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PubMed1992

Neuroradiology of the immunosuppressed state.

In recent years, one of the most common reasons for neuroimaging has become the evaluation of the immunosuppressed patient. In this review the radiographic appearances of the common inflammatory and neoplastic conditions affecting the central nervous system in patients with HIV infection, as well as the AIDS-dementia complex, are discussed. Non-AIDS immunocompromised neurologic disease is also examined, with particular emphasis on the effect of various immunosuppressive medications on the brain and spine.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Nitric oxide synthase expression and apoptotic cell death in brains of AIDS and AIDS dementia patients.

OBJECTIVES: To determine the occurrence and cellular localization of inducible nitric oxide synthase (iNOS), NOS activity and its association with cell death in brains of AIDS and AIDS dementia complex (ADC) patients. DESIGN AND METHODS: Post-mortem cerebral cortex tissue of eight AIDS patients, eight ADC patients and eight control subjects was processed for iNOS immunocytochemistry, NADPH-diaphorase activity staining as an index of NOS activity, and in situ end-labelling to detect cell death. RESULTS: iNOS-positive cells were present in the white matter of 14 out of 16 AIDS and ADC patients, whereas two out of eight control subjects showed iNOS-positive cells. iNOS immunoreactivity was exclusively localized in activated macrophages and microglial cells that both showed NADPH-diaphorase activity. In addition, NADPH-diaphorase activity, not related to iNOS immunoreactivity, was observed in astrocytes in both white and grey matter of AIDS and ADC patients. All AIDS and ADC patients, and only one control subject showed characteristic features of apoptotic cell death. CONCLUSIONS: Different forms of NOS are present in microglial cells and astrocytes of AIDS and ADC patients but are largely absent in control subjects. Although more NOS-expressing cells occur in ADC than in AIDS patients, apoptotic cell death was found in both patient groups to the same extent. We postulate that NO production in brains of AIDS patients results in cumulative cortical cell loss, which becomes neurologically evident at later stages of disease and is expressed as ADC.

AIDS Dementia Complex↗
PubMed2005

Human immunodeficiency virus infection and acquired immunodeficiency syndrome dementia complex: role of cells of monocyte-macrophage lineage.

The entry of human immunodeficiency virus (HIV) into the central nervous system (CNS) causes both the establishment of a lifelong viral reservoir in the brain and symptoms of neurological dysfunction that have an AIDS dementia complex (ADC) clinical appearance. Neurological dysfunction in ADC patients still remains an unresolved problem. However, ADC pathogenesis may be a multistep process that starts with HIV invasion of CNS by crossing the blood-brain barrier (BBB). It progresses by developing a chronic inflammatory status that can cause dysfunction in neurons and astrocytes that result in apoptotic death. Monocytes-macrophages (M/M) may play an important role by concealing the HIV transfer across the BBB. Furthermore, HIV-infected M/M could produce and release neurotoxic factors. In this review the main mediators and cells involved in pathogenesis and development of ADC are highlighted. A better understanding of the mechanisms involved in this process may help in a successful therapeutic approach to the neuropathogenesis of HIV infection.

AIDS Dementia Complex↗
PubMed1992

Cerebral metabolic dysfunction in AIDS: findings in a sample with and without dementia.

Positron-emission tomography was coupled with neurological and neuropsychological evaluation to study regional cerebral activity and neurologic status in two groups. Seventeen patients with full-blown AIDS and 14 seronegative control subjects were studied using [18F]2-fluoro-2-deoxy-D-glucose in a resting state. The AIDS group had relative regional hypermetabolism in the basal ganglia and thalamus; stepwise multiple-regression analyses revealed a significant relationship for the AIDS group between temporal lobe metabolism and severity of dementia on the AIDS Dementia Complex Rating Scale. These results suggest that the basal ganglia, thalamus, and temporal lobes are differentially affected in AIDS.

AIDS Dementia Complex↗
PubMed1994

Clinical comparison of adult and pediatric NeuroAIDS.

