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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus (HIV) was detected ultrastructurally and immunohistochemically in the brain of a Japanese hemophiliac presenting AIDS encephalopathy. The encephalopathy was characterized by the multifocal occurrence of multinucleated giant cells mainly in the subcortical areas. The giant cells were identified immunohistochemically to be macrophages. HIV particles were observed in and out of the giant cells, and most of the particles ingested in the cells were membrane-bound. Some virus particles were found in pinocytic vesicles or phagocytic vacuoles, whereas the others were degradated in the lysosomes of the cells. Budding of HIV particles from the cell surface was also observed, indicating replication of the virus in vivo. These findings suggest ingestion, digestion, and replication of HIV by brain macrophages in AIDS.
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PMID:Ultrastructural behavior of human immunodeficiency virus (HIV) in multinucleated giant cells in the brain of a Japanese hemophiliac presenting AIDS encephalopathy. 276 79

Neurological disease occurs frequently in patients infected with the human immunodeficiency virus. Disorders may affect either the central or peripheral nervous systems and may be the presenting manifestation of human immunodeficiency virus-related disease. Opportunistic infections and lymphomas are major causes of central nervous system disease. Increasingly, however, human immunodeficiency virus infection of the central nervous system is being recognized and is now associated with a syndrome of progressive dementia in adults, referred to as the acquired immunodeficiency syndrome dementia complex, and an encephalopathy in infants born to human immunodeficiency virus-infected mothers. Whether brain disease related to this virus will respond to antiretroviral drugs will be a major focus of future research. Although less frequent than central nervous system disease, disorders of the peripheral nervous system are increasingly being recognized, including cases that probably have an autoimmune basis.
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PMID:AIDS and neurological disorders: an overview. 283 2

The biological properties of the ruminant animal lentiviruses, visna and caprine arthritis-encephalitis viruses, closely resemble those of their human counterparts, the human immunodeficiency viruses (HIV). All of these viruses are morphologically identical and are disseminated from host to host in nature during exchange of body fluids. Artificial conditions that favor excess exchange of such fluids precipitate epidemics by these viruses. The strategy of replication of the animal viruses in tissue culture and in vivo are very similar to that of the human virus. Virus replication is highly productive in tissue culture and leads to cytopathic effects characterized by fusion. In vivo, the rate of virus replication is restricted and lesions, suggestive of an immunopathological origin, develop after prolonged periods of subclinical infection. Similar to the animal viruses, the human viruses have a tropism for macrophages in vivo, and this leads somehow to a loss of T helper lymphocytes and proliferation of cytotoxic lymphocytes. In addition, the viruses are highly neurotropic and this results in acute fulminating disease in neonatal hosts and chronic encephalopathy in adults. Both animal and human viruses cause persistent infections and have similar strategies for eluding host immune responses. These include sequestration of neutralizing epitopes, induction of low titers of neutralizing antibodies, and antigenic drift during persistent infection. Despite close homology between genetic sequences of HIV-I and -II, these two viruses seem to have as much biological disparity from each other as does visna virus from caprine arthritis-encephalitis virus. The latter two viruses induce neutralizing antibodies that are highly strain specific and show no cross protection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lentivirus-host interactions: lessons from visna and caprine arthritis-encephalitis viruses. 283 8

The acquired immunodeficiency syndrome (AIDS) is a devastating new disease caused by the human immunodeficiency virus (HIV). This retrovirus causes profound immunoincompetence in its infected hosts, who are thereafter susceptible to develop myriad severe and relapsing protozoal, fungal, bacterial, viral, and arthropodal opportunistic infections, as well as unusual malignancies. The more than 50,000 patients who have developed AIDS in the United States have produced a sudden unexpected deluge of diagnostic dilemmas that are stressing laboratories of pathology everywhere. This paper describes the gross and microscopic pathology of the numerous complications in patients infected by HIV: (a) the prodromal AIDS-related complex with persistent generalized lymphadenopathy, (b) lymphoid infiltration of salivary gland and lung, including the complex of lymphoid interstitial pneumonitis-pulmonary lymphoid hyperplasia, (c) extranodal non-Hodgkin's lymphomas, (d) multifocal mucocutaneous and visceral Kaposi's sarcoma, (e) small cell undifferentiated (oat cell) carcinomas, (f) protozoal infections caused by Pneumocystis carinii, Toxoplasma gondii, Acanthamoeba, Cryptosporidium species (sp.), and Isospora belli, (g) the causes of chronic enteritis, (h) mycotic infections caused by Candida sp., Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, and Sporothrix schenckii, (i) bacterial infections caused by Mycobacterium avium-intracellulare, M. tuberculosis, M. kansasii, Nocardia sp., Listeria monocytogenes, Legionella sp., Treponema pallidum, and others, (j) viral infections caused by cytomegalovirus, herpes simplex and zoster, polyomavirus (progressive multifocal leukoencephalopathy), hepatitis B, molluscum contagiosum, and papillomavirus, (k) oral hairy leukoplakia, (l) subacute encephalopathy, and (m) Norwegian scabies.
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PMID:The pathology of AIDS. 283 78

