Neurologic complications of HIV-1 infection and its treatment in the era of antiretroviral therapy

Abstract

Purpose of review: Neurologic complications of HIV infection are unfortunately common, even in the era of effective antiretroviral treatment (ART). The consulting neurologist is often asked to distinguish among neurologic deterioration due to opportunistic infection (OI), immune reconstitution, or the effect of the virus itself, and to comment on the role of immunomodulatory agents in patients with HIV infection. Additionally, as successful virologic control has extended the life span of patients with HIV infection, neurologists are called upon to manage long-term complications, such as neurocognitive disorders and peripheral neuropathy.

Recent findings: Despite the use of ART, significant numbers of patients continue to be affected by HIV-associated neurocognitive disorders, although with milder forms compared to the pre-ART era. Regimens of ART have been ranked according to CNS penetration and are being studied with regard to neuropsychological outcomes. Nucleoside analogs with the greatest potential for peripheral neurotoxicity are no longer considered first-line agents for HIV treatment. Efavirenz, a non-nucleoside reverse transcriptase inhibitor, has the greatest frequency of neurologic side effects among newer ART regimens. The spectrum of clinical manifestations of immune reconstitution inflammatory syndrome (IRIS) continues to grow, including IRIS without underlying OI. A greater understanding of pathophysiology and risk factors has shown that while HIV should be treated early to prevent severe immunocompromise, delayed initiation of ART may be helpful while treating OIs.

Summary: This article reviews the neurologic complications of HIV infection, or its treatment, most commonly encountered by neurologists.

FIGURE 4-1

Fluid-attenuated inversion recovery sequence of MRI shows hydrocephalus ex vacuo, diffuse leukoencephalopathy (A), and diffuse, generalized atrophy (B). This degree of leukoencephalopathy is not a cardinal imaging feature of HIV encephalopathy but is commonly found in patients with advanced HIV infection and likely represents axonal injury.

FIGURE 4-2

Fluid-attenuated inversion recovery sequence of MRI shows diffuse bilateral hyperintense signal in the basal ganglia (A) and periventricular white matter (B).

FIGURE 4-3

Fluid-attenuated inversion recovery (A, B) and T1 postgadolinium (C) sequences of MRI show hyperintense signal in the bilateral mesial temporal cortex (A) and the periventricular white matter of the left subinsular cortex (arrow, B). The signal abnormality in the left subinsular cortex is found to have very subtle enhancement on the postgadolinium image. Increased vascular markings are also seen in the right basal ganglia (arrow, C). While the enhancement is subtle, early intervention with corticosteroids reversed the encephalopathy in this case, providing further evidence that early inflammation was developing.