Exam V Flashcards
alpha motor nerves are associated with what?
Extrafusal muscle fibers
beta motor nerves are associated with what?
intrafusal, with collaterals to extrafusal
gamma motor nerves are associated with what?
intrafusal muscle fibers
Describe the vascular supply of peripheral nerves
Rich vascular supply makes them resistant to ischemia. Vessel are coiled when limb is in shortened position, becomes uncoiled during movement, so vasculature is not stretched/damaged during movements
3 categories of severity in PNIs
Neuropraxia
Axonotmesis
Neurotmesis
Neurapraxia
Typically a result of mild blunt injury, compression, ischemia or disease
-Results in temporary weakness and/or sensory loss, Axons remain intact and myeline can get damaged (segmental demyelination. Slows/block local conduction at the site of injury, conduction above and below is normal. no atrophy of muscles and recovery can happen through re-myelination. Typically rapid full recovery of function (6-8 weeks)
Axonotmesis
When axon gets damaged/disconnected, but outer coverings (endo-, peri- or epineurium) remain intact
Neurotmesis
When axon along with all its coverings (endo-, peri- and/or epineurium) are severed
Risk factors for CTS
neuropathic conditions, arthritic conditions, metabolic conditions, smoking, structural abnormalities, occupation (repetitive gripping, hand held heavy tools that vibrate), working in extreme cold temps, and sedentary lifestyle
CTS clinical manifestations
Pain, paresthesia, numbness and weakness in the distribution of median nerve, Sensory symptoms precede motor. Nocturnal pain is hallmark, thenar weakness in advanced stages that can lead to atrophy if not addressed.
Thoracic outlet syndrome
entrapment or compression syndrome caused by pressure on nerve fibers of brachial plexus or vascular structures at some point between the interscalene triangle and inferior border of axilla. Vague symptoms
What are the 3 categories of TOS
Neurogenic (compression of brachial plexus), Vascular (subclavian artery/vein), nonspecific (disputed etiology)
Risk factors for TOS
congenital abnormalities and posture associated with growth (cervical rib, elevated first rib, or scalene muscle anomalies. Can also be due to trauma or certain occupations. Women > men
Clinical manifestations of TOS
May have vague symptoms (difficult to interpret), pain, tingling, paresthesia in arm particularly at end of day. Can also cause paresis and atrophy in severe cases.
If upper nerve plexus (C5-7) is involved in TOS, it results in…
pain in neck, radiate to face (sometimes ear), anterior chest, scapula
If lower plexus (C7-T1) is involved in TOS, it results in…
pain/numbness in shoulder, arm, ulnar digits of hand
Neural involvement with TOS symptoms
pressure over lateral neck/clavicle elicits pain/tingling; pain with head turned/tilted to opposite side; numbness/hypoesthesia in radial/ulnar nerve distribution; weakness in biceps/triceps/wrist/hand, color and temperature changes
Vascular involvement with TOS symptoms
Swelling of arm/hand, discoloration of hand, UE claudication, skin temperature changes, cold intolerance
Bells Palsy/Facial nerve paralysis risk factors
Triggered by viral infections, re-activation of a latent virus, or HSV, mumps, rubella. Also metabolic factors or demyelination and axonal degeneration
Bells Palsy/Facial nerve paralysis clinical manifestations
Unilateral facial paralysis, symptoms develop rapidly often overnight. Corner of mouth droops, nasolabial fold flattens, eyelids do not close. Autonomic involvement causes dry/red eyes (lack of tearing). in severe and chronic cases, pain contractures, and hemi-facial spasms.
How can you lose taste sensation with facial nerve paralysis?
If compression is proximal to chorda tympani branch
What happens if stapedius muscle innervation is lost with facial nerve paralysis?
Sounds become louder
What is Bell’s Reflex?
rolling up of eye ball during attempts to close eye, upper eyelid does not close far enough (is physiologic protective reflex, but becomes more apparent following orbicularis oculi muscle weakness)
Synkinesis
After severe injury, axonal regrowth/rewiring could be misdirected. Synkinesis is involuntary and undesirable facial movements associated with voluntary facial movements.
