterior
Cerebral Artery
Anterior Cerebral Artery CVA
Middle Cerebral Artery CVA
Posterior Cerebral Artery CVA
Visual agnosia
(objects)
Prosopagnisia( face)
Thalamus leads to
persistent pain
Case Study 2
• A patient presents with left-sided
weakness. The weakness thought of
following a really bad headache. Upon
examination you notice the following.
– 3+ reflexes left side
– Clonus left ankle
– Lower extremities tested more than half of
extremities
– Difficulty concentrating and impulsivity
Case Study 3
• 58 y/o with c/o vertigo especially with turning
her head to the right. She have a history of
falls, DM and dyslipidemia. She had previously
been ruled out for cerebrovascular accident
and cerebellar dysfunction. What’s a possible
diagnosis?
Vertebral Arteries
Vertebrobasilar Insufficiency
• Vertigo with associated
Neurological signs
• Diplopia (double vision)
• Ataxia
• Lateral nystagmus
• Drop attacks
• Dysarthria
• Paralysis/weakness/Nu
mbness
• Risk factors (HTN,
Diabetes, Coronary
artery disease and DJD)
– Look at the relationship
the symptoms and the
part of the brain effected.
Case Study 4
• A patient was in an MVA suffered a T12
fracture. Following the accident the patient
has difficulty walking.
• Exam results:
– Hyper-reflexia in lower extremities.
– Sensory loss in the lower extremities.
– Strength 5/5(normal)
Spinal Cord Trauma: Transection
• Cross sectioning of the spinal cord at any
level results in total motor and sensory loss
in regions inferior to the cut
• Paraplegia – transection between T1 and L1
• Quadriplegia – transection in the cervical
region
SCI: Subtypes
•
Complete: complete transection of motor
and sensory tracts
•
Incomplete:
– Anterior Cord Syndrome
– Central Cord Syndrome
– Posterior Cord Syndrome
– Brown Sequard Syndrome
Picture
Anterior Cord Syndrome
• Results from
compression or hyper
flexion injury.
• Loss of motor, pain
and temperature.
• Proprioception and
vibratory sense
preserved
Central Cord Syndrome
• Central cord may
result from
compression of spinal
cord, intramedullary
tumors or ischemia.
• Upper extremities
more involved then
lower extremities.
• Sensory less then
motor
Posterior Cord Syndrome
• May result from hyper
flexion injury.
• Profound sensory
loss
• Ataxic presentation
without procrioceptive
feed back ascending
the cord.
• Motor functions is
spared.
Brown Sequard Syndrome
• Damage to half the SC
usually from a gun shot or a
knife.
• Contralateral presentation:
– Loss of pain and temp
• Ipsilateral presentation:
–
–
–
–
–
Motor loss
Sensation
Proprioception
Hyperreflexia
+ babinski
Why is it worse to have a disease that
attacks the CNS vs. PNS
Lower Motor Neuron Lesion
(LMN)
Lesions affecting the ant. horn cell
or peripheral nerve
1.
2.
3.
4.
Atrophy
Weakness
Decreased or absent tone
Hypo-reflexia
LMN Associated Conditions
•
•
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Bell’s Palsy
Poliomyelitis
Guillain-Barre syndrome
ALS
Myasthenia Gravis
Duchenne Muscular Dystrophy
Traction Nerve Injuries (Whiplash)
Herniated disc
Case Study 5
• The patient presents with 6/10 LBP pain
that radiates to the left foot. Pain is worse
with prolonged sitting and bending over.
The patient noticed the symptoms
following shoveling snow.
• Your exam reveals the following.
– Painful straight leg raise test to 30°.
– L4 and L5 vertebrae very tender to touch
– Tingling along the dorsal surface of the foot.
Parkinson's Disease
• Results from a loss of
dopamine production in the
Substantia Nigra
• This effects the other nuclei in
the basal ganglia related to
voluntary movement and
postural adjustments.
• These pathways can both
stimulate wanted movements
(direct pathway) and inhibit
unwanted movements( indirect
pathways)
• Some common signs and
symptoms include
– Akinesia, rigidity
– Pill rolling tremor
– Fesitinating gait
Pain
•
Pain receptors are the most primitive
receptors.
–
•
•
They respond to a broad spectrum of stimuli
Pain has a sensory component :allow you to
localize it.
