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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors review the cases of 40 patients with AIDS who died in 1989, in order to establish the relationships between clinical picture, neuroradiological features and neuropathological findings. Neurological involvement was present in over 75% of the patients, with HIV-related encephalopathy and toxoplasmosis as the most frequent diseases (52.5% and 20.0%). With regard to the cases of AIDS dementia complex (ADC) the authors observed a good correlation between the severity of the clinical manifestations, central nervous system atrophy as observed on computed tomography scan and pathological findings. The survival of AIDS patients with ADC was higher when compared to patients without ADC, suggesting the time-relationship of ADC. AS in the case of toxoplasma encephalitis, a strong relationship between radiological and pathological findings was observed. The presence of toxoplasma encephalitis in patients with radiologic features of healed lesions confirms the need for life-long prophylaxis.
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PMID:[AIDS and the central nervous system: correlations between clinical, radiological and anatomo-pathological aspects. A critical review of 40 personal cases]. 166 Jul 20

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.
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PMID:AIDS dementia complex and HIV-1 infection: a view from the clinic. 166 4

The early manifestation of HIV infection of the brain, HIV encephalitis, is due to the invasion of HIV infected mono- and multinuclear macrophages into the brain tissue and cerebrospinal fluid. These cells are intensely PAS reactive, auto-fluorescent and express the macrophage antigen CD68. They clearly prefer the white matter of cerebral hemispheres, corpus callosum and internal capsule. Lymphocytic infiltrates and microglial nodules are additional, unspecific changes. HIV encephalopathy following HIV encephalitis is patho-anatomically characterized by brain tissue damage. Its clinical correlate is so-called AIDS dementia complex. It presumably is caused by neurocytotoxic and myelinotoxic factors released by activated macrophages and/or by shedding HIV retrovirus proteins. HIV encephalopathy includes leukoencephalopathy, diffuse poliodystrophy, disseminated basal ganglia damage and brain atrophy. In some cases, granulomatous angiitis may occur.
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PMID:[HIV encephalopathy]. 172 52

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.
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PMID:Medical management of AIDS patients. Central and peripheral nervous system abnormalities. 172 42

The clinical and social consequences of AIDS dementia complex/HIV-1 associated cognitive/motor complex (ADC/HACC) in drug users have not been well documented. The value of prospective serial neuropsychological, neuroradiological and neurophysiological measurements to assist diagnosis of ADC/HACC in patients with premorbid personality disorder and intercurrent drug use is demonstrated. The psychosocial problems resulting from ADC/HACC with respect to community care and the location of hospitalization is considered. The relevance of the 1984 Mental Health Act (Scotland) with regard to drug users with ADC/HACC is discussed.
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PMID:HIV-1 associated cognitive/motor complex in an injecting drug user. 178 69

Studies of smooth pursuit eye movements were conducted in 30 ambulatory drug-free HIV-1 seropositive patients who did not yet manifest marked clinical signs of the AIDS Dementia Complex. Seropositive patients demonstrated disturbances in pursuit eye movements that were correlated with extent of immunosuppression, with impairments on neuropsychological tests of fine motor control/speed, and with independent clinical staging of the AIDS Dementia Complex. The results provide quantitative evidence that oculomotor disturbances are present in HIV-1 seropositive individuals before the manifestation of marked AIDS Dementia Complex. For this reason, and because more severe eye movement impairments have been observed in patients with AIDS, quantitative eye movement studies may provide a useful neurobehavioral procedure for characterizing and monitoring progression of CNS involvement associated with HIV-1 infection from early in its course.
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PMID:Pursuit eye movement dysfunction in HIV-1 seropositive individuals. 179 99

Subjects were 21 men with persistent generalized lymphadenopathy (PGL, n = 13) or AIDS-related complex (ARC, n = 8), who were not receiving anti-retroviral medication, and 21 controls. At baseline, mild cognitive impairment was detected in language, memory, attention, and visual and auditory processing, primarily in patients with ARC. On follow-up, the ARC group showed continued impairment and abnormalities on new measures of distractibility and activities of daily living. Although mild decline in verbal memory was noted for some patients, overall neuropsychological profiles did not show deterioration. Nomenclature for the pattern of mild, stable neuropsychological changes in patients with cognitive symptoms is discussed. Two interdisciplinary panels have recommended the term HIV-1-associated minor cognitive/motor disorder. Unlike the term AIDS dementia, it does not imply progression or a diagnosis of AIDS.
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PMID:Longitudinal evaluation of neuropsychological function in homosexual men with HIV infection: 18-month follow-up. 182 Dec 45

