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

Single photon emission computed tomography (SPECT) using N-isopropyl-p-(123I)iodoamphetamine (123I-IMP) and 99Tcm-hexamethylpropyleneamine oxime (99Tcm-HMPAO) was performed in 25 patients with different clinical stages of AIDS encephalopathy. The average interval between the two examinations was 7 days. In 15 of the 25 cases (60%) 99Tcm-HMPAO scans were different from 123I-IMP scans. Uptake defects of different extent were observed in 8 of 25 cases (32%), of different extent and different location in 3 of 25 cases (12%) and of identical extent but of different location in 4 of 25 cases (16%). Differences in the uptake patterns of 123I-IMP and 99Tcm-HMPAO with regard to extent and/or location were more commonly shown in patients with early acquired immunodeficiency syndrome (AIDS) encephalopathy (P = 0.0372). In this group, 99Tcm-HMPAO showed uptake defects of greater extent more frequently than did 123I-IMP (P = 0.0156). Our data indicate different brain uptake mechanisms of 123I-IMP and 99Tcm-HMPAO in early and advanced AIDS encephalopathy.
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PMID:Double-tracer SPECT in patients with AIDS encephalopathy: a comparison of 123I-IMP with 99Tcm-HMPAO. 151 20

To investigate the epidemiology of human immunodeficiency virus (HIV) encephalopathy, we analyzed cases of acquired immunodeficiency syndrome (AIDS) reported to the Centers for Disease Control (CDC) from September 1, 1987, through August 31, 1991. Of 144,184 persons with AIDS (PWAs), 10,553 (7.3%) were reported to have HIV encephalopathy. The proportion of PWAs with HIV encephalopathy was highest at the extremes of age: in PWAs less than 15 years old the proportion was 13%, and in PWAs greater than or equal to 15 years old the proportion progressively increased with age, from 6% in PWAs 15 to 34 years old to 19% in PWAs greater than or equal to 75 years old (p = 0.00001, chi 2 test for linear trend in proportions). The reported annual incidence of HIV encephalopathy per 100,000 population aged 20 to 59 years was 1.4 in 1988, 1.5 in 1989, and 1.9 in 1990. This analysis best provides estimates for HIV encephalopathy as the initial manifestation of AIDS because the CDC AIDS reporting system often does not ascertain diagnoses after the initial AIDS report. These data suggest that age (very young or old) is associated with the development of HIV encephalopathy and that HIV encephalopathy is a common cause of dementia in adults less than 60 years old in the United States.
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PMID:Epidemiology of human immunodeficiency virus encephalopathy in the United States. 164 Nov 38

The ventricular area at the level of the foramen of Monro was measured from axial x-ray computed tomography (CT) scans obtained prior to and 6 months after the initiation of continuous infusion of zidovudine (ZDV) in eight children with human immunodeficiency virus-induced encephalopathy. Evidence of moderate to severe central atrophy was present on initial CT scans (p less than 0.05). Ventricular area and ventricular brain area ratio (VBR) decreased after ZDV therapy in seven of eight children (mean decrease of 21.5 and 20%, respectively, p less than 0.05). The degree of decrease in VBR correlated with reductions in cerebrospinal fluid (CSF) protein concentration (r = 0.93, p less than 0.01), but not lymphocyte T4 or T8 counts. Intelligence quotients (IQs) improved in all seven children tested (mean improvement of 17.7%, p less than 0.01) and correlated significantly with reductions in CSF protein concentration (r = -0.85, p = 0.003). The magnitude of IQ changes was not significantly correlated with the magnitude of changes in ventricular area. We conclude that the cognitive improvement of HIV encephalopathy seen after 6 months of continuous infusion of ZDV is accompanied by reduction in brain atrophy and decreased CSF protein, suggesting an ameliorating effect of ZDV on the pathogenesis of AIDS encephalopathy in children.
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PMID:Brain growth and cognitive improvement in children with human immunodeficiency virus-induced encephalopathy after 6 months of continuous infusion zidovudine therapy. 167 12

The neurological findings in 41 HIV-seropositive children are described. 23 children were symptomatic, eight seropositive but without symptoms and 10 seropositive children less than 15 months of age had no other evidence of immunodeficiency. Acquired microcephaly, developmental regression and progressive motor deterioration indicated HIV encephalopathy, as did developmental delay, mental retardation, cerebellar symptoms and behavioural changes. Three children with progressive encephalopathy improved after treatment with azidothymidine (AZT). In eight children treated with prophylactic intravenous immunoglobulin therapy (IVIG) and seven treated with both IVIG and AZT, no mental deterioration has been observed since the beginning of therapy. One child with advanced encephalopathy and severe pyramidal tract involvement did not improve.
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PMID:Central nervous system involvement of children with HIV infection. 186 79

HIV induces severe dementia in about 20% of adult AIDS patients. In children HIV-infected at birth, the incidence of specific neurological complications is still higher since severe encephalopathy occurs in almost all children who develop an early and severe immunosuppression. In all cases, the brain monocytes/macrophages and the microglial cells are the only cells which replicate HIV in the central nervous system (CNS) of these patients, and the appearance of neurological symptoms seems induced by an interaction between HIV-infected macrophages with neurons and glial cells. AIDS encephalopathy is related to two properties of HIV: to the viral tropism for monocytes/macrophages/microglial cells, which allow the brain infection, and to HIV tropism for CD4+ lymphocytes responsible for the appearance of immunosuppression, which trigger viral dissemination in the CNS. However, childhood encephalopathy is not always associated with HIV replication in the CNS at the time of death, and mild dementia in HIV-infected adults were described without signs of HIV replication in autopsy CNS samples. Those findings suggest that persistent, productive viral infection is not required for the development of HIV encephalopathy. Therefore, if the relationship between HIV CNS infection and AIDS encephalopathy in adults and children is clearly demonstrated, the pathogenesis of the neurological disease and the kinetics of HIV replication in the CNS are unclear. In addition, the very high incidence of AIDS encephalopathy in children could be related to HIV infection of microglia which is differentiating in fetal or newborn brain.
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PMID:AIDS encephalopathy and tropism of HIV for brain monocytes/macrophages and microglial cells. 188 16

