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

The epidemiologic, neuropsychiatric, and medical data on AIDS and HIV infection that are relevant to state psychiatric facilities are reviewed. The epidemiologic data suggest that a larger than expected number of AIDS patients may be seen in these facilities. Patients who are severely disturbed and psychotic may present to state hospitals with HIV encephalopathy. In patients who are chronically and severely ill, physical symptoms, including oral and cutaneous conditions, the HIV wasting syndrome, and lymphadenopathy, may provide early clues to HIV infection. The early neuropsychiatric and medical findings in HIV infection are discussed, and a clinical case is presented.
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PMID:Clinical presentations of AIDS and HIV infection in state psychiatric facilities. 265 84

Central nervous system (CNS) involvement is very frequently observed in pediatric AIDS. Clinical manifestations include encephalopathy, cognitive deficits, acquired microcephaly, neurological signs, myelopathy, and peripheral neuropathy. Neurological complications can be related to opportunistic viral infections such as encephalitis, atypical aseptic meningitis, progressive multifocal leukoencephalopathy, and myelitis. Nonviral syndromes include: toxoplasmosis, cryptococcal meningitis, candidiasis, Mycobacterium tuberculosis meningitis, and Mycobacterium avium subacute encephalitis. Bacterial infections, tumors, cerebrovascular complications, and peripheral neuropathies are not frequently observed in pediatric AIDS. The most severe complications of HIV infection is encephalopathy resulting from HIV infection of brain tissue. Direct HIV invasion of the CNS has been demonstrated. Clinical features of HIV encephalopathy are classified into three categories: (1) normal neurological findings; (2) static encephalopathy; and (3) progressive encephalopathy. AIDS dementia complex can be differentiated from the predominance of behavioral and cognitive disabilities.
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PMID:Acquired immune deficiency syndrome in childhood. Neurological aspects. 268 79

Involvement of the central nervous system with the human immunodeficiency virus is thought to underlie the clinical and pathologic features of acquired immunodeficiency syndrome (AIDS) encephalopathy. Although morphologic, immunocytochemical, and molecular data point to predominant human immunodeficiency virus infection of multinucleated and mononuclear macrophages, neuroglial and other cells are thought to be involved as well. Electron microscopic studies of biopsy tissue that might further define the neuropathologic changes have been limited. The opportunity to study well-preserved biopsy tissue from a 38-year-old man with the acute onset of dementia and AIDS encephalopathy prompted this report. Human immunodeficiency virus was seen budding from the surface of multinucleated and mononuclear cells with morphologic features of macrophages; a rare astrocyte process showed evidence of viral infection as well. Macrophages were noted within the walls of blood vessels and in intimate contact with lymphocytes within the neuropil. Notably rare were tubuloreticular inclusions, interferon-related cytoplasmic structures commonly found in systemic endothelial cells and lymphocytes in AIDS. Their relative scarcity may signify reduced interferon production in AIDS encephalopathy.
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PMID:The fine structure of acquired immunodeficiency syndrome encephalopathy. 275 85

In order to determine if ocular motor disturbances due to brainstem and cerebellar dysfunction provide a frequent and early marker for HIV infection of the brain, neurological examination was performed in 133 HIV-infected persons who were consecutively admitted to our hospital. In 22 patients (17%) we found no other reason for cerebellar or pontomesencephalic signs than HIV encephalopathy. Ocular motor disorders accounted for the most frequent signs of cerebellar and pontomesencephalic dysfunction. Ocular motor disorders mainly consisted of dissociated nystagmus (n = 12), gaze-evoked nystagmus (n = 10) and impaired smooth pursuit (n = 6). Cerebellar ataxic gait and dysmetria were present in 3 patients. Since dissociated nystagmus was the primary ocular motor disorder, we assume that the medial longitudinal fasciculus may be a predilected circumscribed area for HIV infection of the brain. We suppose that cerebellar and pontomesencephalic disorders may be an early marker for HIV encephalopathy because they were the only neurological signs found in 12 patients.
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PMID:Dissociated nystagmus as a common sign of ocular motor disorders in HIV-infected patients. 279 47