Human Immunodeficiency Virus type-1 (HIV-1)-associated neurologic disease occurs as the initial presenting clinical manifestation of acquired immunodeficiency syndrome (AIDS) in 3-7% of infected patients, but in up to 18% of children and adolescents (Janssen, 1992; Janssen et al., 1992; Scott et al., 1989; Mintz et al., 1989a; Epstein et al., 1986). The overall prevalence of dementia in adult AIDS patients is 7.3-11.3% (Janssen, 1992), but up to 30-60% of children with AIDS manifest an analogous progressive encephalopathy (Epstein et al., 1986; Belman et al., 1988; Mintz, 1992; The European Collaborative Study, 1990). As a result of both direct and indirect effects of HIV-1 infection of the central nervous system (CNS), a distinct clinical and pathologic picture has emerged of insidious and severe neurologic deterioration, termed "AIDS Dementia Complex" (ADC) in adults, and "HIV-1-associated Progressive Encephalopathy" (PE) in children (Working Group, 1991) (see Table 1). In the severe manifestations of this pariah, there is little dispute as to the necessity of CNS HIV-1 infection for precipitating the cascade of adverse neurologic symptoms, although the pathogenic mechanisms of neurologic dysfunction and destruction--whether a result of direct cellular infection of HIV, secondarily produced and upregulated cytotoxic cytokines, or co-infection with opportunistic pathogens--remains an area of active research (Epstein and Gendelman, 1993; Fiala et al., 1993; Wiley and Nelson, 1988; Saito et al., 1994; Koenig et al., 1986; Sharer, 1992). Furthermore, the existence of systemic immune deficiency renders the CNS susceptible to opportunistic infection (OI), particularly in adult patients, adding further to morbidity and mortality (Clifford and Campbell, 1992). With the introduction of antiretroviral nucleoside analogues, there have been reports of a decreasing incidence of ADC (Portegies et al., 1989; Day et al., 1992), and amelioration--at least temporarily--of PE in children (Pizzo et al., 1988; Mintz and Epstein, 1992; Brouwers et al., 1990; Mintz et al., 1990). This appends further evidence to the central precipitating role of CNS HIV-1 infection.

AIDS Dementia Complex↗
PubMed1998

Cerebrospinal fluid mononuclear cell counts influence CSF HIV-1 RNA levels.

This study evaluated the relation between cerebrospinal fluid (CSF) mononuclear cells (MNC) and CSF HIV-1 RNA levels. HIV-1 RNA levels in plasma and CSF were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) in 58 consecutive patients with neurologic symptoms and late HIV-1 infection. The majority of the patients had no central nervous system (CNS) complication (n = 36), 11 had AIDS dementia complex (ADC) and 11 had CNS opportunistic infection (CNS OI). CSF cell counts were analyzed using a method that also evaluated hypocellular CSF (i.e., from 0.1 x 10(6) cells/L). A strong correlation was found between CSF MNC and CD4+ lymphocyte counts in blood (r = 0.58; p < .0001). HIV-1 RNA was detected in all plasma samples and in 38 of 58 (66%) of the cell-free CSF samples. CSF HIV-1 RNA was less frequently detected in patients with hypocellular CSF than in patients with normocellular or pleocytic CSF (13 of 28 patients [46%] versus 10 of 14 patients [71%] versus 15 of 16 patients [94%], respectively). The levels of CSF HIV-1 RNA correlated with the CSF MNC count (r = 0.61; p < .0001). The correlation also remained strong within the clinical subgroups of CNS asymptomatic patients (r = 0.55; p < .001) and ADC patients (r = 0.79; p < .001), but not among CNS OI patients (r = 0.19). Patients with CNS OI were found to have higher CSF HIV-1 RNA levels than the patients without evidence of CNS complication. Thus, a close relation was found between CSF HIV-1 RNA levels and CSF MNC counts. These data support the hypothesis that a substantial part of the virus in the CSF of HIV-1-infected patients is locally produced by CSF MNC.

AIDS Dementia Complex↗
PubMed1992

Medical management of AIDS patients. Central and peripheral nervous system abnormalities.

This article discusses the wide range of neurologic complications of HIV infection according to degree of advancement of systemic HIV disease. The focus is principally on those disorders that appear at least in part to be directly related to HIV: AIDS dementia complex, peripheral neuropathy, and myopathy. Unusual disturbances such as seizures and transient neurologic disorders are also discussed.

AIDS Dementia Complex↗
PubMed1995

[AIDS dementia. Prognosis and therapeutic perspectives].

AIDS dementia complex is a severe complication related to HIV infection of the central nervous system. It has been estimated to affect about 7% of AIDS patients, with an increased frequency in very young and old patients. In most cases, it appears in severely immuno-deficient patients. Typically, AIDS dementia presents as a subcortical dementia with cognitive, behavioural and motor decline. The mechanism of the dementia remains unclear; the neuronal loss is controversial and a neurotoxicity due to NMDA receptor activation is likely. No treatment proved to be efficient. Beneficial effect of anti-NMDA receptor antagonists are under investigation.

