title: Structural and metabolic brain changes in the striatum associated with methamphetamine abuse.
abstract: OBJECTIVE
  To review structural, chemical and metabolic brain changes, particularly those in the basal ganglia, in individuals who used methamphetamine, as well as in children with prenatal methamphetamine exposure.
  
  
  METHODS
  Magnetic resonance imaging (MRI) and positron emission tomography (PET) studies that evaluated brain structural, chemical and metabolite changes in methamphetamine subjects, or children with prenatal methamphetamine exposure, were reviewed and summarized. Relevant pre-clinical studies that provided insights to the interpretations of these imaging studies were also reviewed.
  
  
  RESULTS
  In adults who used methamphetamine, MRI demonstrates enlarged striatal volumes, while MR spectroscopy shows reduced concentrations of the neuronal marker N-acetylasparate and total creatine in the basal ganglia. In contrast, children with prenatal methamphetamine exposure show smaller striatal structures and elevated total creatine. Furthermore, PET studies consistently showed reduced dopamine transporter (DAT) density and reduced dopamine D(2) receptors in the striatum of methamphetamine subjects. PET studies also found lower levels of serotonergic transporter density and vesicular monoamine transporter (VMAT2) across striatal subregions, as well as altered brain glucose metabolism that correlated with severity of psychiatric symptoms in the limbic and orbitofrontal regions.
  
  
  CONCLUSIONS
  Neuroimaging studies demonstrate abnormalities in brain structure and chemistry convincingly in individuals who used methamphetamine and in children with prenatal methamphetamine exposure, especially in the striatum. However, many important questions remain and larger sample sizes are needed to validate these preliminary observations. Furthermore, longitudinal studies are needed to evaluate the effects of treatment and abstinence on these brain changes and to determine whether imaging, and possibly genetic, markers can be used to predict treatment outcome or relapse.
authors.affiliation: Department of Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. LChang@hawaii.edu
authors.forename: Linda
authors.initials: L
authors.lastname: Chang
authors.forename: Daniel
authors.initials: D
authors.lastname: Alicata
authors.forename: Thomas
authors.initials: T
authors.lastname: Ernst
authors.forename: Nora
authors.initials: N
authors.lastname: Volkow
mesh_terms: D000293:Adolescent; D000328:Adult; D019969:Amphetamine-Related Disorders / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D001479:Basal Ganglia / Q000187:drug effects* / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001927:Brain Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D000697:Central Nervous System Stimulants / Q000009:adverse effects*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008694:Methamphetamine / Q000009:adverse effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
chemical_list: D000697:Central Nervous System Stimulants; D008694:Methamphetamine; D005947:Glucose