[Increased sensory nerve action potential amplitudes after plasma exchanges in a patient with acute sensory neuropathy].

Acute sensory neuropathy (ASN) is characterized by rapidly progressive sensory ataxia and areflexia without motor weakness. The disease has been thought to be due to dorsal root ganglionitis which leads to secondary sensory nerve axonal degeneration. In contrast, we here report a patient with ASN, in whom results of nerve conduction study pointed to a direct involvement of the sensory nerve axons. A 33-year-old man was admitted to our hospital because of a few days history of progressive numbness in his extremities and unsteadiness of gait. The results of motor nerve conduction studies were normal. Amplitudes of sensory nerve action potentials (SNAPs) decreased within a few days after admission, whereas sensory nerve conduction velocities were preserved. Cerebrospinal fluid examination showed an elevated protein level without pleocytosis. He was diagnosed as having ASN, and was treated with four times of plasma exchange which rapidly restored SNAP amplitudes to normal. However, a few days after the plasma exchanges, SNAP amplitudes decreased again. Second series of plasma exchanges one month after admission transiently increased SNAP amplitudes again but not to normal range. These electrophysiologic changes were not associated with clinical improvement. A sural nerve biopsy one month after admission revealed axonal degeneration. These findings suggest that our patient's sensory impairment is caused by reversible sensory axonopathy due to humoral factors that can be removed by plasma exchange, as well as acute irreversible ganglionopathy which may lead to secondary axonal degeneration as shown by sural nerve biopsy.