46 Diseases of the Peripheral Nerves Flashcards
(32 cards)
The most frequent electrodiagnostic findings in GBS?
- ) Reduction in the amplitude of muscle action potentials
- ) Slowed conduction velocity
- ) Conduction block in motor nerves
p. 1324
Acute motor axonal variety has tendency to be associated with which antibodies?
GM1 or GD1a
p.1325
Pharyngeal-cervical brachial associated with which antibody
GT1a
p.1325
Many patients with bizarre waking dreams or hallucinations after weeks of immobilization, seen in GBS
Oneiric hallucinations
p.1328
Plasma Exchange in GBS
removes a total of 200 to 250ml/kg of plasma in 4 to 6 treatments
p.1329
Dose of IvIg in GBS
0.4 g/kg per day for 5 days
A fairly consistent predictor of residual weakness and muscle atrophy?
Reduced amplitude of muscle action potentials; Widespread denervation p.1330
An acute or subacute symmetrical polyneuropathy frequently seen in critically ill and septic patients, particularly those with failure of multiple organs
Critical illness polyneuropathy
p.1330
Findings in critical illness polyneuropathy
Primary axonal process with early denervation, and normal CSF
The many systemic mediators of sepsis are toxic to the peripheral nervous system, _______________has been proposed as one such endogenous toxin causing neuropathy
Tumor Necrosis Factor p.1330
2 main presentations in Acute Sensory neuronopathy
Limb ataxia with no dysarthria or nystagmus
Generalized facial and truncal numbness that involved proximal and distal sensory areas
p.1331
Most salient identifying feature for gangliopathy
Early proximal symptoms
p.1331
Electrophysiologic studies in acute sensory neuronopathy
Absent or slowed sensory conduction, no abnormalities in motor nerve conduction or signs of denervation p.1331
A severe, rapidly advancing, symmetrical and mainly motor polyneuropathy-often with abdominal pain, psychosis and convulsions
Porphyric polyneuropathy p.1331
Metabolic defect in acute porphyria
Defect in the liver, marked by increased production and urinary excretion of Porphobilinogen, and porphyrin precursor 🔺aminolevulinic acid p.1331
Most characteristic features of porphyric neuropathy
Relapsing nature, acute onset, abdominal pain, psychotic symptoms, predominant motor neuropathy, often with bibrachial distribution of weakness, truncal sensory loss and tachycardia
p.1332
Therapy for porphyric neuropathy
IV Glucose a s IV hematin (4mg/kg daily for 3-14 days) p.1332
CA most related to paraneoplastic polyneuropathy
Small cell CA of lung p.1334
Antibody in paraneoplastic polyneuropathy
Anti-Hu antibody or ANNA-1 antinuclear neuronal antibody p.1334
Subacute neuropathy assoc with anemia, jaundice, brownish cutaneous pigmentation, hyperkeratosis of palms and soles, and later with white transverse banding of nails (Mees lines)
Arsenic polyneuropathy p.1335
Pathology in arsenic polyneuropathy
Dying back-axonal degeneration type p.1335
Acute or subacute evolution of complete or almost complete sensorimotor paralysis in the distribution of a single peripheral nerve
Mononeuritis multiplex p.1341
Medical findings of anemia, basophilic stippling of red blood cell precursors in the bone marrow, colicky abdominal pain, constipation
Lead toxicity p.1335
Blood lead level toxicity
more than 70 micorgram/dL
