Promoting the Importance of Addiction Neuropsychology

Introduction

In Canada and the United States, the prevalence of substance use disorders (SUDs) is among the highest of all psychiatric disorders (Statistics Canada, 2023; Grant et al., 2015; 2016: Tam et al, 2020). Despite its prevalence, clinical psychology training programs allocate disproportionately less time to SUDS than other mental health disorders, resulting in a knowledge gap and a shortage in skilled clinical providers (Burrow-Sánchez, et al., 2020). For example, in a 2017 study, less than 40% of programs had even a single faculty member studying addiction, and less than one-third of respondents offered any specialty clinical training in addiction (Dimoff et al., 2017). In addition, while there is growing recognition that neuropsychologists should possess a strong understanding of how substance use impacts the brain, many feel ill-equipped to assess, conceptualize, and treat substance-related cognitive dysfunction, leaving the profession underprepared to address one of the most prevalent and consequential contributors to brain and behavioral impairments (e.g., Verdejo-Garcia, 2018).

This gap – the intersection between substance use disorders and brain dysfunction, or addiction neuropsychology – represents a convergence of two ABPP specialties (clinical neuropsychology, addiction psychology). While the concept is well established scientifically in both fields (e.g., Koob & Le Moal, 2006;  Yucel et al., 2018), most professionals specialize in one or the other. In this brief article, based on a workshop presented at the June 2025 American Academy of Neuropsychology conference (MacKillop & MacKillop, 2025), we highlight the importance of addiction neuropsychology as an emerging interdisciplinary field and the ways researchers and clinicians in both fields can benefit from insight from the other.

For Neuropsychologists, Unique Insights into Diagnosis and Comorbidity

The DSM-5-TR recognizes that “An important characteristic of substance use disorders is an underlying change in brain circuits that may persist beyond detoxification” (American Psychiatric Association, 2022, p. 544) and separates disorders related to substance use into two categories: substance use disorders and substance-induced mental disorders (i.e., symptomatic effects of substances) – each being relevant to neuropsychology in terms of etiology and the nature of the impact on the brain. Substance use produces both acute (state-like) and chronic (trait-like) cognitive effects. Acute effects include intoxication, residual post-intoxication states (e.g., “hangovers”), withdrawal syndromes, and post-acute withdrawal syndrome, while chronic effects encompass etiological factors, acute brain injury, progressive neurodegenerative changes, and teratogenic consequences. In addition to dementias associated with substance use. Individuals with SUD commonly experience neurocognitive difficulties, such as noted impairments in attention, memory, and executive functioning, which may either precede or result from substance use (e.g., Ramey & Regier, 2019; Dominguez-Salas et al., 2016; Bruijnen et al., 2019). Substances also alter immune response and compromise the blood–brain barrier, compounding cognitive effects of co-occurring conditions (e.g., postoperative complications, chronic disease) —factors highly relevant to neuropsychologists but often overlooked in practice (Guerri et al., 2019; Pimentel et al., 2020).

Brain dysfunction that occurs after addiction develops is also highly relevant to neuropsychology, as SUDs are prevalent among routinely referred patient populations (e.g., ADHD, TBI, dementia, chronic pain; NIDA, 2020). For example, individuals with ADHD are 2–3 times more likely to develop SUDs, with both conditions marked by impulsivity, poor self-control, impaired decision-making, and emotional dysregulation (Wilens & Morrison, 2011). Differentiating attention deficits is of clinical importance given that stimulants are first-line ADHD treatment. A similar comorbidity exists with TBI, as 20–50% of individuals with TBI have a history of substance misuse (e.g., Weil et al., 2016), while also those with SUD face greater risk of TBI from accidents, violence, and risky behaviors. Both TBI and SUD share vulnerabilities in impulsivity and self-regulation, thought to contribute to their high comorbidity (e.g., Bjork & Grant, 2009). Finally, SUDs accelerate aging processes, producing premature neurocognitive decline, neuroinflammation, and brain changes associated with dementia (Bachi et al., 2007; Shi & Wiers, 2025; Battista, et al., 2025). Recognizing these complex relationships is essential for neuropsychologists, as substance use disorders complicate differential diagnosis, heighten vulnerability to age-related conditions, and implicate etiology and the trajectory of cognitive and behavioral impairments.

