Emotionalpersonality Functions

SDM IV Interview Schedules

Beck Scales

Symptom Checklist 90-Revised Millon Clinical Mulhaxial Inventory

Minnesota Multiphasic Personality Inventory-Second Edition (MMPI-2)

disease processes may present with a similar neurocognitive picture. Consideration of this issue is particularly important because HIV-infected individuals quite often present with histories that include other problems (e.g., alcohol/drug abuse, depression and other psychiatric disorders, learning disabilities, head injury). In addition, concurrent CNS processes such as metabolic encephalopathy and OIs can also overlap with respect to cognitive deficits.

In addition to mental changes, central nervous system- based motor complications are also frequently seen in association with HIV dementia, especially myelopathies. Myopathies (see later discussion) and neuropathies (see later

discussion) can also occur but are considered as additional complications within the realm of ADC. Cerebrospinal fluid in HIV dementia is typically remarkable for elevated beta-2 microglobulin, as well as elevated total protein and increased total IgG fraction. Of these, elevated beta-2 microglobulin has the greatest diagnostic value, particularly in cases of mild dementia. The latter two findings are not specific to HIV dementia and may be seen in normal HIV carriers. Work by Martin and colleagues^1 has also suggested that elevated CSF quinolinic acid concentrations in HIV-infected individuals are associated with deficits in motor learning and reaction time.

Imaging studies may not show abnormalities in persons with HIV-associated minor cognitive and motor disorder, despite positive neuropsychological findings. In mild HIV dementia, neuroimaging suggests subcortical and cortical atrophy with MRI abnormalities seen in deep white matter. White matter abnormalities, which may represent disruptions of the blood-brain barrier, progress and are more diffuse with increasing severity of dementia. [io&i There appears to be a positive relationship between MRI findings and neuropsychological impairment,^1 and the diffuse, ill- defined nature of the MRI lesions also serves to differentiate HIV dementia from other CNS processes. Volumetric MRI indicates caudate atrophy as well as decreased gray matter. [io91 , y?1 PET studies have suggested that subcortical hypermetabolism occurs during early HIV dementia, particularly in the basal ganglia and thalamus. This hyper- metabolism later appears to progress to subcortical and cortical hypometabolism.[iii] , [ii21 SPECT indicates abnormalities in cerebral blood flow in both neurologically normal HIV carriers and in demented patients. However, cocaine ingestion may also produce similar PET and SPECT patterns and should be ruled out.

EEG abnormalities have been reported in some asymptomatic seropositive patients, [iia] but this is not the experience of all investigators. y] Early dementia may be associated with EEG abnormalities, but up to 50 percent of these patients may be normal. y As dementia becomes severe, diffuse slowing is frequently noted, consistent with widespread dysfunction.^

Management. It is unclear if antiretroviral drug therapy initiated before the development of AIDS can prevent (or delay) the onset of HIV dementia. Portegies and associates reported a decline in the number of new cases with HIV dementia after the introduction of zidovudine therapy in 1987. y The dose was 1000 to 1200 mg/d, and other groups reported a decrease in the number of patients developing new HIV-1 dementia when treated with zidovudine 1200 mg/d compared with patients taking lower doses.y1 However, these reports should be viewed with caution because long-term, large cohort studies are limited. Moreover, other studies have shown no significant decline in incidence rates in the past several years. y , y

Antiretroviral therapy is recommended as the first-line treatment. The optimal dose has not been determined. Zidovudine regimens of 1000 to 1500 mg daily were used in the early clinical trials and were reduced to 600 mg daily, because the lower dose was found to have equivalent efficacy as the higher dose in preventing systemic infections. Results from the only U.S. placebo-controlled trial of this antiretroviral in HIV dementia suggested that neurocognitive improvement might be seen with high doses of ZDV. For patients with dementia and no prior treatment with ZDV, current recommendations include ZDV daily and regular blood count monitoring. If anemia or neutropenia develops, a dose reduction or treatment with erythropoietin or granulocyte colony stimulating factor (GCSF) can be instituted. In most cases, however, HIV dementia patients will have been treated with ZDV already, and in these patients, or those who are ZDV intolerant, ddI in a dose of 200 mg bid or d4T 40 mg twice a day may be tried.

It is as yet unclear why some demented patients respond whereas others do not. In one study, neurological improvement was noted in patients with mild neurological abnormalities, but no relationship could be found between treatment response and cumulative antiretroviral dose or CSF concentrations of antiretroviral or HIV levels. There is still very limited information about the therapeutic effects of ddI, d4T, ddC, or the protease inhibitors for the treatment of dementia. In addition to antiretroviral agents, other therapies (inflammatory, platelet activating factor, and N- methyl-D-aspartate (NMDA) antagonists) are currently or will be in clinical trials.

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