CROSSED-CEREBELLAR DIASCHISIS IN CEREBRAL INFARCTION - TECHNETIUM-99M-HMPAO SPECT AND MRI

Citation
Se. Kim et al., CROSSED-CEREBELLAR DIASCHISIS IN CEREBRAL INFARCTION - TECHNETIUM-99M-HMPAO SPECT AND MRI, The Journal of nuclear medicine, 38(1), 1997, pp. 14-19
Citations number
31
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
ISSN journal
01615505
Volume
38
Issue
1
Year of publication
1997
Pages
14 - 19
Database
ISI
SICI code
0161-5505(1997)38:1<14:CDICI->2.0.ZU;2-R
Abstract
We studied 26 patients with a single supratentorial infarction using T c-99m-HMPAO SPECT and MRI to investigate the phenomenon of crossed-cer ebellar diaschisis (CCD). Methods: From the total single-photon emissi on counts obtained from each cerebellar hemisphere, the percent differ ence between the contralateral (CCH) and ipsilateral (ICH) cerebellar hemispheres [Delta%(cbll) = (CCH-ICH)/ICH x 100] was calculated. Both SPECT (SVD) and MRI volume deficit (MVD) were measured to examine thei r relationship with CCD. Results: A CCD was observed in 12 of the 26 p atients (46%) with cerebral infarction. There was no significant corre lation between SVD and Delta%(cbll) or MVD and Delta%(cbll) in the pat ients with cerebral infarction. There were no significant differences in SVD and MVD between the patients with and without CCD. The frequenc y of CCD was significantly higher in the patients whose infarctions we re in the frontoparietal robes or the deep middle cerebral artery terr itory, including the basal ganglia and internal capsule (11/19) than i n the patients whose infarctions were in other regions (1/7) (p = 0.04 8). The severely hemiparetic patients had a higher frequency of CCD an d lower Delta%(cbll), than the patients with milder or no hemiparesis (frequency, 5/5 compared with 6/18, p = 0.008; Delta%(cbll), -21.4% +/ - 3.8% compared with -8.3% +/- 11.1%, p = 0.018). However, CCD also oc curred in 5 of the 14 patients without hemiparesis and was not seen in 5 of the 12 hemiparetic patients. None of the patients with CCD demon strated the apparent clinical signs of cerebellar dysfunction. Conclus ion: The location rather than the extent and severity of the lesion ma y be the major determinant for the occurrence and magnitude of CCD in patients with cerebral infarction. Our results also support the notion that CCD is a consequence of the interruption of the corticopontocere bellar pathway at the supratentorial level.