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.