Charcot Marie Tooth disease
Inherited motor and sensory neuropathy (HMSN), slowly progressive disorder characterized by distal limb weakness and wasting, skeletal deformities, distal sensory loss and reduced DTRs. Cna present as foot deformities
Charcot Marie Tooth disease clinical manifestations
Distally symmetric muscle weakness, Fibularis/Peroneal muscles affected causing weakness and wasting of dorsiflexors/evertors, intrinsic foot muscles. As the disease progresses, weakness/wasting of intrinsic muscles of hand. Symptoms progress proximally.
Sensory symptoms with Charcot Marie Tooth disease
loss of proprioception/vibration followed by decrease in pain/temperature, parasthesia, in feet/hands - presents in ‘stocking and glove’ pattern
Rapidly reversible neuropathy
in those who have been newly diagnosed. Symptoms disappear when blood sugar gets controlled although NCV abnormalities may persist. Distally symmetric sensory changes like burning, paresthesia, and tenderness in feet/legs.
Generalized symmetric polyneuropathies
Acute sensory neuropathy
Rapid onset of severe burning pain, deep aching pain, sharp ‘electric shock-like’ sensations, hypersensitivity of feet worse at night, allodynia
Motor exam is mostly normal
Recovery can occur within 1 year if individual can maintain good blood sugar
Chronic sensorimotor neuropathy (DPN)
The most common type, onset is mostly insidious, and slowly progressive. Clinical features depend on selective fiber-type involvement. Typically glove and stocking pattern. Loss of ankle DTR, motor weakness mostly in hands/feet, is mostly milder but can cause deformities
Small fiber involvement for DPN
Small fibers involvement causes burning pain, paresthesia, more profound at night
Large fiber involvement for DPN
Large fiber involvement causes painless paresthesia, impaired proprioception, vibration sense, may feel like ’walking on cotton’.
Autonomic involvement for DPN
sweating (less or more), OH, resting tachycardia
Autonomic neuropathy
Sympathetic and parasympathetic involvement. With autonomic denervation, heart rate becomes fixed
may not feel ischemic angina - can suffer silent MI
Focal neuropathies (mononeuropathies)
Occurs less often than generalized symmetric patterns
May involve nerves in limbs or CNs –median, ulnar, peroneal nerves most commonly affected, somatic division of oculomotor nerve
Anterior Vestibular Artery
supplies the vestibular nerve, utricle, horizontal and anterior semicircular canals. Can become occluded due to cardioembolic source and not often visible on MRA. No auditory symptoms
Main Cochlear Artery
supplies the cochlea
vestibulocochlear artery
supplies parts of the cochlea, inferior saccule, and posterior semicircular canal
Posterior vestibular artery
supplies the saccule and the posterior semicircular canal
Vestibular Nuclear Complex
Superior and Medial Vestibular Nuclei are relays for the VOR. MVN is also involved in VSR and coordinates eye/head movements that occur together. Lateral vestibular nucleus is principle nucleus for VSR
Otoliths: Utricle and Saccule
Responds to both linear head motions and static tilt with respect to gravity. Also responds to changes in velocity (acceleration/deceleration). Saccule is oriented vertically while utricle is oriented horizontally.
Striola
separates the direction of hair cell polarization on each side of the otolithic organ
Alexander’s law
States that in individuals withnystagmus, the amplitude of the nystagmusincreases when the eye moves in the direction of the fast phase. Nystagmus increases when visual fixation is blocked.
Ewald’s laws
Law 1: A stimulation of the semicircular canal causes a movement of the eyes in the plane of the stimulated canal
Law 2: In the horizontal semicircular canals, an ampullopetal endolymph movement causes a greater stimulation than an ampullofugal one.
Law 3: In the vertical semicircular canals, the reverse is true.
Cerebellar Vermis (Midline)
responds to vestibular stimulationhas inhibitory influence on the vestibular nuclear complex. Helps to calibrate/modulate vestibular outflow improve accuracy of vestibular reflexes.