AIDS Dementia Complex↗
PubMed1990

Brain imaging in acquired immunodeficiency syndrome dementia complex.

Human immunodeficiency virus (HIV) infections are accompanied by many different types of neurological complications. Opportunistic infections and neoplasms, particularly lymphoma, are often an underlying cause for these complications in patients with acquired immunodeficiency syndrome (AIDS). Frequently, these can be detected by cerebrospinal fluid (CSF) examination, double-dose contrast transmission computed tomography (CT), and/or magnetic resonance imaging (MRI). It has become apparent that the HIV itself is responsible for a significant percentage of neurological disease in the HIV-seropositive individual. The onset may be subtle and may occur before the onset of frank immunosuppression. Diagnosis of HIV encephalitis or AIDS dementia complex (ADC) is complicated by the frequent coexistence of opportunistic infections. Structural neuroimaging (CT or MRI) shows atrophy and in some case white matter abnormalities, but imaging-pathological correlation suggests that these modalities are relatively insensitive to the presence of HIV brain infection. Functional neuroimaging, both 18fluorodeoxyglucose positron emission tomography (PET) for evaluation of glucose metabolism and 123I iodoamphetamine or 99mTc-HMPAO single-photon emission computed tomography (SPECT) for evaluation of cerebral perfusion, can demonstrate abnormalities in the subcortical gray matter structures and the cerebral cortex in patients with ADC. These abnormalities may be observed early in the course of ADC even when MRI is negative and the patient is relatively asymptomatic. Also, PET and SPECT may be useful to follow progression of the dementia or response to therapy.

AIDS Dementia Complex↗
PubMed1998

Cerebrospinal-fluid HIV-1 RNA and drug concentrations after treatment with lamivudine plus zidovudine or stavudine.

BACKGROUND: Treatment and prevention of HIV-1-related central-nervous-system disease may be dependent on penetration of antiretroviral drugs into the central nervous system. Few data are available about cerebrospinal-fluid penetration and concomitant changes of HIV-1-RNA concentrations during treatment with antiretroviral agents. We investigated these effects in HIV-1-infected people. METHODS: 28 antiretroviral-naive individuals with CD4 cell counts of 200/microL or more and plasma HIV-1-RNA concentrations of 10,000 or more copies/mL who were free of neurological symptoms were randomly assigned lamivudine plus either stavudine (n = 17) or zidovudine (n = 11). We did lumbar punctures on 28 individuals before and 22 individuals after 12 weeks of treatment to assess HIV-1-RNA and drug concentrations in cerebrospinal fluid. FINDINGS: All 28 individuals had detectable HIV-1-RNA concentrations in the cerebrospinal fluid (median 4.64 log10 copies/mL and 4.20 log10 copies/mL in the lamivudine plus zidovudine and lamivudine plus stavudine groups, respectively). There was no correlation between plasma and cerebrospinal-fluid HIV-1-RNA concentrations (r = 0.18, p = 0.35). After 12 weeks of treatment none of the individuals had detectable HIV-1-RNA concentrations in the cerebrospinal fluid. The highest drug concentration in the cerebrospinal fluid was for lamivudine followed by stavudine and zidovudine. Concentrations were consistent over time, unlike plasma concentrations. Therefore, we found time-dependent cerebrospinal-fluid to plasma drug-penetration ratios, which were highest for zidovudine followed by stavudine and lamivudine. INTERPRETATION: The two drug combinations were equally effective in the decrease of cerebrospinal fluid HIV-1-RNA concentrations. All drugs penetrated the cerebrospinal fluid. Antiretroviral drugs other than zidovudine might be useful in the prevention of AIDS dementia complex.

AIDS Dementia Complex↗
PubMed1993

Potent stimulation of monocytic endothelin-1 production by HIV-1 glycoprotein 120.

Monocytes/macrophages play a critical role in the pathogenesis of HIV infection, both as targets for virus replication and as sources of production of multifunctional cytokines. Endothelins, peptides with potent vasoconstricting activities originally isolated from endothelial cells, are also produced and secreted by macrophages in a manner similar to that of other cytokines. In an attempt to explore the potential role of endothelins in HIV-infection, we investigated the effect of the HIV-1 envelope glycoprotein, glycoprotein 120, on monocytic endothelin-1 production. This glycoprotein has been identified as a potent stimulator of monokines such as TNF-alpha and IL-6, which have been implicated as potential mediators of HIV-encephalopathy. We found that glycoprotein 120, similar to LPS, stimulates the secretion of endothelin-1, as well as TNF-alpha, from macrophages in a concentration-dependent manner. Using reverse transcriptase polymerase chain reaction, we found that circulating monocytes in HIV-infected individuals show a distinct expression of the endothelin-1 gene that is not detectable in healthy controls, indicating chronic activation of this gene in HIV-infection. In addition, cerebral macrophages in patients with HIV-encephalopathy were strongly positive for endothelin. Thus, monocytic endothelins appear to be stimulated during HIV infection. Their potent vasoactive properties render them potential candidates for mediating alterations in the cerebral perfusion pattern associated with the AIDS dementia complex.

