PubMed HealthSearch

SEARCH · PubMed Health

Results for “AIDS Dementia Complex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Detection of a vigorous HIV-1-specific cytotoxic T lymphocyte response in cerebrospinal fluid from infected persons with AIDS dementia complex.

AIDS dementia complex is a common neurologic disorder in later stages of HIV-1 infection. Because virus-specific CTL have been shown to contribute to neurologic disease in certain viral illnesses, we examined the cerebrospinal fluid of HIV-1-infected persons with various stages of AIDS dementia complex for the presence of HIV-1-specific CTL. In five of six subjects studied, HIV-1-specific CTL were identified in the cerebrospinal fluid. These CTL were directed at epitopes within the gag, reverse transcriptase, envelope, and nef proteins and restricted by HLA class I Ag. In four of these subjects, virus-specific CTL were detected in higher numbers in the cerebrospinal fluid compared to the peripheral blood, suggesting a specific recruitment to or local induction within the nervous system. These studies demonstrate the presence of a vigorous and broadly directed CTL response to HIV-1 in the central nervous system of infected persons with AIDS dementia complex, and provide immunologic evidence of localized intrathecal infection. Although HIV-1-specific CTL may serve to inhibit viral replication in the central nervous system, the presence of a persistent CTL response in the central nervous system may also contribute to the neurologic disorders characteristic of HIV-1 infection.

AIDS Dementia Complex

[AIDS dementia complex].

The AIDS dementia complex (ADC) is the SNC complaint that appears most frequently in AIDS patients. ADC is characterized by a subacute onset of dementia accompanied by motor disturbance and changes in behaviour and is considered to be directly caused by HIV-1. Very frequent in advanced stages of AIDS, it can also be the way in which the illness appears. In 90% of the necropsies of these patients a diffuse demyelination of the white substance is observed with multinucleate cells appearing in 40% of the cases. Up to now, the factors triggering this disease are not well understood, nevertheless, the immunosuppression present in these individuals could act as a factor favouring the appearance of ADC. A specific marker does not exist and, therefore, the complementary studies can only help to eliminate other causes of neurological complaints. Successful tests of treatment with zidovudine have been made, although it would be necessary to carry out studies with a larger number of patients to be able to evaluate its long-term efficacity.

AIDS Dementia Complex

Prevalence of neuropsychological deficit in HIV infection. Incipient signs of AIDS dementia complex in patients with AIDS.

The present study attempts to estimate the prevalence of Aids Dementia Complex assessed by neuropsychological testing in Norwegian patients with AIDS using a clinical control group with acute leukemia and an asymptomatic HIV-positive group as reference groups. Newly diagnosed patients with AIDS and not receiving zidovudine or other anti-viral drugs, patients with asymptomatic HIV infection, and newly diagnosed patients with acute leukemia, were studied with a battery of neuropsychological tests. Speeded tests and composite non-verbal measures discriminated significantly between groups. The results indicate higher than 50% prevalence of ADC in newly diagnosed Norwegian patients with AIDS. Our findings indicate that the AIDS population may contain two distinct groups, a subgroup with ADC and a subgroup with persistently normal neuropsychological function. The group with asymptomatic HIV infection showed normal neuropsychological performance.

AIDS Dementia Complex

Declining incidence of AIDS dementia complex after introduction of zidovudine treatment.

