The neurological manifestations of HIV infection

Renaud A. Du Pasquier*, I. J. Koralnik

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


At the end of 2002, an estimated 42 million people worldwide were living with human immunodeficiency virus (HIV). In Switzerland, the number of newly diagnosed HIV infections had been declining between 1992 and 1999. However, since the year 2000, this trend has not continued and more than 50% of these new infections are now due to heterosexual contact. This increased risk-taking behaviour comes in large part from the fact that highly active anti-retroviral therapy (HAART) is perceived by many in the general population as a cure for HIV, which, unfortunately, is not true. Nevertheless, HAART has brought a major improvement in the prognosis of HIV+ people who can afford these costly drugs. As a result of this longer survival, the number of people living with HIV has increased. In this context, the neurological manifestations of HIV infection continue to represent a diagnostic and therapeutic challenge. Indeed, most antiretroviral medications have a poor ability to cross the blood-brain barrier and some subtypes of HIV seem to have a higher affinity for the central nervous system (CNS). Thus, the CNS may serve as a sanctuary for the virus. In addition, novel neurological syndromes have recently been recognised: such as a severe demyelinating leukoencephalopathy in AIDS patients receiving antiretroviral therapy as well as paradoxical reaction against known opportunistic infections in the context of the immune reconstitution inflammatory syndrome. Finally, antiretroviral therapies themselves can cause neurological dysfunction. Knowledge of the patients' level of immunosuppression, as reflected by their CD4+ T lymphocytes count is of paramount importance. At the time of seroconversion, a patient can present with aseptic meningitis, mononeuritis such as peripheral facial nerve palsy, or inflammatory demyelinating polyradiculopathy, similar to Guillain-Barré syndrome. It is important for the clinician to recognise these conditions since they can be the lead to the diagnosis of HIV infection. Mononeuritis multiplex, myopathy or distal sensory polyneuropathy can occur in patients with CD4+ T cells <500/μl. Myopathy can be caused by HIV itself or by zidovudine. When the CD4+ T cells count goes below 200/μl, opportunistic infections and tumours of the brain have to be expected. In this category of patients, neurological complications directly attributable to HIV include HIV-associated dementia and its lesser form, HIV-associated minor cognitive/motor disorder, and vacuolar myelopathy. The diagnosis of an intracranial mass lesion in an HIV+ patient with a CD4+ T cells count less than 200/μl can be particularly challenging. Indeed, several types of opportunistic infections or tumours can present as a space-occupying lesion. In addition, two or more pathogenic processes can coexist in the brain of an HIV+ individual, and these can also be superimposed to HIV encephalopathy (HIVE). We here review the diagnostic criteria and therapeutic modalities concerning the major neurological opportunistic infections, which include toxoplasma encephalitis and progressive multifocal leukoencephalopathy (PML), as well as primary CNS lymphoma. We propose an algorithm for the clinical management of such patients and discuss new trends in HIV-associated neurological disorders.

Original languageEnglish (US)
Pages (from-to)178-185
Number of pages8
JournalSchweizer Archiv fur Neurologie und Psychiatrie
Issue number4
StatePublished - 2003


  • AIDS
  • CNS mass lesion
  • Dementia
  • HIV
  • Highly active antiretroviral therapy

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health


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