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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of important neurological diseases, including HIV-1 encephalitis, Alzheimer's disease, and brain trauma, are associated with increased cerebral expression of the multifunctional cytokine transforming growth factor-beta 1 (TGF-beta 1). To determine whether overexpression of TGF-beta 1 within the central nervous system (CNS) can contribute to the development of neuropathological alterations, a bioactive form of TGF-beta 1 was expressed in astrocytes of transgenic mice. Transgenic mice with high levels of cerebral TGF-beta 1 expression developed a severe communicating hydrocephalus, seizures, motor incoordination, and early runting. While unmanipulated heterozygous transgenic mice from a low expressor line showed no such alterations, increasing TGF-beta 1 expression in this line by injury-induced astroglial activation or generation of homozygous offspring did result in the abnormal phenotype. Notably, astroglial overexpression of TGF-beta 1 consistently induced a strong upmodulation of the extracellular matrix proteins laminin and fibronectin in the CNS, particularly in the vicinity of TGF-beta 1-expressing perivascular astrocytes, but was not associated with obvious CNS infiltration by hematogenous cells. While low levels of extracellular matrix protein expression may assist in CNS wound repair and regeneration, excessive extracellular matrix deposition could result in the development of hydrocephalus. As an effective inducer of extracellular matrix components, TGF-beta 1 may also contribute to the development of other neuropathological alterations, eg, the formation of amyloid plaques in Alzheimer's disease.
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PMID:Increased central nervous system production of extracellular matrix components and development of hydrocephalus in transgenic mice overexpressing transforming growth factor-beta 1. 760 85

Cerebral infarction is an uncommon complication of AIDS in pediatric patients. We have seen three HIV-infected children who developed acute neurological deficits due to stroke. Cerebral infarction must be considered in the work-up of a child with AIDS who presents with focal neurological deficit, seizure or mental status change. Stroke is a complication of HIV infection that occurs in approximately 1% of affected children [1]. At autopsy, evidence of cerebral infarction was documented in 10-30% of children with HIV infection [2]. We have seen three children with focal infarction who are HIV positive.
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PMID:Cerebral infarction in pediatric acquired immunodeficiency syndrome. 772 94

The full range and occurrence of medical conditions in persons infected with human immunodeficiency virus (HIV) before they develop illnesses that define acquired immunodeficiency syndrome (AIDS) have not been systematically or completely described. In a retrospective and prospective cohort study, 1,073 homosexual and bisexual men in three US cities were interviewed and examined twice per year from January 1988 to September 1992. Study participants were from San Francisco, California (273 HIV-seropositive and 432 HIV-seronegative men), Denver, Colorado (107 positive and 129 negative men), and Chicago, Illinois (54 positive and 78 negative men). A total of 305 HIV-positive men had specifiable dates of HIV seroconversion (mean of 15.3 months between the last negative and the first positive HIV antibody test). Besides much increased incidences of thrush (incidence relative risk (IRR) = 23.3) and hairy leukoplakia (IRR = 551), the following conditions also occurred significantly more frequently in HIV-positive men than in HIV-negative men: anal herpes (incidence density (ID) = 10.7/100 person-years; IRR = 7.7); sinusitis requiring antibiotics (ID = 6.2/100 person-years; IRR = 2.1); anal warts (ID = 5.8/100 person-years; IRR = 2.7); seborrhea (ID = 3.8/100 person-years; IRR = 6.6); community-acquired pneumonia (ID = 1.4/100 person-years; IRR = 2.7); skin cancers (ID = 1.0/100 person-years; IRR = 2.2); and seizures, often apparently "breaking through" prior anticonvulsant therapy (ID = 0.8/100 person-years; IRR = 5.6). First episodes of hairy leukoplakia, thrush, and skin cancer occurred at low mean CD4 counts (mean counts were less than 350 cells/microliters) and late in HIV infection (mean times were more than 8 years after HIV seroconversion). Many medical problems, some not widely appreciated, occur in HIV-infected men before they develop AIDS-defining illnesses, signifying considerable morbidity from pre-AIDS HIV infection.
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PMID:The spectrum of medical conditions and symptoms before acquired immunodeficiency syndrome in homosexual and bisexual men infected with the human immunodeficiency virus. 853 42

