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In all patients sensory neuropathy was sudden at onset and peaked to maximal deficit within 4 weeks. In five (63&) cases, there was an antecedent viral illness. All patients had objective sensory loss and diminished or absent reflexes. No ne showed any muscle weakness. In all four patients in whom the spinal fluid was examined during the first 4 weeks, there was albuminocytologic dissociation. All of the patients had electrophysiologic evidence of demyelination in at least two nerves. D emyelination was demonstrated in motor nerve conduction in seven patients and in sensory nerve conduction in one, indicating that motor nerve conduction studies were the key for the diagnosis of demyelinating neuropathy. All patients had sensory nerve co nduction abnormalities in at least one nerve. Three patients responded to immunotherapies. All had a favorable outcome, with a monophasic course of disease and no sign of relapse. The current study confirms the existence of sensory GBS. |
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areflexia
cerebrospinal fluid,elevated protein of
Guillain Barre syndrome
Guillain Barre syndrome,differential diagnosis of
Guillain Barre syndrome,sensory
Guillain Barre syndrome,variant forms of
hyporeflexia
misdiagnosis
nerve conduction studies
neuromuscular disease,electrodiagnosis of
neuronopathy
neuronopathy,sensory
polyneuritis
polyneuritis,acute sensory
polyneuropathy,acute sensory
prognosis
sensory loss
sensory polyneuropathy
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