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

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.
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PMID:[AIDS dementia complex]. 270 Feb 97

Although merging clinically within the spectrum of the AIDS dementia complex, vacuolar myelopathy is a pathologically distinct entity detected in up to 30% of autopsied patients succumbing to the late complications of human immunodeficiency virus type 1 (HIV-1) infection. Using immunohistochemistry and in situ hybridization to detect an HIV-1 core protein and viral mRNA, respectively, in tissue sections, and culture isolation to assess infectious virus in tissue homogenates, we found that vacuolar myelopathy was independent of productive HIV-1 infection of the spinal cord and brain. These results indicate that AIDS-associated vacuolar myelopathy is either not related directly to spinal cord HIV-1 infection or involves nonproductive infection and pathobiological processes distinct from those responsible for the multinucleated-cell inflammatory infiltrates that serve as histopathologic markers of productive CNS HIV-1 infection.
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PMID:Dissociation of AIDS-related vacuolar myelopathy and productive HIV-1 infection of the spinal cord. 273 16

The neurological features of 10 patients with HIV-related disease seen in Glasgow between July 1984 and May 1988 are described. Two of these patients presented with ARC and eight with AIDS. Six patients showed features consistent with a diagnosis of AIDS-dementia complex, one had cerebral toxoplasmosis, one had CNS lymphoma, one had a probable drug-induced encephalopathy and one patient had a meningoencephalitis of undetermined cause. Seven of these patients have now died. The implications of these findings are discussed.
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PMID:Neurological features of HIV-related disease in Glasgow. 274 Aug 91

The results are described of a retrospective multicentric CT/MR study of 141 neuro-AIDS patients (IV group CDC classification); 114 patients were drug addicted, 13 homosexual, 8 polytransfused, and 6 had other risk factors. The mean age was 29.6 years. The pathologic agent was identified in 47 cases by c.s. fluid examination, biopsy, autopsy or specific treatment response: it was HIV in 20 cases, toxoplasmosis in 11, cryptococcosis in 9, leishmaniasis, salmonella and papovavirus in single cases. In the follow up of 2 cases, a Kaposi's sarcoma and a primitive CNS lymphoma occurred. The main clinical features were AIDS-dementia complex (45% of cases) and focal neurologic manifestations (36%). The neuroradiological protocol consisted of 238 CT exams (97 controls), most of them with DDD (delayed double dose) technique, 7 MR exams (0.15 T) and 2 angiographies. CT findings were divided into 3 groups: negative (16%), atrophic (47%) and focal lesions (37%). In the first and second group, HIV and cryptococcal infections were the main pathologic agents. In the third group toxoplasma infections were discovered, and TB granulomas and other pathologic conditions, with ring-like or nodular enhancement, in cortical/cortico-medullary location. In follow-up patients a high tendency of evolution towards focal lesions was observed, even in negative cases. The DDD enhancement technique allowed in most cases both the demonstration of very small lesions and their grading. According to the literature CT, though a highly sensitive method, is inferior to MR imaging; however our experience in this field is currently insufficient. The specific diagnosis of pathologic agents of neuro-AIDS is difficult, due to the high number of opportunistic AIDS-related infections and neoplasms, with overlapping features: differential diagnostic criteria can be assessed only by comparing the clinical, microbiological, topographic, CT and MR findings. CT and MR exams are necessary to guide and monitor therapy and to plan stereotaxis biopsy.
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PMID:[Neuro-AIDS: a multicenter neuroradiological study]. 275 76

1. With the awareness that the population of older adults with whom nurses and other health-care workers come in contact may indeed be HIV infected, the need for universal precautions becomes imperative in all health-care settings. 2. The subpopulations of older adults in which HIV infection is most likely to be concentrated are the same as those for any other age group; ie, homosexual and bisexual men, IV drug users and their partners, people who have received blood products, and sexual partners of people who are HIV infected. 3. It is important for nurses to recognize that older adults may be manifesting the signs of symptoms of AIDS; for example, some people diagnosed with Alzheimer's disease may actually have AIDS-related dementia. 4. Gerontological nurses need to be the initiators of implementing universal precautions in their health-care settings.
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PMID:HIV and the older adult taking the necessary precautions. 277 72

Infection with the AIDS virus itself (HIV, HTLV-III, LAV, ARV) is associated with a full spectrum of neurological disorders. The application of diagnostic studies for HTLV-III infection has demonstrated that these neurologic disorders can be the first manifestation of AIDS or occur in the absence of AIDS. The most common conditions associated with HTLV-III infection alone are a subacute encephalopathy (AIDS dementia) and peripheral neuropathy; however, vacuolar myelopathy and both acute and chronic aseptic meningitis are also common. Congenital (or neonatal) transmission of the virus can result in a mental retardation syndrome of delayed onset. The AIDS virus is neurotropic as well as targeting T-helper lymphocytes. The virus has been readily identified in neural tissues and cerebrospinal fluid, including instances in which other central nervous system infections, such as toxoplasmosis, coexist. Hence, recognition of an appropriate syndrome, neurodiagnostic studies, and exclusion (or treatment) of other infections, as well as evidence for HTLV-III infection are required for diagnosis. The development of successful therapy will require agents which cross the blood-brain barrier.
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PMID:Neurology of AIDS virus infection: a clinical classification. 282 50

