Substance/Medication-Induced Major or Mild Neurocognitive Disorder 631
Development and Course
Substance use disorders tend to commence du ring adolescence and peak in the 20s and
30s. Although longer history of severe substa nce use disorder is associated with greater
likelihood of NCD, the relationships are not straightforward, with substantial and even
complete recovery of neurocognitive func tions being common among individuals who
achieve stable abstinence prior to age 50 ye ars. 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 becaus e of a combination of lessened neural plas-
ticity and beginnings of other age-related br ain 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 and Prognostic Factors
Risk factors for substance/medication-induced  NCDs include older age, longer use, and
persistent use past age 50 years. In additi on, for alcohol-induced NCD, long-term nutri-
tional deficiencies, liver disease, vascular r isk factors, and cardiovascular and cerebrovas-
cular disease may contribute to risk. 
Diagnostic Markers
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-