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

The amount of human immunodeficiency virus (HIV) type 1 RNA and the presence of a codon 215 mutation indicative of zidovudine resistance were evaluated in cerebrospinal fluid (CSF) and plasma obtained from HIV-1-infected children. The level of HIV-1 RNA in CSF was highest in children with severe encephalopathy (n = 25; median, 430 copies/mL; range, 0-2.2 x 10(5) copies/mL) followed by the moderately encephalopathic (n = 7; median, 330; range, 0-1130) and nonencephalopathic groups (n = 9; median, 0; range, 0-566) (P = .007). There was no correlation between CSF and plasma HIV-1 RNA levels. Five of 7 children with the codon 215 mutation in CSF had a progression of encephalopathy, while all 8 children with wild type codon 215 had improved or stable disease during zidovudine treatment (P = .007). These findings suggest that increased viral replication and emergence of drug-resistant HIV-1 variants within the central nervous system may play a role in progression of HIV encephalopathy.
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PMID:Evaluation of human immunodeficiency virus (HIV) type 1 RNA levels in cerebrospinal fluid and viral resistance to zidovudine in children with HIV encephalopathy. 894 Feb 9

The first case of one of the most frequent intestinal microsporidians, Encephalitozoon intestinale, is reported from an AIDS patient in the Czech Republic. The patient experienced diarrhoea and was found to have microsporidia spores in stool. Species determination by electron microscopy confirmed the diagnosis of the microsporidian, E. intestinale. The CD4-count at the time of the diagnosis was 73 cells/mm3, IRI = 0.21. Only after symptomatic therapy and rehydration the patient stopped the complaining, and although he refused an antimicrosporidial therapy, the CD4-count one month later increased to 200 cells/mm3 and patient didn't suffered from diarrhoea. Six months after the first finding of microsporidia, the patient was admitted to the hospital care for progressive encephalopathy and developing wasting syndrome again with the intermittent diarrhoea. The patient was treated with albendazole at that time. Nevertheless, after 14 days of albendazole therapy, he still remained positive for E. intestinale spores in the stool (urine specimens remained negative for all the time). The patient died after a two-month hospitalisation and the apparent cause of death was purulent bronchopneumonia, wasting syndrome with microsporidiosis, and HIV encephalopathy. Generalised mycobacteriosis (MAC) was also found from the autopsy material.
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PMID:Encephalitozoon intestinale infection in an AIDS patient--a case report. 1008 22

Human immunodeficiency virus (HIV)-associated dementia (HIVD) has been reported in up to 15% of HIV-infected adult patients. Although the pathogenesis of HIVD remains unclear, HIV probably plays an important role in the syndrome, as evidenced by the correlation between cerebrospinal fluid (CSF) HIV load and neuropsychological functioning. Although a large number of antiretrovirals are used to treat HIVD, zidovudine is the best studied. Zidovudine therapy has been associated with reduced levels of HIV RNA in CSF, fewer HIV-related changes in brain tissue at autopsy, and time-limited improvements in neurological function among AIDS and HIVD patients. More recent studies have investigated the penetration into CSF of other antiretrovirals, including protease inhibitors, and the clinical efficacy of abacavir in the treatment of dementia. HIV encephalopathy may occur in 30%-60% of children with AIDS and causes significant disability. Zidovudine has been associated with improved neuropsychological functioning in children with progressive encephalopathy, but optimum dosing levels, duration of effect, and prophylactic potential remain to be demonstrated.
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PMID:Human immunodeficiency virus-associated dementia: review of pathogenesis, prophylaxis, and treatment studies of zidovudine therapy. 1043 61

