Dataset Information

Laterality of Brain Activation for Risk Factors of Addiction.

ABSTRACT:

Background

Laterality of brain activation is reported for tests of risk factors of addiction- impulsivity and craving-but authors rarely address the potential significance of those asymmetries.

Objective

The purpose of this study is to demonstrate this laterality and discuss its relevance to cognitive and neurophysiological asymmetries associated with drug abuse vulnerability in order to provide new insights for future research in drug abuse.

Method

From published reports, brain areas of activation for two tests of response inhibition or craving for drugs of abuse were compiled from fMRI activation peaks and were tabulated for eight sections (octants) in each hemisphere. Percent asymmetries were calculated (R-L/R+L) across studies for each area.

Results

For impulsivity, most activation peaks favored the right hemisphere. Overall, the percent difference was 32% (Χ2 = 16.026; p < 0.0001) with the greater asymmetry for anterior peaks (46.8%; Χ(2) = 17.329; p < 0.0001). The asymmetries for cue-induced craving were opposite, favoring the left hemisphere by 6.7% (Χ(2) = 4.028; p < 0.05). The consistency of left asymmetry was found for almost all drugs. For nicotine, studies where subjects were not allowed to smoke (deprived) prior to measurement had the same left hemisphere activation but those who smoked (satiated) before the fMRI measure showed right asymmetry.

Conclusion

Brain activation studies demonstrate different left/right hemispheric contributions for impulsivity versus craving-factors related to addiction. Failure to take laterality into consideration is a missed opportunity in designing studies and gaining insight into the etiology of drug abuse and pathways for treatment.

SUBMITTER: Gordon HW

PROVIDER: S-EPMC4811731 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundsInternet addiction (IA) has become a major public health issue worldwide and is closely linked to psychiatric disorders and suicide. The present study aimed to investigate the prevalence of IA and its associated psychosocial and psychopathological determinants among internet users across different age groups.MethodsThe study was a cross-sectional survey initiated by the Taiwan Suicide Prevention Center. The participants were recruited from the general public who responded to the online questionnaire. They completed a series of self-reported measures, including Chen Internet Addiction Scale-revised (CIAS-R), Five-item Brief Symptom Rating Scale (BSRS-5), Maudsley Personality Inventory (MPI), and questions about suicide and internet use habits.ResultsWe enrolled 1100 respondents with a preponderance of female subjects (85.8%). Based on an optimal cutoff for CIAS-R (67/68), the prevalence rate of IA was 10.6%. People with higher scores of CIAS-R were characterized as: male, single, students, high neuroticism, life impairment due to internet use, time for internet use, online gaming, presence of psychiatric morbidity, recent suicide ideation and past suicide attempts. Multiple regression on IA showed that age, gender, neuroticism, life impairment, internet use time, and BSRS-5 score accounted for 31% of variance for CIAS-R score. Further, logistic regression showed that neuroticism, life impairment and internet use time were three main predictors for IA. Compared to those without IA, the internet addicts had higher rates of psychiatric morbidity (65.0%), suicide ideation in a week (47.0%), lifetime suicide attempts (23.1%), and suicide attempt in a year (5.1%).ConclusionNeurotic personality traits, psychopathology, time for internet use and its subsequent life impairment were important predictors for IA. Individuals with IA may have higher rates of psychiatric morbidity and suicide risks. The findings provide important information for further investigation and prevention of IA.

Project description:During critical illness, impaired endothelial vascular reactivity predicts prolonged acute brain dysfunction, but relationships between endothelial activation, blood-brain barrier/neurological injury, and acute brain dysfunction, including delirium, remain unexamined. We tested the hypothesis that elevated plasma markers of endothelial activation and blood-brain barrier/neurological injury are associated with delirium duration during critical illness.Prospective cohort study.Medical and surgical ICUs in an academic medical center.Adults in acute respiratory failure and/or shock.None.We enrolled subjects within 72 hours of organ failure diagnosis in the ICU. We measured plasma concentrations of plasminogen activator inhibitor-1, E-selectin, and angiopoietin-2 as markers of endothelial activation and S100B as a marker of blood-brain barrier/neurological injury in blood collected at enrollment. We assessed patients for delirium and coma twice daily after enrollment using the Confusion Assessment Method for the ICU and the Richmond Agitation-Sedation Scale. Among 134 patients with a median (interquartile) age of 57 years (46-66 yr) and Acute Physiology and Chronic Health Evaluation II of 26 (19-31), delirium occurred in 94 patients (70%) with a median duration of 2 days (0-4 d). Higher plasminogen activator inhibitor-1 (p = 0.002), E-selectin (p = 0.02), and S100B (p < 0.001) concentrations were associated with fewer delirium/coma-free days after adjusting for age, Charlson comorbidity index, modified Sequential Organ Failure Assessment score, and severe sepsis. Similarly, higher plasminogen activator inhibitor-1 (p = 0.007) and S100B (p = 0.01) concentrations were associated with longer delirium duration in survivors. Adjusting for S100B did not alter plasminogen activator inhibitor-1 and E-selectin associations with delirium, suggesting that these associations were not mediated by blood-brain barrier/neurological injury.Elevated plasma markers of endothelial activation and blood-brain barrier/neurological injury during critical illness are associated with prolonged delirium after biomarker measurement. Future research is needed to determine whether these processes have pathophysiologic roles in delirium and whether therapies targeted at the endothelium or blood-brain barrier can prevent and/or treat delirium during critical illness.