Human immunodeficiency virus antigen (HIV-Ag) was detected in the serum of most adult (13/16) and paediatric (6/6) AIDS patients and rarely in the serum of symptomless seropositive controls (1/13). It was present in the cerebrospinal fluid (CSF) of all 5 children and most (5/9) adults with AIDS-related encephalopathy, but not in the CSF of 13 symptomless seropositive controls, of whom 8 had antibody in the CSF. A longitudinal study of 1 of the controls with antibody in the CSF showed that HIV-Ag in CSF was present transiently before the occurrence of antibody in the CSF. In serial samples of serum from 35 men who seroconverted HIV-Ag was detected in 11 persons--in 5 before seroconversion and in 6 after. 3 of the 6 who became antigenaemic after seroconversion remained so for the rest of the follow-up. AIDS was diagnosed in 1 patient, 3 months after HIV-Ag was first detected in serum and 6 months after seroconversion. The findings suggest that HIV-Ag appears early and transiently in primary HIV infection. Antibody production follows, after which HIV-Ag may disappear. Its persistence or reappearance seems to correlate with clinical, immunological, and neurological deterioration.
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PMID:Expression of human immunodeficiency virus antigen (HIV-Ag) in serum and cerebrospinal fluid during acute and chronic infection. 287 36

The neurologic sequelae of human immunodeficiency virus (HIV) infection may be divided into primary (= HIV-induced) and secondary (= opportunistic infections and malignancies) manifestations. Our experience with 215 HIV-infected patients indicates that major clinical symptoms are due to a few, albeit important, neurologic diseases, although in a given patient rare and sometimes multiple complications have to be considered. The clinical features of acquired immunodeficiency syndrome (AIDS) encephalopathy and CNS toxoplasmosis that represent the major primary and secondary neurologic manifestations of AIDS are discussed in detail.
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PMID:Primary and secondary involvement of the CNS in HIV infection. 305 40

Nearly 40% of AIDS patients develop neurological complications during the course of their illness, and about 10% experience neurological symptoms as the initial manifestations of AIDS. The most common neurological complication (14% of AIDS patients) is human immunodeficiency virus (HIV) encephalopathy, but opportunistic viral and nonviral infections and neoplasms are also quite common; the most frequent among these are cryptococcal meningitis, toxoplasmosis, primary central nervous system (CNS) lymphoma, progressive multifocal leukoencephalopathy, and herpesvirus infections. Most of the nonviral infections and neoplasms are potentially treatable. Neurological syndromes include diffuse and regional encephalopathies, myelopathy, meningitis, intraaxial cranial neuropathies, and retinopathy. About 10% of AIDS patients develop a CNS mass lesion; the chief causes of these lesions are toxoplasmosis and primary CNS lymphoma. Since the clinical profiles of the various diseases overlap to a great extent, differential diagnosis requires a thorough workup, including magnetic resonance imaging or computed tomography brain scanning, examination of the cerebrospinal fluid, and, frequently, brain biopsy. Because AIDS patients have a high incidence of multiple intracranial pathologies, the diagnostic workup may have to be repeated to identify all of the diseases present.
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PMID:Central nervous system dysfunction in acquired immunodeficiency syndrome. 306 5