We prospectively studied a cohort of 25 HIV-1 infected individuals with no clinical signs of encephalopathy with 99mTc-HMPAO-SPECT. The findings were correlated with magnetic resonance imaging (MRI), neuropsychological testing and clinical staging aiming at the early diagnosis of HIV encephalopathy by single photon emission computed tomography (SPECT). A total of 25 matched seronegative controls were subject to neuropsychological testing only. A total of 24 patients and controls were monitored for 6-46 months (mean and median 26 months). No patients developed AIDS dementia complex during the study; 3 patients developed minimal symptoms (MSK classification stage 0.5). There was a significant decline in 99mTc-HMPAO uptake over time and neuropsychological abnormalities progressed. Unexpectedly, there was a correlation of high cortical and subcortical 99mTc-HMPAO uptake and low performance in cognitive dysfunction tests, indicating a possible inflammatory reaction in the brain with increased blood flow due to HIV infection. We conclude that, in non-demented HIV-infected individuals, both the 99mTc-HMPAO uptake and functional level slowly decrease over time, but the regional cerebral blood flow decrease could be masked by a direct HIV-induced inflammatory reaction in the brain, which gives a 99mTc-HMPAO hyperfixation.
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PMID:SPECT with 99mTc-HMPAO in subjects with HIV infection: cognitive dysfunction correlates with high uptake. 1052 71

With the recent improvements in treatment of HIV, the disease has become a chronic one. The mean survival time of HIV-infected children is now 9-10 years, which is more than 4 times the mean age of such children who died in 1990. Yet, the prevalence of HIV encephalopathy has not decreased despite use of HAART. Rather, it is expected that as patients live longer, the prevalence of CNS manifestations will actually increase. Thus, more children can be expected to manifest encephalopathy, cerebral aneurysms and CNS lymphoma. As AIDS patients live longer, newer and more effective drugs to combat the neurological effects of HIV infection will be required. There is little evidence that HIV damages neurons directly; rather, the damage appears to occur indirectly via viral proteins or neurotoxic factors causing excessive stimulation by excitatory amino acids such as glutamate and quinolinate. This common pathway is similar to that seen in acute neuronal injury and CNS degenerative diseases and may make HIV encephalopathy amenable to pharmacotherapy. The very complexity of HIV CNS entry mechanisms and neuropathogenesis provides a host of sites for potential therapeutic interventions and hope for the future.
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PMID:Central nervous system abnormalities in pediatric human immunodeficiency virus infection. 1070 51

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

In a cross-sectional, non-randomized, prospective study in an outpatient clinic a possible relationship between the cerebrospinal fluid (CSF) concentrations of the potent vasoconstrictor peptide endothelin-1 (ET-1) and prevalence and degree of HIV-encephalopathy was studied. Forty-eight CSF samples from HIV-infected patients undergoing lumbar punction for diagnostic reasons were investigated for ET-1 concentrations. In 37 patients ET-1 was also measured in plasma. Patients were investigated clinically and staged with respect to HIV encephalopathy. Patients with arterial hypertension, diabetes or acute opportunistic infections were excluded from the study. In the remaining, 18 of the CSF samples were from patients with normal neurological findings (grade 0-0.5), whereas 30 were from patients with HIV encephalopathy (grade 1-3). The mean CSF ET-1 concentration was significantly elevated (P = 0.001) in patients with HIV encephalopathy (1.97 +/- 2.33 pmol/l) as compared to those patients without encephalopathy (0.57 +/- 0.67 pmol/l). Moreover, there was a significant correlation between ET-1 CSF concentrations and the degree of HIV encephalopathy (r = 0.49, P < 0.001). In addition, there was a significant correlation between ET-1 levels in the CSF and the IgG serum to CSF ratio. However, we found no correlation between HIV encephalopathy and neither CSF total protein, IgG, albumin or the serum to CSF ratio of IgG or albumin. In conclusion, we could demonstrate a close relationship between CSF ET-1 concentrations and the degree of HIV encephalopathy. Thus, by virtue of its long-lasting and potent vasoconstrictor activity ET-1 might contribute to the pathogenesis of HIV encephalopathy.
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PMID:Endothelin-1 is elevated in the cerebrospinal fluid of HIV-infected patients with encephalopathy. 1088 34

