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

The authors describe two siblings affected by an immunodeficiency state characterized by low IgA and IgM levels in serum, and an early encephalopathy with infantile spasms and hypsarrhythmia. The nosography of this unusual association and the relationship to ataxia telangiectasia and allied disorders are briefly discussed.
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PMID:Primary immunodeficiency with early encephalopathy in two siblings. An anatomo-clinical study. 108 Apr 62

Four patients with acquired immunodeficiency syndrome, a 27-year-old female intravenous drug abuser and three males (two drug addicts aged 27 and 33 years and a 40-year-old homosexual) presented with a rapidly progressive encephalopathy. Two had generalized varicella-zoster virus skin infection, one had had a regressive thoracic zoster rash 7 months previously and one had no history of cutaneous eruption. Neuropathological examination revealed, in each case, multifocal necrotic changes with numerous, intranuclear Cowdry type A inclusion bodies in glial cells, endothelial cells, macrophages and neurons, within and around the lesions. These inclusion bodies were stained positively for varicella-zoster virus by immunocytochemistry and contained herpes virus nucleocapsids by electron microscopy. Molecular biology using the polymerase-chain-reaction method demonstrated viral genome. In one case, zoster-induced non-inflammatory vasculopathy involved medium sized leptomeningeal vessels and was associated with circumscribed areas of cortico-subcortical infarction. In another case, varicella-zoster virus encephalitis was associated with human immunodeficiency virus encephalitis and a secondary cerebral lymphoma. Multinucleated giant cells expressing human immunodeficiency virus proteins in their cytoplasm, were found in the lymphomatous deposits and in the varicella-zoster virus necrotic lesions. In these latter lesions, Cowdry type A inclusion bodies could be seen in the nuclei of some multinucleated giant cells confirming previous observations of MGCs co-infected by HIV and CMV, and supporting the hypothesis that DNA viruses interact with HIV, thus increasing its effect.
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PMID:Varicella-zoster virus encephalitis in acquired immunodeficiency syndrome: report of four cases. 133 72

Human immunodeficiency virus (HIV) infects cells of the monocyte/macrophage lineage in addition to lymphocytes, and infection of these cells may be responsible for viral persistence and dissemination, encephalopathy of the acquired immunodeficiency syndrome and other sequelae of HIV infection. We have developed an in vitro model utilizing peripheral-blood monocyte-derived macrophages to study HIV-1 infection of macrophages. HIV-1 isolates vary greatly in their ability to infect and replicate in macrophages, from highly restricted to highly productive infection. Productively infected macrophages undergo syncytium formation but remain viable in culture and support sustained levels of virus production for prolonged periods. Transformed monocytoid and lymphoid cell lines, however, show very different patterns of permissiveness for HIV-1 strains and do not reflect their corresponding primary cell types in studies of host cell tropism. Studies on viral entry show that the CD4 molecule, known to be the HIV receptor on lymphoid cells, is expressed at low levels on the surface of macrophages as well, where it functions as the receptor for viral entry. Therefore, differential host cell tropism does not result from the use of an alternative macrophage-specific receptor instead of CD4.
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PMID:Human immunodeficiency virus type 1 tropism for human macrophages. 138 18

Central nervous system disease has emerged as an important manifestation of acquired immunodeficiency syndrome in both the adult and pediatric populations, with neurologic abnormalities occurring in up to 90% of pediatric patients in some series. Neuropathologic studies, based primarily on the autopsy, have provided valuable insights into the spectrum and pathogenesis of acquired immunodeficiency syndrome-associated neurologic disorders, including primary human immunodeficiency virus encephalopathy and as the spectrum of infectious, neoplastic, and cerebrovascular diseases that may complicate the course of acquired immunodeficiency syndrome. Progressive encephalopathy represents the single most common neurologic disorder in pediatric acquired immunodeficiency syndrome and appears to be caused in most cases by direct infection in brain parenchyma by human immunodeficiency virus. Central nervous system lymphoma and cerebrovascular disease continue to account for most focal central nervous system lesions in the pediatric population. In contrast to adults with acquired immunodeficiency syndrome, opportunistic central nervous system infections remain relatively uncommon in the pediatric population. Our understanding of acquired immunodeficiency syndrome-associated neurologic disease remains far from complete. A plea is made for regular postmortem examination of the central nervous system in all patients dying with human immunodeficiency virus infection.
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PMID:The neuropathology of pediatric acquired immunodeficiency syndrome. 146 39

