Antiretroviral treatment is associated with increased attentional load-dependent brain activation in HIV patients.

Full Abstract

OBJECTIVE: The purpose of this paper was to determine whether antiretroviral medications, especially the nucleoside analogue reverse transcriptase inhibitors, lead to altered brain activation due to their potential neurotoxic effects in patients with human immunodeficiency virus (HIV) infection. METHODS: Forty-two right-handed men were enrolled in three groups: seronegative controls (SN, n = 18), HIV subjects treated with antiretroviral medications (HIV+ARV, n = 12), or not treated with antiretroviral medications (HIV+NARV, n = 12). Each subject performed a set of visual attention tasks with increasing difficulty or load (tracking two, three or four balls) during functional magnetic resonance imaging. RESULTS: HIV subjects, both groups combined, showed greater load-dependent increases in brain activation in the right frontal regions compared to SN (p-corrected = 0.006). HIV+ARV additionally showed greater load-dependent increases in activation compared to SN in bilateral superior frontal regions (p-corrected = 0.032) and a lower percent accuracy on the performance of the most difficult task (tracking four balls). Region of interest analyses further demonstrated that SN showed load-dependent decreases (with repeated trials despite increasing difficulty), while HIV subjects showed load-dependent increases in activation with the more difficult tasks, especially those on ARVs. INTERPRETATION: These findings suggest that chronic ARV treatments may lead to greater requirement of the attentional network reserve and hence less efficient usage of the network and less practice effects in these HIV patients. As the brain has a limited reserve capacity, exhausting the reserve capacity in HIV+ARV would lead to declined performance with more difficult tasks that require more attention.

Author information

Author/s: Chang, L (L); Yakupov, R (R); Nakama, H (H); Stokes, B (B); Ernst, T (T);

Affiliation: Department of Medicine, Division of Neurology, John A. Burns School of Medicine, University of Hawaii at Manoa, The Queen's Medical Center University Tower, 1356 Lusitana Street, Honolulu, HI 96813, USA. lchang(-atsign-)hawaii.edu

Grants: 2R01MH61427 (Agency:NIMH NIH HHS) ; 5P20-RR11091 (Agency:NCRR NIH HHS) ; G12 RR003061-23 (Agency:NCRR NIH HHS) ; G12-RR003061 (Agency:NCRR NIH HHS) ; K02 DA016991-04 (Agency:NIDA NIH HHS) ; K02-DA16991 (Agency:NIDA NIH HHS) ; K24 DA016170-05 (Agency:NIDA NIH HHS) ; K24-DA16170 (Agency:NIDA NIH HHS) ; P20 RR011091-14 (Agency:NCRR NIH HHS) ; R01 MH061427-08 (Agency:NIMH NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.

Journal: Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology (J Neuroimmune Pharmacol), published in United States. (Language: eng)

Reference: 2008-Jun; vol 3 (issue 2) : pp 95-104

Dates: Created 2008/05/12; Completed 2008/10/08; Revised 2009/09/18;

PMID: 18247124, status: MEDLINE (last retrieval date: 9/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

External Links for this article
(including full text providers, if available):

Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.

This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.