Significance of postoperative crossed cerebellar hypoperfusion in patients with cerebral hyperperfusion following carotid endarterectomy: SPECT study

被引:18
|
作者
Ogasawara, Kuniaki
Kobayashi, Masakazu
Suga, Yasunori
Chida, Kohei
Saito, Hideo
Komoribayashi, Nobukazu
Otawara, Yasunari
Ogawa, Akira
机构
[1] Iwate Med Univ, Cyclotron Res Ctr, Morioka, Iwate 0208505, Japan
[2] Iwate Med Univ, Dept Neurosurg, Morioka, Iwate 0208505, Japan
关键词
carotid endarterectomy; cerebral hyperperfusion; cognition; crossed cerebellar hypoperfusion; brain SPECT;
D O I
10.1007/s00259-007-0588-x
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Purpose Cerebral hyperperfusion after carotid endarterectomy (CEA) results in cerebral hyperperfusion syndrome and cognitive impairment. The goal of the present study was to clarify the clinical significance of postoperative crossed cerebellar hypoperfusion (CCH) in patients with cerebral hyperperfusion after CEA by assessing brain perfusion with single-photon emission computed tomography (SPECT). Methods Brain perfusion was quantitatively measured using SPECT and the [I-123]N-isopropyl-p-iodoamphetamine-autoradiography method before and immediately after CEA and on the third postoperative day in 80 patients with ipsilateral internal carotid artery stenosis (>= 70%). Postoperative CCH was determined by differences between asymmetry of perfusion in bilateral cerebellar hemispheres before and after CEA. Neuropsychological testing was also performed preoperatively and at the first postoperative month. Results Eleven patients developed cerebral hyperperfusion (cerebral blood flow increase of >= 100% compared with preoperative values) on SPECT imaging performed immediately after CEA. In seven of these patients, CCH was observed on the third postoperative day. All three patients with hyperperfusion syndrome exhibited cerebral hyperperfusion and CCH on the third postoperative day and developed postoperative cognitive impairment. Of the eight patients with asymptomatic hyperperfusion, four exhibited CCH despite resolution of cerebral hyperperfusion on the third postoperative day, and three of these patients experienced postoperative cognitive impairment. In contrast, four patients without postoperative CCH did not experience postoperative cognitive impairment. Conclusions The presence of postoperative CCH with concomitant cerebral hyperperfusion reflects the development of hyperperfusion syndrome. Further, the presence of postoperative CCH in patients with cerebral hyperperfusion following CEA suggests development of postoperative cognitive impairment, even when asymptomatic.
引用
收藏
页码:146 / 152
页数:7
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