AIDS Dementia Complex↗
PubMedDate not supplied

Evidence of neuronal degeneration in C57B1/6 mice infected with the LP-BM5 leukemia retrovirus mixture.

Mice infected with LP-BM5 develop a severe immunodeficiency accompanied by learning and memory deficits, gliosis, and neurotransmitter abnormalities. The neurochemical alterations are consistent with elevated excitotoxin levels, suggesting that infected mice may incur neuronal damage. Although the number of neocortical neurons was unchanged in mice 12 wk after LP-BM5 infection, the expression of cytoskeletal proteins declined, particularly in the frontal and parietal cortex as indicated by MAP2, NF-200, and synaptophysin immunoreactivity. In contrast, the number of striatal neurons decreased 19%. The remaining neurons were smaller, with fewer synaptic boutons, and showed decreased synaptophysin and NF-200, immunoreactivity. Immunoblots of cortex and striatum confirmed decreases in MAP2, NF-200 and synaptophysin expression. Finally, although NCAM expression decreased in the striatum, it increased in the cortex. These results indicate that LP-BM5-infected mice sustain significant neuronal damage, which may contribute to their behavioral deficits. Moreover, the increase in cortical NCAM expression suggests active synaptic remodeling to compensate for the persistent excitotoxic environment in these mice, whereas striatal neurons degenerate. These concurrent degenerative and compensatory processes may also occur in the brains of patients with AIDS dementia complex (ADC), who suffer extensive degeneration of the basal ganglia and cerebral cortex.

AIDS Dementia Complex↗
PubMed1990

Mental changes in patients with AIDS.

Mental changes are common in patients with acquired immunodeficiency syndrome (AIDS). Neuropsychological data of 32 patients with AIDS and cognitive symptoms were reviewed. All patients were neurologically examined and ancillary investigations were performed. According to the neuropsychological data three groups could be distinguished: I) 4 patients with dementia and cortical deficits; II) 16 patients with subcortical dementia; III) 12 patients with subcortical cognitive deficits without global intellectual deterioration. AIDS Dementia Complex (ADC) was diagnosed in 12 patients and occurred in all three groups. The most frequent form of dementia in patients with AIDS is of a subcortical type. Impaired memory or reduced psychomotor speed, or both, are common in patients without global intellectual deterioration. ADC seems an unlikely diagnosis in patients with cortical dementia. Neuropsychological examination is important for diagnosing ADC but the diagnosis cannot be made without regarding the neurological findings and ancillary investigations.

AIDS Dementia Complex↗
PubMed1996

Pathogenesis of HIV-1 associated neurodegeneration.

A significant number of people infected with the human immunodeficiency virus (HIV) develop neurologic complications. The AIDS dementia complex is frequently accompanied by HIV encephalitis, which is characterized at the neuropathologic level by loss of neuronal subpopulations in the neocortex, limbic system, and basal ganglia in association with synaptic and dendritic damage, astrogliosis, and formation of microglial nodules and multinucleated giant cells. Recent studies have shown that the extent of neurodegeneration in this condition correlates directly with the amount of HIV-1 antigen in the brain. HIV-1 infection of the brain could result in neurodegeneration via neurotoxic effects of viral products (e.g., gp 120, Nef, Tat) and/or via alterations in the expression of host factors. The latter may include increased production of potentially detrimental factors such as cytokines, excitotoxic amino acids, free oxygen radicals, and bioactive lipid mediators as well as interference with the production or action of neurotrophic/protective factors. Derangements of the neuronal calcium homeostasis, lipid peroxidation, and induction of programmed cell death (apoptosis) may all play a role as final common pathogenetic pathways in HIV-1-induced neurodegeneration. Recent studies in transgenic mice (over)expressing HIV- or host-derived proteins in their central nervous system indicate that distinct neuronal populations may differ in their susceptibility to specific pathogenic factors. For example, glutamate-receptor-bearing pyramidal neurons were particularly susceptible to neurodegeneration promoted by HIV-1 products, whereas interneurons were more sensitive to the neurotoxic effects mediated by cytokines. For the design of effective treatments for the HIV-1-associated cognitive/motor complex, it will be important to determine whether the neurologic deficits in this entity result from global neuronal dysfunction or relate more specifically to the impairment of distinct neuronal subpopulations. It will also be critical to examine diverse in vitro and in vivo models to help decide which of the many pathogenetic processes that may be at work in this complex disease constitute the most promising therapeutic targets.