One common blind spot among neuropsychologists is in the formal assessment of substance use and SUDs. Although neuropsychologists routinely inquire about substance use during interviews, research indicates they rely primarily on unstructured patient reports, as standardized or high-resolution substance use measures  are not as commonly included in typical test batteries as other mental health measures (e.g., Rabin et al., 2016). Guidelines emphasize taking a history (Heilbronner et al., 2009), but do not require standardized substance use screening, creating highly variable practices across clinicians. Surveys of cognitive assessment clinics similarly show inconsistent alcohol and drug screening, especially in older adults (Alhalaseh et al., 2025). Urine drug screening is objective, quick, easy,  inexpensive and quite sophisticated, which include novel drug biomarkers and sample validity tests, but is seldom used in neuropsychological evaluations. Collectively, substance use is not commonly objectively assessed, increasing the risk of overlooking substance-related cognitive effects or misattributing test findings.

Although neurocognitive impairment can arise from substance use, its effects can also be underappreciated in a neuropsychological assessment – particularly when SUD was not part of the referral question. Beyond recognizing brain dysfunction secondary to substance use, neuropsychologists are responsible for evaluating how such dysfunction influences cognition, emotion, and behavior persisting after prolonged, chronic use. While testing is vital, common neuropsychological assessment instruments and procedures are limited in capturing several constructs implicated in addiction (Bigler, 2024). These constructs, established by a Delphi consensus study, include reward valuation, expectancy/reward prediction error, action selection/preference-based decision-making, reward learning; habit, response selection/inhibition, and compulsivity (Yucel et al., 2018). In addition to considering substance use screening as part of routine clinical practice, the neuropsychologist should also consider understanding patterns of performances related to SUD across more traditional assessment tools. Combining knowledge of acute and chronic substance use (e.g., direct and indirect laboratory biomarkers, breathalyser tests, urine drug screening), with test performances is critical to making an informed diagnosis.

For Addiction Psychologists, Unique Insights into the Manifestations of Neurobiological Changes

Addiction is now recognized as a brain disorder characterized by enduring neurobiological changes in circuits regulating reward, motivation, emotion, and executive control (Koob & Volkow, 2016; Heilig et al., 2023). At its core, addiction involves the hijacking of ancient brain circuits (basal ganglia, amygdala, and prefrontal cortex) subserving classical fitness drives, redirecting them toward compulsive substance use and maladaptive reward seeking (Koob & Volkow, 2016). The basal ganglia, especially the nucleus accumbens, mediate the acute rewarding effects of substances and support reinforcement learning. Over time, habitual drug-seeking behavior becomes encoded in the dorsal striatum, making use increasingly compulsive (Everitt & Robbins, 2016). The extended amygdala contributes to the negative emotional states and stress responses associated with withdrawal, which further drive substance use through negative reinforcement (Koob & Schulkin, 2019). Addictive substances also produce supraphysiological dopamine release in the pathways from the ventral tegmental area to the nucleus accumbens, reinforcing drug use and strengthening cue associations. Over time, dopamine receptor downregulation reduces reward sensitivity, driving escalating use and contributing to anhedonia (Volkow et al., 2016). Glutamatergic dysregulation in prefrontal-striatal circuits further impairs cognitive control and heightens cue reactivity (Kalivas & Volkow, 2005). The prefrontal cortex — including the orbitofrontal, ventromedial, and dorsolateral regions — is critical for decision-making and self-control. Chronic substance exposure impairs these regions, weakening inhibitory control and promoting impulsive, maladaptive behaviors (Bechara, 2019; Goldstein & Volkow, 2011).

