Article abstract-Objective: To report eight cases of sensory Guillain-Barré syndrome (GBS). Background: The concept of sensory equivalent to ascending paralysis of GBS was raised in 1958, and the diagnostic criteria for a sensory loss and areflexia variant of GBS were proposed in 1981. However, clinical cases meeting these criteria have been relatively scarce. Methods: During a 13-year period between 1986 and 1999, the authors collected eight cases of an acute sensory demyelinating neuropathy that met most of the proposed diagnostic criteria of a sensory variant of GBS. Results: 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. None 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. Demyelination 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 conduction 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. Conclusion: The current study confirms the existence of sensory GBS.

The authors present two cases that provide the first autopsy findings in multifocal acquired demyelinating sensory and motor neuropathy (MADSAMN). Both cases documented multifocal but asymmetric demyelinating neuropathy with rare axonal degeneration. One case clearly documented an inflammatory polyradiculoplexoneuropathy, confirming the inflammatory nature of this neuropathy. This study showed that MADSAMN is an inflammatory demyelinating polyradiculoneuropathy that shares histologic features observed in chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy (MMN), suggesting a similar immunopathogenesis for these entities.