Greater activation of the "default" brain regions predicts stop signal errors

Previous studies have provided evidence for a role of the medial cortical brain regions in error processing and post-error behavioral adjustment. However, little is known about the neural processes that precede errors. Here in an fMRI study we employ a stop signal task to elicit errors approximately half of the time despite constant behavioral adjustment of the observers (n=40). By comparing go trials preceding a stop error and those preceding a stop success, we showed that (at p<0.05, corrected for multiple comparisons) the activation of midline brain regions including bilateral precuneus and posterior cingulate cortices, perigenual anterior cingulate cortices and transverse frontopolar gyri precedes errors during the stop signal task. Receiver operating characteristic (ROC) analysis based on the signal detection theory showed that the activity in these three regions predicts errors with an accuracy between 0.81 and 0.85 (area under the ROC curve). Broadly supporting the hypothesis that deactivation of the default mode circuitry is associated with mental effort in a cognitive task, the current results further indicate that greater activity of these brain regions can precede performance errors.     

Eating Pathology among Women with Alcoholism and/ or Anxiety Disorders

Two hundred one non-treatment seeking women with alcoholism, anxiety disorders, alcoholism and anxiety disorders, or neither alcoholism nor anxiety disorders were interviewed to assess core psychopathology associated with eating disorders using the Eating Disorders Examination and DSM-IIIR psychiatric diagnoses using the Schedule of Affective Disorders and Schizophrenia-Lifetime version. Alcoholic women had significantly higher mean scores on each of the Eating Disorders Examination subscales of Restraint, Overeating, Eating Concern, Shape Concern, and Weight Concern compared with nonalcoholic women. Women with anxiety disorders had significantly elevated scores on subscales of Overeating, Eating Concern, and Weight Concern compared with women without anxiety disorders. Women with both alcoholism and anxiety disorders had higher rates of bulimia nervosa and/or eating disorder NOS compared with women with either disorder alone. Implications of these findings are discussed in the context of the co-morbid association between alcoholism, eating disorders, and anxiety disorders.     

How does stress increase risk of drug abuse and relapse?

RATIONALE: The notion that stress leads to drug abuse in vulnerable individuals and relapse in addicts is not new. Most major theories of addiction postulate that stress plays an important role in increasing drug use and relapse. Several animal studies and some human laboratory studies have shown that stress exposure enhances drug self-administration. Although clinical observations suggest that exposure to stress increases drug use, and are associated with craving and relapse in addicts, human research in this area is largely correlational and at times contradictory. OBJECTIVE: Given the growing preclinical evidence that supports the key role of stress in substance abuse, careful examination of this research area in humans is warranted. This paper examines empirical evidence on how stress may increase the vulnerability to drug abuse, and explores whether chronic drug abuse alters the stress response and coping in addicts, thereby increasing the likelihood of drug seeking and relapse. Unanswered questions on the association between stress and substance abuse in humans are identified. CONCLUSION: Preclinical research has shown that stress, in addition to drug itself, plays a key role in perpetuating drug abuse and relapse. However, the mechanisms underlying this association in humans remain unclear. A greater understanding of how stress may perpetuate drug abuse will likely have a significant impact on both prevention and treatment development in the field of addiction.     

Performance monitoring and stop signal inhibition in abstinent patients with cocaine dependence

Impulsivity has been associated with drug abuse and relapse. As a measure of impulsivity, response inhibition in a stop signal task is impaired in substance abusers compared to healthy control subjects. However, cognitive processes besides response inhibition can affect performance in the stop signal task. Greater response readiness to the go signal increases stop signal reaction time (SSRT) and greater performance monitoring elicited by the stop signal decreases SSRT. Prolonged SSRT, therefore, may reflect differences in these other task-related cognitive processes rather than impaired response inhibition. Using a tracking stop-signal task, we compared 18 abstinent cocaine dependent patients with 41 age- and education-matched healthy controls. We computed SSRT for each individual subject on the basis of the horse race model. We also computed the fore-period (FP) effect to measure response readiness to the go signal and the post-signal slowing (PSS) effect to measure performance monitoring to the stop signal. Cocaine subjects showed increased SSRT and decreased PSS effect, compared to healthy controls. Covariance adjustment for the PSS effect eliminated the SSRT difference from healthy controls. These results suggest that diminished performance monitoring can be a critical cognitive mechanism underlying impaired response inhibition in cocaine dependent patients.     

Selective cocaine-related difficulties in emotional intelligence: relationship to stress and impulse control

Emotional Intelligence (EI) comprises the ability to perceive, use, understand, and regulate emotions and may potentially contribute to variability in risk-related factors such as stress perception and impulse control in cocaine dependent individuals. The main objective of the current study is to better define EI in cocaine dependent individuals compared with healthy controls, using the Mayer, Salovey, and Caruso Emotional Intelligence Test (MSCEIT). Secondary analysis investigates the association between EI, IQ factors, perceived stress, and impulse control in both populations. Seventy-two abstinent treatment-seeking cocaine patients and 52 healthy controls were administered the MSCEIT as well as measures of IQ, perceived stress, and impulse control. Findings showed that cocaine dependent participants demonstrated highly selective EI difficulties compared with healthy controls, specifically with regard to higher-level emotional reasoning including the understanding, management, and regulation of emotion. These EI problems were associated with increased perceived stress and impulse control difficulties. IQ was significantly associated with all MSCEIT measures in the cocaine dependent participants, but not controls. Findings indicate that specific aspects of EI may be of clinical importance to cocaine dependent populations, impacting relapse-related factors such as stress dysregulation and impulse control.     

New Findings on Biological Factors Predicting Addiction Relapse Vulnerability

Relapse is a highly prevalent phenomenon in addiction. This paper examines the new research on identifying biological factors that contribute to addiction relapse risk. Prospective studies examining relapse risk are reviewed, and clinical, biological, and neural factors that predict relapse risk are identified. Clinical factors, patient-related factors, and subjective and behavioral measures such as depressive symptoms, stress, and drug craving all predict future relapse risk. Among biological measures, endocrine measures such as cortisol and cortisol/corticotropin (ACTH) ratio as a measure of adrenal sensitivity and serum brain-derived neurotrophic factor were also predictive of future relapse risk. Among neural measures, brain atrophy in the medial frontal regions and hyperreactivity of the anterior cingulate during withdrawal were identified as important in drug withdrawal and relapse risk. Caveats pertaining to specific drug abuse type and phase of addiction are discussed. Finally, significant implications of these findings for clinical practice are presented, with a specific focus on determining biological markers of relapse risk that may be used to identify those individuals who are most at risk of relapse in the clinic. Such markers may then be used to assess treatment response and develop specific treatments that will normalize these neural and biological sequelae so as to significantly improve relapse outcomes.