Fourteen patients with AIDS were treated for 23 neurologic complications: four episodes of acute meningoencephalitis; eight episodes of subacute encephalopathy; two cases of progressive multifocal leukoencephalopathy; and nine cases of polyneuropathy. Nine patients were treated with 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG), one with 3'-azido-3'-deoxythymidine (AZT), and four initially with DHPG directed against cytomegalovirus (CMV) retinitis or encephalitis and subsequently with AZT against human immunodeficiency virus (HIV) encephalopathy. CMV retinitis was a helpful clinical observation indicating neurologic involvement. DHPG produced improvement in two of three cases of acute meningoencephalitis but was ineffective in cases of subacute encephalopathy or neuropathy. AZT therapy resulted in resolution in both of the two treated cases of acute confusional state and in two of the four treated cases of polyradiculoneuropathy with paraparesis but was ineffective in the late stage of subacute encephalopathy. These results suggest that CMV is important in some cases of acute meningoencephalitis, whereas HIV is a dominant pathogen in subacute dementia and polyneuropathy in patients with AIDS. DHPG may be beneficial in the former, whereas AZT appears to be effective in the latter complications.
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PMID:Responses of neurologic complications of AIDS to 3'-azido-3'-deoxythymidine and 9-(1,3-dihydroxy-2-propoxymethyl) guanine. I. Clinical features. 316 17

Eight children with acquired immunodeficiency syndrome (AIDS), aged four months to 12 years, were treated with zidovudine (azidothymidine) 100 mg/m2 intravenously every six hours for 14 days, followed by oral zidovudine at the same dose for a total of six months. Of the eight, six were infected at birth and two were contaminated by blood transfusion at ages eight and nine years, respectively; seven of the eight showed specific neurologic impairment consisting of encephalopathy (six children) and myelopathy (one child). In two children, a dramatic improvement of clinical status occurred, including neurologic progress in one; in three, the improvement was dissociate or transient and in the other three, no modification was observed. A marked increase of total lymphocyte and CD4(+) cell counts occurred in four children but was transient without modification of in vitro antigen-induced lymphocyte proliferation; p24 human immunodeficiency virus serum antigens were detected in seven of eight children, then transiently disappeared in all children during intravenous therapy but reappeared progressively during the oral regimen in all but one. Progressive modification of human immunodeficiency virus serology was noted in five children, mainly characterized by the finding of anti-core antibodies. The hematologic toxicity of zidovudine was comparable with that observed in adults. These preliminary results support the need for further studies in order to delineate the optimal regimen of zidovudine in children with AIDS.
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PMID:Zidovudine therapy in children with acquired immunodeficiency syndrome. 316 4

To produce concentrations of zidovudine (AZT) in plasma and cerebrospinal fluid that would provide constant inhibition of the replication of human immunodeficiency virus (HIV), we gave AZT by continuous intravenous infusion to 21 children ranging in age from 14 months to 12 years who had acquired HIV infection through transfusions or perinatally. All patients were symptomatic before AZT treatment (Class P2 of the Centers for Disease Control); 13 (62 percent) had evidence of neurodevelopmental abnormalities. The mean CD4/CD8 ratio was 0.18; 11 patients had CD4 counts below 0.2 x 10(9) per liter. We administered AZT at four dose levels: 0.5, 0.9, 1.4, and 1.8 mg per kilogram of body weight per hour. The plasma drug concentrations achieved at the respective dose levels were 1.9 +/- 0.3, 2.8 +/- 1.4, 3.1 +/- 1.1, and 4.5 +/- 1.0 microM. The steady-state cerebrospinal fluid:plasma ratio was 0.24 +/- 0.07. The only evidence of toxicity was bone marrow suppression. Transfusion was required in 14 patients because of low levels of hemoglobin (5 mmol per liter [less than 8 g per deciliter]). Dose-limiting neutropenia (less than 0.5 x 10(9) polymorphonuclear leukocytes per cubic millimeter) occurred in most patients who received doses of 1.4 mg per kilogram per hour or more. Improvement in neurodevelopmental abnormalities occurred in all 13 children who had presented with encephalopathy before treatment. Serial measurements of IQ before therapy and after three and six months of continuous therapy with AZT showed that IQ scores, including those for verbal and performance IQ, rose in these 13 patients and in 5 other children who had no detectable evidence of encephalopathy before treatment. Most patients also had increased appetite and weight, decreased lymphadenopathy and hepatosplenomegaly, decreased immunoglobulin levels, and increased numbers of CD4 cells. In some patients the improvement in the features of encephalopathy occurred despite the absence of immunologic improvement. We conclude that AZT is beneficial in children with symptomatic HIV infection, especially those with encephalopathy (which may be subclinical), and that the optimal continuous intravenous dose of AZT in children is between 0.9 and 1.4 mg per kilogram per hour.
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PMID:Effect of continuous intravenous infusion of zidovudine (AZT) in children with symptomatic HIV infection. 263 49


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