Cerebral Cortex, Vol. 9, No. 7, 712-721,
October 1999
© 1999 Oxford University Press
Patterns of Age-related Shrinkage in Cerebellum and Brainstem Observed In Vivo Using Three-dimensional MRI Volumetry
Department of Neuroradiology and , 2 Department of Neurology, University of Tübingen, Hoppe Seyler-Strasse 3, 72076 Tübingen, Germany
This study investigates the time course and regional differences in age-related volume loss in cerebellum and brainstem. Threedimensional (3D) magnetic resonance imaging (MRI) volumetry was used to measure the volumes of 11 regions in the cerebellum and three regions in the brainstem in 48 healthy volunteers (age 19.8–73.1 years). Landmark-adjusted lattices were used to divide the cerebellum into three radial (lobules I–V = lingula/lobulus/culmen, lobules VI–VII = declive/folium/tuber, lobules VIII–X = pyramis/ uvula/nodulus) and three transverse subdivisions (vermis, medial, lateral hemisphere). The radial sectors extended laterally throughout the vermis and the medial hemisphere. The brainstem was divided into midbrain, metencephalon (pons and tegmentum pontis) and medulla. Total cerebellar volume marginally declined with age using a linear regression model. An exponential model better described the age dependency of total cerebellar volume. The curve predicted that the volume remained stable until age 50 years and declined thereafter. Volume loss in the cerebellar vermis was striking. Shrinkage in the medial hemisphere was markedly less and only the inferior sector showed a trendwise negative association with age. The lateral hemisphere was not affected by age. No age effects were found for total brainstem volume, metencephalon and medulla. Only the mid-brain showed a trend for age-related shrinkage. The mediolateral gradient of decreasing age effects is similar to the histological pattern of alcoholic cerebellar atrophy (although our subjects were non-alcoholics according to DSM-IIIR criteria and laboratory data) suggesting that a common factor is involved in both processes. In search for a cause of the regional vulnerability, vascular, functional, structural and molecular/genetic factors may be considered.
1 Present address: Division of Neurosciences Critical Care, Department of Neurology, Johns Hopkins University, 600 N. Wolfe Street, Meyer 8-140, Baltimore, MD 21287-7840, USA
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