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

Many HIV-infected children have neurological involvement. We present our observations in 49 cases, 58% of which had some form of clinical neurological impairment. Most of the patients affected (71%) presented with progressive encephalopathy, characterized by developmental delay with loss of acquisitions and cognitive decline, an impaired growth curve, microcephaly and corticospinal dysfunction. CT-scan imaging shows cerebral atrophy in all cases and basal ganglia calcifications in 29%. Non-specific abnormalities are found on the EEG in two-thirds of cases and in the CSF in slightly less than half the cases. Pathological studies sometime revealed HIV encephalitis or lateral corticospinal tracts degeneration. Neurological impairment secondary to vascular events, neoplasms or opportunistic infections were rare, especially when compared with the adult HIV population.
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PMID:Neurological findings in HIV-infected children: a review of 49 cases. 138 47

Experimental and clinical evidence indicates that all lentiviruses of animals and humans are neurotropic and potentially neurovirulent. The prototypic animal lentiviruses, visna virus in sheep and caprine arthritis encephalitis virus in goats have been known for decades to induce neurologic disease. More recently, infection of the brain with the human immunodeficiency virus (HIV) has been linked to an associated encephalopathy and cognitive/motor complex. While the visna virus and caprine arthritis encephalitis virus are important models of neurologic disease they are not optimal for the study of HIV encephalitis because immune deficiency is only a minor component of the disease they induce. By contrast, the recently isolated lentiviruses from monkeys and cats, the simian and feline immunodeficiency viruses (SIV and FIV respectively), are profoundly immunosuppressive as well as neurotropic. SIV infection of the central nervous system of macaques now provides the best animal model for HIV infection of the human brain due to the close evolutionary relationship between monkeys and man, the genetic relatedness of their respective lentiviruses, and the similarities in the neuropathology. This chapter will compare and contrast the neurobiology of SIV and FIV with HIV.
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PMID:Neurobiology of simian and feline immunodeficiency virus infections. 166 9

A female infant born pre-term to a HIV seropositive mother presented at birth with seropositivity for HIV and CMV viruria. At five months of age she developed an AIDS-related complex. Six months later she died from rapidly progressive diffuse encephalopathy. Post mortem examination revealed generalized CMV infection. Neuropathological examination showed a nodular encephalitis with occasional cytomegalic cells containing characteristic CMV inclusion bodies. There was no evidence of HIV encephalitis; immunostaining for HIV antigen (gp 41) was negative. Opportunistic infections in infants with congenital AIDS are the exception. To our knowledge, only one case of CMV encephalitis in an infant with congenital AIDS has been reported previously. In that case, as in the present one, a reactivation of a congenital CMV infection is likely.
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PMID:Cytomegalovirus encephalopathy in an infant with congenital acquired immuno-deficiency syndrome. 217 57

The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.
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PMID:Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion. 317 3

We have examined 9 healthy volunteers and 63 HIV-patients (16 asymptomatic patients and 47 patients with clinical AIDS-dementia complex, ADC) by magnetic resonance spectroscopy (MRS) and imaging (MRI) on a Siemens Magnetom SP63 (1.5 T). Proton MRS of the brain was performed at 63 MHz using the PRESS sequence (echo time = 135 ms, TR = 1.6 s). Four main results have been found: (1) HIV-related encephalopathy induces significant modifications of brain metabolism analyzed by MRS and the most sensitive metabolic parameter is the N-acetyl-aspartate/Choline ratio, (2) the correlation between MRS and MRI is good in 75% of patients, (3) in 4 of the 16 neuro-asymptomatic patients (i.e. 25%) a metabolic encephalopathy was found while MRI was still normal, and (4) MR spectra describe 3 different pathological metabolic patterns in the brain of HIV patients. Two patterns might correspond to the two entities of HIV-induced lesions i.e. HIV encephalitis and HIV-related progressive leukoencephalopathy.
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PMID:Localized brain proton MRS metabolic patterns in HIV-related encephalopathies. 788 65

The neuropathologic examination of symptomatic perinatal HIV infection was performed using a large group of cases from New York Medical Centers. Macroscopic evaluation demonstrated many cases with microencephaly and others with brain atrophy. Microscopically in a part of them, as far as in others without microencephaly/atrophy changes corresponding to HIV encephalitis were found, including multinucleated giant cells, microglial nodules and perivascular infiltrations. In other brains in which inflammatory changes were minimal, myelin lesions were also observed and the picture corresponded to the diagnosis of encephalopathy. In addition lesions of cortico-spinal tracts, mineralization within the basal ganglia and changes of vascular walls with secondary parenchymal lesions were found. Opportunistic infections and neoplastic changes were rare. The review demonstrated the picture of neuropathological changes in pediatric cases that died of AIDS.
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PMID:[Nervous system changes in infants with HIV virus. Neuropathological picture]. 808 64

