Clinical Considerations of the Nervous System

• The Neurological exam should consist of the following six subdivision: – Mental status – Cranial nerves – Motor exam – Reflexes – Coordination and gait – Sensory exam

Neurologic Examination

• 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.

Mental Status

I. Olfactory: identify familiar smellsII. Optic: SeeingIII. Oculomotor: Eye movement, opening of eyelid, constriction of pupil,

focusingIV. Trochlear Nerve: Eye movementV. Trigeminal Nerve: Sensory to face (touch, pain and temperature) and

muscles of masticationVI. Abducens Nerve: lateral eye movementVII. Facial : Motor - facial expressions; salivary glands and tear, nasal and

palatine glands Sensory - taste on anterior 2/3’s of tongueVIII. Vestibulocochlear Nerve: Provides hearing and sense of balanceIX. Glossopharyngeal Nerve: Swallowing, salivation, gagging, control of BP

and respirationX. Vagus: Swallowing, speech, regulation of visceraXI. Accessory Nerve: Swallowing, head, neck and shoulder movementXII. Hypoglossal Nerve: Tongue movements for speech, food manipulation

and swallowing.

Cranial Nerves Review

• 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

Reflex Test

• 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

Reflexes

• 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.

Coordination Test

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.

• Multiple Sclerosis

• Cerebral Vascular Accident ( Stroke)

• Traumatic Brain Injury

• Spinal Cord Injury

• Cerebral Palsy

• Amyotrophic Lateral Sclerosis (ALS)

UMN Associated Conditions

• A motor dysfunction associated with lesions of cortical, subcortical, or spinal cord structures:

1. Muscle weakness to paralysis

2. Hyperreflexia, (spasticity and clonus)

3. (+) Babinski sign in LE

4. (+) Hoffman's sign in UE

Upper Motor Neuron Lesion (UMN)

• 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.

Spasticity

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.

• 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 Vascular Accidents( Stroke)

Cerebral Circulatory System

Blood Supply to the Brain

• Anterior cerebral artery

• Middle Cerebral Artery

• PosteriorCerebral Artery

http://www.cnsforum.com/content/pictures/imagebank/hirespng/brain_struc_stroke.png

http://www.cnsforum.com/content/pictures/imagebank/hirespng/brain_struc_stroke.png

Anterior Cerebral Artery CVA

Middle Cerebral Artery CVA

Posterior Cerebral Artery CVA

Visual agnosia (objects)

Prosopagnisia( face)

Thalamus leads to persistent pain

• 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 2

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/Numbness

• 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)

• 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

Spinal Cord Trauma: Transection

• Complete: complete transection of motor and sensory tracts

• Incomplete:– Anterior Cord Syndrome– Central Cord Syndrome– Posterior Cord Syndrome– Brown Sequard Syndrome

SCI: Subtypes

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

Lesions affecting the ant. horn cell or peripheral nerve

1. Atrophy

2. Weakness

3. Decreased or absent tone

4. Hypo-reflexia

Lower Motor Neuron Lesion (LMN)

• Bell’s Palsy • Poliomyelitis• Guillain-Barre syndrome• ALS• Myasthenia Gravis• Duchenne Muscular Dystrophy • Traction Nerve Injuries (Whiplash)• Herniated disc

LMN Associated Conditions

• 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.

Case Study 5

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 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

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

• 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.

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

CNS Modulation of Pain

Spinal Gating of Pain Signals

• 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)

Central Spinal Gating

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

External Gaiting Techniques

• 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.

Anatomy of ANS

• 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

Case Study 5

1. Diaphoresis / Night sweats2. Nausea3. Diarrhea4. Pallor5. Dizziness / Syncope6. Fever7. Fatigue8. Weight loss9. Night pain / Painless weakness10. Motor and Sensory changes associated with changes

in 1 or more DTR’s

The Red Flags- For Systemic Pathology

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

• 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.

Referred Pain

Sympathetic preganglionics from T1 to T4(5)

T1

T2

T3

T4

Cutaneous Innervation and Dermatomes

• (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.

Benign Paroxysmal Positional Vertigo (BPPV)

BPPV Diagnosis: Dix-Hallpike Manoeuvre

BPPV: Therapy

Eply Manuaver Brandt-Daroff

• 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 , alcohol-withdrawal, acetazolamide, betahistine

4. Menière disease

• Cervical spondylosis• Neuropathy• Visual impairment• Anemia• Hypoglycemia• Orthostatic hypotension• VBI/CVA

Common Causes of Vertigo

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.

• 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?

Plasticity Throughout the Life Span

• 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

Necessary for Plasticity

• 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.

Plasticity in Rehabilitation