Brains from AIDS patients with an HIV-induced encephalopathy but without opportunistic infections or indications for an inflammation were studied by immuno- and enzyme-histochemical methods. It was found that the macrophages of these brains expressed a lysosomal tartrate-resistant acid phosphatase which gave a good immunological cross-reaction with an antibody to the well-characterized iron-containing bovine spleen purple acid phosphatase, belonging to the group of purple phosphatases, which are regarded as a marker for a special phenotype of activated macrophages. It was discussed that the numerous brain macrophages found in AIDS encephalopathy derive from latently infected monocytes which are believed to be drawn to the brain from the bloodstream.
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PMID:Purple acid phosphatase of human brain macrophages in AIDS encephalopathy. 279 17

In conclusion, there are a number of neurological manifestations of HIV infection, affecting both the central and peripheral nervous systems. Involvement of the CNS may occur very early in the course of infection and manifest itself as an acute aseptic meningitis. HIV encephalopathy is currently the most commonly diagnosed neurologic disorder associated with HIV and may in fact occur as a direct result of HIV infection in the brain. In years to come, HIV encephalopathy may assume epidemic proportions. Thus, nurses and other health care workers will have to be well versed in the major symptoms as well as the subtleties associated with this disease. Any drugs effective in treating these neurologic disorders must be capable of crossing the blood-brain barrier. AZT is currently being evaluated in the treatment of HIV encephalopathy. Only carefully designed prospective studies will define the natural history of neurologic disorders seen with HIV infection, as well as drugs effective in their treatment.
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PMID:Human immunodeficiency virus and the nervous system. 284 27

In a study of treatment by zidovudine in 106 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex, an acute meningo-encephalitic illness developed in 4 of 21 patients within 17 days after the dose of zidovudine had had to be reduced because of myelotoxicity. 3 of the 4 patients had previous clinical evidence of HIV encephalopathy. AIDS-related opportunist infection of the central nervous system was excluded. This acute meningo-encephalitic illness probably results from an increase in HIV replication following dose reduction.
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PMID:Acute meningo-encephalitis on dose reduction of zidovudine. 289 18

The pathogenesis of CNS damage by human immunodeficiency virus infection is unclear. Because there is little detectable virus within the CNS, we evaluated the role of the humoral immune system in mediating CNS tissue destruction. The paucity and nonspecific nature of immunoglobulin deposition rules against significant involvement of humorally mediated injury in the pathogenesis of AIDS encephalopathy.
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PMID:Absence of humorally mediated damage within the central nervous system of AIDS patients. 291 1

Reported in this paper are postmortem findings recorded from the central nervous system of 51 HIV carriers, among them 43 with clinically manifest AIDS. Opportunistic infections and tumours were established in 24 cases, including toxoplasmosis, cytomegaly, progressive multifocal leucoencephalopathy, and lymphomas. Findings obtained from 5 patients were restricted to unspecific alterations. No pathological findings at all were recordable from 8 HIV carriers without AIDS. So-called subacute microglial encephalitis (SME) was detected in 26 cases. SME was found to provide for the morphological substrate of genuine HIV encephalopathy. It was characterised by occurrence of mononuclear and even multinucleated cells which were macrophages and obviously served as virus carriers. Multinucleated cells are pathognomonic of HIV encephalopathy. No unambiguous evidence has so far been produced to primary invasion of neurons or glial cells by HI viruses.
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PMID:[The morphology of HIV encephalopathy]. 292 83

Clinical symptoms of the central and peripheral nervous system occur in about 40% of patients wit HIV infection. At autopsy, CNS lesions can be demonstrated in even higher percentages. Primary sequelae of HIV infection--either due to direct viral effects or the immunopathologic response of the human host--are acute aseptic meningitis or mengingo-encephalitis, HIV encephalopathy, myelopathy, neuropathy, and myositis. Secondary consequences of immunodeficiency in AIDS are opportunistic infections with other viruses, bacteria, fungi, and protozoa, e.g. CMV, HSV and HZV encephalitis, mycobacterial CNS infections, neurosyphilis, cryptococcal meningitis, and last but not least cerebral toxoplasmosis. The main secondary malignoma of the CNS is lymphoma. Together these disorders form a complex spectrum of central and peripheral neurological symptoms.
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PMID:[Neurologic complications of AIDS]. 304 48


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