HIV-Associated Sensory Neuropathies

Sanjay C. Keswania, Carlos A. Pardoa, Catherine L. Cherry, Ahmet Hokea, Justin C. McArthura

Disclosures

AIDS. 2002;16(16) 

In This Article

Introduction

Peripheral neuropathy has emerged as the most common neurological complication of HIV infection.[1,2,3,4] There are several discrete types of HIV-associated neuropathy, which can be classified according to the timing of their appearance during HIV infection, their etiology and whether they are primarily axonal or demyelinating ( Table 1 ). Some represent a consequence of HIV infection producing neuropathological damage [e.g., distal symmetrical polyneuropathy (DSP)], while others are related to opportunistic pathogens [e.g., cytomegalovirus (CMV) polyradiculitis]. An increasingly common group is that which occurs as a result of treatment toxicity [e.g., toxic neuropathy from antiretroviral drugs (TNA) and lactic acidosis syndrome].

HIV-Associated Sensory Neuropathies

The HIV-associated sensory neuropathies include both DSP due to HIV infection per se, and TNA associated with the use of dideoxynucleoside reverse transcriptase inhibitors (NRTI), particularly zalcitabine (ddC), stavudine (d4T) and didanosine (ddI). These two conditions are phenotypically identical, and together form the commonest neurological disorder affecting people with HIV/AIDS. This review shall focus primarily on these neuropathies as they form the bulk of peripheral nervous system disease encountered in HIV clinical practice today.

Inflammatory Demyelinating Polyradiculoneuropathies

Acute and chronic inflammatory demyelinating polyradiculoneuropathies (AIDP and CIDP, respectively) occur with increased frequency in people with HIV, particularly in the early stages of infection, and probably represent autoimmune phenomena.[5] The clinical and electrophysiological features, as well as the response to immunomodulating therapies are indistinguishable from those seen in non-HIV associated AIDP and CIDP. However the classic finding of 'dissociation albuminocytologique', where cerebrospinal fluid (CSF) protein is elevated but the CSF is acellular, may be absent, because typically in HIV-associated IDP, there is a lymphocytic pleocytosis in addition to elevated CSF protein.

Mononeuropathy Multiplex

Mononeuropathy multiplex (MM) can occur both early in infection, due to dysimmune or vasculitic mechanisms,[6,7] and also in advanced AIDS associated with a low CD4 cell count, usually from opportunistic pathogens such as CMV and varicella-zoster virus (VZV).[8] MM can also occur secondary to hepatitis B and C viruses, particularly when there is an associated cryoglobulinemia.[9] Electrophysiological studies are helpful in diagnosis, often demonstrating multiple, asymmetric mononeuropathies that cannot be localized to typical sites of entrapment. A nerve/muscle biopsy is usually necessary to distinguish between etiologies that require very different therapies (e.g., immunosuppression for vasculitis versus ganciclovir therapy for CMV neuritis).

Progressive Polyradiculopathy

Progressive polyradiculopathy presents characteristically with lumbosacral pain, 'saddle' anesthesia, a rapidly progressive flaccid paraparesis and urinary retention.[10,11] The most common cause is CMV infection occurring in the advanced stages of immunodeficiency, and it is important to note that early anti-CMV therapy may prevent a neurologically devastating outcome. Other causes of this syndrome are VZV infection, neurosyphilis and leptomeningeal lymphoma.[12,13]

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