OBJECTIVE: To assess the incidence of the AIDS dementia complex and the presence of HIV I p24 antigen in cerebrospinal fluid in relation to zidovudine treatment. DESIGN: Retrospective study of a consecutive series of patients with AIDS from 1982 to 1988. SETTING: An academic centre for AIDS. PATIENTS: 196 Patients with AIDS and neurological symptoms examined from 1982 to 1988. INTERVENTIONS: Zidovudine treatment, which was introduced to The Netherlands on 1 May 1987 for patients with severe symptoms of HIV infection (Centers for Disease Control groups IVA, B, C, and D). MAIN OUTCOME MEASURES: Diagnosis of AIDS dementia complex and presence of HIV I p24 antigen in cerebrospinal fluid. RESULTS: The AIDS dementia complex was diagnosed in 40 of the 196 (20%) patients with AIDS. Thirty eight of 107 patients with AIDS (36%) not taking zidovudine developed the AIDS dementia complex compared with two of the 89 (2%) taking the drug (p less than 0.00001). The incidence of the AIDS dementia complex increased to 53% in the first half of 1987, after the introduction of zidovudine in May 1987, decreasing to 10% in the second half of 1987 and to 3% in 1988. Dementia was diagnosed before definition of the AIDS dementia complex (1986) according to DSM-III criteria and there was good agreement between diagnosis before and after 1986. Sixteen of 61 samples of cerebrospinal fluid (26%) from patients with AIDS (10 with the AIDS dementia complex) not taking zidovudine were positive for HIV I p24 antigen, whereas none of 37 cerebrospinal fluid samples from patients with AIDS (two with the AIDS dementia complex) taking zidovudine were positive. CONCLUSIONS: The incidence of AIDS dementia complex in patients with AIDS declined after the introduction of systematic treatment with zidovudine; the AIDS dementia complex might be prevented by inhibiting viral replication in the central nervous system.

AIDS Dementia Complex

The acquired immunodeficiency syndrome (AIDS) dementia complex.

The acquired immunodeficiency syndrome (AIDS) dementia complex is a frequent and devastating complication of infection with human immunodeficiency virus-type 1 (HIV-1). Features of the AIDS dementia complex include decreased memory, the inability to concentrate, apathy, and psychomotor retardation. Typical neuropathologic findings include gliosis, focal necrosis of neurons, perivascular inflammation, formation of microglial nodules, multinucleated giant cells, and demyelination. That HIV-1 is the direct cause of this neurologic syndrome is strongly supported by the available evidence. In addition, several studies have identified the monocyte-macrophage as the predominant cell type in the brain infected with HIV-1. However, the mechanisms by which the infected monocytes-macrophages mediate neurologic dysfunction and destruction have not been elucidated.

Acquired Immunodeficiency Syndrome

Evaluation of the AIDS dementia complex in clinical trials.

The AIDS dementia complex (ADC) is one of the most common and important causes of morbidity associated with infection by human immunodeficiency virus type 1 (HIV-1). The evaluation of ADC in clinical trials is significant not only because of the clinical impact of this syndrome, but also because of the value of measuring its cardinal features as an index of drug efficacy and because of its emerging role as a major clinical end point. The objectives of therapy include both prevention of ADC in the presymptomatic patient and alleviation of established disease. At present, the pathogenesis of ADC is incompletely understood in several critical aspects, particularly the processes underlying the clinical manifestations of central nervous system (CNS) HIV-1 infection and, further, how such processes are related to systemic disease. Consequently, it is not yet clear to what extent, or in which patients, it is necessary to achieve "therapeutic" drug levels within the CNS. Nevertheless, the assessment of ADC prevention and treatment relies principally on the complementary approach of neurological examination for diagnosis and neuropsychological testing for quantitative serial measurement of treatment effects. Additionally, surrogate markers in cerebrospinal fluid (CSF) may hold promise for objective, rapid assessment of treatment response and dose adjustment. Other measurements, including more routine CSF analysis, neuroimaging, and neurophysiological assessments, are used principally for differential diagnosis rather than for monitoring ADC status. Accumulating experience with available antiviral agents suggests that ADC can be effectively prevented and treated, at least for some period of time, and that assessment of this condition is indeed a valuable approach for measuring antiviral therapy.

AIDS Dementia Complex

Neuropsychological characterization of the AIDS dementia complex: a preliminary report.

The AIDS dementia complex (ADC) is a frequent complication of advanced HIV infection. In order to better define the neuropsychological character and progression of the ADC, four groups of subjects were studied with a battery of neuropsychological tests: an HIV-seronegative comparison group (n = 20), asymptomatic HIV-seropositive patients (n = 16), newly diagnosed AIDS patients (n = 44) and AIDS patients who were referred for neurological consultation (n = 40). Results showed significant reductions in performance in the two AIDS groups, with impairment being most prominent in tests that assessed motor speed and fine control, concentration, problem solving and visuospatial performance. This pattern of neuropsychological dysfunction is consistent with the characterization of the ADC as a subcortical dementia.

Acquired Immunodeficiency Syndrome

Single photon emission computed tomography in AIDS dementia complex.

