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.