Quinolinic acid is an "excitotoxic" metabolite and an agonist of N-methyl-D-aspartate receptors. Of patients infected with human immunodeficiency virus type 1 (HIV-1) who were neurologically normal or exhibited only equivocal and subclinical signs of the acquired immunodeficiency syndrome (AIDS) dementia complex, concentrations of quinolinic acid in cerebrospinal fluid (CSF) were increased twofold in patients in the early stages of disease (Walter Reed stages 1 and 2) and averaged 3.8 times above normal in later-stage patients (Walter Reed stages 4 through 6). However, in patients with either clinically overt AIDS dementia complex, aseptic meningitis, opportunistic infections, or neoplasms, CSF levels were elevated over 20-fold and generally paralleled the severity of cognitive and motor dysfunction. CSF concentrations of quinolinic acid were significantly correlated to the severity of the neuropsychological deficits. After treatment of AIDS dementia complex with zidovudine and treatment of the opportunistic infections with specific antimicrobial therapies, CSF levels of quinolinic acid decreased in parallel with clinical neurological improvement. By analysis of the relationship between levels of quinolinic acid in the CSF and serum and integrity of the blood-brain barrier, as measured by the CSF:serum albumin ratio, it appears that CSF levels of quinolinic acid may be derived predominantly from intracerebral sources and perhaps from the serum. While quinolinic acid may be another "marker" of host- and virus-mediated events in the brain, the established excitotoxic effects of quinolinic acid and the magnitude of the increases in CSF levels of the acid raise the possibility that quinolinic acid plays a direct role in the pathogenesis of brain dysfunction associated with HIV-1 infection.
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PMID:Quinolinic acid in cerebrospinal fluid and serum in HIV-1 infection: relationship to clinical and neurological status. 182 18

All presently available replication-competent proviral clones of human immunodeficiency virus type 1 (HIV-1) are derived from cell culture-amplified virus. Since tissue culture is highly selective for viral strains with an in vitro growth advantage, such clones may not be representative of the biologically relevant virus present in vivo. In this study, we report the molecular cloning and genotypic characterization of 10 HIV-1 genomes directly from uncultured brain tissue of a patient with AIDS dementia complex. Targeting unintegrated circular HIV-1 molecules for recombinant lambda phage cloning, we obtained four full-length genomes with one or two long terminal repeats (LTRs), three defective genomes with internal deletions, two rearranged genomes with inverted LTR sequences, and one integrated proviral half with flanking cellular sequences. Nucleotide sequence analysis of these clones demonstrated chromosomal integration, circle formation, genomic inversion, and LTR-mediated autointegration of HIV-1 genomes in vivo. Comparison of a 510-bp hypervariable envelope region among 8 lambda phage-derived and 12 polymerase chain reaction-derived clones from the same brain specimen identified a predominant viral form as well as genetically divergent variants. Variability among 19 of 20 clones ranged between 0.2 and 1.2%. One clone exhibited 8.2% nucleotide sequence differences consisting almost exclusively of G-to-A changes. Transfection of the four full-length HIV-1 genomes identified one clone (YU-2) as replication competent and exhibiting growth characteristics similar to those of tissue culture-derived macrophage tropic strains of HIV-1. These results demonstrate, for the first time, that replication-competent HIV-1 genomes, complex mixtures of defective viral forms, and chromosomally integrated provirus persist in vivo. In addition, the brain-derived viral clones are expected to prove valuable for future studies of macrophage and neurotropism as well as for the analysis of other viral properties that are subject to in vitro selection pressures.
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PMID:Molecular characterization of human immunodeficiency virus type 1 cloned directly from uncultured human brain tissue: identification of replication-competent and -defective viral genomes. 183 Jan 10

Neuropsychiatric problems have assumed an increasingly prominent role in HIV-infected individuals. Disease occurs at all levels of the central and peripheral nervous systems by a variety of mechanisms. The AIDS dementia complex is the prototypical example of "direct" effects of HIV on the neuraxis, while infections such as toxoplasmosis and cryptococcal meningitis are complications of HIV-induced immunosuppression. Neurologic manifestations vary in frequency depending upon the overall stage of HIV disease; diagnostic difficulties may be encountered because of HIV's effect on cerebrospinal fluid parameters. The uncertainties of management of neurosyphilis in this setting provide and example of these problems. As is the case with other organ systems, the main goal of neurodiagnostic efforts is to find the increasing number of treatable components of neuropsychiatric dysfunction.
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PMID:Neurologic and psychiatric manifestations of HIV disease. 184 9


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