The detrimental effects of emotional process dysregulation on decision-making in substance dependence

Abstract

Substance dependence is complex and multifactorial, with many distinct pathways involved in both the development and subsequent maintenance of addictive behaviors. Various cognitive mechanisms have been implicated, including impulsivity, compulsivity, and impaired decision-making. These mechanisms are modulated by emotional processes, resulting in increased likelihood of initial drug use, sustained substance dependence, and increased relapse during periods of abstinence. Emotional traits, such as sensation-seeking, are risk factors for substance use, and chronic drug use can result in further emotional dysregulation via effects on reward, motivation, and stress systems. We will explore theories of hyper and hypo sensitivity of the brain reward systems that may underpin motivational abnormalities and anhedonia. Disturbances in these systems contribute to the biasing of emotional processing toward cues related to drug use at the expense of natural rewards, which serves to maintain addictive behavior, via enhanced drug craving. We will additionally focus on the sensitization of the brain stress systems that result in negative affect states that continue into protracted abstinence that is may lead to compulsive drug-taking. We will explore how these emotional dysregulations impact upon decision-making controlled by goal-directed and habitual action selections systems, and, in combination with a failure of prefrontal inhibitory control, mediate maladaptive decision-making observed in substance dependent individuals such that they continue drug use in spite of negative consequences. An understanding of the emotional impacts on cognition in substance dependent individuals may guide the development of more effective therapeutic interventions.

Keywords: addiction; cognition; decision-making; emotion; reward; stress.

Figure 1

Reward system changes associated with substance dependence. Enhanced brain response and craving elicited by drug cues supports the incentive sensitization view of addiction. This theory suggests that repeated exposure to drugs of abuse causes neuroadaptations within mesolimbic dopamine neurons that results in pathological levels of incentive salience being attributed to drugs and their associated stimuli. In contrast, reduced brain responses for natural rewards, and blunted dopaminergic functioning in the absence of drug cues, are suggestive of deficient reward functioning. This deficient reward signaling is hypothesized to result in the seeking of drug rewards as natural rewards do not adequately stimulate the deficient reward system.

Figure 2

Example of a drug word emotional Stroop task showing drug words (A) and neutral words (B). Participants are required to identify the color of the text as quickly as possible. Successful performance of this task requires the suppression of emotional responses to word meaning, and a direction of attention toward non-emotional content (word color). Slower reaction times are assumed to indicate a greater degree of emotional interference on cognitive processing. Panel (C) demonstrates that heroin dependent individuals have significantly slower reaction times for drug words compared to neutral words (Murphy et al., 2011), reflecting the emotional significance of the drug words compared to neutral words.

Figure 3

Neurotransmitter changes within the brain stress system that are associated with withdrawal and stress-induced reinstatement of drug-seeking. Neurochemical changes are proposed to occur within the extended amygdala in order to overcome the chronic presence of drugs of abuse. Withdrawal from all major drugs of abuse is associated with CRF and NA release within the CeA that produces anxiety like responses that are thought to drive drug seeking via negative reinforcement mechanisms. CRF and noradrenaline release within the BNST is considered to be important for mediating drug seeking in response to a stressor, such as a footshock (Koob, 2008). Abbreviations: CRF, Corticotrophic releasing factor; NA, Noradrenaline; CeA, central nucleus of the amygdala; BNST, bed nucleus of the stria terminalis.

Figure 4

Hypothetical relationship of the effect of stress on cognitive performance in substance dependence according to different trait levels of stress sensitivity. Mild stress improves performance in those of low and medium AS traits by enhancing arousal and sensitivity to punishment signals. Increasing stress results in an increasing need for affect regulation, thus resulting in reduced task-related cognitive resource allocation and impaired performance. High trait AS is associated with impaired decision-making performance before stress induction (Lemenager et al., 2011) and thus further increases in stress are likely to lead to further significant task impairments. Abbreviations: AS, Anxiety Sensitivity.