AIDS Dementia Complex↗
PubMed1993

HIV-1-related neurological disease.

Infection due to human immunodeficiency virus type 1 (HIV-1) frequently leads to neurological complications that may involve each part of the neuraxis. A brief discussion is presented of the nature of involvement, appropriate treatment modalities, and the diagnostic approach to such problems. Emphasis will be placed on AIDS dementia complex (ADC). A summary of the current understanding of the pathogenesis of ADC will be presented and used as a platform for discussion of future therapeutic interventions.

AIDS Dementia Complex↗
PubMedDate not supplied

[Dementia associated with AIDS].

INTRODUCTION: Dementia associated with AIDS or AIDS dementia complex (ADC) is characterized by neurocognitive defects with disorders of the functional ability of the patient for work and the activities of everyday life. The increasing number of AIDS patients has led to a significant rise in those with neurological involvement, especially in poorer countries. DEVELOPMENT: At present no data on the incidence of ADC is available. The prevalence varies with the population studied and criteria used for diagnosis. Some authors have suggested a frequency of 8 to 16%. However, other reports mention an incidence of up to 20.7% of encephalopathy in AIDS patients. The mechanism by which ADC occurs is still not clear. Many factors have been suggested but none confirmed as causal. CLINICAL FEATURES: symptoms are due to subcortical dementia with difficulty in concentration, memory and learning whilst language, recognition, basic attention and executive function are relatively well preserved. DIAGNOSIS: this is essentially clinical, by exclusion, in cases of HIV+ patients with marked immunological deterioration and compatible clinical features. TREATMENT: current clinical guidelines recommend that most AIDS/HIV patients, if not all, should receive treatment with potent combinations of anti retroviral drugs. CONCLUSION: Even in the age of modern, highly active anti retroviral treatment, ADC is still a devastating complication of HIV infection.

AIDS Dementia Complex↗
PubMed1991

Dementia in patients with the acquired immunodeficiency syndrome.

Central nervous system (CNS) manifestations are common in patients with the acquired immunodeficiency syndrome (AIDS). The most common CNS syndrome is a dementing illness referred to as the AIDS dementia complex, in which motor and cognitive changes may also be seen. Neurodiagnostic studies are fairly characteristic, though highly nonspecific. Dementia may precede overt manifestations of AIDS, and either an insidious or a fulminant course may be seen. Appropriate management of the patient with AIDS includes differentiating dementia from psychologic responses to the disease.

AIDS Dementia Complex↗
PubMed1996

Abnormal cerebral glucose metabolism in HIV-1 seropositive subjects with and without dementia.

UNLABELLED: This study was undertaken in order to extend our previous finding of relative basal ganglia hypermetabolism in AIDS dementia complex (ADC) and to develop clinically useful metabolic indices of CNS involvement in HIV-seropositive (HIV+) subjects. METHODS: Twenty-one HIV+ subjects (11 with AIDS) underwent FDG-PET scanning; 12 had a follow-up scan at 6 mo and 4 had a third scan at 12 mo. Forty-three age-matched heterosexual volunteers served as controls. FDG-PET scanning was performed with arterial blood sampling, and scan data were analyzed using the Scaled Subprofile Model (SSM) with principal component analysis. RESULTS: SSM/principal component analysis of the combined (HIV+ and controls) FDG-PET dataset extracted two major disease-related metabolic components: (a) a nonspecific indicator of cerebral dysfunction, which was significantly correlated with age, cerebral atrophy and ADC stage and (b) the striatum, which was heavily weighted (relatively hypermetabolic) and appeared to provide a disease-specific measure of early CNS involvement. CONCLUSION: FDG-PET scans provide quantitative measures of abnormal functional connectivity in HIV-seropositives-with or without AIDS or ADC. These measures, which are robust across centers with respect to instrumentation, scanning technique and disease severity, appear to track the progression of CNS involvement in patients with subclinical neurologic or neuropsychologic dysfunction.

AIDS Dementia Complex↗