In order to obtain information on neurologic AIDS, 54 white caucasian children infected by nosocomial route with a median age of 46.2 +/- 7 months were followed up prospectively for a median of 12 months with three months Denver tests neurologic evaluation and six months serologic investigations in CSF and sera. Paired CSF and serum samples, collected on the same day, from children with AIDS encephalopathy, were analysed for the permeability of the blood brain barrier (BBB) and for intrathecal production of anti HIV specific antibodies. A prospective follow-up and repeated comparison of WB profiles and the presence of anti V3 antibodies in CSF and sera was done, as well as an evaluation of the modification in the CSF antibody specificity (anti gag Western Blot scoring) with disease progression. An increased intrathecal synthesis of IgG was recorded in all subjects, in spite of an unaltered BBB permeability. No significant differences were recorded for the anti gag score in the serum samples, which was stable between 9.1-10.4. By contrast, the score for CSF samples decreases significantly with disease progression, from 8.7 in children without encephalopathy, to 6.5 in those with stationary disease and 3.6 in the progressive encephalopathy group. A strong correlation was found between the level of anti p24 antibodies determined by ELISA and the anti gag score quantified by WB for the same CSF samples. The p24 antigen was found to be positive only in 3 cases, even after immune complex dissociation. Anti V3 antibodies were not detected in CSF samples from patients with functional BBB. The decline in anti-gag antibody reactivity in CSF is an early indicator of disease progression, reflecting a severe course of neurological impairments. The absence of anti V3 antibodies in the CSF samples suggests that the PND of neurotropic strains mapped in distinct positions into the V3 loop. These results reflect the selection of antigenic escape mutants which evolve in the CNS, distinct from the blood lymphotropic isolates.
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PMID:Cerebrospinal fluid western Blot profiles in the evolution of HIV-1 pediatric encephalopathy. 1089 27

Cytomegalovirus (CMV) infections of the central nervous system (CNS) could be the most underrecognized neurologic complication of AIDS. CMV can cause a number of distinct neurologic syndromes in addition to retinitis. The actual rate of CMV CNS infection is unclear: studies show CMV encephalopathy exists in anywhere from 20 percent of the brains studied in autopsies to as high as 75 percent of cases involving more advanced cases of retinitis. Whatever the actual rate may be, unrecognized CMV encephalitis my cause both mild and severe neurocognitive impairment in patients with advanced HIV infection. CMV encephalitis symptoms are abrupt, progress rapidly, and occur late in the course of HIV disease, although signs of the most common alternate diagnosis, HIV encephalopathy, appear earlier and more gradually. There have been no prospectively controlled studies of the treatment of CMV CNS disease. Standard treatments for CMV retinitis may be inadequate as therapy for CMV infections in the brain. One explanation is that there is no treatment recovery for the extensive damage to the nerves that can be caused by the disease. ACTG 305, a 6-month, high dose, aggressive combination foscarnet/ganciclovir therapy has been developed to answer many of the nagging treatment issues surrounding CMV CNS disease as well as evaluate both quantitative CMV DNA PCR and CMV bDNA as assays for disease severity, progression, and response to therapy.
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PMID:Responding to CMV neurologic infections. 1136 10

HIV-related encephalopathy is an important problem in vertically infected children with HIV. Infected infants may manifest early, catastrophic encephalopathy, with loss of brain growth, motor abnormalities, and cognitive dysfunction. Even without evidence of AIDS, infected infants score lower than serorevertors on developmental measures, particularly language acquisition. Children with perinatal or later transfusion-related infection generally are roughly comparable developmentally to their peers until late in their course. Symptoms similar to adult AIDS dementia complex are occasionally seen in adolescents with advanced AIDS, including dementia, bradykinesia, and spasticity. Opportunistic CNS infections such as toxoplasmosis and progressive multifocal leukoencephalopathy are less common in children and adolescents than in adults. Increasing evidence suggests that aggressive antiretroviral treatment may halt or even reverse encephalopathy. Neuroimaging changes may precede or follow clinical manifestations, and include early lenticulostriate vessel echogenicity on cranial ultrasound, calcifying microangiopathy on CT scan, and/or white matter lesions and central atrophy on MRI. Differential diagnosis of neurological dysfunction in an HIV-infected infant includes the effects of maternal substance abuse, other CNS congenital infections, and other causes of early static encephalopathy. Initial entry of HIV into the nervous system occurs very early in infection. The risk of clinical HIV encephalopathy increases with very early age of infection and with high viral loads. Virus is found in microglia and brain derived macrophages, not neurons. The neuronal effect of HIV is probably indirect, with various cytokines implicated. Apoptosis is the presumed mechanism of damage to neurons by HIV.
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PMID:Neurological and developmental effects of HIV and AIDS in children and adolescents. 1155 37


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