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At vero eos et accusamus et iusto odio dignissimos ducimus qui blanditiis praesentium voluptatum deleniti atque corrupti quos dolores et quas. In This Article. The pathology and pathogenesis of this disorder are discussed to highlight the theme of molecular mimicry. There are several variants of this condition, and a classification of this syndrome is included in Table 1.
This is distinguished from acute inflammatory demyelinating polyneuropathy primarily by electrophysiological studies. Autopsy on one patient showed significant and marked axonal degeneration in the ventral roots and peroneal nerves without demyelination. In addition, Electrodiagnostic studies in 22 of 37 patients showed reduction in compound muscle action potential amplitudes, suggesting axonal abnormalities. There was little to no prolongation of distal motor latencies or slowing of motor nerve conduction velocities suggesting demyelination, except in one patient who also had abnormal sensory studies.
These findings indicate that this patient had acute inflammatory demyelinating polyneuropathy Although Griffin and colleagues suggest patients with acute motor-sensory axonal neuropathy may have a more severe disease than acute motor axonal neuropathy, they also recognize similar pathological characteristics of the motor and sensory fibers.
The disorders may be within the same disease spectrum. Sensory impairment is minimal, and autonomic involvement less common. Peak severity is reached within 5 to 9 days Weakness may involve dysphagia, dysarthria, and facial diplegia and may progress to flaccid quadriplegia and respiratory failure.
