title: [Clinical and etiological study of crossed cerebellar diaschisis. Report of two cases].
abstract: With the great progress in the imaging technique of cerebro-cerebellar perfusion and metabolism, it has been revealed that supratentorial cerebrovascular disorders often cause some reduction of contralateral cerebellar blood flow and metabolism. The phenomenon, termed crossed cerebellar diaschisis (CCD), is interpreted to be brought about by transneuronal deactivation of cerebellum via the corticopontocerebellar pathway and usually not to accompanied by limb-incoordination. We have experienced 2 cases presenting ataxia clinically and CCD in positron emission tomography (PET) which are thought to be caused by the interruption of two distinctive neural pathways, the corticopontocerebellar and cerebellorubrothalamic pathways. Case 1 was a 34-year-old housewife with cerebral infarction which magnetic resonance imaging disclosed in the left parietal cortex and subcortical white matter. She showed mild right-sided hemiataxia featured by dysarthria, hypermetria, dysrhythmia, decomposition, dysdiadochokinesis and rebound phenomenon. Cheirooral syndrome, a hand-pronation sign and defects of combined sensation were present on the right but not accompanied by any disturbances of deep sensation. PET with 15O-labeled CO2 and O2 demonstrated the left frontoparietooccipital and contralateral cerebellar hypoperfusion and hypometabolism. Case 2 was a 69-year-old female suffering from aftereffects of old thalamic hemorrhage. Neurological examination revealed moderate degree of right-sided hemiataxia suggesting a cerebellar type of dysfunction like in case 1. Muscle power and sensory system were well-preserved. Brain CT revealed a small and restricted low density area in the left posterolateral thalamus indicating destruction of the Vim nucleus. PET study confirmed reduced blood flow and oxygen metabolism in the left thalamus and contralateral cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: S
authors.initials: S
authors.lastname: Hirai
authors.forename: M
authors.initials: M
authors.lastname: Morimatsu
authors.forename: H
authors.initials: H
authors.lastname: Kanai
authors.forename: Y
authors.initials: Y
authors.lastname: Mizuno
mesh_terms: D000328:Adult; D000368:Aged; D002526:Cerebellar Diseases / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D002531:Cerebellum / Q000000981:diagnostic imaging; D002540:Cerebral Cortex / Q000000981:diagnostic imaging; D002543:Cerebral Hemorrhage / Q000150:complications / Q000503:physiopathology; D002544:Cerebral Infarction / Q000150:complications* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D005260:Female; D006801:Humans; D013786:Thalamic Diseases / Q000150:complications / Q000503:physiopathology; D014055:Tomography, Emission-Computed