Chapter 32 Substance Use Disorders: Cognitive Sequelae, Behavioral Manifestations, Neuroimaging Correlates, and Novel Interventions James J. Mahoney III, Kirk R. Bryant, and Marc W. Haut The United States is currently in the midst of a substance abuse crisis. According to the 2016 National Survey on Drug Use and Health (NSDUH), approximately 20.1 million people had a substance use disorder (SUD) in 2016 [1]. Specifically, 15.1 million people met criteria for alcohol use disorder and 7.4 million people met criteria for an illicit SUD, the most common being for marijuana (4.0 million people) and opioids (2.1 million people). Unfortunately, the number of individuals with SUD far exceeds the number of patients receiving substance use treatment. Specifically, of the 20.1 million people with SUD, only 3.8 million people received any form of substance use treatment with only 2.2 million receiving treatment at a specialty facility [1]. Further complicating matters is the high comor- bidity between SUD and other psychiatric disor- ders. In 2016, an estimated 8.2 million adults (3.4 percent of all adults) had both mental illness and SUDs in the past year, and 2.6 million adults (1.1 percent of all adults) had co-occurring serious mental illness and SUDs. About half of those with co-occurring mental illness and a SUD did not receive either mental health care or specialty substance use treatment, and approximately one-third of those with co-occurring serious mental illness and a SUD did not receive either type of care [1]. Another factor impeding on SUD is the lack of medication-assisted treatments (MAT) for SUDs, other than MAT for alcohol and opioids, especially given the rise of other sub- stances of abuse such as methamphetamine. The current conceptualization regarding the immediate and long-term neural effects of sub- stance use focuses on dopamine (DA), and the nucleus accumbens (NAc), which is the center in the reward circuitry [2–6]. The NAc maintains direct and indirect involvement in several brain regions associated with emotions, self-regulation, disinhibition, insight, craving, and habit forming, which include the dorsal striatum, amygdala, hippocampus, and prefrontal cortex [3]. The acute effects of substance use result in a surge of DA throughout the reward circuitry. Given the reinforcing effects of this surge of DA, the probability of continued and future substance use is subsequently increased. Chronic substance use eventually leads to a suppression of DA availability over time secondary to the persistent release of dopamine caused by substance use. As a J. J. Mahoney III (&) Department of Behavioral Medicine and Psychiatry, West Virginia University School of Medicine, Morgantown, WV, USA e-mail: james.mahoney@hsc.wvu.edu K. R. Bryant Clinical Neuropsychologist, WellStar Medical Group, Marietta, GA, USA M. W. Haut Departments of Behavioral Medicine and Psychiatry, Neurology, and Radiology, West Virginia University School of Medicine, Morgantown, WV, USA © Springer Nature Switzerland AG 2019 C. L. Armstrong and L. A. Morrow (eds.), Handbook of Medical Neuropsychology, https://doi.org/10.1007/978-3-030-14895-9_32 697