Single photon emission computed tomography (SPECT) studies were performed in AIDS dementia complex using IMP in 12 patients (and HM-PAO in four of these same patients). In all patients, SPECT revealed either multiple or focal uptake defects, the latter corresponding with focal signs or symptoms in all but one case. Computerized tomography showed a diffuse cerebral atrophy in eight of 12 patients, magnetic resonance imaging exhibited changes like atrophy and/or leukoencephalopathy in two of five cases. Our data indicate that both disturbance of cerebral amine metabolism and alteration of local perfusion share in the pathogenesis of AIDS dementia complex. SPECT is an important aid in the diagnosis of AIDS dementia complex and contributes to the understanding of the pathophysiological mechanisms of this disorder.

Acquired Immunodeficiency Syndrome

AIDS dementia complex. Characteristics of a unique aspect of HIV infection.

A common complication of acquired immunodeficiency syndrome (AIDS) is being increasingly recognized. Known as AIDS dementia complex, the disorder is characterized by global impairment of intellectual and cognitive functions, personality and behavioral disturbances, and motor dysfunction manifested by impaired speech, gait, and coordination. AIDS dementia complex progresses rapidly and inexorably from psychomotor slowing to dementia, then to an akinetic mute state in which the patient becomes immobile and incapable of speaking, and finally to coma. Differentiation of AIDS dementia complex from a potentially treatable condition, such as reactive depression, is important. Zidovudine (Retrovir), the drug currently used to treat AIDS, has shown promise in the treatment of AIDS dementia complex. Clinical trials are now under way to determine its efficacy in this application.

Acquired Immunodeficiency Syndrome

AIDS dementia complex in the elderly. Diagnosis and management.

Ten percent of acquired immunodeficiency syndrome cases are reported in people 50 years of age or older. These older people have been infected with the human immunodeficiency virus primarily through homosexual contact, heterosexual contact or blood transfusion. AIDS in the elderly can be described as the new great imitator, often manifesting as an undetected dementia. This article focuses on the diagnosis and management of the AIDS dementia complex, a subcortical dementia with subtle and variable manifestations. The pathogenesis of AIDS dementia complex is not well understood; however, studies have shown that two-thirds of patients with AIDS exhibit overt dementia, and less than 10 percent of the brains of AIDS patients are found to be normal upon post-mortem examination. Clinical features of AIDS dementia complex include impairment in cognitive, motor and behavioral function. Since the primary care practitioner is the first line of defense in controlling the AIDS epidemic, including AIDS in the differential diagnosis for dementia is imperative.

AIDS Dementia Complex

[Neurophysiological diagnosis of AIDS dementia complex: importance of electroencephalography].

This study reports the results obtained by an Electroencephalographic screening of 450 HIV-seropositive patients, belonging to different stages of infection. The major bioelectrical changes of cerebral activity were evident in AIDS group (87.2%) and in ARC group (64.5%), whereas mild abnormalities were present in LAS group (38.8%) and in asymptomatic infection (19.2%), often without any evidence of neuropsychological impairment. Therefore, we emphasize the usefulness and the sensibility of Electroencephalography and, in particular, of Electroencephalography coupled with Computerized Spectral Analysis with the aim of identifying the subclinical stages of AIDS Dementia Complex.

AIDS Dementia Complex

Neuropsychiatric aspects of AIDS dementia complex: a report on a clinical series.

The AIDS Dementia Complex (ADC) frequently occurs in individuals with Acquired Immunodeficiency Syndrome (AIDS). We report on a clinical series of 33 patients with either AIDS or AIDS-Related Complex (ARC), who were referred for neuropsychological evaluation. This clinical series supports the developing understanding that AIDS spectrum patients often demonstrate impairment on tasks involving abstract reasoning, memory, speeded mental processing and motoric slowing. This series helps to draw attention to a small subgroup of patients, with no previous psychiatric history, who after infection with the human immunodeficiency virus (HIV), present with hyperactivity, euphoria and grandiose delusions. ADC would appear to bear with it the increased possibility of the development of secondary mania.

Acquired Immunodeficiency Syndrome

The AIDS dementia complex: some current questions.

The acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) commonly complicates the course of human immunodeficiency virus (HIV) infection and AIDS. Although many of its clinical aspects have recently been brought into clearer focus, and pathogenetic evidence has accrued implicating direct HIV brain infection, there remain a number of fundamental aspects of ADC and HIV nervous system infection that require clarification. These include clearer definition of the clinical syndrome and its variants; development of instrumentation for diagnosis and monitoring the disorder; definition of the epidemiology and natural history of both central nervous system HIV infection and ADC, which may seemingly be discordant; and understanding of both the viral pathogenesis and the biology of resultant brain dysfunction. Elucidation of these fundamental issues will enhance rational development and evaluation of therapy.

Acquired Immunodeficiency Syndrome

The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex.

Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. This dementia is due partially or wholly to a direct effect of the virus on the brain rather than to opportunistic infection, but its pathogenesis is not well understood. Productive HIV-1 brain infection is detected only in a subset of patients and is confined largely or exclusively to macrophages, microglia, and derivative multinucleated cells that are formed by virus-induced cell fusion. Absence of cytolytic infection of neurons, oligodentrocytes, and astrocytes has focused attention on the possible role of indirect mechanisms of brain dysfunction related to either virus or cell-coded toxins. Delayed development of the AIDS dementia complex, despite both early exposure of the nervous system to HIV-1 and chronic leptomeningeal infection, indicates that although this virus is "neurotropic," it is relatively nonpathogenic for the brain in the absence of immunosuppression. Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.

Acquired Immunodeficiency Syndrome

[Decrease in notifications of AIDS dementia complex in 1989-1990 in Italy: possible role of the early treatment with zidovudine].

We evaluated the incidence of AIDS dementia complex (ADC) in groups of patients who acquired infection through different risk behaviours, and attempted to evaluate the possible role of zidovudine (AZT) treatment in preventing or delaying the onset of ADC. The Italian National AIDS Registry was used to study patients with AIDS for whom ADC was reported as an index disease. Relative risk of presenting ADC between different patient categories has been determined. Logistic regression was used to analyse temporal trends in the proportion of AIDS cases presenting with ADC. Of the 6466 cases reported between August '87 and August '90, ADC was seen in 640 (9.9%). I. V. drug addicts had twice the risk (estimated odds ratio: 1.9; 95% confidence interval: 1.5-2.6, p less than 0.001), compared to homo/bisexuals, of presenting with ADC. There is significant evidence (p less than 0.0001) that after a progressive increase in the period '87-'89, it began a definite decrease in the monthly proportion of ADC cases, starting August '89. AZT was introduced in Italy in July 1987 for patients with AIDS or advanced ARC. The incidence of AIDS dementia complex at the moment of AIDS diagnosis in our population of patients, began to decline 24 months after the introduction of systematic AZT treatment in Italy. This could have been due to inhibition of HIV replication in the Central Nervous System among patients who initiated AZT-treatment before developing full-blown AIDS.

AIDS Dementia Complex

AIDS dementia complex and HIV-1 infection: a view from the clinic.

The AIDS dementia complex (ADC) is a clinical syndrome which characteristically presents as a "subcortical dementia" with cognitive, motor and behavioral changes. While the pathogenesis remains puzzling in a number of critical aspects, ADC likely relates in a fundamental way to HIV-1, itself, rather than to a secondary, opportunistic condition. This review focuses on some of the clinical information which bears on the pathogenesis of this syndrome and its relation to HIV-1 infection. This information derives from studies of the clinical character of ADC, its epidemiology and natural history, cerebrospinal fluid analysis, neuroimaging results, clinical correlates of pathological findings and its response to antiviral therapy.

AIDS Dementia Complex

Brain-reactive antibodies and the AIDS dementia complex.

To determine the role of autoantibodies in the development of the AIDS dementia complex, brain-reactive antibodies (BRAs) were assayed in 30 sera samples obtained from AIDS patients. Eighteen samples were obtained from AIDS patients with neuropsychological complications, and 12 samples were obtained from patients without any neuropsychological involvement. BRAs were analyzed using strips of nitrocellulose electroblots as a source of antigen, and were prepared from a sample of normal human parahippocampal tissue subjected to SDS-PAGE. Fourteen of 18 patients with neuropsychological complications and 4 of 12 patients without such complications were positive for BRAs to a protein with Mr of 45,000-50,000.

AIDS Dementia Complex