Disorders of the Peripheral Nervous system (PNS)
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21 terms
Terms | Definitions |
|---|---|
Class 1 -Neurapraxia | nerve entrapment(damages the myelin sheath), affects large diameter axons first (motor, touch, proprioception, reflexes) but not nerve fibers of axon, can progress to axonotmesis or recover in 4-6 weeks) |
Class 2 (Axonotmesis) | crush injury with damage to nerve fibers, immediate loss of nerve function followed by Wallerian degeneration of the axons distal to the injury, connective tissues and Schwan cells are intact, so axons can regenerate to appropriate target tissues (1mm/day) |
Class 3 (Neurotmesis) | nerves are severed by excessive stretch or laceration, connective tissues and myelin are also damaged along with the axon, immediate loss of nerve function followed by Wallerian degeneration of the axons |
Multiple Mononeuropathy | random, asymmetrical involvement of more than one nerve |
Polyneuropathy | symmetrical involvement, distal to proximal (stocking/glove), involves sensory impairments, motor weakness and atrophy, Causes-toxicity, nurtitional deficiencies, diabetes and autoimmune disorders |
Signs and symptoms of Mononeuropathy | REMEMBER, symptoms occur in the peripheral nerve distribution, NOT a dermatomal or myotomal distribution |
Sensory-Neuronal Hypoactivity | decreae or lack of sensation (touch, pain, pressure or proprioception) |
Sensory- Neuronal Hyperactivity | Pain, dysesthesia or hyperesthesia |
Motor Neuronal Hypoactivity | Paresis, paralysis, hypotonia or muscle atropy |
Motor Neuronal Hyperactivity | spasm, Fasiculations, and fibrillations |
Autonomic-Neuronal Hypoactivity | Edema, flush skin and no sweating |
Autonomic Neuronal Hyperactivity | vasoconstriction, cold skin, cyanosis, perpetuations of pain and increased swelling |
Reflexes-neuronal Hypoactivity | Decreased or absent |
Refexes-Neuronal Hyperactivity | Normal |
Bells Palsy | annual incidence is 20 cases per 100,000 people, entrapment of facial nerve, unilateral facial paralysis with normal sensation, may also affect taste, salivation and tear production, Treatment- during paralysis, estim to maintain muscular tone and facilitate function, AROM for facial muscles affected (shouldn't be too strenuous), after recovery, retraining and strengthening of nuscles affected as needed, typically recover in several weeks to months |
Charcot-Marie-Tooth disease | affects 1 and2500 people in the US, inherited disorder with several forms caused by differen charomosomal abnormalities, it is a demyelination or axonal degerneration of peripheral nerves, affects the peroneal nerves first (DF and evertors), symmetrical weakness and atrophy with loss of reflexes, weakness of dorsifelexors causes foot drop and steppage gait, feet develop a pes cavas deformity with hammer toes, treatment and progression involves use of orthotics for gait and stretching to prevent contractures, slowly progressive with symptoms appearing distally in the UE's with progression |
Trigeminal Neuralgia | demyelinated fibers of CN 5 become hyperexcitable, possible causes- Herpes Zoster (Shingles), MS, vascular lesions or tumors, unkown in some, attacks of sharp facial pain that can be triggered by chewing, smiling, remissions occur spontaneoulsy and medication is used to control symptoms |
Guillain-Barre; Syndrom (acute Inflammatory demyelinating Polyradiculoneuropathy) | Annual incidence is 1-2 cases per 100,000 people, autoimmune disorder, often triggered by an acute viral or bacterial infection, Macrophages strip myelin from axons in the PNS, symmetrical motor weakness, distal to proximal with distal sensory impairment up to 30% of pt's require mechanicall ventilation, |
Treatment of Guillain-Barre' Syndrome | symptoms progress 2-4 weeks, followed by recovery progressing proximal to distal, by the third week of the illness 90 % of all pt's are at their weakest, During actue phase- monitor and facilitate respiratiory functioning (O2 sat, cough, airwary clearance), PROM to maintain muscle length, teach postiong to avoid skin breakdown, During early rehabilitation- don't overstretch or overwork affected muscles, pool exercise facilitates muscle strengthening, As function returns- muscle reeducation(PNF) beginning active and progressing to resistive, moderate level intensity to increae cardiovascular functioning, teaxch energy conservation techniqus, Prognosis- 67% have complet recovery after 1 year, 30% have residual weakness after 3 years, 3% suffer a relapse of muscl weakness and tngling sensations years after the intial attack |
Postpolio Syndrome-Acute pliomyelitis (Polio)- | caused by a virus in the 1950's and1960's) that destroys brain and spinal cord motor neurons, surviving neurons sprouted reinnervate surrounding fibers-> overly large motor units, occurs decades after episode as nevous systmes purges axonal sprouts it can't support, severe fatigue that dosen't improve with rest, even in previously strong muscles, functional limitaions will occur secondary to mucle weakness, Treatment- submaximal exercise shouyld be used-avoid overuse by teaching inergy conservation, address functional limitations, consider orthotic use to decrease foot drop (therby increasing function) |
Myasthenia Gravis | Autoimmune disorder of neuromuscular junction resulting in decreased number of ACh receptors, causes muscle weakness and fatigue, increases as muscles contract repeatedly, most noticeable in proximal muscles, muscles controlling eye movement and the eyelids are affectd first, which results in Diplopia and Ptosis (drooping eyelid), may spread to other cranial nerves, which cause problems with chewing and swallowing, and even to the respiratory muscles, Treatment and progression- address functional limitations that occur secondary to muscle weakness, teach energy conservation, pacing and importance of rest periods, the course of the disease is slowly progressive with exacerbations and remissions, symptoms typically decrease with rest and anticholinesterase drugs |
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