HIV-infected patients are at markedly increased risk for neurological dysfunction, which may occur at any level of the neuraxis (see Table 1). The most common syndromes--AIDS dementia complex, vacuolar myelopathy, and possibly distal symmetric peripheral neuropathy--appear to be related to HIV infection within the nervous system, rather than due to the immunoincompetence caused by HIV. However, the mechanism(s) by which HIV causes these syndromes, e.g., infecting neurons or oligodendroglia directly, interfering with neurotrophic factors, effecting toxic monokine production, etc., is unknown. Early, albeit incomplete, success with azidothymidine is encouraging. Less commonly, neurological syndromes may be secondary to the immunoincompetence produced by HIV. Many different etiologies--most of which are treatable--have been encountered, but a few of these (cerebral toxoplasmosis, cryptococcal meningitis, primary CNS lymphoma, and progressive multifocal leukoencephalopathy) are responsible for most of the opportunistic complications. Marked differences in symptoms and signs between AIDS patients and immunologically normal patients may complicate recognition of some of these diseases (e.g., herpes simplex encephalitis). Finally, some HIV-associated syndromes, e.g., inflammatory demyelinating polyradiculoneuropathy and retinal microvasculopathy, are of unknown etiology.
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PMID:The neurology of human immunodeficiency virus infection. 285 54

The present study evaluates the utility of the dihydropyridine in equilibrium pyridinium salt redox system for the specific delivery and sustained release of a model 2',3'-dideoxynucleoside to the brain of mice as the initial effort in a search for agents that may prove effective in reversing the complicating neurological disorders of AIDS. The unsaturated nucleoside 2',3'-didehydro-2',3'-dideoxythymidine (1), which is effective in protecting ATH8 cells against the cytopathogenicity of HIV-1, was converted to the corresponding N-methyl-1,4-dihydronicotinate derivative, 4, in three steps. The 5'-O-nicotinate ester, 2, obtained by reaction of 1 with nicotinyl chloride, was converted in quantitative yield to the N-methylpyridinium salt 3 on treatment with MeI in acetone. Reduction of the latter with Na2S2O4 gave 4 in 50% yield. Pseudo-first-order rate constants for the oxidation of 4 to 3 were observed in plasma (k = 3.54 x 10(-5) s-1) and in homogenates of mouse liver (k = 9.2 x 10(-5) s-1) and brain (k = 8.85 x 10(-5) s-1). None of the chemical delivery system 4 could be detected in the brain of female BDF/1 mice at 1 h postinjection. The peak level of 3 in the brain occurred at 3 h with a half-life of 25 h. Both 1 and N-methylnicotinic acid (trigonelline, 5) were readily identified by HPLC in a brain homogenate derived from mice injected (25 mg/kg) with 4. TLC showed a low level penetration of mouse brain by 1 (0.44 microgram/g wet tissue) following injection of the corresponding labeled [methyl-3H]-2',3'-unsaturated nucleoside (25 mg/kg). The data indicate that 4 crosses the blood-brain barrier to be oxidized by cerebral tissue to the ionic structure 3, which is "locked therein". The sustained local release of a 2',3'-dideoxynucleoside, such as 1, from a chemical delivery system (4) represents a potentially useful approach to the treatment of AIDS dementia complex.
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PMID:A dihydropyridine carrier system for sustained delivery of 2',3'-dideoxynucleosides to the brain. 291 10

In a 36-year-old patient an acute onset of psychosis occurred, probably due to HIV infection. For one year HIV-infection with reduced T4/T8 ratio had been known without clinical manifestation (stage IV B of the CDC-classification). He developed chronic delusional hallucinations, which persisted for more than one year in spite of adequate psychoactive drug therapy. So far AIDS-related dementia has not become evident. Focal lesions caused by opportunistic infections or tumour were excluded by computed tomography and magnetic resonance imaging. The latter revealed several small lesions and the brain scan showed a nonhomogeneous pattern of cerebral blood flow. CSF-examination disclosed a mild lymphocytosis and raised protein concentration. A classification as an organic, HIV-induced delusional hallucination seems to be justified.
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PMID:[Chronic paranoid-hallucinatory psychosis as the initial manifestation of an HIV infection?]. 292 4

Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.
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PMID:Functional interaction and partial homology between human immunodeficiency virus and neuroleukin. 303 62


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