For individuals quitting cocaine, methamphetamine, opioids, phencyclidine, and sed- ative, hypnotics, or anxiolytics, substance / medication-induced mild NCD of intermediate duration may occur in one-third or more, and there is some evidence that these substances may also be associated with persistent mild NCD. Major NCD associated with these sub- stances is rare, if it occurs at all. In the case of methamphetamine, cerebrovascular disease can also occur, resulting in diffuse or focal brain injury that can be of mild or major neu- rocognitive levels. Solvent exposure has been linked to both major and mild NCD of both intermediate and persistent duration.
The presence of NCD induced by cannabis and various hallucinogens is controversial.
With cannabis, intoxication is accompanied by various neurocognitive disturbances, but these tend to clear with abstinence.
Substance use disorders tend to commence during adolescence and peak in the 205 and 30s. Although longer history of severe substance use disorder is associated with greater likelihood of NCD, the relationships are not straightforward, with substantial and even complete recovery of neurocognitive functions being common among individuals who achieve stable abstinence prior to age 50 years. Substance/medication—induced major or mild NCD is most likely to become persistent in individuals who continue abuse of sub- stances past age 50 years, presumably because of a combination of lessened neural plas- ticity and beginnings of other age-related brain changes. Earlier commencement of abuse, particularly of alcohol, may lead to defects in later neural development (e.g., later stages of maturation of frontal circuitries), which may have effects on social cognition as well as other neurocognitive abilities. For alcohol-induced NCD, there may be an additive effect of aging and alcohol-induced brain injury.
Risk factors for substance/medication—induced NCDs include older age, longer use, and persistent use past age 50 years. In addition, for alcohol—induced NCD, long-term nutri— tional deficiencies, liver disease, vascular risk factors, and cardiovascular and cerebrovas- cular disease may contribute to risk.
Magnetic resonance imaging (MRI) of individuals with chronic alcohol abuse frequently reveals cortical thinning, white matter loss, and enlargement of sulci and ventricles. While neuroimaging abnormalities are more common in those with NCDs, it is possible to ob- serve NCDs without neuroimaging abnormalities, and vice versa. Specialized techniques (e.g., diffusion tensor imaging) may reveal damage to specific white matter tracts. Mag- netic resonance spectroscopy may reveal reduction in N-acetylaspartate, and increase in markers of inﬂammation (e.g., myoinositol) or white matter injury (e.g., choline). Many of cessful abstinence. In individuals with methamphetamine use disorder, MRI may also re— veal hyperintensities suggestive of microhemorrhages or larger areas of infarction.
Functional Consequences of SubstancelMedication-
The functional consequences of substance/medication—induced mild NCD are sometimes in many other NCDs. In addition, at both major and mild levels, substance/medication- induced NCDs may have associated motor syndromes that increase the level of functional impairment.
Individuals with substance use disorders, substance intoxication, and substance withdrawal are at increased risk for other conditions that may independently, or through a compounding effect, result in neurocognitive disturbance. These include history of traumatic brain injury and infections that can accompany substance use disorder (e.g., HIV, hepatitis C virus, syph- ilis). Therefore, presence of substance/medication—induced major or mild NCD should be differentiated from NCDs arising outside the context of substance use, intoxication, and with- drawal, including these accompanying conditions (e.g., traumatic brain injury).