Abstract
Neurocognition is a key factor in the development and maintenance of Substance Use Disorders (SUD). However, there are still several aspects that need to be studied in this area. In this study, we elucidate the influence of age of onset of substance use (OSU) on the clinical course and neuropsychological performance of substance use disorder (SUD) patients, as well as to explore the influence of years of education, duration of drug use and premorbid intelligence quotient (IQ) on the cognitive results obtained. An exhaustive neuropsychological battery was used to assess different cognitive domains in 80 male polyconsumers, 41 with earlier OSU (16 years or before: OSU ≤ 16) and 39 with later OSU (17 years or later: OSU ≥ 17). The patients were under treatment with at least 4 months of abstinence confirmed by urinalysis. The OSU ≤ 16 group presented a worse clinical state, as well as a lower premorbid IQ and worse performance in processing speed, visual perception and planning skills. The duration of drug use may account for the differences in planning and processing speed. In this work we discuss the premorbid or acquired nature of the cognitive deficits found.
Highlights
Neurocognition is a key factor in the development and maintenance of Substance Use Disorders (SUD)
This study examines, for the first time, the possible existence of clinical and neurocognitive differences in polydrug addicts depending on whether their substance use began at age or earlier, or at age or later
We assess the effect of age of onset, age, years of education, duration of drug use and premorbid intelligence quotient (IQ) on cognitive performance for the total sample
Summary
Neurocognition is a key factor in the development and maintenance of Substance Use Disorders (SUD). Despite the improvements in prevention and treatment of Substance Use Disorders (SUD), the world levels of consumption are significantly high[2] This may be partly due to the fact that several genetic and environmental factors intervene in the onset and maintenance of SUD3, which in turn causes a wide array of clinical symptomatology[4] and response to intervention[5]. Scarce but promising, indicate that incorporating cognitive rehabilitation in the treatment of addiction optimizes the results of traditional interventions[6,7] This is consistent with current models of development and maintenance of SUD where the role of biological and neurocognitive factors stands, in addition to environmental factors[3]. Patients to focus attention and direct their behavior to new and alternative goals which are incompatible with substance use-related behaviors[15]
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