serve NCDs without neuroimaging abnormalitie s, 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
these brain imaging changes and neurocogniti ve manifestations reverse following suc-
cessful abstinence. In individuals with meth amphetamine use disorder, MRI may also re-
veal hyperintensities suggestive of microhem orrhages or larger areas of infarction.
Functional Consequences of Substance/Medication-
Induced Major or Mild Neurocognitive Disorder
The functional consequences of substance/ medication-induced mild NCD are sometimes
augmented by reduced cognitive efficiency an d difficulty concentrating beyond that seen
in many other NCDs. In addition, at both major and mild levels, substance/medication-
induced NCDs may have associated motor syndro mes that increase the level of functional
impairment. 
Differential Diagnosis
Individuals with substance use disorders, substance intoxica tion, and substance withdrawal
are at increased risk for othe r conditions that may independently, or through a compounding
effect, result in neurocognitive  disturbance. These include hi story of traumatic brain injury
and infections that can accompany substance use disorder (e.g., HIV, hepatitis C virus, syph-
ilis). Therefore, presence of substance/medi cation-induced major or mild NCD should be
differentiated from NCDs arising outside the co ntext of substance use, intoxication, and with-
drawal, including these accompanying cond itions (e.g., traumatic brain injury).