CH43: Peripheral Nerves Flashcards
Differentiate central and peripheral nerve (p. 1310)
Myelin of centrally located fibers: oligodendrocyte
Myelin of peripheral: Schwann cells
Support central:astroyctes
Supprt peripheral: Fibroblasts
Disease mechanism is producing toxin that directly acts on the membrane of the Schwann cells near the DRG(p. 1311)
Diphteria
Disease mechanism is occlusion of vasa nerosum (p. 1311)
Polyarteritis nodosa
Disease mechanism is treponemal meningoradiculitis (p. 1311)
Tabes dorsaleis
Disease mechanism is combination of toxin with axoplasm of the largest sensory and motor nerves via sulfhydryl bonds (p. 1311)
Arsenic
Disease mechanism is damaging the microtubular transport (p. 1311)
Vincristine toxicity
Retrograde changes consisting of swwelling of the cell cytoplasm and marginalization and dissolution of the NIssl substance (p. 1312)
Chromatolysis
Exception wherein an axonal process is seen presenting as proximal weakness (p. 1312)
Porphyria
Compare polyneuropathies vs multifocal. (p. 1313)
The multifocal nature of lesions and blocakge of electrical conduction often leads to weakness of proximal limb and muscles before or at the same time as distal parts are affected.
Disuse vs Denervation atrophy (p. 1313)
In dususe, the muscle does not reduce its size by ore than 25 to 30%.
As a rule, neuropathies are associated with a reduction or loss of tendon reflexes EXCEPT (p. 1314)
small fiber neuropathies; in which DTR may be retained even with marked loss of perception of painful stimuli.
Characteristic of sensory ataxic gait (p. 1315)
brusque, flinging, slapping movements
NO NYSTAGMUS, DYSARTHRIA
Two most frequent manifestation of autonomic failure (p. 1315)
Anhidrosis
Orthostatic hypotension
Is there dysautonomia in radicular diseases? (p.1316)
No. Because the autonomic fiebrs join the spinal nerves from the sympathetic chain and parasympathetic ganglia more distally.
Fasciculations and cramps are NOT prominent features in polyneuropathies (they are in anterior horn cell diseases) EXCEPT (p. 1316)
Chronic spinal motor root compression leads to fasciculations or painful spams in the innervated muscles
TREATMENT: Carbamazepine, Phenytoin
Differentiate an L5 vs peroneal nerve lesion. (p. 1318)
Check INVERSION. If spared, lesion is in the peroneal nerve.
Check sensory:
L5 extends almost up to the knee on the anterior surface of the foreleg
Peroneal: it ends a limited distance above the ankle
Infections associated with GBS(p. 1321)
C jejuni
Herpes family (CMV EBV HIV)
Campylobacter- Mycoplasmae and Lyme
Not infection: lymphoma and systemic autoimmune
GBS: Antibody (p. 1323)
acute motor axonal- GM1
PCB- GT1b, GD1a
MFS- GQ1B
Pathologic findings in GBS (p.1323)
endoneural perivascular lymphocytic infiltrates
In GBS, the CSF is under normal pressure or contains only a few lymphocytes in all but __%of patients (p. 1323)
`10%
Very earliest changes in pathology of GBS(p. 1325)
deposition of compleemnt on the innner layer of myelin
Differentiate Tick paralysis vs GBS (p.1325)
Sensory loss is not a usual feature of tick paralysis and CSFprotein is normal
MG vs GBS (p. 1326)
The mandibular muscles remain relatively stron in GBS
Botulism vs GBS (p.1326)
Bradycardia in botulism
The ability to reach a count of 20 generally corresponds to a vital capacity of greater than (p.1326)
1.5L
Dysautonomia in how many percent of GBS patients (p. 1326)
10%
Bizarre waking dreams or hallucinations after weeks of immobilization (p. 1326)
Oneiric hallucinations
Dose of plasma exchange (p. 1327)
200 to 250ml/kg in 4 to 6 treatments on alternate days; onset less than 2 weeks
Dose of IvIg (p. 1327)
0.4g/kg per day for 5 consecutive days
How many percent of GBS who intiially improve will relapse with treatment (p. 1327)
10%
Differentiate between acute sensory neuronopathy and GBS (p. 1329)
In GBS, there is usually some degree of proximal wekaness and sensory changes do not extend to the face and trunk
Important pathologic change in diphtheria (p. 1330)
segmental demyelination without inflammatory reaction of spinal roots, sensory ganglia, and adjacent spinal nerves
Anterior horn cells, axons, peripheral nerves distally and muscle fibers remain normal
Treatment for diphtheria (p. 1330)
Diphtheria antitoxin within 48 hours
This disease is due to a metabolic defect in the liver marked by increased production and urinary excretion of porphobilinogen and porphyrin precurose alpha aminolevulenic acid (p. 1330)
Porphyria
Characteristics of porphyric neuropathy (p. 1330)
relapsing nature acute onset abdominal pain psychotic symtoms predominant motor neuropathy- often bibrachial distrubution of weakness truncal sensory loss tachycardia
Treatment for porphyria (p. 1331)
IV glucose and IV hematin