Pain has a drive like qualities:
–
–
Pain pathways also go to the midbrain (arousal)
Limbic system (motivational) makes you deal with it.
Pain Signal Destinations
• General pathway –
conscious pain
– 2nd order neurons
decussate and send fibers
up spinothalamic tract or
through medulla to
thalamus
– 3rd order neurons from
thalamus reach primary
somesthetic cortex as
sensory homunculus
• Spinoreticular tract
– pain signals reach reticular
formation, hypothalamus
and limbic
– trigger visceral, emotional,
and behavioral reactions
Pain
• Nociceptors – allow awareness of tissue injuries
– found in all tissues except the brain
• Somatic pain from skin, muscles and joints
– Fast pain travels in smaller myelinated fibers at 30 m/sec
– sharp, localized, stabbing pain perceived with injury
• Visceral pain from stretch, chemical irritants or
ischemia of viscera (poorly localized)
– Slow pain travels unmyelinated fibers at 2 m/sec
– longer-lasting, dull, diffuse feeling
• Injured tissues release chemicals that stimulate pain
fibers (bradykinin, histamine, prostaglandin)
– Anti-inflammatory medication inhibit the production of these
substances.
CNS Modulation of Pain
• Intensity of pain - affected by state of mind
• Endogenous opiods (enkephalins,
endorphins and dynorphins) act as
neuromodulators block transmission of pain
– produced by CNS and other organs under stress
• This is why you don’t feel pain right after a car accident.
– Spinal gating is the process of blocking
transmission of pain
– Occurs in the dorsal horn of spinal cord
Spinal Gating of Pain Signals
Central Spinal Gating
• Stops pain signals at dorsal horn
– descending analgesic fibers from reticular
formation travel down reticulospinal tract to
dorsal horn
• secrete inhibitory substances
(enkephalins and serotonin)
– block pain fibers from secreting substance P
» pain signals never ascend
» Opioids such as morphine also block receptors for
pain transmission within the brain and spinal cord.
» Can be very addictive because its effect on reward
centers ( Nucleus Accumbens)
External Gaiting Techniques
Nociceptors (smaller unmyelinated ) will be inhibited by
input from mechanoreceptors which are ( large
mylinated)
– Cutaneous stimulation is transmitted toward the CNS
via large mylinated A-delta fibers
– Pain fibers travel via small unmyelinated C –fibers
– Substantia gelatinosa appears to act as a gate
– Excitation of Substantia gelatinosa closes the gait.
• We uses counter-irritants such as
– Acupuncture ,hot packs, cold packs ,massage and
vibrating devices, vigorous activities (Runners High)
• These all excite large mylinated fibers
Anatomy of ANS
• We must look at the underline mechanics.
• Many symptoms patients experience and side
effects of medications are directly connected to
the ANS.
• ANS regulates all of the bodies major organ
systems.
• Understanding this system has lead to drugs
used to treat dysfunctions of cardiac, respiratory
,urinary ,reproductive to name a few.
Case Study 5
• Patient presents with left shoulder pain
and occasional jaw pain. Pain is provoked
with activity. Your exam reveals the
following.
– Range of motion and strength WNL
– Skin temperature was slightly cool and
diaphoretic.
– Pupils dilated
The Red Flags- For Systemic
Pathology
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Diaphoresis / Night sweats
Nausea
Diarrhea
Pallor
Dizziness / Syncope
Fever
Fatigue
Weight loss
Night pain / Painless weakness
Motor and Sensory changes associated with changes
in 1 or more DTR’s
Referred Pain
• Pain stimuli arising from the viscera are perceived as
somatic in origin
• This may be due to the fact that visceral pain afferents
travel along the same pathways as somatic pain fibers
Referred Pain
• Misinterpreted pain
– brain “assumes” visceral pain is coming from
skin
– Heart pain may be felt in shoulder, Upper
back, chest or and medial arm share
sympathetic input at spinal cord segments T1 to
T5
– Heart pain can also be perceived as nausea,
indigestion and throat tightness due to
parasympathetic input via the vagus nerve.
Sympathetic preganglionics from T1 to T4(5)
T1
T2
T3
T4
Cutaneous Innervation and Dermatomes
Benign Paroxysmal Positional Vertigo
(BPPV)
• (BPPV) dizziness results from debris "ear rocks",
(otoconia). They are small calcium carbonate crystals
from the utricle get lodged in one of the semi circular
canals.
