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PubMed1993

AIDS dementia complex complicated by cytomegalovirus encephalopathy.

We have studied longitudinally ten patients with AIDS encephalopathy with respect to pathogenetic roles of human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Three patients manifested typical AIDS dementia complex (ADC) (initially without retinitis and with slowly progressive cognitive, motor and behavioral abnormalities which were zidovudine-responsive, and relatively preserved CD4+ T cells), and seven patients presented with AIDS dementia complex complicated by CMV encephalopathy (ACE) (with CMV retinitis, peripheral neuropathy, altered sensorium, and rapidly declining clinical and immunological status). Whereas only HIV antibody was elevated in the spinal fluid of patients with ADC, both virus infections were active in the central nervous system of patients with ACE as shown by HIV p24 antigenemia and antigenrrhachia, elevated HIV and CMV antibody in the spinal fluid, disseminated CMV infection with retinitis, and basilar ventriculoencephalitis with multinucleated cytomegalic cells containing CMV and HIV proteins and CMV DNA. The recognition of ADC and ACE is important, since some patients with ACE may respond to ganciclovir or foscarnet.

AIDS Dementia Complex↗
PubMed1988

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↗
PubMed2001

Cerebrospinal fluid S-100beta and its relationship with AIDS dementia complex.

BACKGROUND: The astrocyte is thought to be important in AIDS dementia complex (ADC) pathogenesis on the basis of ADC neuropathology and cell culture models putatively because HIV can infect astrocytes leading to a compromise of their physiological detoxifying and neuronal support functions. Confirmatory in vivo data are lacking. Currently, the only widely available marker of the astrocyte is the protein S-100beta. OBJECTIVE: The aims of this study were to determine whether cerebrospinal fluid (CSF) levels of S-100beta correlate with the presence, severity and rapidity of ADC progression. STUDY DESIGN: Fourty nine CSF samples from HIV-1 seropositive individuals with either no ADC (ADC stage 0) or varying degrees of ADC (ADC stages 1-3) were analysed in this study. An immunoradiometric assay was used to quantify levels of S-100beta in the CSF. All individuals in this study were receiving antiretroviral therapy. In addition, individuals with ADC were grouped as either rapid ADC progressors or slow ADC progressors depending on the period of time from ADC diagnosis to death. RESULTS: CSF S-100beta levels in individuals with either ADC stage 2 or 3 were significantly elevated compared to those with stage 0 or 1. Moreover, CSF S-100beta levels were significantly higher in individuals with rapid ADC progression compared with slow progressors. CONCLUSIONS: This study shows that CSF S-100beta levels predict those patients in whom ADC will progress rapidly.

AIDS Dementia Complex↗
PubMedDate not supplied

[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↗
PubMed1994

SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression.

OBJECTIVE: Chronic fatigue syndrome is an illness of unknown origin that begins abruptly with a flulike state and has symptoms suggesting both a chronic viral encephalitis and an affective disorder. We compared single-photon emission computed tomography (SPECT) scans of patients with chronic fatigue syndrome with those of patients with AIDS dementia complex and unipolar depression. SUBJECTS AND METHODS: We used 99mTc-hexamethylpropyleneamine oxime to examine 45 patients with chronic fatigue syndrome, 27 patients with AIDS dementia complex, and 14 patients with major unipolar depression. Scans of 38 healthy persons were used as controls. Comparison of regional defects between groups, as well as midcerebral uptake indexes (an objective measure of global radionuclide uptake), was performed by using analysis of variance with the Student-Newman-Keuls option. Correlation between the number of regional defects and the midcerebral uptake index was determined by using the Spearman rank-correlation test. RESULTS: Patients with AIDS dementia complex had the largest number of defects (9.15 per patient) and healthy patients had the fewest defects (1.66 per patient). Patients with chronic fatigue syndrome and depression had similar numbers of defects per patient (6.53 and 6.43, respectively). In all groups, defects were located predominantly in the frontal and temporal lobes. The midcerebral uptake index was found to be significantly lower (p < .002) in the patients with chronic fatigue syndrome (.667) and patients with AIDS dementia complex (.650) than in patients with major depression (.731) or healthy control subjects (.716). Also, a significant negative correlation was found between the number of defects and midcerebral uptake index in patients with chronic fatigue syndrome and AIDS dementia complex, but not in depressed patients or control subjects. CONCLUSION: These findings are consistent with the hypothesis that chronic fatigue syndrome may be due to a chronic viral encephalitis; clinical similarities between chronic fatigue syndrome and depression may be due to a similar distribution and number of defects in the two disorders.

AIDS Dementia Complex↗
PubMed1991

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↗
PubMed1989

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↗
PubMed2000

Human Herpesvirus 8 and Protection from AIDS Dementia Complex.

