Neuropsychological and Neurological Function of Human Immunodeficiency Virus Seropositive Asymptomatic Individuals

Goethe, Katherine E.; Mitchell, John C.; Marshall, Douglas W.; Brey, Robin L.; Cahill, William T; Leger, G. D.; Hoy, L. J.; Boswell, R N

doi:10.1001/archneur.1989.00520380029008

Cited by 142 publications

(29 citation statements)

References 14 publications

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“…O u r results are also consistent with those from the neurological, neuroradiologicd, and neuropsychological arms of our multidisciplinary study [lo] and with the growing number of studies that have detected n o evidence of a clinically significant neuropsychological o r electrophysiological abnormality in asymptomatic seropositive subjects 118, 19, 2.3, 30,35,36). This suggests that the early and persistent involvement of the CNS during the asymptomatic stages of H I V disease does not result in discernible cognitive dysfunccion.…”

Section: Discussionsupporting

confidence: 88%

Long‐latency event‐related potentials in asymptomatic human immunodeficiency virus type 1 infection

Connolly¹,

Manji²,

McAllister³

et al. 1994

Annals of Neurology

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As part of the Medical Research Council prospective study of the neurological and neuropsychological complications of human immunodeficiency virus (HIV) infection, long-latency event-related potentials were recorded in a cohort of homosexual and bisexual men. The latencies and amplitudes of the potentials, recorded from three scalp sites, were compared with the scores from neuropsychological tests of memory, attention, and concentration and with markers of immune function. The findings from 94 men were analyzed in the cross-sectional study of whom 47 were HIV seropositive without symptoms or signs of HIV type 1 (HIV-1) infection, 24 had progressed to the symptomatic stages of the disease, and 23 were persistently HIV seronegative. There were no consistently significant differences between the three subject groups in mean latencies and amplitudes of the P300 and N200 or in the numbers of abnormal P300 latencies. There were no significant correlations between either the neuropsychological tests scores or the immune measures (CD4 lymphocyte count and beta 2 microglobulin level) and the neurophysiological parameters. On repeated testing an average of 2 years later, there was no evidence of a significant trend towards deterioration in 30 HIV-seropositive subjects who remained asymptomatic compared with 22 HIV seronegatives. These findings indicate that there is no neurophysiological evidence of cognitive dysfunction in the asymptomatic stages of HIV-1 infection.

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Section: Discussionsupporting

confidence: 88%

Long‐latency event‐related potentials in asymptomatic human immunodeficiency virus type 1 infection

Connolly¹,

Manji²,

McAllister³

et al. 1994

Annals of Neurology

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“…HIV-1 encephalopathy typically occurs in the context of advanced immunosuppression and coexistent systemic disease (136,139,300,301,333,339,364) (22,52,267). Approximately 3% of adults with AIDS present with dementia (177,242,267).…”

Section: Hiv-1 Encephalopathy (Hiv-1-associatedmentioning

confidence: 99%

Human immunodeficiency virus type 1 infection of the brain

et al. 1993

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Direct infection of the central nervous system by human immunodeficiency virus type 1 (HIV-1), the causative agent of AIDS, was not appreciated in the early years of the AIDS epidemic. Neurological complications associated with AIDS were largely attributed to opportunistic infections that arose as a result of the immunocompromised state of the patient and to depression. In 1985, several groups succeeded in isolating HIV-1 directly from brain tissue. Also that year, the viral genome was completely sequenced, and HIV-1 was found to belong to a neurotropic subfamily of retrovirus known as the Lentivirinae. These findings clearly indicated that direct HIV-1 infection of the central nervous system played a role in the development of AIDS-related neurological disease. This review summarizes the clinical manifestations of HIV-1 infection of the central nervous system and the related neuropathology, the tropism of HIV-1 for specific cell types both within and outside of the nervous system, the possible mechanisms by which HIV-1 damages the nervous system, and the current strategies for diagnosis and treatment of HIV-1-associated neuropathology.

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“…The detection of HIV-positive isolates from the cerebrospinal fluid (CSF) in asymptomatic HIV-seropositive individuals indicates that the virus replication may start a latent and slowly progressing infection in the central nervous system (CNS) long before other manifestations of disease appear (Chiodi et al, 1988). Abnormalities in cognitive, behavioural , and motor functions are frequently reported in patients with AIDS (Goethe et al, 1989), and dementia is commonly seen during the late stages of the disease (Navia et al, 1986). We have recently reported deficiencies in the CSF and serum indole amine system in HIV-infected patients (Larsson et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal fluid catecholamine metabolites in HIV‐infected patients

Larsson

Hagberg²,

Forsman

et al. 1991

J of Neuroscience Research

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Twenty-eight HIV-seropositive individuals--11 asymptomatic cases, 8 with lymphadenopathy syndrome (LAS), and 9 with AIDS--were investigated. Clinical staging of the AIDS dementia complex was done in the 9 AIDS patients. The catecholamine metabolites 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) in CSF were determined in all the HIV patients and in 20 healthy volunteers. The CSF MHPG levels did not differ significantly between healthy subjects and HIV-infected patients at any stage of the infection. The CSF concentrations of HVA differed between the groups only during the AIDS stage. The mean CSF HVA value in the AIDS patients was 42% lower than in the healthy subjects and significantly lower than in any other stage of HIV infection (P less than .01). Patients with signs of the AIDS dementia complex had reduced CSF HVA levels, but there was no clear relationship between HVA concentration and stage of the AIDS dementia complex.

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Neuropsychological and Neurological Function of Human Immunodeficiency Virus Seropositive Asymptomatic Individuals

Cited by 142 publications

References 14 publications

Long‐latency event‐related potentials in asymptomatic human immunodeficiency virus type 1 infection

Long‐latency event‐related potentials in asymptomatic human immunodeficiency virus type 1 infection

Human immunodeficiency virus type 1 infection of the brain

Cerebrospinal fluid catecholamine metabolites in HIV‐infected patients

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