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

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

We report the neurological findings in two children with AIDS and one child with lesser AIDS. The first patient developed acute encephalopathy 37 months after having received a blood transfusion from a HTLV-III positive donor. CCT showed ring-enhancement and hypodense lesions with homogenous enhancement. Autopsy revealed CNS toxoplasmosis. The second child with AIDS, born to an iv drug-addicted mother, had one seizure at four months of age, but other neurologic signs were absent. She died of pneumonia due to Pneumocystis carinii at seven months of age. Postmortem examination of the brain revealed extensive nerve cell damage in the cerebral cortex and cerebellum, probably due to terminal hypoxemia and not AIDS-related. In both children clinical features of childhood AIDS like failure to thrive, lymphadenopathy, oral thrush and chronic pulmonary infiltrates were absent. The hallmark of the third child's clinical course was a progressive loss of psychomotor abilities with onset of the neurological symptoms nine months before other signs of AIDS occurred. AIDS should be suspected or excluded in children at increased risk for AIDS presenting with either acquired atypical CNS infection or unexplained developmental regression, even in the absence of other clinical symptoms of pediatric AIDS.
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PMID:Neurological manifestations in three German children with AIDS. 347 44

Recent studies in our laboratory and that of Dr. Howard Gendelman have revealed two important pathways for neuronal damage during HIV-1 encephalopathy in children. First, substantial numbers of astrocytes are actively or latently infected with HIV-1. Astrocyte infection may lead to neuronal dysfunction through loss of supporting growth factors, excitotoxicity due to dysregulation of neurotransmitter reuptake, and loosening of the blood-brain barrier permitting further seeding of HIV-1 in the CNS. Significantly, infection of astrocytes is marked by near-exclusive synthesis of early regulatory gene products of HIV-1, while structural proteins characteristic of productive infection are found in macrophages, microglia and multinucleated giant cells. We propose the term 'restricted' to denote the non-productive infection found in astrocytes. Second, HIV-1-infected macrophages initiate inflammatory processes which are amplified through cell-cell interactions with astrocytes. Macrophage-astrocyte interactions produce arachidonic metabolites and potentially neurotoxic cytokines (TNF-alpha and IL-1 beta), leading to astroglial activation and proliferation which then amplifies these cellular processes. These new findings suggest that two major pathways leading to neurotoxicity in pediatric AIDS encephalopathy are linked to HIV-1 infection through astrocyte-mediated processes, and help explain how small numbers of productivity infected cells indirectly cause widespread tissue pathology and elicit profound neurological impairment.
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PMID:HIV-1 infection of the developing nervous system: central role of astrocytes in pathogenesis. 806 56

Encephalopathy and neurological disorders are a major manifestation of pediatric AIDS. Although HIV-1 can replicate in cells of neuronal and glial origin, it is yet unclear whether immature neural cells, which are present during nervous system development, can support HIV-1 replication and whether neurotrophic factors can modulate HIV-1 gene expression. In this study we show that a glial cell line with a phenotype closely resembling immature glial cells is more permissive to HIV-1 infection and replication than a neuroblastic cell line. After HIV-1 infection or after transfection of these cells with the HIV-1 LTR-CAT reporter gene alone or in the presence of Tat, both HIV-1 replication and viral gene expression progressively decrease in the neuronal cell line, while they increase in the glial cell line. In both cell types viral gene expression and replication are augmented by the addition to the cells of nerve growth factor (NGF) at concentrations which induce neuronal differentiation. However, these effects are again more evident with the glial cell type, suggesting that immature glial cells may represent one of the major targets and reservoirs of HIV-1 in the developing nervous system. As NGF and Tat act synergistically in inducing HIV-1 gene expression, these data also suggest that during development the presence of high levels of neural trophic factors may activate viral replication and render the CNS more susceptible to the deleterious effects of HIV-1 infection.
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PMID:HIV-1 gene expression and replication in neuronal and glial cell lines with immature phenotype: effects of nerve growth factor. 817 51

MR imaging has firmly established its place as the cornerstone of pediatric neuroimaging. Recent advances in MR imaging have led to decreased imaging time, high resolution studies, and new methods for obtaining tissue contrast. Magnetic resonance angiography (MRA) now obviates the need for angiography in some children, although its extended role is still to be defined. Normal and abnormal development and myelination patterns have been further defined with MR imaging. The patterns of brain injury resulting from hypoxia and ischemia vary with the degree of the insult as well as the gestational age of the child. These patterns of hypoxic-ischemic encephalopathy can be analyzed to determine when the insult occurred. Neuronal migration disorders and phakomatoses can be diagnosed with confidence at an early age, thus facilitating genetic counseling. MR imaging can detect the most common lesions associated with childhood epilepsy, such as hippocampal sclerosis, focal cortical dysplasias, and low-grade tumors. Other areas, including pediatric AIDS, toxicity-related injury, metabolic/mitochondrial conditions, and disorders associated with iatrogenic injury, can be diagnosed with MR. Spectroscopy provides information that should prove useful in evaluating and monitoring neuronal and other brain tissue disorders in children.
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PMID:MR of the brain in children. 887 Jan 79

The predominant cell types infected by HIV-1 in AIDS associated encephalopathy are cells of the macrophage/microglial lineage. There has been consistent evidence, however, that astrocytes also become infected although not at the same frequency or level of multiplication as microglial cells. HIV-1 antigens and/or nucleic acid have been identified in astrocytes in brain autopsy tissue from both adult and pediatric AIDS cases. In cell cultures, HIV-1 infection of astrocytes results in an initial productive but non-cytopathogenic infection that diminishes to a viral persistence or latent state. Understanding the nature of HIV-1 infection of astrocytes, which represents the largest population of cells in the brain, will contribute to the understanding of AIDS encephalopathy and the dementia that occurs in nearly one-quarter of all AIDS patients.
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PMID:Stages of restricted HIV-1 infection in astrocyte cultures derived from human fetal brain tissue. 1087 71

Neurodevelopmental abnormalities associated with HIV infection have been described since the first reports of pediatric AIDS in the 1980s. Before antiretroviral therapy (ART) became widely available, progressive HIV-1 encephalopathy (PHE) was reported in the US in 13-35% of children with HIV-1 infection and in 35-50% of children with AIDS. Introduction of ART can prevent PHE and reverse PHE present at ART initiation, but a high prevalence of residual problems has been described. Even though 90% of HIV-infected children live in the developing world, few children have access to ART and little is known regarding the neurological manifestations of perinatal HIV infection in those regions. Mechanisms of pediatric HIV-1 neuropathogenesis and factors associated with neurodevelopmental abnormalities in perinatally infected children are not yet fully understood. Studies have demonstrated that HIV-1 enters the CNS soon after infection and may persist in this compartment over the entire course of HIV-1 infection. The CNS is a distinct viral reservoir, differing from peripheral compartments in target cells and antiretroviral penetration. Neurotropic HIV-1 likely develops distinct genotypic characteristics in response to this unique environment. We reviewed the literature on pediatric neuroAIDS and identified gaps in the current knowledge.
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PMID:Neurologic and neurodevelopmental manifestations of pediatric HIV/AIDS: a global perspective. 1713 13