Location of lesion determines motor vs. cognitive consequences in patients with cerebellar stroke.
Cerebellar lesions can cause motor deficits and/or the cerebellar cognitive affective syndrome (CCAS; Schmahmann's syndrome). We used voxel-based lesion-symptom mapping to test the hypothesis that the cerebellar motor syndrome results from anterior lobe damage whereas lesions in the posterolateral cerebellum produce the CCAS. Eighteen patients with isolated cerebellar stroke (13 males, 5 females; 20-66 years old) were evaluated using measures of ataxia and neurocognitive ability. Patients showed a wide range of motor and cognitive performance, from normal to severely impaired; individual deficits varied according to lesion location within the cerebellum. Patients with damage to cerebellar lobules III-VI had worse ataxia scores: as predicted, the cerebellar motor syndrome resulted from lesions involving the anterior cerebellum. Poorer performance on fine motor tasks was associated primarily with strokes affecting the anterior lobe extending into lobule VI, with right-handed finger tapping and peg-placement associated with damage to the right cerebellum, and left-handed finger tapping associated with left cerebellar damage. Patients with the CCAS in the absence of cerebellar motor syndrome had damage to posterior lobe regions, with lesions leading to significantly poorer scores on language (e.g. right Crus I and II extending through IX), spatial (bilateral Crus I, Crus II, and right lobule VIII), and executive function measures (lobules VII-VIII). These data reveal clinically significant functional regions underpinning movement and cognition in the cerebellum, with a broad anterior-posterior distinction. Motor and cognitive outcomes following cerebellar damage appear to reflect the disruption of different cerebro-cerebellar motor and cognitive loops.
Department of Psychology and Center for Behavioral Neuroscience, American University, Washington, DC, USA.
Catherine J
CJ
Stoodley
Ataxia Unit, Cognitive Behavioral Neurology Unit, Laboratory for Neuroanatomy and Cerebellar Neurobiology, Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Jason P
JP
MacMore
Center for Morphometric Analysis, Departments of Psychiatry and Neurology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
Nikos
N
Makris
Psychology Assessment Center, Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA.
Janet C
JC
Sherman
Ataxia Unit, Cognitive Behavioral Neurology Unit, Laboratory for Neuroanatomy and Cerebellar Neurobiology, Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Jeremy D
JD
Schmahmann
D000328:Adult; D000339:Affect; D000368:Aged; D002545:Brain Ischemia / Q000150:complications / Q000473:pathology; D002524:Cerebellar Ataxia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000523:psychology; D002526:Cerebellar Diseases / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology* / Q000523:psychology*; D003072:Cognition Disorders / Q000209:etiology / Q000473:pathology; D056344:Executive Function; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009043:Motor Activity; D000068079:Motor Disorders / Q000209:etiology / Q000473:pathology; D009483:Neuropsychological Tests; D020521:Stroke / Q000150:complications* / Q000473:pathology; D055815:Young Adult
Ataxia; Cerebellar cognitive affective syndrome; Cerebellum; Cognition; MRI; Stroke