Understanding these mechanisms is essential for developing targeted interventions and integrating neurobiological insights into clinical assessment and treatment. A critical element that is missing for addiction psychologists, however, is clinically assessing the expression of these underlying neurobiological adaptations. Neuropsychological tests can provide high-resolution characterization of inhibition, cognitive flexibility, adaptive decision making, and other features of executive function that can illuminate both areas of weakness, but also where functioning is preserved. Consistent patterns of findings across neuropsychological research demonstrate deficits in attention, working memory, and inhibitory control among individuals with substance use disorders (e.g., Yücel et al., 2007;Verdejo-Garcia  & Albein-Urios,  2021). It has been suggested that such deficits are related to structural and functional changes in the prefrontal cortex and related networks that sustain addictive behaviours , consistent with the models explaining the neurobiology of addiction (Goldstein & Volkow, 2011). This information in turn, can be integrated into assessment and intervention. Furthermore, neurocognitive testing can clarify functional capacity and, as alluded to above, the extent to which additional rehabilitation services are needed, such as for TBI or other comorbid neurocognitive disorders. On balance, even a relatively brief neuropsychological screening or assessment has the potential to be highly revealing about an SUD patient’s cognitive capacities and constraints. 

Future Addiction Neuropsychology Research Applications

There is a clear and growing need to develop and refine neuropsychological assessment tools that can accurately evaluate the cognitive and behavioral impact of addiction within both clinical and research contexts (e.g., Domínguez-Salas et al., 2016; Goldstein & Volkow, 2011). Among the most promising approaches are paradigms that examine decision-making processes implicated in substance use disorders, particularly delay discounting tasks — which assess the tendency to devalue future rewards in favor of immediate gratification — and gambling paradigms such as the Iowa Gambling Task, which measure reward sensitivity, risk–reward evaluation, and deficits in feedback-based learning (Bechara, 2003; Bickel et al., 2014; MacKillop et al., 2011; Verdejo-García et al., 2006). The principles underlying these measures hold significant promise for enhancing the assessment and understanding of cognitive networks associated with addictive behaviors.

In addition, the use of brain stimulation as an intervention for addictive behaviors is becoming increasingly prominent (e.g., Ekhtiari et al., 2019; Salling & Martinez, 2016). There is an essential role for neuropsychological assessment in characterizing cognitive functioning before, during, and after treatment with neuromodulation (e.g., repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), deep brain stimulation (DBS)). Ongoing evaluation of cognitive profiles — both those that precede intervention and those that evolve throughout the course of recovery — will be critical for advancing our understanding of the mechanisms underlying treatment response and outcomes. Treatment interventions intended to reverse these neuroadaptations also show promise as therapeutic approaches for addiction (Volkow et al., 2019). These are but a few examples of manifold opportunities for research in addiction neuropsychology.

Conclusion 

Clinical neuropsychology is a longstanding specialty centered on the scientific investigation and clinical application of the relationship between brain function and behavior. It involves the assessment, diagnosis, treatment, and rehabilitation of individuals across the lifespan with neurological, medical, developmental, or psychiatric conditions that impact cognition, emotion, personality, and behavior. More recently, addiction psychology has become a recognized specialty reflecting an evidence-based approach to the assessment, diagnosis, and treatment of SUDs and other addictive behaviors. At the intersection of these two established domains lies addiction neuropsychology, an emerging specialty area that addresses a critical knowledge gap and responds to pressing clinical needs that are often not currently met. Addiction neuropsychology focuses on causes and contributions to substance use – including the impact of substance use on brain structure and function — and how these neurobiological changes, in turn, influence cognition, emotion, and behavior across a range of neurological, medical, developmental, and comorbid psychiatric conditions. Prioritizing the expertise of both clinical neuropsychologists and addiction psychologists is critical for optimal assessment, conceptualization, and treatment of substance use and brain dysfunction.