Peripheral neuropathies associated with human immunodeficiency virus infection

Abstract

Peripheral neuropathies may complicate all stages of infection with human immunodeficiency virus (HIV). Acute inflammatory demyelinating polyneuropathy, sensory ganglioneuritis, and acute cranial nerve palsy all may occur 2 to 3 weeks after acute HIV infection. Acute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, and polyradiculopathy may occur with otherwise asymptomatic HIV virus infection. Neuropathy is one of the most common neurological manifestations of the acquired immunodeficiency syndrome (AIDS)-related complex, occurring in as many as 20% of these patients. Acute or chronic inflammatory demyelinating polyneuropathy (38%) and mononeuropathy multiplex (29%) are most frequently seen, and usually there is a good prognosis, with the neuropathy resolving spontaneously or with steroids or plasmapheresis. Neuropathy occurring with AIDS is reportedly uncommon but probably is underreported, especially in seriously ill patients. By contrast with AIDS-related complex, the neuropathy associated with AIDS is usually a distal symmetrical polyneuropathy (72%), with inflammatory neuropathy, mononeuropathy multiplex, and polyradiculopathy occurring rarely. The pathogenesis of acute or chronic inflammatory demyelinating polyneuropathy and possibly of mononeuropathy multiplex is probably autoimmune. The pathogenesis of distal symmetrical polyneuropathy is less clearly established and may be infectious, toxic, or nutritional. Polyradiculopathy most likely is infectious; cytomegalovirus is a leading contender for infectious agent, but herpes simplex virus and HIV are other possibilities.