Advances in the fields of neuropsychological assessment and neuroimaging have enormously expanded our knowledge about the profile and severity of cognitive deficits in patients with substance use disorders. Neuroscience studies have complemented this knowledge by revealing the neural adaptations induced by different substances (dopamine, glutamate, or serotonin) on specific cellular systems and by showing the structure and dynamics of brain systems, including frontostriatal systems and paralimbic networks involved in motivation and cognitive control.1,2
Typical cognitive deficits
Patients with substance use disorders have common cognitive impairments in frontal-executive control skill centers related to planning, working memory, inhibition, and decision making, as well as alterations in episodic memory, selective attention, and emotional processing.3 Moreover, certain drugs have more robust effects on particular cognitive functions3:
• Psychostimulants, on inhibition and flexibility
• Opiates, on planning and fluency
• Cannabis, on episodic memory
• Alcohol, on a wide range of executive functions as well as on visual-spatial and psychomotor skills
These deficits are not ubiquitous among patients with substance use disorders, and there is considerable variability in the degree of cognitive dysfunction depending on a number of drug use parameters, such as quantity, frequency, and duration of use. Heavier users typically display greater impairments. Greater quantity and longer duration of cocaine use are associated with poorer response inhibition and flexibility; longer duration of heroin use is associated with poorer flexibility; heavier cannabis use is linked to poorer episodic memory, working memory, and reasoning; and heavier alcohol use relates to poorer updating of information and less adaptive decision making.4
The causality of these deficits is still disputed, since a certain degree of cognitive dysfunction (linked to disinhibition) may preexist and be further exacerbated by drug exposure.5 Current neurobiological models assume that impulsivity (as a trait) may confer vulnerability for the onset and progression of substance use disorders, whereas prolonged exposure may induce relatively persistent deficits in memory, attention, and different executive functions (as a state).2,5 This evolution is mediated by neuroadaptations in the frontostriatal systems that provoke a transition from goal-directed (impulsive) toward outcome-detached (compulsive) behavior.6,7
Individual differences in genetic makeup (including genes involved in cognitive functioning or those involved in drug pharmacodynamics) and in rates of cognitive maturation and ageing are also thought to contribute to the differential impact of vulnerability as well as drug exposure in the cognitive status of patients with substance use disorders.8,9
Relevant to both causal pathways (vulnerability and neuroadaptations) is the neuropsychological concept of executive functions, which refers to a group of abilities involved in the production, monitoring, and readjustment of goal-directed behavior. Executive functions are directly involved in planning, updating of relevant information (working memory), control of prepotent inappropriate responses (inhibition), detection and correction of errors (flexibility), and adaptive decision making.10 They are also indirectly involved in successful encoding and retrieval of information (episodic memory), attentional control (sustained, selective, and dual attention), affective responsiveness, and self-awareness.11 Anatomically, they are tightly associated with the functioning of the frontostriatal systems.12
It is not surprising that study results have shown that patients with disorders related to different substances have common cognitive impairments in planning, working memory, inhibition, and decision making (core executive functions), as well as in episodic memory, selective attention, and emotional processing (executive function–related processes). Partial spontaneous recovery of cognitive function is manifest during abstinence, although different profiles of drug use and different cognitive skills are associated with different rates of recovery.3 However, certain skills, such as response inhibition, self-regulation, and decision making, are persistently impaired even after several months of abstinence.3,13
? Patients with substance use disorders have cognitive impairments in frontal-executive control skill centers related to planning, working memory, inhibition, and decision making, as well as in episodic memory, selective attention, and emotional processing.
? This article provides prevalence rates for cognitive dysfunction in individuals with substance-related disorders; profiles of cognitive dysfunction associated with the use of different psychoactive substances, including cannabis, psychostimulants, opiates, and alcohol; and data on the timing and rates of recovery of diverse cognitive deficits across abstinence. There are key recommendations for selection and appropriate administration of a brief cognitive screening battery to detect cognitive dysfunction secondary to substance abuse. Information on novel therapies to address cognitive dysfunction in individuals with substance-related disorders is supplied.
? Clinicians need to be mindful about and carefully screen for cognitive dysfunction in patients with substance-related disorders. They need to refer for thorough neuropsychological assessment and tailored rehabilitation therapies those patients with significant cognitive dysfunction.
Overall, the prevalence of executive deficits in inpatients with substance use disorders (abstinent for at least 3 months) is approximately 30% in patients with moderate to severe impairment and 70% in those with mild impairment, compared with demographically matched controls.13 It is noteworthy that these data were obtained after excluding drug users with other CNS pathologies (such as head injury).
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