Cerebellar Flocculus
adjusts and maintains the gain of VOR
Cerebellar Nodulus
adjusts the duration of VOR responses and is responsible for processing otolithic input
Lesions to the anterior/superior vermis cause…
affect the VSR -> Profound gait ataxia and truncal instability (Excessive ETOH intake)
Neuritis
inflammation of the nerve,affects the branch associated with balance, resulting in dizziness or vertigo but no change in hearing.
Labyrinthitis
inflammation of the labyrinth,occurs when an infection affects both branches of the vestibulo-cochlear nerve, resulting in hearing changes as well as dizziness or vertigo.
Vestibular neuritis
onset is often preceded by presence of a viral infection of the upper respiratory or GI tracts. The chief symptom is the acute onset of prolonged severe rotational vertigo that is exacerbated by movement of the head. Associated with spontaneous horizontal rotatory nystagmus beating toward the good ear
H.I.N.T.S.
Head impulse, nystagmus, test of skew
For patients with acute vestibular syndrome, need to rule out central causes indicated by the following clinical findings:
Normal head impulses
Direction changing nystagmus in different directions of gaze (gaze evoked nystagmus)
-Nystagmus may also be pure vertical or pure torsional
-Nystagmus is not suppressed with visual fixation
Vertical skew
If there is no chance in quality of nystagmus with vision blocked, what is it indicative of?
With this, the diagnosis of vestibular neuritis is excluded. It is indicative of central lesion
I.N.F.A.R.C.T.
For stroke screening,
I.N. -> Impulse Normal (HIT negative bilaterally)
F.A. ->Fast-phase Alternating (direction changing nystagmus)
R.C.T -> Refixation on Cover Test (skew deviation)
H.I.N.T.S. “Plus”- PERIPHERAL FINDINGS
Must have ALL of the following
-Unidirectional Nystagmus–> direction-fixed
-No Skew Deviation
-Abnormal Head Impulse Test -> unilateral, away from fast phase of nystagmus
-No new hearing loss
H.I.N.T.S. “Plus” – CENTRAL FINDINGS
Stroke is suspected if ANY of the following exist:
-Normal head impulse test
-Direction changing nystagmus in eccentric gaze (gaze evoked nystagmus)
-Skew deviation (vertical ocular misalignment)
-New hearing loss
Lateral Medullary Syndrome patient complaints
aka Wallenberg’s or PICA syndrome,
Vertigo/dysequilibrium
Altered perception of verticality
Loss of pain and temperature:
-Ipsilateral on face
-Contralateral on body
Lateral Medullary Syndrome clinical findings
aka Wallenberg’s or PICA syndrome,
Central nystagmus
Ipsiversive OTR
Ipsipulsion on saccades
Lateropulsion of body
Ipsilateral dysmetria, dysrhythmia, and dysdiadochokinesia
Ipsilateral Horner’s Syndrome (droopy eyelid, decreased pupil size and sweating on affected side)
Lateral Pontomedullary Infarct(AICA Infarction) patient complaints
Vertigo/Dysequilibrium
Altered perception of verticality
Loss of pain & temperature
-Ipsilateral on face
-Contralateral on body
Hearing loss
Lateral Pontomedullary Infarct(AICA Infarction) clinical findings
Gaze evoked (direction changing) nystagmus
Unilateral hearing loss is more common with AICA than PICA infarcts
Cerebellar infarction
initial symptoms may include vertigo, N/V, and ataxia. May be confused with peripheral vestibular loss but should see cerebellar signs
Benign Paroxysmal Positional Vertigo (BPPV)
A mechanical disorder of the labyrinths in which otoconia become displaced in the semicircular canals and cause asymmetric vestibular excitatory output with head movement contributing to episodic, intense, vertigo related to head position
Canalithiasis
free-floating particles (otoconia) that have moved from the utricle and collect near the cupula of the affected canal, causing forces in the canal leading to abnormal stimulation of the vestibular apparatus. (takes a little while for nystagmus and dizziness to start also more brief duration)
Cupulolithiasis
otoconial debris attached to the cupula of the affected semicircular canal cause abnormal stimulation of the vestibular apparatus. (starts immediately)
Superior semicircular canal dehiscence
Syndrome of vertigo and oscillopsia induced by loud noises or by stimuli that change middle ear or intracranial pressure. Symptoms with loud noises and valsalva.
