Journal of neuro-AIDS最新文献

Objective: To identify clinical, laboratory and demographic markers which are associated with the presence of dementia and neuropsychological impairment in severely immunodeficient patients.

Method: Fifty-nine HIV+ patients participated in the study. Patients were assessed neurologically and neuropsychologically, and a subset of patients underwent lumbar punctures. Logistic regression was used to determine which variables from a set including age, education, IQ, depression, anxiety, CD4 cell counts, haemoglobin, serum and CSF â2 microglobulin and neopterin, constitutional symptoms, past opportunistic infections and use of antiretroviral therapy was associated with the occurrence of dementia and neuropsychological impairment.

Results: An increased likelihood of neurological and neuropsychological dysfunction was associated with diarrhoea at some time in the recent past, elevated serum neopterin at the time of assessment, and increased age. A decreased likelihood of impairment was associated with a higher estimated IQ, more years of education, and the presence of an AIDS-defining illness at the time of assessment.

Conclusion: Recent diarrhoea, elevated serum neopterin, advanced age and low education and IQ can serve as ''signals'' for the presence of neurological and neuropsychological dysfunction.

A prospective, case-control study was undertaken to characterise seizures occurring in the context of human immunodeficiency type-1 (HIV-1) infection. Fifty consecutive patients with a documented seizure were enrolled along with fifty control patients. Among cases the median CD4 cell count was 8/mm3 and 84% had a prior AIDS defining illness; 14/mm3 and 80% among the control group. Generalised seizures were seen in 84%, partial with secondary generalisation in 10% and partial in 6%. Associated conditions included cerebral toxoplasmosis (22%), cryptococcal meningitis (8%), progressive multifocal leukoencephalopathy (6%), cytomegalovirus encephalitis (6%), central nervous system (CNS) lymphoma (2%), and other causes (14%) including pre-HIV epilepsy. No associated condition was identified in 42% of patients of whom 18% were receiving foscarnet therapy at the time of seizure, compared with 4% of control patients (p < 0.001). Concentrations of cerebrospinal fluid â2-microglobulin and neopterin, markers that have been associated with HIV-1 involvement of the CNS, were elevated in 12/12 and 13/13 patients, respectively, of the group with no identifiable cause for their seizure. We conclude that seizures occur principally in patients with advanced HIV-1 disease, with opportunistic infections of the CNS the predominant underlying condition. In the group with no identifiable cause foscarnet therapy and subclinical HIV-1 involvement of the CNS may be factors responsible for seizure activity.

Unlabelled: Objective. To examine the cross-sectional prevalence of neurological symptoms and signs in a large cohort of human immunodeficiency virus (HIV)-seropositive men, and determine the relationship of the symptoms to disease stage, immunologic markers, and independent variables from neuropsychological (NP) testing and psychiatric interview.

Methods: One hundred-nine controls and 386 HIV-infected volunteers enrolled in the HIV Neurobehavioral Research Center (HNRC) longitudinal study. The majority, without acquired immune deficiency syndrome (AIDS), were screened for alcohol/substance abuse; previous diagnosis of HIV-associated dementia; and HIV-unrelated developmental, neurological, medical, and neurobehavioral conditions which potentially impair cognition; and underwent a structured neurological interview and examination, standardized NP testing, and psychiatric interview as part of a more extensive battery. A large subset (N = 377) underwent lumbar puncture for cerebrospinal fluid (CFS) examination. We examined the relationship of sixteen select but independent variables, using stepwise multiple regressions, from demographic/staging, immunological, NP, and psychiatric domains to neurological symptoms in an effort to identify possible predictors of subclinical nervous systems involvement. Results. All categories of neurological symptoms were significantly more prevalent among medically asymptomatic (CDC stage A) subjects than controls, with a further rise in prevalence in those with more advanced stages of infection. The most marked rise was seen in cognitive and sensorimotor complaints. In contrast, significant findings on neurological examination were evident in only the sicker (stage C) subjects. Stage of illness, serum β2-microglobulin, psychiatric indices of depressed mood or anxiety, and NP "motor" performance were the most significant independent variables associated with the presence of neurological symptoms. CSF pleocytosis was seen early (CDC stage A), and may reflect the presence of HIV in the central nervous system (CNS) at the least stages of infection. We also confirmed the value of CSF β2m and neopterin as important markers of advancing disease stage. Whether they predict subclinical CNS involvement is to be determined by longitudinal observations. Conclusion. Neurological complains are common in medically asymptomatic HIV subjects whereas signs are not. The symptoms correlate with commonly determined independent measures of depression, anxiety, NP tests of fine motor speed and strength, as well as indices of disease worsening (CDC stage, serum β2m).

This study assesses the integrity of the blood-brain barrier (BBB) in human immunodeficiency virus (HIV) seropositive individuals to magnetic resonance imaging (MRI) contrast agent Gd-DTPA. Twelve HIV seropositive patients and six control subjects had T2-weighted and serial pre- and post-contrast TI-weighted MRI. Ten of the twelve seropositive patients demonstrated white matter hyperintensity with or without atrophy on T2-weighted MRI and 8/10 who underwent neurological examination demonstrated neurological abnormalities. No statistically significant differences of trends in white matter pixel values were observed between pre- and post-contrast scans in any of the patients or controls. Serial T1-weighted MRI does not demonstrate any change in the integrity of the BBB to Gd-DTPA in HIV seropositive patients, regardless of the presence or absence of white matter hyperintensity with or without atrophy on T2-weighted MRI or clinical signs of HIV-I associated with cognitive/motor complex.

Purpose: T2 shortening (hypointensity) in magnetic resonance (MR) images of the putamen, which may be associated with iron deposition, only occurs in normal subjects over the age of 60 years. Increased or premature putaminal iron deposition may be related to brain injury. We sought to determine the correlation between MR putaminal hypointensity in HIV-infected patients and brain iron deposition.

Methods: Eleven T2-weighted axial MR scans were retrospectively rated for the extent of putaminal hypointensity from patients who also had neuropathological examination for the extent of putaminal iron disposition. Correlations between MR putaminal hypointensity and brain iron were obtained.

Results: Neuropathological examination in 9 of 10 patients with putaminal hypointensity demonstrated putaminal iron deposition, predominantly in a perivascular pattern.

Conclusions: Premature putaminal iron deposition occurs in patients with HIV infection and may be detected by MR imaging.

We have theorized a direct relationship between viral burden and deleterious effects on the central nervous systems. It was hypothesized that HIV+ individuals would manifest poorer neuropsychological functioning after increased viral load. To address this, we compared viral burden to neuropsychological performance in subjects who participated in ACTG 116-118. Plasma samples and neuropsychological assessments completed at the same time were available for 64 observations on 21 subjects. Subjects who had a viral peak of over 1000 TCID per ml were classified as high viral load, those who did not as low viral load. Mean performances of the high viral load subjects were poorer, even though baseline performances were slightly poorer in the low viral load group. Mean post-viral peak performances were poorer than pre-viral peak performances. Declines in neuropsychological performance were found significantly more often in the high viral load group. These findings support the viral load hypothesis.