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Background
Since the development and practice of combining different classes of antiretrovirals (ARVs) for individualized regimens of highly active antiretroviral therapy (HAART), survival and disease progression of human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS) has drastically improved patient outcomes. Prior to the advent of HAART in the late 1990s, most patient deaths were attributable to opportunistic infections and neoplasms due to a loss of CD4 receptor-positive T lymphocytes and collapse of the immune system. Approximately 63% of autopsied patients with AIDS had evidence of nervous system involvement, and before the use of HAART, neurologic manifestations of HIV or associated neuropathologies were the first symptoms of HIV infection in up to 20% of patients. The most common pathologies implicated were HIV encephalitis (HIVE) and opportunistic infections of the CNS, including cytomegalovirus encephalitis (CMVE), non-Hodgkin’s lymphoma (NHL), cryptococcus, toxoplasmosis, and progressive multifocal leukoencephalopathy (PML). This review focuses on imaging findings of the CNS manifestations of HIV/AIDs in the post-HAART era.

Educational Goals / Teaching Points
Currently, with the introduction of HAART, treatment of HIV/AIDS has been shown to decrease plasma viral loads and the incidence of such opportunistic infections. However, the incidence of HIVE and HIV-associated dementia (HAD) remains high, with a prevalence of up to 25% reported in HAART autopsy studies, in part likely due to increased longevity in the post-HAART era. An additional early complication of HAART is the immune reconstitution inflammatory syndrome (IRIS), which is in part a recovery of a preexisting immune response, following the improvement in immune function with therapy. The median time of onset of HAART-associated IRIS is 1–10 months following therapy initiation; however, ranges vary as wide as a few days up to 3 years.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Individuals affected by HIVE show patterns of global brain atrophy, evidenced by dilated ventricles and prominent sulci. HIV predominantly affects the deep white matter in a symmetric pattern. CT manifestations include atrophy advanced for patient age, as well as lesions of decreased attenuation in the periventricular white matter. Lesions are not associated with mass effect. Consistent with CT findings, MRI reveals diffuse atrophy, and T2-weighted imaging shows periventricular hyperintensities. Manifestations of IRIS are similar to the preexisting immune response; some have worsening of the condition based on the radiologic findings. Neuropathological correlation also may display worsening responses based on histological samples.

Conclusion
In conclusion, treatment with HAART has altered neurologic imaging trends in patients with HIV/AIDS, with fewer opportunistic infections. The prevalence of HIVE remains elevated, and IRIS is an additional neurological imaging manifestation to come about since the widespread adoption of HAART.