Dehiscence creates a defect in bone overlying the superior semicircular canal creating a “third mobile window”
Tullio phenomenon
increased pressure in external auditory canal produce nystagmus consistent with superior canal involvement
Perilymphatic Fistula
rare condition often caused by head trauma/barotrauma, violent exercise, heavy lifting, and sneezing. Abnormal communication of the inner and middle ear and commonly at round and oval windows of middle ear. May experience increased symptoms with exertion or loud noises (“Tullio” phenomenon)
Common symptoms associated with BPPV
intense vertigo with head position changes and sensations stop 20-30 seconds after the head is in static position. Complaints of waking up dizzy after rolling over in bed and during head movement or when bending forwards.
Vertebrobasilar Insufficiency symptoms
vertigo (most common), dizziness/syncope, drop attacks where people suddenly feel weak in the knees and fall. Also include ataxia, contralateral motor weakness, and dysphagia/dysarthria
what two things help differentiate Vestibular Migraine vs Meniere’s Disease?
With migraine, usually short naps are helpful, and visual auras are common. With Meniere’s disease short naps are not beneficial and visual auras are uncommon.
Endolymphatic Hydrops
consists of abnormal fluctuations in the endolymph fluid, which fills the hearing and balance structures of the inner ear. These fluctuations cause an increase in pressure in the endolymphatic system of the inner ear. The Patient could complain of pressure or fullness in the ears, tinnitus (ringing in the ears), hearing loss, and balance problems.
Meniere’s Disease
has the following spells: aural fullness/tightness, fluctuating hearing loss, tinnitus, vertigo
Vertigo peaks within minutes and last for several hours and dysequilibrium can last for several days. Asymptomatic in between spells
Persistent Postural Perceptual Dizziness (3PD)
The main clinical characteristics of this disorder include:
-Persisting subjective non-rotational vertigo or dizziness
-Hypersensitivity to motion stimuli (patients own movement, motion of objects in the visual surround)
-Difficulties with precision visual tasks.
Typically have normal values in clinical balance tests, some patients can develop secondary features of functional gait disorder.
Acoustic Neuroma
Slow-growing tumor that develops from the balance and hearing nerves supplying the inner ear. The tumor comes from an overproduction of Schwann cells
As the acoustic neuroma grows, it compresses the hearing and balance nerves, usually causing unilateral (one-sided) hearing loss, tinnitus (ringing in the ear), and dizziness or loss of balance.
As it grows, it can also interfere with the facial sensation nerve (the trigeminal nerve), causing facial numbness.
It can also exert pressure on nerves controlling the muscles of the face, causing facial weakness or paralysis on the side of the tumor.
Guillian-Barre Syndrome
rapidly evolving inflammatory PND characterized by rapid-onset motor paresis and sensory deficits. Autoimmune inflammatory disorder where body’s immune system mistakenly attacks the PNS. Can be triggered/preceded by respiratory/GI infections
Guillian-Barre Syndrome clinical manifestations
rapid onset of symmetric weakness, beginning distally in legs or arms, progressing to trunk, reaching peak weakness in 2-3 weeks. Initial symptoms are often tingling/paresthesia often in toes. progression of symptoms stop by 4 weeks, then a static phase lasts for 2-4 weeks, then recovery begins in proximal to distal direction. Recovery may take months to years. Respiratory muscles can also be involved.
Prognosis of Guillian-Barre Syndrome and factors to predict poor outcomes
Most people recover completely. Complications that can persist (distal weakness, neuropathic pain, autonomic changes).
Factors that predict poor outcomes – onset at older age, protracted time before recovery begins, need for artificial respiration
Modified Erasmus GBS Outcome Score (EGOS)
Prediction tool for walking, higher the score (0-9 or 0-12), higher the probability of inability to walk in weeks and months.