This study analyzes the correlation of basic laboratory test results with clinical outcome in 94 children with perinatally acquired human immunodeficiency virus 1 infection who did not receive zidovudine during the study period of 1983 to 1988. Two life-threatening conditions highly correlated with survival, opportunistic infection and severe encephalopathy, were the end points of the study. At a median age of 25 months 30 (32%) of the 94 children had developed such conditions (Group I), and their survival at 3 years of age was 48% (95% confidence interval, 24 to 72%), contrasting with the 97% survival rate (95% confidence interval, 94 to 100%) of the remaining 64 (68%) children who had not developed such conditions by age 25 months. (Group II). Compared with children in Group II, children with life-threatening complications were more likely at the onset of symptoms to be younger and have a lower CD4 count, an impaired in vitro lymphocytic proliferation and a lack of p18 or p25 antibodies in the Western blot profile and, during the progression of the disease, a negative slope of the subsequent CD4 counts. These results highlight the need for an early diagnosis of the human immunodeficiency virus 1 infection in children and demonstrate that it is possible to determine the prognosis of their disease as early as in the first year of life.
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PMID:Natural history of human immunodeficiency virus type 1 infection in children: prognostic value of laboratory tests on the bimodal progression of the disease. 152 73

The sedative thalidomide was withdrawn from the market 30 years ago because of its teratogenic and neurotoxic adverse effects. The compound was later discovered to be extremely effective in the treatment of erythema nodosum leprosum, a complication of lepromatous leprosy. This effect is probably due to a direct influence on the immune system, because thalidomide possesses no antibacterial activity. The compound is presently used as an experimental drug in the treatment of a variety of diseases with an autoimmune character, including recurrent aphthosis of nonviral and nonfungal origin in human immunodeficiency virus (HIV) patients. This article reviews the most important chemical and pharmacokinetic properties of thalidomide. The possible mechanisms of the nonsedative effects of thalidomide with respect to the safety of its use in HIV patients are discussed. Because the mechanism of the immunomodulatory effect of thalidomide is unknown, the possibility that the administration of this compound will accelerate the deterioration of the immunological status of HIV patients cannot be excluded. Clinical evidence suggests that thalidomide may aggravate the condition of patients with preexisting peripheral neuropathy. Hypersensitivity reactions to thalidomide may occur more frequently in HIV patients than in other patient groups. Because of the teratogenic activity of thalidomide, reliable contraception must be provided to female patients of childbearing age. Before the introduction of thalidomide therapy to an HIV patient presenting with oral ulcers, a fungal or viral origin of the lesions should be excluded. Thalidomide should not be used in patients with preexisting HIV-related peripheral polyneuropathy, polyradiculopathy or encephalopathy. In patients experiencing a complete remission, the discontinuation of thalidomide treatment and its reintroduction in the case of a relapse are preferable to maintenance therapy.
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PMID:Thalidomide in human immunodeficiency virus (HIV) patients. A review of safety considerations. 160 98

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

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

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

We evaluated cerebrospinal fluid (CSF) antibody levels against a lipid-free, denatured form of myelin basic protein (LF-MBP) in 11 patients with AIDS dementia complex (ADC) by using an enzyme-linked immunosorbent assay (ELISA). In 9 out of 11 patients, anti-LF-MBP antibody levels were significantly higher than those observed both in 15 human immunodeficiency virus (HIV)-infected patients without neurological disorders and in 9 anti-HIV-negative subjects affected by other neurological diseases. Furthermore, we followed up anti-MBP levels in 5 out of the 11 ADC patients and detected a strict relationship with the encephalopathy progression. At the same time, with the aim to detect early demyelinating events we investigated CSF antibody levels against a lipid-bound, native-like form of MBP (LB-MBP). Results did not show any significant difference between LF-MBP and LB-MBP in terms of antibody reactivity. The detection of anti-MBP antibodies in CSF may provide the opportunity to assess a diagnostic tool for discovering demyelinating lesions in ADC patients.
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PMID:Detection of cerebrospinal fluid antibodies against myelin basic protein in patients with AIDS dementia complex. 172 Mar 16


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