– This may result from head injury, infection, or other disorder of
the inner ear.
• BPPV include dizziness or vertigo, lightheadedness,
imbalance, and nausea
• Treatment includes:
– diagnosis with Dix-Hallpike manoeuvre.
– Treatment included Eply maneuver and Brandt-Daroff
exercises.
BPPV Diagnosis: Dix-Hallpike
Manoeuvre
BPPV: Therapy
Eply Manuaver
Brandt-Daroff
4. Menière disease
• Disorder of the inner ear that can affect hearing
and balance.
• Patients may experience episodes of tinnitus,
dizziness, nausia,vomiting,nystagmus and
progressive hearing loss.
• Results from an increase in volume and
pressure of the endolymph of the inner ear.
• Therapy: salt free diet, nicotine , alcoholwithdrawal, acetazolamide, betahistine
Common Causes of Vertigo
•
•
•
•
•
•
•
Cervical spondylosis
Neuropathy
Visual impairment
Anemia
Hypoglycemia
Orthostatic hypotension
VBI/CVA
Psychological Disorders
• Anxiety: involves the
hippocampus and
Amygdala of the limbic
system.
– Characterized as an intense
fear, apprehension, or
worrying.
– Neural connections to the
hypothalamus result in a
sympathetic response.
• Increases in
– Heart rate (palpations)
– Blood pressure (Headache)
– Excessive sweating
(diaphoreses)
Psychological Disorders
– Depression: prolonged feeling
of sadness, hopelessness,
pessimism, guilt, often often
accompanied with multiple
musculoskeletal complaints.
– Obsessive Compulsive
Disorder (OCD)
• Defect in the ability to make
decisions
– Schizophrenia: Progressive
neurological condition destroys
brain matter. Results in the
following:
• delusions, hallucinations
(visual or auditory)
Insomnia
•
•
Defined as a persistent difficulty falling asleep or
staying asleep despite the opportunity.
The suprachasmatic nuclei in the hypothalamus
is your biological clock.
– At night less input from your eyes triggers melatonin
which reduces sensory input to the cortex.
– Day time the brain produces serotonin which wakes
us up.
– The ability to over ride your sleep cycle was
important from an evolution stand point.
– During sleep we go through different stages. That
gives you the ability to respond to your environment.
– Stress is a leading cause of insomnia. This may
have kept you out of the tiger’s stomach.
– Stress today is more mental then physical.
– The primitive pathways that saved us in the past
prevent us from getting to bed now.
Plasticity Throughout the Life Span
• At birth there are less neural pathways
developed.
– A rapid increase in both the production of
neurons and their synaptic connections.
• In early childhood we have the greatest
amount of synaptic connections.
– By adolescence we strengthen synaptic
connections that we frequently use and loose
synaptic connections that we don’t use.
– Why do teenagers do really stupid things?
Plasticity Throughout the Life Span
– Historically it was thought that only the young
brain could only rewire itself and creates new
neurons up to the first few years of life.
– Recent studies have demonstrated that even
the brain of the elderly could create new
synapses and neurons.
• Remodeling will be based on the stresses and
areas of the brain you use.
– What areas of the brain my overly develop in the blind?
– How may a spinal cord injury effect the primary sensory
cortex?
Necessary for Plasticity
• The brain must be focused.
– This will allow for maximum synaptic connection.
– Neurons the fire together get stronger together.
• Initial changes are temporary.
• Cardiovascular exercise will ensure the brain receives
enough oxygen.
– Exercise is better for maintaining your brain than doing
a crossword puzzle.
• Memory and motivations are critical for learning and
developing more skilled movement brain plasticity can be
a double edge sword.
– Chronic pain syndromes and bad habits.
– Rehabilitation of patients with CVA, TBI
Plasticity in Rehabilitation
• Following a CVA it is critical to get the patient to use the
effected limb
– Repetition stimulates descending cortical fibers to
undergo synaptogenesis ( make new synapses)
around the alpha motor neuron in the anterior horn.
– Without descending input ( disuse) muscle spindle
circuit synaptogenesis will dominate resulting in
increased spasticity.
– The bottom line is synaptogenesis can be beneficial if
the descending cortical neurons are sprouting
collaterals. With disuse the monosynaptic reflex will
undergo this same process further limiting volitional
use.