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

Early Clinical Neurologic Manifestations

At the time of seroconversion to HIV-positive status, some patients remain asymptomatic, while others have symptoms reminiscent of mononucleosis (fever, sore throat, lymphadenopathy, myalgias, anorexia, fatigue, headache, and retro-orbital pain), frequently with skin rash.[4,5] One third of patients may have HIV-related "aseptic" meningitis at or around the time of seroconversion, with a typically normal opening pressure on lumbar puncture[6,7] and CSF findings of lymphocytic pleocytosis, elevated protein content, normal glucose content, negative serologic results, and cultures negative for other potential infectious etiologies. Human immunodeficiency virus antibodies and p24 antigen may be detected in the CSF at this stage.[8,9]

Patients may have prominent and severe headache in early HIV infection. The headache mechanism may be cytokine-mediated and may occur in patients whose CSF reveals pleocytosis or is acellular. If the CD4 lymphocyte count is greater than 400, fungal or tuberculous meningitis is seen rarely but should be excluded. Symptomatic headache treatment should be prescribed, consisting of abortive and prophylactic treatment similar to that used for migraine patients.[7,8] In patients with a history of substance abuse, opiate medication use should be carefully monitored. Because of a high index of suspicion of intracranial lesions in these HIV patients, computed tomography (CT) or magnetic resonance imaging (MRI) must be done.[10] The CT or MRI studies may also show evidence of "cerebral atrophy" in patients who are simply dehydrated, malnourished, protein-depleted, or alcoholic, all conditions that occur with increased frequency in HIV-positive patients. Evidence of cerebral atrophy by brain imaging does not indicate acquired immunodeficiency syndrome (AIDS) dementia complex or any other process directly related to HIV infection, and the abnormal scan findings may reverse with hydration and improved nutrition.

When patients become aware of their HIV-positive status, they may complain of cognitive impairment, including difficulty thinking, impaired concentration and attention, and poor memory. If careful mental status testing detects no objective cognitive abnormality and the patient and others (family, friends, employers) have observed no specific cognitive "failures" (eg, forgetting to pay bills, missing appointments, failing to complete tasks), the clinician should consider a diagnosis of "pseudodementia" and inquire about the presence of behavioral, autonomic, or vegetative symptoms of depression. Effective treatment of depression may eliminate "neurologic symptoms" and preclude the need for CSF analysis, CT, or MRI. In addition, one should carefully question the patient about non-HIV-related causes of memory loss that may predate HIV infection, eg, traumatic brain injury or alcoholism.

Neuropsychologic decline in asymptomatic HIV-positive patients has been reported, a finding that would have important implications for HIV-positive individuals in the work force, but multiple other studies failed to confirm this.[11,12,13] Brain imaging (CT, MRI) and neurophysiologic studies (electroencephalogram [EEG], evoked potentials) of HIV-positive, neurologically asymptomatic patients as compared with HIV-negative controls have failed to show evidence of brain dysfunction in the infected group.[14] In particular, MRI studies have shown no difference in the prevalence of cerebral atrophy or high-signal intensity white matter lesions in HIV-positive individuals.[15] Magnetic resonance spectroscopy surveys biochemical markers of neuronal or white matter function and has shown no difference in HIV-positive neurologically asymptomatic patients compared with normal controls.[4]

Less common neurologic manifestations of early HIV infection include unilateral or bilateral facial weakness, brachial plexitis (weakness in the shoulder girdle), inflammatory demyelinating polyneuropathy (identical to Guillain-Barré syndrome, except weakness descends in HIV-positive patients), mononeuritis multiplex, and radiculopathy.[16] In such conditions, MRI may show white matter lesions in the brain or spinal cord consistent with inflammatory demyelination. Management of certain of these peripheral nervous system disorders begins with exclusion of other infections (herpes simplex, cytomegalovirus [CMV]) by serologic tests. Treatment with plasma exchange or intravenous immune globulin may be effective if no specific infectious etiology is identified for the polyneuropathy, polyradiculopathy, or mononeuritis multiplex, but these disorders frequently recur and may require repeated treatment. Corticosteroids should be used carefully in HIV-positive patients to avoid unmasking latent infection (eg, fungal, tuberculous).

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