Peripheral Nerve Disorders Flashcards
Wallerian degeneration
Involves axon and sheath distal to site of interruption.
Sheath doesn’t regenerate
Segmental demyelination
Involves sheath. It remyelination can occur to restore function.
(Guillain barre)
Axonal degeneration
Involves sheath and axon. Distal to proximal.
Peripheral neuropathy
Polyneuropathy
Bilateral symmetrical nerve involvement.
Legs more than arms, distal before proximal.
Radiculopathy
Involvement of the nerve root
neuropraxia
temporary disruption of nerve function (compression)
axonotmesis
axon interruption and loss of function (crush injury)
regen possible
neurotmesis
severance of the nerve. regen fails without surgery
Trigeminal Neuralgia
degeneration or compression (tumor, age) of the trigeminal nerve
Characteristics: UNILATERAL neuropathic pain along mandibular and maxillary branches. Autonomic involvement: worse with stress and cold, better with relaxation.
Bell’s Palsy
CN VII lesion by unknown acute inflammatory compression.
Characteristics: UNILATERAL facial muscle weakness or paralysis, loss of salivation control, acute onset with weeks-month recovery. Change in taste of ant 2/3 tongue. No loss of sensation.
Bulbar Palsy
weakness or paralysis to mm innervated by nerves with nuclei of the lower brainstem: face, tongue, larynx, pharynx.
Differentiate bulbar palsy from myasthenia gravis
both involve bulbar system but bulbar palsy doesn’t affect the ocular muscles***
Guillain-Barre
LMN polyneuritis affecting all peripheral nerves and CN.
Etiology: unknown, usually occurs after illness or infection of GI or resp
Characteristics: bilateral distal to proximal, motor > sensory, quick progression and slow but usually complete recovery
Medical: plasmapheresis, IVG, analgesics
PT: pulmonary PT, energy conservation, avoid overuse
ALS
Amyotrophic Lateral Sclerosis: progressive UMN and LMN degeneration (anterior horn cells including CST and CBT)
Etiology: unknown, some viral or autoimmune, 5-10% genetic
Characteristics: death in 2-5 years, variable symptoms, muscular weakness spreads over time, spasticity and hyperreflexia, usually no sensory involvement, pain, respiratory involvement, sparing of bowel and bladder, normal cognition, depression common.
Stages of ALS
I. early, focal weakness, hand cramping and fasciculations
II. moderate weakness in mm groups, some atrophy, MOD I
III. Severe weakness, increased fatigue, moderate functional limitations but ambulatory.
IV. severe weakness and wasting LE, mild UE, MOD A and wheelchair used.
V. deterioration of mobility and endurance, severe weakness of UE and LE. UMN signs, loss of head control, MAX A
VI. bedridden, dependent, progressive respiratory distress.
Role of Riluzole
glutamate antagonist - may help to delay disability and prolong survival with ALS, especially pseudo bulbar type
Postpolio Syndrome
New onset of weakness in patient with confirmed hx of polio.
Etiology: unknown - may be due to hyper functioning of nerves leading to denervation
Characteristics: asymmetrical weakness in weak mm groups, abnormal fatigue, myalgia and hypersensitivities, slow progression, cold intolerance, damage to reticular formation - change in concentration, attention. NO sensory involvement.
PT:
