Carolien Zeetsen

18 Substance–induced neurocognitive disorder What all substances have in common, is that they act directly on the reward system of the brain, which may result in brain changes that are sometimes irreversible (APA, 2013). Chronic substance (ab)use has acute and long–term effects on cognitive functioning. In the DSM–5 these effects are classified as either mild or major substance–induced Neurocognitive Disorders (NCD; APA, 2013), based on the severity of the cognitive decline from a previous level of performance. The cognitive sequelae can be present in various domains, including complex attention (e.g. sustained attention, divided attention, selective attention, processing speed), executive function (e.g. planning, decisionmaking, working memory, error correction, inhibition, mental flexibility), learning and memory (e.g. working memory, short–termmemory, long–term memory), language (e.g. expressive and receptive language, such as fluency, grammar and syntax), perceptual motor abilities (e.g. visual perception, visuo–construction, praxis, gnosis), and social cognition (e.g. recognition of emotions, theory of mind). As these effects vary per substance, both quantitatively and qualitatively, a brief summary of the evidence for the different substances is now provided. Alcohol In alcohol use disorder (AUD), it is estimated that about half of all patients seeking treatment have cognitive deficits (Rourke & Grant, 2009). In about 10% of cases these deficits are very severe, and also include for instance patients with Korsakoff’s Syndrome (KS). The effects of alcohol on cognitive performance have been widely studied, possibly because it is the most widely used legal drug. Mild NCD may be the result of the direct effects of long–term alcohol abuse, like the toxic actions of alcohol itself or the consequences of alcohol withdrawal, but also by indirect effects of alcohol use, such as thiamine deficiency or liver cirrhosis. Acute alcohol intoxication primarily acts upon rather specific neuropsychological functions associated with the prefrontal cortex, such as planning, verbal fluency, memory and complex motor control, both in experimental (Peterson et al., 1990) and naturalistic settings (Lyvers & Tobias–Webb, 2010). On the contrary, the effects of alcohol on cognitive functioning post–detoxification are diffuse across 12 cognitive domains (Stavro et al., 2013). After one to three weeks of abstinence, chronic alcohol use is associated with decrements in memory, visuospatial abilities and inhibition (van Holst & Schilt, 2011). After six months of abstinence, the most enduring deficits have been reported in the domains of visuospatial ability and decision making (Fernández– Serrano et al., 2011). Although partial and sometimes full recovery occurs after abstinence, effects may endure at least up to one year after abstinence (van Holst et al., 2011; Stavro et al., 2013; Crowe et al., 2020). On the extreme end of the alcohol–induced NCD–spectrum lies KS: a neuropsychiatric disorder that is caused by thiamine deficiency and mostly associated with chronic alcohol use (Arts et al., 2017). Well–known symptoms of KS include severe memory deficits, confabulations, apathy, disorders of affect, social–cognitive problems and impaired insight into the illness (Arts et al., 2017; Rensen et al., 2017).