There are no neurophysiologic features characteristic of "axonal" Guillain-Barré syndrome.
Classical views hold Guillain-Barré syndrome (GBS) as a primary inflammatory-demyelinating neuropathy in which secondary axonal degeneration may occur, particularly when inflammatory lesions are severe. Feasby and colleagues proposed that primary axonal degeneration can also cause GBS characterized by inexcitable motor nerves and poor outcome. This hypothesis rests largely on the results of a single autopsy in which no inflammation or demyelination were found. Using an illustrative case report confirming earlier studies, we point out that inexcitable motor nerves (or low amplitude compound muscle action potentials [CMAPs]) are of ambiguous significance and may reflect distal demyelination, causing conduction block between distal stimulation sites and target muscles, a pattern not uncommon in GBS. Recovery from such lesions may occur within weeks with restoration of CMAP amplitudes. The recognition of a yet unproven axonal variant of GBS cannot be based solely on documentation of inexcitable motor nerves in the context of rapidly developing weakness.
Cros
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Department of Neurology, Massachusetts General Hospital, Boston 02114.
Triggs
W J
WJ
D000200:Action Potentials; D001369:Axons / Q000502:physiology*; D004576:Electromyography; D006801:Humans; D007136:Immunoglobulins / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000503:physiopathology; D009420:Nervous System / Q000503:physiopathology*; D009431:Neural Conduction; D011129:Polyradiculoneuropathy / Q000503:physiopathology* / Q000628:therapy
D007136:Immunoglobulins