The effects of HIV on P300 are moderated by familial risk for substance dependence: Implications for a theory of brain reserve

2011

Psychiatry Research

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In view of the rising prevalence of an overweight body mass among patients living with HIV/AIDS, clinicians must now be mindful of possible adverse outcomes resulting from the co-occurrence. The present study was designed to examine the additive and interactive effects of HIV/AIDS and an excess body mass, as well as the additional contributions of substance abuse or dependence. The dependent variable was brain function estimated by the measurement of P300 electroencephalographic potentials. P300 potentials were recorded during a task designed to elicit subcomponents with frontal (P300a) and both frontal and nonfrontal (P300b) generators. Analyses revealed greater frontal P300a latencies among the 102 HIV-1 seropositive versus the 68 seronegative participants. In addition, frontal P300a latency was further increased by a synergistic interaction of HIV-1 serostatus with a body mass index (BMI) ≥ 25 kg/m2. A history of substance abuse/dependence did not alter these changes. However, it did combine with HIV/AIDS to produce a smaller P300a amplitude than was seen in participants with neither disorder. The findings suggest that white matter changes accompanying an excess BMI may exacerbate those that attend HIV/AIDS and thereby slow frontal brain function. Substance abuse likewise interacts with HIV/AIDS but may impair frontal brain function via a different mechanism.

Section: Methodsmentioning

confidence: 99%

Interactive effects of HIV/AIDS, body mass, and substance abuse on the frontal brain: A P300 study

2011

Psychiatry Research

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“…But, there is disagreement on this point (Heaton et al , 2011). The likely source of the disagreement is the inadequate control employed in some studies over the influence of other contributors, including substance abuse (Archibald et al , 2012; Bauer, 1998; Bauer and Shanley, 2006; Gongvatana et al , 2014; Morgan et al , 2012), familial/genetic risk (Bauer, 2008a; Bauer, 2008b; Bauer, 2013), and comorbid medical disorders (Dufouil et al , 2015; McCutchan et al , 2012; Rodriguez-Penney et al , 2013; Vance et al , 2016). As a result, the literature is clouded with higher-than-expected rates of impairment.…”

Section: Introductionmentioning

confidence: 99%

HIV/AIDS and an overweight body mass are associated with excessive intra-individual variability in response preparation

2018

J. Neurovirol.

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Factors other than HIV/AIDS may influence the cognitive function of patients living with this disease. The present study tested the influence of a common comorbid problem-an overweight body mass. It also examined intra-task variabilities in performance and brain activation as potentially more sensitive indicators of dysfunction than their mean levels. One-hundred seventy-eight participants were recruited and categorized by HIV-1 serostatus (-/+) and body mass (BMI < 26/≥ 26 kg/m). They performed a simple time estimation task during which response time accuracy and electroencephalographic readiness potentials were recorded. A few hours later, they completed a battery of tests measuring balance and gait. The analyses revealed an advantage of variability over the mean in differentiating groups: the presence of HIV-1 and an overweight body mass were independently and additively associated with greater variability across trials in readiness potential amplitude and response accuracy. The analysis also showed that intra-task variability in the readiness potential, but not in response accuracy, was predictive of decrements in single and tandem leg balance and gait velocity. The present findings suggest that an elevated body mass is associated with, and may contribute to, problems in brain function and motor behavior experienced by patients in the current era. The findings recommend a careful consideration of the manner in which these problems are measured. When the problems are episodic and subtle, measures of central tendency may be less than ideal.

“…Because neurophysiological differences are covert and objective, they may constitute a more sensitive index of disordered control less affected by demand characteristics, observer bias and measurement error. The differences were expected to involve P300 and N450 event-related potentials (ERP), which have been shown to be delayed in latency or altered in amplitude by the introduction of response conflict [9,10,30,31] during the Stroop task. Admittedly, the association between these ERP components and response conflict is not consistent across all studies.…”

mentioning

confidence: 99%

P300 and the Stroop Effect in Overweight Minority Adolescents

Kaplan²,

Hesselbrock³

2010

Neuropsychobiology

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Aim: The goal was to examine the relationship between a risk factor for poor cognitive control and a health outcome of growing public significance – an excess body mass – among adolescents. Methods: To this end, 109 adolescents aged 14–20 years were recruited and assigned to 1 of 4 groups defined by the crossing of the absence versus presence of a parental history (PH) of externalizing disorders with a body mass index (BMI) percentile (BMIP) <85 versus ≧85. The principal measure estimating cognitive control was the P300 event-related electroencephalographic response recorded during the Stroop task. Results: The analyses revealed a synergistic interaction between BMIP rank, PH and trial type: the increase in P300 latency and the decrease in response accuracy, elicited by the presence of interfering information, were markedly greater in high-BMIP subjects with a PH of externalizing disorders than in the other subject groups. Analyses of a later component, the N450, previously associated with the Stroop interference effect, revealed no effect of BMI or PH. Conclusions: We conclude that subjects with both a PH of externalizing disorders and an excess BMI constitute a unique group that is less able to resolve cognitive conflict than others. The excessive delay in P300 evoked by conflicting response demands in these subjects may be a marker of a heritable factor that increases risk for both excess body mass and substance use disorders.