The encephalopathy resulting from direct infection of the brain by human immunodeficiency virus (HIV), which correlates clinically with the AIDS dementia complex, has been reported as being localized to the white matter where it induces myelin loss, gliosis and perivascular infiltration by mononuclear macrophages and multinucleated giant cells. Damage to the cortical grey matter in HIV encephalopathy was investigated in nine randomly selected HIV-positive cases with or without clinical or morphological evidence of encephalopathy and in five age-matched controls, using routine histology and immunohistochemical methods [glial fibrillary acidic protein (GFAP), microglia and HIV antibodies]. Increased numbers of GFAP-expressing astrocytes and Ricinus communis agglutinin 1-120-expressing microglial cells were found in all the HIV-positive cases (including asymptomatic) and their severity could be correlated with the severity of the encephalopathy in the white matter; the increase in number of cells expressing GFAP was diffuse and the intensity of the staining higher than that of microglial cells. The subpial region was the most severely involved. It is suggested that involvement of the cortical grey matter is more common in HIV infection than previously suspected and that clinical evidence of a dementing process in AIDS is not necessarily due only to white matter lesions.
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PMID:The involvement of the cerebral cortex in human immunodeficiency virus encephalopathy: a morphological and immunohistochemical study. 208 94

The appearance on magnetic resonance (MR) and computed tomographic (CT) images of specific central nervous system disorders associated with acquired immunodeficiency syndrome in 12 cases was correlated with autopsy findings. There were three cases of human immunodeficiency virus (HIV) encephalopathy; three, primary lymphoma; three, toxoplasmosis; one, cryptococcosis; one, cytomegalovirus infection; and one, progressive multifocal leukoencephalopathy. MR imaging demonstrated the various cranial lesions more clearly than did CT. On the basis of MR imaging characteristics, HIV encephalopathy could be distinguished from other lesions, particularly progressive multifocal leukoencephalopathy. Basal ganglia were the most common sites of involvement in opportunistic infections and primary lymphoma. Reliable distinguishing features among lesions of the basal ganglia were not found, except for cryptococcal lesions, which had a unique appearance.
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PMID:Acquired immunodeficiency syndrome: correlation of radiologic and pathologic findings in the brain. 232 12

Brains of AIDS patients do often display characters of HIV specificity, in the presence or not of opportunistic lesions. Mesodermal nodules with giant cells, and a peculiar primary demyelination, the progressive diffuse leukoencephalopathy of Kleihues et al., which can be found only in brains with giant cells, have been pointed out as typical. In 100 intra venous drug user patients, younger than 32 years (mean age: 26) the HIV specificity described was observed on 49 occasions. All these patients presented with Seitelberger's glio-neuronal poliodystrophy (GP), quite similar to that encountered in several kinds of encephalopathies. Nevertheless, in 35 of the patients with HIV typical findings, there was in the cortex and some other grey matter regions, an amount of diffuse mesodermal elements uncommon in encephalopathies, and so relevant as to contradict the notion itself of this kind of cerebral lesion, where "inflammatory" events ought not to appear. This aspect of HIV encephalopathy was indicated by us as "GP plus". An optic microscopy examination of the cortex allowed us to establish how in GP plus the neuronal changes are more severe and apparently older than in the other patients considered. The fact that the astrocytes did not behave differently in the two aspects of encephalopathy lead us to conclude that GP plus sets in through processes distinct from those in encephalopathy tout-court, and to put forward that it is a further character of HIV specificity.
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PMID:[Cerebral cortex and HIV lesion specificity. A neuropathological study of the brain of 100 drug addicts]. 253 92

Fifty to ninety percent of pediatric AIDS cases are complicated by neurologic dysfunction. We present a case of a 5-year-old black female with AIDS encephalopathy and Mycobacterium avium intracellulare. Her initial presentation was that of neuroencephalopathy with loss of developmental milestones, pyramidal tract signs, and subsequent evidence of cortical atrophy. Her initial CT scan at the time of frank encephalopathy was normal, whereas 18 months into the clinical course of her encephalopathy, her CT scan of the head demonstrated typical ventricular dilatation and severe cortical atrophy consonant with her clinical picture. She subsequently developed Mycobacterium avium intracellulare documented by gastric aspirate culture and other opportunistic infections including Candida esophagitis. Her neuroencephalopathy plateaued with continued evidence of immune dysfunction and mycobacterium by gastric aspirate, despite triple antibiotic therapy with INH, streptomycin, Pyrazinamide with later addition of Rifampin and final substitution of the investigational congener Rifabutin. AIDS encephalopathy and Mycobacterium intracellulare are discussed in terms of their prognosis and therapy, particularly in view of new reports of the application of AZT and immunoglobulin therapy.
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PMID:Encephalopathy as a presentation of pediatric AIDS: case report. 255 69

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


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