Although it is usually accepted that the pathogeny of HIV infection is related to the direct cytotoxic effect of the virus or indirectly by the invasion of T4 cells altering the T4/T8 ratio, clinical and serological and biochemical manifestations of the B cell polyclonal activation were described early in HIV infection epidemy. It is postulated that the central pathophysiologic mechanism in HIV infection is a high and inefficient production of interferon-gamma, genetically determined, leading to a production of autoantibodies that blocks the target organs even the immune system as well as a progressive interleukins levels increase, including tumor necrosis factor-alpha (TNF-alpha), responsible for many of the symptoms of these patients like fever, headache, fatigue, myalgia, hypotension, seizure and other neurological disorders, hematologic and hepatic disorders. Thalidomide reduces polyclonal hypergammaglobulinemia, that is associated with a clinical and laboratorial improvement, in a dose dependent manner as well as TNF-alpha levels. It seems that HIV infection is more a disease of abnormal host response triggered by HIV than an HIV disease.
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PMID:Autoimmunity in human immunodeficiency virus infection and the use of thalidomide. 809 May 35

A presumptive diagnosis of toxoplasmic encephalitis was made in 73 of the 428 AIDS patients followed in the Bordeaux Regional Hospital between 1985 and 1990. The sex ratio (M:F) was 2.8:1. The mean age was 36.2 years. Forty-three percent were homosexuals, 30 percent intravenous drug abusers. The encephalitis revealed the HIV infection in 10 percent of the cases; it was the first opportunistic infection in 27 percent. The clinical manifestations were: focal neurologic deficit (62 percent), fever (58 percent), headaches (47 percent), altered consciousness (45 percent), seizures (18 percent). The CT scan findings were focal lesions with (60 percent) or without (40 percent) ring enhancement. Oedema was present in 58 percent of the lesions, and multiple lesions in 59 percent. At the time of diagnosis, the mean CD4 lymphocyte count was 72 per mm3. The initial therapeutic regimens were: pyrimethamine (P) plus sulfadiazine (n = 57), P plus clindamycin (n = 11) and P plus clarithromycin (n = 5). Following acute therapy the patients had a complete (64 percent) or partial (18 percent) response, and 18 percent died. Adverse reactions were noticed in 53 percent. Sixty patients received a maintenance therapy; after a mean follow-up of 8 months, 12 relapsed and died of toxoplasmic encephalitis; 17 died of another cause. The median survival after toxoplasmosis was diagnosed was 7.5 months.
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PMID:[Cerebral toxoplasmosis in AIDS. 73 cases. Clinical Epidemiology Group on AIDS in Aquitania]. 837 80

Several problems are presented in differential diagnosis between cerebral tuberculomas and other brain lesions. Eight cases of cerebral tuberculomas diagnosed in our hospital between 1962 and 1992 were studied. Data about age, sex, HIV antibodies, clinical manifestation, tomographic images, non cerebral locations, diagnostic method, evolution and treatment resolution were collected. Eight cases were diagnosed, seven men and one woman, age 40.75 +/- 10 HIV antibodies in three patients were positive. Meningitis (4 cases) and weight loss (4 cases) were the first clinical features. Confusional state, fever and seizures were presented in three cases one (37.5%), ataxia in two cases (25%) and headache in one (12.5%). Lesions were sole in 62.5% of cases, and several in 37.5%. Were high density in 25.9% and low density in 75%. All patients presented a other localization of tuberculosis. Mycobacterium tuberculosis was isolated in sputum in 75% of cases. After six month, most of the lesions improved.
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PMID:[Clinico-radiologic characteristics of 8 cases of brain tuberculoma]. 851 37