Postpolio syndrome/Post-polio muscular atrophy
PPS refers to new neuromuscular symptoms that occur to polio survivors decades after recovery from the acute paralytic episode of poliomyelitis infection
Clinical presentation following initial polio attack
focal asymmetric motor involvement without any sensory deficits
Postpolio syndrome/Post-polio muscular atrophy clinical manifestations
New weakness, muscle atrophy, pain and fatigue in the limbs that were originally affected, or in limbs that were not affected previously. Very slowly progressing condition, deterioration of strength occurs faster than normal aging. Excessive fatigue, pain, and problems swallowing and breathing.
Myasthenia Gravis
Most common disorder of the NMJ. Chronic autoimmune disorder characterized by fluctuating weakness and fatigability of skeletal muscles. Can affect any age group
Myasthenia Gravis clinical manifestations
Cardinal features are fluctuating muscle weakness and fatigability. Repetition of activity causes fatigue, rest restores normal activity.
Complex regional pain syndrome (CRPS)
A group of chronic pain syndromes that often worsens with time, generally characterized by severe pain out of proportion to the original injury,
Characterized by sensory, motor and sympathetic dysfunction w/ or w/o known trauma
CRPS I (formerly RSD)
caused by injury that did not directly damage the nerves in the affected limb, most (90%) CRPS is of this type.
CRPS II (formerly causalgia)
associated with known nerve trauma
CRPS clinical manifestations
Abnormally exaggerated pain processing (hyperalgesia, allodynia) – may spread proximally, and also from ipsi to contra side. Edema, skin color and temp changes, trophic changes, motor dysfunctions, bone changes.
Acute inflammation stage of CRPS
pain, swelling, redness, sensitivity to touch
Dystrophic stage of CRPS
alternating between sweaty and cold, skin color changes from red-to-white-to-blue
Atrophic stage of CRPS
severe muscle and bone changes, atrophy, osteoporosis, contractures
Meningitis
Inflammation of the meninges of brain and spinal cord secondary to infection which needs to be treated quickly. It can also extend to 1st and 2nd layers of cortex and spinal cord. Increased chance of tissue infarction, scar tissue formation, which can restrict CSF flow, resulting in hydrocephalus. Cardinal sign is headache (sudden).
meningitis clinical manifestations
Primary signs - Headache, sudden high fever, stiff neck. Positive meningeal signs include nuchal rigidity, Kernigs sign, and Brudzinski’s sign.
In severe cases - opisthotonus, seizures, reduced level of consciousness (sleepiness)
Kernigs sign
In supine position, after thigh is flexed at the hip and knee kept at 90 degree angles, subsequent extension of the knee causes pain (leading to resistance)
Brudzinski’s sign
In supine, flexion of neck produces flexion of hips and knees
Encephalitis
Acute inflammatory disease of the brain parenchyma (brain tissue), is caused by direct viral or bacterial invasion or by hypersensitivity initiated by virus. primarily in gray matter but meninges could also be affected.
Encephalitis clinical manifestations
In general, fever, headache, nausea, vomiting are followed by altered mental status (lethargy, confusion, memory disturbances), seizures. Depending on the brain area involved, there may be focal signs, hemiparesis, aphasia, sensory deficits, ataxia, chorea, athetosis
West Nile virus can cause…
fever, headache, stiff neck, photophobia, lesion of anterior horn cells cause paralysis and diminished reflexes similar to polio which plateaus within hours
Herpes simplex can cause…
seizures, hallucinations, memory disturbances.
Primary tumors
Develop in brain, spinal cord or surrounding structures
benign or malignant
Secondary tumors
Metastatic
Spread to CNS from another site, such as lung or breast
Paraneoplastic syndromes
May occur because of remote effects or indirect effects on CNS from cancer elsewhere in body (possibly from abnormal immune reaction of body when fighting the cancer)
Leptomeningeal carcinoma
When cancer metastasizes to pia and arachnoid with multiple lesions in meninges and CSF pathways
CNS neoplasms clinical manifestations
Initial signs are related to generalized effect of increased ICP – headache, nausea, vomiting, AMS. Tension type headache, migraine, papilledema (swelling in optic disc)
As tumor grows, it causes progressive tissue destruction in specific locations, CN VI highly susceptible to ICP elevations (causing diplopia)
seizure activity - may be the first sign of tumor in them (or stroke)
