Neuropsychological Consequences of Chronic Drug Use: Relevance to Treatment Approaches

Abstract

Heavy use of drugs impacts of the daily activities of individuals in these activities. Several groups of investigators have indeed documented changes in cognitive performance by individuals who have a long history of chronic drug use. In the case of marijuana, a wealth of information suggests that heavy long-term use of the drug may have neurobehavioral consequences in some individuals. In humans, heavy cocaine use is accompanied by neuropathological changes that might serve as substrates for cognitive dysfunctions. Similarly, methamphetamine users suffer from cognitive abnormalities that may be consequent to alterations in structures and functions. Here, we detail the evidence for these neuropsychological consequences. The review suggests that improving the care of our patients will necessarily depend on the better characterization of drug-induced cognitive phenotypes because they might inform the development of better pharmacological and behavioral interventions, with the goal of improving cognitive functions in these subsets of drug users.

Self‐reported cognitive scales in a US National Survey: reliability, validity, and preliminary evidence for associations with alcohol and drug use

“…The longitudinal ABCD study could determine the direction of effect between cognition and substance use/disorders, and if specific substances influence particular aspects of cognition by affecting specific areas of the developing brain. However, regardless of direction, poorer cognitive functioning negatively impacts daily life [4,5] and may cause lack of insight into one’s substance use as a source of problems, impeding treatment utilization [80,81] or decreasing the likelihood of effective treatment [1,3]. While abstinence or reduced substance use may partially improve cognition [69,82], future research should determine whether factors shown to protect against cognitive impairments in aging adults, e.g., healthy diet [83,84], physical activity [85], and intellectual activities [86], also protect against cognitive impairments in populations with difficulties in reducing substance use.…”

“…NESARC-III included 12 items from the Strategic Planning and Organization EFI sub-scales to provide brief assessment of domains with widely-established impairments among patients in treatment for substance use [3,6,7]. These subscales previously evidenced good reliability (α=.70 and .75, respectively [44]), and correlated as predicted to demographic characteristics, other cognitive measures, and psychological attributes [44,50,51].…”

“…Neuropsychological and neuroimaging evidence indicates impaired cognitive functioning in adult patients treated for substance use disorders (SUD) [1], potentially impacting their ability to utilize treatment [2,3] or function well in important interpersonal or occupational areas [4,5]. These cognitive impairments are associated with many substance disorders [6], including alcohol [7–10], cannabis [11–15], cocaine [16–24], and others [25–29].…”

On the necessity of translational cognitive-neurotoxicological research in methamphetamine abuse and addiction

“…This ultimately contributes to maintaining continuous drug-seeking behaviors (Cadet and Bisagno 2015), and thus indirectly enhances all of the toxicological effects of METH abuse. METH is often consumed for its effects which, among others, include increased energy levels and decreases in fatigue, increased psychomotor activity and alertness, anorectic effects, increases in sex drive, and euphoria.…”

“…METH is often consumed for its effects which, among others, include increased energy levels and decreases in fatigue, increased psychomotor activity and alertness, anorectic effects, increases in sex drive, and euphoria. Yet, irritability, agitation, risky sexual behaviors, (motor) stereotypies, psychosis, seizures, hyperthermia and other systemic effects are also common acute (side) effects of METH consumption (Panenka et al 2013;Cadet and Bisagno 2015;Chomchai and Chomchai 2015). Those effects are mainly attributed to increases in both central and peripheral monoaminergic signaling, with strong effects in the noradrenergic (NA) and dopaminergic (DA) systems (5-HT) (Schep et al 2010;Carvalho et al 2012).…”