The importance of the EEG for the investigation of neurological diseases in the neonatal period has been largely discussed, since it is often the only way to approach cerebral function in newborns with severe pathologies or under drug effect. The present study was carried out with 85 newborns (NB) who presented perinatal dysfunctions and were submitted to neurological and electroencephalogram (EEG) or polysomnography (PS) evaluation. EEG/PS alterations, pathologies and prognosis were reported. The EEG were classified according to basal activity alterations, presence of paroxysmal activity and sleep stages organization and maturity. The most frequent pathology was perinatal asphyxia (40%) followed by intraventricular hemorrhage (HIV, 16%). The most frequent complaint for exam indication was apnea (71%) followed by convulsion (19%). Fifty-five percent of the exams exclusively required because apnea complaint were considered normal and out of all exams required because seizures only 31% were normal. The EEG alteration most frequently related to perinatal asphyxia, HIV and intrauterine growth delay was immaturity and in the NB with seizures immature EEG and abnormal paroxysms. Many different alterations were registered in the NB with nervous system infection. The EEG findings more correlated with unfavorable prognosis were isoelectricity and abnormal paroxysmal activity including positive sharp waves (100%).
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PMID:[Value of EEG in the characterization and prognosis of neurological diseases in premature infants]. 858 21

A serendipitous discovery during early AIDS investigations was human herpes virus type 6 (HHV-6). Two years later (1988) it was shown that HHV-6 and later on also HHV-7 are the causes of exanthema subitum, a childhood disease with previously unknown causation. HHV-6 and HHV-7 are the main cause of febrile seizures. It is assumed that 90% of children are infected before they are three years old. The viruses are also found in adults; HHV-6 may cause mononucleosis and hepatitis. HHV-6 and HHV-7 infect CD4+ cells and may influence the course of HIV infection. In AIDS patients HHV-6 and cytomegalovirus are often isolated together from the lungs, possibly because they activate each other. Another possibility is that the circumstances in the lungs are favourable to both. HHV-6 and HHV-7 infection may be serologically diagnosed. There is little experience with antiviral treatment.
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PMID:[Human herpes viruses type 6 and 7; causative agents of, among others, exanthema subitum]. 861 28

We reviewed the records and radiologic studies of eight patients who developed new focal neurologic abnormalities while receiving interleukin-2 (IL2)-based immunotherapy for malignancy or HIV infection. Initial confusion and delirium in the patients evolved into coma, ataxia, hemiparesis, seizures, and cortical syndromes including aphasia, apraxia, and cortical blindness. Imaging studies showed multiple white and gray matter lesions with a predilection for the occipital poles, centrum semiovale, and cerebellum. After cessation of IL2 treatment, seven patients improved to normal or near-normal neurologic function paralleled by resolution of the lesions on scans. One patient improved only minimally. Possible etiologies for the lesions include an IL2-induced cerebral vasculopathy, a direct toxic effect of IL2, or immunologically mediated damage.
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PMID:Multiple cerebral lesions complicating therapy with interleukin-2. 875 14

Human immunodeficiency virus type-1 (HIV-1)-associated neurologic disease, known as "HIV-1-associated progressive encephalopathy" (PE), is a common concomitant in the progression towards AIDS. PE, characterized by a triad of symptoms including impaired brain growth, progressive motor dysfunction, and loss or plateau of developmental milestones, is believed to result from both direct and indirect effects of HIV-1 infection on the central nervous system (CNS). Consequent to the hallmark systemic immune deficiency of HIV infection, the CNS becomes susceptible to opportunistic infections which add further morbidity and mortality, and may contribute either directly or indirectly to neurologic symptoms which can often mimic PE. Static encephalopathies (SE) represent fixed, nonprogressive neurologic or neurodevelopmental deficits in HIV-infected children. SE may or may not be caused by HIV infection but are often associated with such identifiable insults as prematurity, in utero exposure to toxins or infectious agents, or head trauma. Additional neurological manifestations of HIV infection are seizures, cerebrovascular complications (i.e., stroke), myelopathies, neuromuscular syndromes, and CNS complications of opportunistic infections. Neurobehavioral aberrations have also been observed in pediatric HIV infection. In addition to the neuropathogenesis, theories regarding the timing and detection of the neurological problems associated with pediatric HIV infection are discussed along with a presentation of current treatment paradigms and their rationales. The importance of identifying the numerous environmental factors, including nutritional status, that may confound the ability to discriminate between a primary or secondary role of HIV infection in the various neurological problems of HIV infection is discussed.
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PMID:Neurological and developmental problems in pediatric HIV infection. 886 30


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