HIV peripheral neuropathy: pathophysiology and clinical implications

Abstract

One of the most debilitating neurological complications of human immunodeficiency virus (HIV), affecting nearly one in three patients, is painful peripheral neuropathy. Although HIV infection can cause distal sensory polyneuropathy (DSP), the advent of highly active antiretroviral therapy (HAART) to treat HIV infection has resulted in a significant number of patients developing a clinically indistinguishable form of toxic neuropathy. The predominant symptom, regardless of etiology, is excruciating unremitting pain, resistant to pharmacological treatments, that leads to a reduction in the ability to conduct activities of daily living and, eventually, inability to ambulate. Since withdrawal from nucleoside therapy is not typically recommended, a more thorough understanding of the etiology and pathophysiology underlying nucleoside-induced peripheral neuropathy, through basic and clinical research endeavors, will aid in the development of new therapeutic treatments aimed at alleviating or ameliorating pain. This article provides the latest information regarding the pathophysiology and clinical implications of HIV peripheral neuropathy.