Edith V Sullivan1, Ty Brumback2, Susan F Tapert3, Sandra A Brown4, Fiona C Baker5, Ian M Colrain5, Devin Prouty5, Michael D De Bellis6, Duncan B Clark7, Bonnie J Nagel8, Kilian M Pohl9, Adolf Pfefferbaum9. 1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California. Electronic address: edie@stanford.edu. 2. Department of Psychological Science, Northern Kentucky University, Highland Heights, Kentucky. 3. Department of Psychiatry, University of California, San Diego, La Jolla, California. 4. Department of Psychiatry, University of California, San Diego, La Jolla, California; Department of Psychology, University of California, San Diego, La Jolla, California. 5. Center for Health Sciences, SRI International, Menlo Park, California. 6. Healthy Childhood Brain Development Research Program, Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, North Carolina. 7. Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania. 8. Departments of Psychiatry and Behavioral Neuroscience, Oregon Health & Sciences University, Portland, Oregon. 9. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California; Center for Health Sciences, SRI International, Menlo Park, California.
Abstract
BACKGROUND: The cerebellum is a target of alcoholism-related brain damage in adults, yet no study has prospectively tracked deviations from normal cerebellar growth trajectories in adolescents before and after initiating drinking. METHODS: Magnetic resonance imaging tracked developmental volume trajectories of 10 cerebellar lobule and vermis tissue constituents in 548 no/low drinking youths age 12 to 21 years at induction into this 5-site, NCANDA (National Consortium on Alcohol and NeuroDevelopment in Adolescence) study. Over the 3- to 4-year longitudinal examination yielding 2043 magnetic resonance imaging scans, 328 youths remained no/low drinkers, whereas 220 initiated substantial drinking after initial neuroimaging. RESULTS: Normal growth trajectories derived from no/low drinkers indicated that gray matter volumes of lobules V and VI, crus II, lobule VIIB, and lobule X declined faster with age in male youths than in female youths, whereas white matter volumes in crus I and crus II and lobules VIIIA and VIIIB expanded faster in female youths than in male youths; cerebrospinal fluid volume expanded faster in most cerebellar regions of male youths than female youths. Drinkers exhibited accelerated gray matter decline in anterior lobules and vermis, accelerated vermian white matter expansion, and accelerated cerebrospinal fluid volumes expansion of anterior lobules relative to youths who remained no/low drinkers. Analyses including both alcohol and marijuana did not support an independent role for marijuana in alcohol effects on cerebellar gray matter trajectories. CONCLUSIONS: Alcohol use-related cerebellar growth trajectory differences from normal involved anterior lobules and vermis of youths who initiated substantial drinking. These regions are commonly affected in alcohol-dependent adults, raising the possibility that cerebellar structures affected by youthful drinking may be vulnerable to age-alcohol interactions in later adulthood.
BACKGROUND: The cerebellum is a target of alcoholism-related brain damage in adults, yet no study has prospectively tracked deviations from normal cerebellar growth trajectories in adolescents before and after initiating drinking. METHODS: Magnetic resonance imaging tracked developmental volume trajectories of 10 cerebellar lobule and vermis tissue constituents in 548 no/low drinking youths age 12 to 21 years at induction into this 5-site, NCANDA (National Consortium on Alcohol and NeuroDevelopment in Adolescence) study. Over the 3- to 4-year longitudinal examination yielding 2043 magnetic resonance imaging scans, 328 youths remained no/low drinkers, whereas 220 initiated substantial drinking after initial neuroimaging. RESULTS: Normal growth trajectories derived from no/low drinkers indicated that gray matter volumes of lobules V and VI, crus II, lobule VIIB, and lobule X declined faster with age in male youths than in female youths, whereas white matter volumes in crus I and crus II and lobules VIIIA and VIIIB expanded faster in female youths than in male youths; cerebrospinal fluid volume expanded faster in most cerebellar regions of male youths than female youths. Drinkers exhibited accelerated gray matter decline in anterior lobules and vermis, accelerated vermian white matter expansion, and accelerated cerebrospinal fluid volumes expansion of anterior lobules relative to youths who remained no/low drinkers. Analyses including both alcohol and marijuana did not support an independent role for marijuana in alcohol effects on cerebellar gray matter trajectories. CONCLUSIONS:Alcohol use-related cerebellar growth trajectory differences from normal involved anterior lobules and vermis of youths who initiated substantial drinking. These regions are commonly affected in alcohol-dependent adults, raising the possibility that cerebellar structures affected by youthful drinking may be vulnerable to age-alcohol interactions in later adulthood.
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