Neurologic Abnormalities in Human Immunodeficiency Virus Infection

, Department of Psychiatry and Neurology, Tulane University School of Medicine, New Orleans, La 

South Med J. 2001;94(3) 

In This Article

Cognitive Symptoms

Cognitive decline due to HIV rarely develops in asymptomatic seropositive patients in the absence of immunosuppression. When immunosuppression develops, however, objective impairment of cognitive and motor function may be detected, though progression to frank dementia and disabling motor impairment does not routinely occur. Patients in whom minor cognitive-motor dysfunction develops have a worse prognosis than those HIV-infected patients without such dysfunction.[20,21,22] Neurologic function improves in patients treated with zidovudine (AZT), and the reduced incidence of HIV dementia complex since introduction of highly active antiretroviral therapy suggests the virus has direct effect on CNS function.[21]

Patients with HIV-associated minor cognitive-motor disorder may report difficulty reading (with poor retention), losing track of conversation, handwriting deterioration, slowness in thinking, or stiffness in the legs. Diagnostic criteria for minor cognitive-motor disorder include the following: (1) acquired cognitive, motor, and behavioral abnormalities confirmed by neurologic and neuropsychologic testing; (2) mild impairment of work performance or activities of daily living (decline in function noticeable to others, but patient can function independently); (3) clinical findings that do not conform to criteria for HIV dementia or myelopathy; and (4) no alternative etiology present to explain clinical findings. Confounding variables that may lead to overdiagnosis of minor cognitive impairment due to HIV include the effect of systemic illness, medication, depression, previous traumatic brain injury, and previous learning disability. Mild cognitive-motor syndrome develops in the later stages of HIV illness, when the viral load is high and the CD4 lymphocyte count is depressed. Antiretroviral and neuroprotective agents (eg, nimodipine, glutamate antagonists) may improve neurologic function; further studies are needed to investigate this possible effect.[22]

Human immunodeficiency virus-associated dementia-motor complex is distinct from minor cognitive motor disorder and does not represent a continuum of that disorder. Diagnostic criteria include the following: (1) acquired abnormality in two or more cognitive functions (dementia) for longer than 1 month, with cognitive dysfunction impairing work and activities of daily living and not solely attributable to systemic illness; (2) acquired abnormality in motor function (gait impairment, myelopathy) verified by neurologic and neuropsychologic tests (slowness in timed tasks) and/or decline in motivation or emotional control or change in social behavior (frontal lobe disinhibition); (3) absence of clouding of consciousness; and (4) no other etiology that would explain these dysfunctions. No CSF or neuroimaging finding can establish diagnosis; however, these are necessary to exclude the presence of an opportunistic infection or neoplasm.[23,24,25]

In AIDS-dementia complex, CT and MRI often show enlarged ventricles and subarachnoid spaces (indicative of cerebral atrophy) and multiple white matter, subcortical gray matter (basal ganglia, thalamus), and non-contrast-enhanced abnormalities. Cerebral atrophy, multifocal hypodense nonenhanced lesions seen on CT, and multiple high-signal-intensity nonenhanced lesions seen in the basal ganglia, thalamus, and white matter on MRI are highly suggestive of direct viral infection of the brain and of "HIV dementia." Neuropathologic findings include multiple nodules of microglia, macrophages, and multinucleated giant cells; reactive gliosis; and diffuse white matter pallor. White matter pallor may be due to cytokine-mediated inflammatory disorder resulting from blood-brain barrier disruption and viral penetration of the CSF protein extravasation and not demyelination. Human immunodeficiency virus has been identified in the brain of AIDS patients with dementia. Possible explanations for HIV dementia include direct HIV neurotoxicity, cytokine-mediated effect, and glutamate neurotoxic effect.[26]

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