It has already been mentioned that HIV infection may present as an acute asymptomatic meningitis with a mild lymphocytic pleocytosis and modest elevation of CSF protein. The acute illness may also take the form of a meningoencephalitis or even a myelopathy or neuropathy (see Myelopathy, Peripheral Neuropathy, and Myopathy). Most patients recover from the initial acute neurologic illnesses; the relationship to HIV may pass unrecognized, as these illnesses are quite nonspecific clinically and may precede or coincide with seroconversion. Once seroconversion has occurred, the patient becomes vulnerable to all the late complications of HIV infection. In adults, the interval between infection and the development of AIDS ranges from several months to 15 years or even longer; the mean latency is 8 to 10 years and 1 year or less in infants.
HIV-2 may display special features of a subacute confusional-dementing illness with deep white matter and basal ganglionic damage.
In the later stages of HIV infection, the most common neurologic complication is a subacute or chronic HIV encephalitis presenting as a form of dementia; formerly it was called AIDS encephalopathy or AIDS dementia complex but it is now generally referred to as HIV encephalopathy. It has been estimated that only 3 percent of HIV cases present in this manner, but the frequency is far higher, close to two-thirds, after the constitutional symptoms and opportunistic infections of AIDS have become established. In children with AIDS, dementia is more common than all opportunistic infections, more than 60 percent of children eventually being affected.
The disorder in adults takes the form of a slowly or subacutely progressive dementia (loss of retentive memory, inattentiveness, language disorder, and apathy) accompanied variably by abnormalities of motor function (see Navia and Price). Patients complain of being unable to follow conversations, taking longer to complete daily tasks, and becoming forgetful. Incoordination of the limbs, ataxia of gait, and impairment of smooth pursuit and saccadic eye movements may be early accompaniments of the dementia. Heightened tendon reflexes, Babinski signs, grasp and suck reflexes, weakness of the legs progressing to paraplegia, bladder and bowel incontinence reflecting spinal cord or cerebral involvement, and abulia or mutism are prominent in the later stages of the disease. In the untreated case, the dementia evolves over a period of weeks or months; survival after the onset of dementia was in the past generally 3 to 6 months but is considerably longer if treatment is instituted. Treatment with antiretroviral drugs can result in cognitive improvement. There is an interest in rare cases of poor penetration of antiretroviral drugs into the central nervous system, allowing for viral replication and reemergence despite elimination of HIV from the peripheral blood.
Tests of psychomotor speed seem to be most sensitive in the early stages of dementia (e.g., trail making, pegboard, and symbol-digit testing). Epstein and colleagues have described a similar disorder in children, who develop a progressive encephalopathy as the primary manifestation of HIV. The disease in children is characterized by an impairment of cognitive functions and spastic weakness and secondarily by impairment of brain growth.
The CSF (including those lacking other manifestations of HIV) may be normal or show only a slight elevation of protein content and, less frequently, a mild lymphocytosis. HIV can be isolated from the CSF. In the CT scan there is widening of the sulci and enlargement of the ventricles; MRI may show patchy but confluent or diffuse white matter changes with ill-defined margins and generally displays cerebral atrophy (Fig. 32-2). These findings are useful in diagnosis, although CMV infection of the brain in HIV produces a similar MRI appearance, as described in the following text.