Infection with human herpesvirus 8 (HHV-8) has been associated with the development of three distinct conditions: Kaposi's sarcoma, body cavitybased lymphoma and Castleman's disease. HHV-8 produces chemokinelike proteins including viral macrophage inflammatory protein II, which has been shown to block human immunodeficiency virus 1 (HIV-1) infection of CD4-positive cells expressing CCR-3. As CCR-3 is a receptor for HIV-1 into microglial cells, it has been hypothesized that HHV-8 infection may inhibit HIV-1 infection of the brain, thereby decreasing the incidence of AIDS dementia complex. We reviewed published studies of the incidence of AIDS dementia complex in individuals with and without Kaposi's sarcoma. The data are consistent in showing a negative association between Kaposi's sarcoma and AIDS dementia complex and, although sparse, support the hypothesis that productive HHV-8 infection decreases HIV-1 infection of the brain sufficiently to decrease the incidence of AIDS dementia complex. This negative association should be examined in further cohorts of HIV-1-infected subjects, to exclude alternative explanations.

Journal Article↗
PubMed1995

Differences in human immunodeficiency virus type 1 V3 sequences from patients with and without AIDS dementia complex.

Paired serum and cerebrospinal fluid (CSF) samples from 10 AIDS patients with and 10 without AIDS dementia complex (ADC) were studied, in an attempt to uncover ADC-associated variation in V3 sequences. Sequences were obtained from four of the patients with and eight of those without ADC. Comparison of the sequences using a resampling technique revealed a significant ADC-associated difference occurring at several amino acid positions. Results from serum and CSF sequences were comparable. These differences may indicate that the virus found in ADC and that in non-ADC patients have different biological properties. Comparison of serum versus CSF sequences within samples from both ADC and non-ADC patients, using the same resampling technique, revealed no clear distinctions. In some patients, the sequence populations in serum and CSF were completely distinct, while in others, there was no difference in distribution. These patterns were not associated with ADC.

AIDS Dementia Complex↗
PubMed2005

The AIDS dementia complex: clinical and basic neuroscience with implications for novel molecular therapies.

The AIDS dementia complex (ADC, also referred to as HIV-associated cognitive impairment) is a common disorder among HIV-infected patients associated with both inflammatory and neurodegenerative processes. This review describes recent advances in the clinical and basic neurosciences of HIV infection and discusses the multivariable nature of what has become a chronic disorder in the context of highly active antiretroviral therapies (HAART). Since its initial description twenty years ago, advances in cell and molecular biology along with those in neuroimaging have furthered our understanding of the underlying pathogenic mechanisms. The clinical and neuropsychological profile of ADC is generally consistent with a "frontal-subcortical" pattern of injury. Neuropathogenesis is largely driven by indirect mechanisms mediated by infected, or more commonly, immune activated macrophages, which secrete viral and host-derived factors. Magnetic resonance spectroscopy (MRS) provides a robust in vivo method to measure the inflammatory and neurotoxic events triggered by these factors and their associated signals. Although the use of combined or highly active antiretroviral therapies (HAART) has significantly improved survival rates, cerebral injury and cognitive impairment remain common events. Factors such as aging and chronic infection will likely impact the course of this disease, its pathogenesis, and treatment. The combined observations presented in this review suggest a number of critical areas for future inquiry.

AIDS Dementia Complex↗
PubMed1997

AIDS dementia complex with generalized myoclonus.

Focal and segmental, but not generalized, myoclonus have been described with human immunodeficiency virus (HIV) infection. We describe three patients with generalized myoclonus and acquired immunodeficiency syndrome (AIDS) dementia complex. In each, myoclonus persisted until death, invariably after a course of a few months. In two patients, myoclonus was elicited by sudden auditory stimuli and resembled a startle response. This form of myoclonus may be subcortical in origin. We suggest that the AIDS dementia complex be included among the causes of myoclonic dementia.

AIDS Dementia Complex↗
PubMed1999

AIDS dementia complex.

Human immunodeficiency virus (HIV) infection is often complicated by the development of AIDS dementia complex (ADC). This article examines the typical and atypical presentations of ADC, along with aspects of the prevalence and natural history of the disorder. Salient aspects of the neuropathology, neurovirology, neuroimmunology, and pathogenesis are also considered. The intricacies of management of ADC, especially in the era of highly active antiretroviral therapy, are fully evaluated. Finally, this information is synthesized into an approach to the diagnosis of ADC in a particular patient.

AIDS Dementia Complex↗
PubMed1997

Functional imaging of the AIDS dementia complex and the metabolic pathology of the HIV-1-infected brain.

The AIDS-dementia complex remains one of the more common neurologic disorders associated with human immunodeficiency virus (HIV) infection. Despite several advances that have been made in elucidating some of its clinical and biological features, pathogenesis is not well understood, and effective treatments are scarce. This article reveals the results of these studies and discusses how these different approaches have already enabled clinicians to study further the effects of HIV infection on brain function and to explore the functional anatomy of this important clinical syndrome.

