Kim S E, Choi C W, Yoon B W, Chung J K, Roh J H, Lee M C, Koh C S
Department of Nuclear Medicine, Samsung Medical Center, Seoul, Korea.
J Nucl Med. 1997 Jan;38(1):14-9.
We studied 26 patients with a single supratentorial infarction using 99mTc-HMPAO SPECT and MRI to investigate the phenomenon of crossed-cerebellar diaschisis (CCD).
From the total single-photon emission counts obtained from each cerebellar hemisphere, the percent difference 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 their relationship with CCD.
A CCD was observed in 12 of the 26 patients (46%) with cerebral infarction. There was no significant correlation between SVD and delta %cbll or MVD and delta %cbll in the patients with cerebral infarction. There were no significant differences in SVD and MVD between the patients with and without CCD. The frequency of CCD was significantly higher in the patients whose infarctions were in the frontoparietal lobes or the deep middle cerebral artery territory, including the basal ganglia and internal capsule (11/19) than in the patients whose infarctions were in other regions (1/7) (p = 0.048). The severely hemiparetic patients had a higher frequency of CCD and 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 occurred 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 demonstrated the apparent clinical signs of cerebellar dysfunction.
The location rather than the extent and severity of the lesion may 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 corticopontocerebellar pathway at the supratentorial level.
我们使用99mTc-HMPAO单光子发射计算机断层扫描（SPECT）和磁共振成像（MRI）研究了26例幕上单发梗死患者，以探究交叉性小脑失联络（CCD）现象。
从每个小脑半球获得的总单光子发射计数中，计算对侧小脑半球（CCH）和同侧小脑半球（ICH）之间的百分比差异[δ%cbll =（CCH - ICH）/ ICH×100]。测量SPECT（SVD）和MRI体积缺损（MVD），以检查它们与CCD的关系。
26例脑梗死患者中有12例（46%）观察到CCD。脑梗死患者中SVD与δ%cbll或MVD与δ%cbll之间无显著相关性。有或无CCD的患者在SVD和MVD方面无显著差异。梗死位于额顶叶或大脑中动脉深部区域（包括基底节和内囊）的患者中CCD的发生率（11/19）显著高于梗死位于其他区域的患者（1/7）（p = 0.048）。重度偏瘫患者的CCD发生率高于轻度偏瘫或无偏瘫患者，且δ%cbll低于后者（发生率，5/5与6/18相比，p = 0.008；δ%cbll，-21.4%±3.8%与-8.3%±11.1%相比，p = 0.018）。然而，14例无偏瘫患者中有5例也出现了CCD，12例偏瘫患者中有5例未出现。所有CCD患者均未表现出明显的小脑功能障碍临床体征。
病变的位置而非范围和严重程度可能是脑梗死患者CCD发生及程度的主要决定因素。我们的结果还支持CCD是幕上水平皮质脑桥小脑通路中断的结果这一观点。
