Although the entire neuraxis is susceptible, the most common neurologic complications of HIV-1 involve the peripheral nervous system. With the advent of highly active antiretroviral therapy (HAART), the incidence of most neurologic complications has declined; however, the incidence of peripheral neuropathy has increased, with distal sensory polyneuropathy and antiretroviral toxic neuropathy being the most frequently reported forms. In this update, the authors review the latest findings on the clinical presentation, management, and pathogenesis of these and other peripheral nerve complications of HIV-1 infection.
Historical note and terminology
Incidence. Neurologic complications of HIV-1 have been reported for over 20 years (Britton et al 1982; Miller et al 1982), and it is widely appreciated that the entire neuraxis is susceptible to complications. With the advent of HAART and prolonged survival, the incidence of most neurologic complications has declined; however, the incidence of distal sensory polyneuropathy has increased, with distal sensory polyneuropathy and antiretroviral toxic neuropathy remaining the most frequently reported neurologic manifestations. Other peripheral nerve complications include acute or chronic demyelinating neuropathies, mononeuritis or mononeuritis multiplex, autonomic neuropathy, and polyradiculopathy (Brew 2003).
In retrospective studies of patients with acquired immune deficiency syndrome, the incidence of peripheral neuropathy syndromes is estimated to be 10% (Snider et al 1983; Levy et al 1985). When including patients with electrophysiologic evidence of polyneuropathy who lack clinical symptoms of peripheral neuropathy, the incidence rises to 40% (Janssen et al 1988; So et al 1988). This figures increases to 48% to 100% in pathologic studies (de la Monte et al 1988; Mah et al 1988).
Prospective series reveal an incidence of peripheral neuropathy of 5% to 60%, depending on the disease stage and neuropathy definition (So et al 1988; Chavanet et al 1989; Hall et al 1991; Husstedt et al 1993; Bacellar et al 1994; Schifitto et al 2002; Ellis et al 2010). A study of 252 patients enrolled in a pre-HAART trial of HIV-infected individuals with memory complaints and CD4 counts less than 300 found a prevalence rate of 20% for asymptomatic neuropathy and 35% for symptomatic neuropathy. The estimated incidence rate of symptomatic distal sensory neuropathy was 36% after 12 months and 52% after 24 months (Schifitto et al 2002). In the age of HAART therapy, the same group found the 1-year incidence of symptomatic distal sensory neuropathy decreased to 21% (Schifitto et al 2005).
When approaching the diagnosis and management of these complications, it is essential to determine 4 things: (1) the specific localization of the lesion (ie, spinal cord, nerve root, plexus, peripheral nerve, or multiple peripheral nerves); (2) the staging of the HIV infection (determined by the total CD4+ lymphocyte cell count, the total HIV viral load, and the patient's clinical condition); (3) the patient's medication regimen; and (4) the presence of concomitant disease processes.
Localizing the lesion may be challenging because multiple points of the neuraxis may be simultaneously involved, resulting in potentially perplexing clinical presentations.
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