We present the clinical, morphological and neuropathological findings in a 44-year-old male suffering from the acquired immunodeficiency syndrome (AIDS) (CDC stage IV C2) who presented with rapidly progressive right-side hemiparesis and developed hemianopia and aphasia. Scans showed multiple, not contrast-enhancing, not space-occupying echo-intensive lesions in T2-weighted MR-imaging. No hint for an opportunistic infection, necrotizing vasculitis or vascular disease was found. All therapeutic regimens failed and 8 weeks after onset of neurological symptoms the patient died because of cardiorespiratory arrest. Post-mortem examination excluded opportunistic infection, progressive multifocal leukoencephalopathy, lymphoma, vasculitis and ischemia of the brain. In the presence of an unusually high amount of HIV-infected macrophages at immunohistochemical examination, the overall pathological findings were atypical both for HIV encephalitis and HIV leukoencephalopathy. We describe a pathologically distinct new form of HIV associated encephalopathy.
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PMID:A pathologically distinct new form of HIV associated encephalopathy. 815 18

The diagnostic approach of focal central nervous system lesions in AIDS patients is now well established. In contrast, it is extremely difficult to determine the cause of diffuse encephalopathies, occurring frequently at the terminal stage of AIDS. Imaging is usually non specific and laboratory investigations are seldom contributive. In most cases, the aetiological diagnosis is provided by post mortem examination. In this first part of the study the authors deal with viral encephalitides which represent a classical and frequent cause of diffuse encephalopathy in AIDS. HIV encephalitis usually causes a progressive brain disease resulting in severe dementia; imaging may show diffuse leucoencephalopathy and/or cortico-subcortical atrophy. CMV encephalitis is often asymptomatic, discovered at autopsy; however, this diagnosis should be considered in patients with an encephalopathy of rapid onset, discrete signs of meningitis, symptoms of myelo-radiculitis, or a systemic CMV infection. Varicella-zoster virus encephalitis is not uncommon and may occur in the absence of characteristic rash. Infections by herpes simplex and measles viruses are exceptional.
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PMID:[Diagnosis of diffuse encephalopathies in adults with HIV infection. I]. 824 44

We report the neuropathological and immunohistochemical findings in the brains of 14 AIDS patients with HIV-related encephalopathy. Clinically, half of the patients presented with severe AIDS dementia complex including advanced psychomotor retardation and behavioural dysfunction. These features correlated with striking cerebral atrophy and subcortical lesions visible in CT and/or MRI scans. In 7 cases early signs of impaired memory and concentration and/or psychomotor slowing were apparent accompanied by subcortical lesions in MRI scans and normal CCTs. In order to investigate the topographical distribution of HIV-1-associated features, in every case tissue samples from the frontal, temporal, parietal, occipital cortex and subcortical white matter, the hippocampus, basal ganglia, midbrain, pons, medulla oblongata and cerebellum were studied. In all patients histological examination disclosed the typical cellular constituents of HIV encephalitis (n = 12) or leukoencephalopathy (n = 2). Antibodies against lymphocyte subsets, CD68 antigen, myelin basic protein and GFAP were used to characterize the phenotype of cells and to highlight the white matter gliosis. The distribution and degree of pathological features were analysed in a semiquantitative scale, based on the number of CD68-positive cells, and disclosed great interindividual differences concerning the affected brain regions which only in part correlated with the severity of the clinical picture. It is noteworthy, that the deep gray matter, in particular putamen and thalamus, was involved in every case, independent from the stage of the disease. In addition, quantity and topographical distribution of HIV-1 core protein p24 were studied by use of two monoclonal antibodies. It is noteworthy, that the number of immunoreactive multinucleated giant cells and microglial cells decreased gradually from the deep gray matter, especially putamen and thalamus, and deep white matter to corpus callosum, cerebellar white matter and subcortical cerebral white matter. The topographical predilection of the deep gray matter even in cases with early cognitive decline indicates that the basal ganglia are affected early in the course of the disease. This observation closely resembles the results of highly sensitive quantitative neuropsychological tests which disclosed slowing and impaired coordination of rapid extremity movements indicating basal ganglia lesions even in early stages of HIV dementia.
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PMID:Frequency and topographical distribution of CD68-positive macrophages and HIV-1 core proteins in HIV-associated brain lesions. 828 24

We analyzed brain tissue from 39 patients for the presence of proviral HIV-1 sequences, using the polymerase chain reaction (PCR) for the amplification of segments of the viral LTR and gag genes. A novel primer extension procedure allowed the detection of a single HIV-1 copy in 1 micrograms DNA. We detected proviral HIV-1 DNA in 16 of 25 brain samples from AIDS patients. Semiquantitative evaluation of the amplified DNAs indicated considerable variation in viral load. Highest levels of proviral DNA were present in brain samples from six patients with clinical evidence of HIV-associated cognitive/motor complex and the histopathologic correlate of HIV leukoencephalopathy or HIV encephalitis. An additional 11 brain samples contained smaller amounts of proviral DNA. In these patients, clinical data were inconclusive regarding the diagnosis of HIV-1 encephalopathy and histopathologically there was no evidence of HIV-1-induced tissue lesions. In nine of 25 seropositive patients with AIDS (36%), brain samples scored negative or did not contain an unequivocal signal indicating the presence of proviral DNA. HIV-1 sequences were not detected in any of 14 control brain samples from HIV-1 seronegative patients. Our data indicate that HIV-1 is present in the central nervous system of the majority (two thirds) of AIDS patients and that the highest levels of proviral DNA in brain tissue are associated with HIV encephalopathy.
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PMID:PCR identification of HIV-1 DNA sequences in brain tissue of patients with AIDS encephalopathy. 841 37


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