HIV is a retrovirus belonging to the subfamily Lentivirus (slow virus), so-called because of the long latency period between primary infection and the CD4+ T-cell depletion that characterizes AIDS. During this latency period, the immune system becomes dysregulated and a chronic proinflammatory state develops, manifesting with hypergammaglobulinemia and an increased secretion of several cytokines. Many neurologic complications, particularly those occurring before the onset of AIDS, are attributable to immune-mediated processes. Without virologic control, eventually all components of the immune system (particularly the cellular response) become deficient, enabling opportunistic infections and malignancies to develop.
It is estimated that at least one third of those with HIV/AIDS are afflicted with an HIV-associated neurologic condition. The epidemiology of these complications has been dramatically altered since the widespread use of combination antiretroviral therapy (CART) in 1996 and the prudent use of other chemoprophylactic agents such as fluconazole and sulfamethoxazole-trimethoprim. In general, the incidence of neurologic complications has declined. But with improved survival, the prevalence of many appears to be rising. Consequently, neurologists are increasingly likely to see a patient with HIV/AIDS for a chronic HIV-associated illness or a non–HIV-related neurologic condition rather than for an acute, life-threatening HIV-related illness.
When approaching an HIV-infected patient, the neurologist must keep in mind the following principles: the entire neuroaxis, from brain to muscle, can be affected; the rule of parsimony is often violated, and more than one process may underlie the clinical picture; and the types of complications tend to be related to duration of HIV infection and degree of immunosuppression (Table 28–1). Early-stage (CD4+ >500/µL) neurologic complications, such as those occurring during primary infection, usually result from HIV itself or as a consequence of an immune-mediated process; middle-stage (CD4+ 200–500/µL) complications tend to result from immune-mediated processes or medication toxicity; and late-stage (CD4+ <200/µL) complications tend to result from opportunistic infections, immune-mediated processes, or medication toxicity. Tantamount to developing a workable differential diagnosis is obtaining a thorough history, and some essential features are outlined in Table 28–2.
Table 28–1.Common neurologic complications of HIV classified by the stage in which each occurs. |Favorite Table|Download (.pdf) Table 28–1. Common neurologic complications of HIV classified by the stage in which each occurs.
|Early Stage (CD4+ > 500) |
|HIV meningitis (acute conversion syndrome) |
|Shingles (varicella-zoster) |
|Acute inflammatory demyelinating polyneuropathy (AIDP) |
|Middle Stage (CD4+ 200–500)a |
|Distal sensory polyneuropathy (DSP) |
|HIV-associated dementia (HIVD) |
|HIV-associated neuromuscular weakness syndrome |
|Mononeuropathy multiplex |
|HIV-associated myopathy |
|Late Stage (CD4+ < 200) |
|CNS toxoplasmosis |
|Cryptococcal meningitis |
|Primary CNS lymphoma (PCNSL) |
|Progressive multifocal leukoencephalopathy |
|HIV-associated myelopathy |
|Varicella-zoster vasculitis |
|CMV ventriculitis or polyradiculitis (CD4+ < 100) |
Table 28–2.Essential clinical information when forming an HIV-related differential diagnosis. |Favorite Table|Download (.pdf) Table 28–2. Essential clinical information when forming an HIV-related differential diagnosis.
|Duration of HIV infection |
|History of HIV-related illnesses |
|CD4+ cell count (current and nadir)...|