________________________________________________________________________ Behavioral Addictions
Compulsivity Compulsivity is less well-defined and investigated than impul- sivity, but it is used to describe repetitive and functionally impairing overt or covert behaviors that lack adaptive function. These habitual, stereotyped behaviors are performed inflexibly to avoid perceived negative consequences and persist despite being harmful [41; 42]. Compulsive behaviors are inappropriate and have no obvious relationship to a goal. When reward-driven substance use or behavioral pursuits persist over an extended period, reward- based learning mechanisms are thought to develop into com- pulsive behaviors [26]. Compulsivity appears distinct from impulsivity, but research demonstrates overlapping neural networks involved in both [4]. Deficits in cognitive flexibility may also serve as markers in disorders of addiction to drug or non-drug rewards. There are two subtypes of compulsivity (reversal learning and attentional set shifting) [43]. Reversal learning is the capacity to flexibly switch choices in response to immediate changes in the envi- ronment or setting. The orbitofrontal cortex are involved in this type of compulsivity. Attentional set shifting is the ability to shift response sets to a previously irrelevant dimension and involves the lateral prefrontal cortex (PFC). EXPLANATORY MODELS OF ADDICTION Explanatory models of psychiatric disorders, including behav- ioral and substance addictions, are developed to provide a conceptual framework for understanding the disorder and identifying an effective treatment approach. Theoretic mod- els can propose an explanatory basis for entire categories of disorders or specific disorders, a pathogenic process within a larger pathophysiology, or a specific symptom or feature. In behavioral addictions, diverse models have been developed to explain symptoms and clinical course and the interpersonal, cognitive, psychological, and neurobiologic dysfunction experienced by patients. The most relevant models serve as an organizing foundation for treatment approaches. GENERAL MODELS OF ADDICTION Reward-seeking is a central component of addictions. Early reward-centric models focused on the nucleus accumbens, where dopamine is released in response to natural rewards like sex or food. Drugs of abuse were thought to “hijack” the nucleus accumbens by triggering dopamine release far exceed- ing that of natural rewards (e.g., food, exercise, sex). The reward deficit disorder model posits that addictive behaviors develop from the need to compensate for impaired reward signaling in the mesolimbic dopamine pathway [44]. Although simplistic based on current understanding, earlier biologic models provided an important foundation for later expansion. For example, nucleus accumbens and dopamine function are now known to be involved in reward-based
learning, reward anticipation and valuation, salience attribu- tion (i.e., assigning degrees of relevance to items, decisions, or behaviors), and loss processing [44]. More recent models include the reward deficit disorder model, Gray’s reinforcement sensitivity theory, the attachment theory development model, and the rejection sensitivity theory. The Reward Deficit Disorder Model The reward deficit disorder model describes addictions as chronic relapsing disorders characterized by a compulsion to seek and take the drug or experience the behavior, loss of control over stimuli intake, and emergence of a negative emotional state (e.g., dysphoria, anxiety, irritability) when unable to access the stimulus. The negative emotional state is termed motivational withdrawal syndrome. A key component of addiction is negative reinforcement, which describes engage- ment in potentially harmful behaviors to alleviate a negative emotional state [45]. “Reward deficit disorder” refers to multiple motivational mechanisms and the progression from impulsivity (positive reinforcement) to compulsivity (negative reinforcement). Compulsivity is thought to result from stress within forebrain structures and dysregulation of neurocircuits involved in reward [45]. Gray’s Reinforcement Sensitivity Theory In Gray’s reinforcement sensitivity theory, behavioral addic- tions are understood from the context of brain system sensi- tivity to punishment and reward. Accordingly, punishment sensitivity regulates responses to stimuli perceived as potentially dangerous, leading to their avoidance (behavioral inhibition). Reward sensitivity directs behavior toward appetitive stimuli that provide immediate compensation (behavioral activation) [46; 47]. The Attachment Theory Developmental Model Behavioral addictions have also been examined through the lens of attachment theory. While not specifically a model of addiction, attachment theory helps explain how early environment experiences may shape beliefs and cognitions that increase risks of behavioral addiction. This model posits that the nature and quality of child attachment to a primary caregiver(s) shape the personality, beliefs in responsiveness and trustworthiness of others, and level of interpersonal security in adolescence and adulthood. The primary attachment relation- ship is thought to form the template from which subsequent relationships are developed [48; 49; 50]. A child with responsive, consistent early caregiving develops an expectation that others will be available and supportive when needed. In contrast, children raised in negligent, reject- ing caregiving environments form negative expectations in future relationships and social interactions. Attachment style influences personality traits, interpersonal behaviors, and
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