AIDS Dementia Complex↗
PubMed1995

Study on didanosine concentrations in cerebrospinal fluid. Implications for the treatment and prevention of AIDS dementia complex.

It has been hypothesized that didanosine has a low efficacy in the prevention and treatment of patients with the dementia complex of acquired immunodeficiency syndrome (AIDS) because "... the drug has not been detected in the cerebrospinal fluid". We investigated didanosine concentrations in cerebrospinal fluid (CSF) and plasma of four patients with AIDS who were using didanosine chronically. Didanosine levels, 4 h after the last drug administration, averaged 0.16 (+/- 0.03) mumol/l in CSF and 0.70 (+/- 0.27) mumol/l in plasma. When compared with historical data from patients using zidovudine, didanosine concentrations in CSF appeared to be approximately half (on a molar base) those of zidovudine concentrations in the CSF. Whether this difference in CSF levels is the explanation for the presumed lower efficacy of didanosine in the prevention and treatment of AIDS dementia complex remains to be proven. However, it is clear from this study, in contrast with earlier suggestions, that didanosine is able to pass the blood-CSF barrier in human immunodeficiency virus-infected individuals.

AIDS Dementia Complex↗
PubMed1994

Envelope glycoprotein gp120 of human immunodeficiency virus type 1 alters ion transport in astrocytes: implications for AIDS dementia complex.

Infection by human immunodeficiency virus type 1 (HIV-1) is often complicated by a variety of neurological abnormalities. The most common clinical syndrome, termed acquired immunodeficiency syndrome (AIDS) dementia complex, presents as a subcortical dementia with cognitive, motor, and behavioral disturbances and is unique to HIV-1 infection. The pathogenesis of this syndrome is poorly understood but is believed to involve interactions among virally infected macrophages/microglia, astrocytes, and neurons. In this study, we show that exposure of primary rat and human astrocytes to heat-activated HIV-1 virions, or to eukaryotically expressed HIV-1 and HIV-2 envelope glycoproteins (gp120) stimulates amiloride-sensitive Na+/H+ antiport, potassium conductance, and glutamate efflux. These effects are blocked specifically by amiloride, an inhibitor of Na+/H+ antiport and by the selective removal of gp120 with immobilized monoclonal antibody. As a result of modulation of astrocytic function by gp120, the ensuing neuronal depolarization and glutamate exposure could activate both voltage-gated and N-methyl-D-aspartate-regulated Ca2+ channels, leading to increases in intraneuronal Ca2+ and neuronal death. These findings implicate the astrocyte directly in the pathogenesis of AIDS dementia complex.

AIDS Dementia Complex↗
PubMed2001

Kaposi's sarcoma and human herpesvirus 8 infection do not protect HIV-1 infected homosexual men from AIDS dementia complex.

OBJECTIVE: To examine the association between Kaposi's sarcoma (KS), human herpes virus 8 (HHV8) and AIDS dementia complex (ADC). DESIGN: A total of 599 HIV-1 infected homosexual men participated in a prospective cohort study (Amsterdam, 1984-1996). METHODS: The risk for ADC in patients with prior KS or HHV8 infection was estimated using the Cox proportional hazards method with adjustments for antiretroviral medication and low CD4 cell counts. RESULTS: Of the 599 participants, 290 (48.4%) had HHV8 antibodies, 99 (16.5%) had KS and 30 (5.0%) had ADC. ADC was diagnosed in 5.2% of participants with KS and 5.0% of those without KS, and in 4.8% of HHV8 seropositive compared to 5.2% seronegative individuals and thus was not associated with KS or HHV8 infection. Using a time-dependent Cox proportional hazards analysis with the date of KS as risk factor, the risk for ADC was 2.7 [95% confidence interval (CI), 0.92-7.96; P = 0.07) and when only definite ADC was considered it was 3.5 (95% CI, 1.00-12.26;P = 0.05). After adjusting for decreases in CD4 cell count and use of medication, the hazards ratio for participants with KS to develop ADC was 2.0 (95% CI, 0.66-5.77; P = 0.23) and 2.6 (95% CI, 0.73-9.12; P = 0.14), respectively. HHV8 seropositivity, adjusted for the same variables, showed a risk for ADC of 0.85 (95% CI, 0.41-1.77;P = 0.66) and for definite ADC 0.69 (95% CI, 0.27-1.73; P = 0.42). The expected neuroprotective effects of antiretroviral medication were observed. CONCLUSIONS: KS or HHV8 does not significantly influence the risk for developing ADC in a group with a uniform risk for developing KS therefore we recommend caution in searching for a KS-associated or HHV8-derived therapy for ADC.

AIDS Dementia Complex↗