OBJECTIVE: In chronic stage of cerebral hemispheric infarction, contralateral cerebellar blood flow and metabolism are depressed, which is known as crossed cerebellar diaschisis (CCD). The present study was performed to elucidate (1) whether the diaschisis occurs in hyperacute stage of ischemic stroke when computed tomography (CT) scans is not able to identify infarction, and (2) which site of lesion in the cerebrum is responsible for the depression in contralateral cerebellar blood flow. METHODS: Single photon emission computed tomography was performed in 21 patients with middle cerebral artery (MCA) embolic infarction within 6 h of the onset (3.2+/-1.1 h, mean+/-S.D.). Regions of interest (ROIs) were symmetrically located in the cerebral hemispheres including cerebral cortex and subcortex, and in the cerebellar hemispheres. RESULTS: The side-to-side ratio of cerebellar blood flow ipsilateral to that contralateral to cerebral infarct was significantly increased compared with that in normal control (P<0.001), indicating that contralateral cerebellar blood flow was significantly depressed. In hyperacute stage, the ratio of cerebellar blood flow appeared to be associated with the ratio of cerebral blood flow in whole hemispheres (r=0.44, P<0.05), in anterior frontal lobe (r=0.44, P<0.05) and in anterior temporal lobe (r=0.58, P<0.01), but not in infarct areas (r=0.26, P=0.3). Stepwise regression analysis revealed that the ratios in cerebellar hemispheres were associated with those in anterior temporal lobe (multiple regression analysis, r=0.58, P<0.01). CONCLUSIONS: Crossed cerebellar diaschisis occurs at hyperacute stage of stroke of the MCA infarction. It may be related to the hypoperfusion in the anterior frontal and anterior temporal lobes of the cerebrum where regional blood flow is decreased by ischemic infarction per se or by ipsilateral hemispheric depression from infarct area (diaschisis mechanism).
OBJECTIVE: In chronic stage of cerebral hemispheric infarction, contralateral cerebellar blood flow and metabolism are depressed, which is known as crossed cerebellar diaschisis (CCD). The present study was performed to elucidate (1) whether the diaschisis occurs in hyperacute stage of ischemic stroke when computed tomography (CT) scans is not able to identify infarction, and (2) which site of lesion in the cerebrum is responsible for the depression in contralateral cerebellar blood flow. METHODS: Single photon emission computed tomography was performed in 21 patients with middle cerebral artery (MCA) embolic infarction within 6 h of the onset (3.2+/-1.1 h, mean+/-S.D.). Regions of interest (ROIs) were symmetrically located in the cerebral hemispheres including cerebral cortex and subcortex, and in the cerebellar hemispheres. RESULTS: The side-to-side ratio of cerebellar blood flow ipsilateral to that contralateral to cerebral infarct was significantly increased compared with that in normal control (P<0.001), indicating that contralateral cerebellar blood flow was significantly depressed. In hyperacute stage, the ratio of cerebellar blood flow appeared to be associated with the ratio of cerebral blood flow in whole hemispheres (r=0.44, P<0.05), in anterior frontal lobe (r=0.44, P<0.05) and in anterior temporal lobe (r=0.58, P<0.01), but not in infarct areas (r=0.26, P=0.3). Stepwise regression analysis revealed that the ratios in cerebellar hemispheres were associated with those in anterior temporal lobe (multiple regression analysis, r=0.58, P<0.01). CONCLUSIONS: Crossed cerebellar diaschisis occurs at hyperacute stage of stroke of the MCA infarction. It may be related to the hypoperfusion in the anterior frontal and anterior temporal lobes of the cerebrum where regional blood flow is decreased by ischemic infarction per se or by ipsilateral hemispheric depression from infarct area (diaschisis mechanism).
Authors: K M Kang; C-H Sohn; B S Kim; Y I Kim; S H Choi; T J Yun; J-h Kim; S-W Park; G J Cheon; M H Han Journal: AJNR Am J Neuroradiol Date: 2015-07-30 Impact factor: 3.825
Authors: D D M Lin; J T Kleinman; R J Wityk; R F Gottesman; A E Hillis; A W Lee; P B Barker Journal: AJNR Am J Neuroradiol Date: 2009-02-04 Impact factor: 3.825