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  • Author or Editor: Akira Ogawa x
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Kuniaki Ogasawara, Keiko Yamadate, Masakazu Kobayashi, Hidehiko Endo, Takeshi Fukuda, Kenji Yoshida, Kazunori Terasaki, Takashi Inoue and Akira Ogawa

Object. Cognitive impairment occurs in 20 to 30% of patients following carotid endarterectomy (CEA). The purpose of the present study was to determine whether postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing that procedure.

Methods. Cerebral blood flow (CBF) was measured using single-photon emission computerized tomography scanning before and immediately after CEA and on the 3rd postoperative day in 92 patients with ipsilateral internal carotid artery stenosis of 70% or greater. Hyperperfusion post-CEA was defined as a 100% increase or greater in CBF compared with preoperative values. Neuropsychological testing was also performed preoperatively and at the 1-, 3-, and 6-month follow-up examinations.

At the 1-month postoperative neuropsychological assessment, 11 patients (12%) displayed evidence of cognitive impairment. In addition, the incidence of postoperative cognitive impairment in patients with post-CEA hyperperfusion (seven [58%] of 12 patients) was significantly higher than that in patients without post-CEA hyperperfusion (four [5%] of 80 patients; p < 0.0001). A logistic regression analysis demonstrated that post-CEA hyperperfusion was the only significant independent predictor of postoperative cognitive impairment. Of the seven patients in whom post-CEA hyperperfusion and cognitive impairment were identified 1 month postoperatively, four (including three patients with hyperperfusion syndrome) remained cognitively impaired at the 3- and 6-month follow-up examinations.

Conclusions. Postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing CEA. Furthermore, the development of hyperperfusion syndrome is associated with the persistence of postoperative cognitive impairment.

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Kuniaki Ogasawara, Hirotsugu Yukawa, Masakazu Kobayashi, Chiaki Mikami, Hiromu Konno, Kazunori Terasaki, Takashi Inoue and Akira Ogawa

Object. The purpose of this study was to determine whether the preoperative measurement of acetazolamide-induced changes in cerebral blood flow (CBF), which is performed using single-photon emission computerized tomography (SPECT) scanning, can be used to identify patients at risk for hyperperfusion following carotid endarterectomy (CEA). In addition, the authors investigated whether monitoring of CBF with SPECT scanning after CEA can be used to identify patients at risk for hyperperfusion syndrome.

Methods. Cerebral blood flow and cerebrovascular reactivity (CVR) to acetazolamide were measured before CEA in 51 patients with ipsilateral internal carotid artery stenosis (≥ 70% stenosis). Cerebral blood flow was also measured immediately after CEA and on the 3rd postoperative day.

Hyperperfusion (an increase in CBF of ≥ 100% compared with preoperative values) was observed immediately after CEA in eight of 12 patients with reduced preoperative CVR. Reduced preoperative CVR was the only significant independent predictor of post-CEA hyperperfusion. Forty-three patients in whom hyperperfusion was not detected immediately after CEA did not exhibit hyperperfusion on the 3rd postoperative day and did not experience hyperperfusion syndrome. In two of eight patients in whom hyperperfusion occurred immediately after CEA, CBF progressively increased and hyperperfusion syndrome developed, but intracerebral hemorrhage did not occur. In the remaining six of eight patients in whom hyperperfusion was detected immediately after CEA, the CBF progressively decreased and the hyperperfusion resolved by the 3rd postoperative day.

Conclusions. Preoperative measurement of acetazolamide-induced changes in CBF, which is performed using SPECT scanning, can be used to identify patients at risk for hyperperfusion after CEA. In addition, post-CEA monitoring of CBF performed using SPECT scanning results in the timely and reliable identification of patients at risk for hyperperfusion syndrome.

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Koji Yoshida, Kuniaki Ogasawara, Hiroaki Saura, Hideo Saito, Masakazu Kobayashi, Kenji Yoshida, Kazunori Terasaki, Shunrou Fujiwara and Akira Ogawa

OBJECT

Cognitive function is often improved or impaired after carotid endarterectomy (CEA) for patients with cerebral hemodynamic impairment. Cerebral glucose metabolism measured using positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) correlates with cognitive function in patients with neurodegenerative diseases. The present study aimed to determine whether postoperative changes in cerebral glucose metabolism are associated with cognitive changes after CEA.

METHODS

In patients who were scheduled to undergo CEA for ipsilateral internal carotid artery (ICA) stenosis (≥ 70% narrowing), cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were assessed preoperatively using brain perfusion single-photon emission computed tomography (SPECT). CBF measurement using SPECT was also performed immediately after CEA. For patients with reduced preoperative CVR to acetazolamide in the cerebral hemisphere ipsilateral to surgery, cerebral glucose metabolism was assessed using FDG-PET before surgery and 3 months after surgery and was analyzed using 3D stereotactic surface projection. Neuropsychological testing was also performed preoperatively and 3 months postoperatively.

RESULTS

Twenty-two patients with reduced preoperative CVR to acetazolamide successfully underwent FDG-PET studies and neuropsychological testing before and after CEA. Seven, 9, and 6 patients were defined as showing improved, unchanged, and impaired postoperative cognition, respectively, based on the neuropsychological assessments. The cortical area with increased postoperative glucose metabolism was greater in patients with improved postoperative cognition than in those with unchanged (p < 0.001) or impaired (p < 0.001) postoperative cognition. The cortical area with decreased postoperative glucose metabolism was greater in patients with impaired postoperative cognition than in those with improved (p < 0.001) or unchanged (p < 0.001) postoperative cognition. All 7 patients with improved cognition exhibited postoperative hemispheric increases in glucose metabolism, while 5 of the 6 patients with impaired cognition exhibited postoperative hemispheric decreases in glucose metabolism. Brain perfusion SPECT revealed that the latter 6 patients experienced postoperative cerebral hyperperfusion, and 2 of the 6 patients exhibited cerebral hyperperfusion syndrome. The cortical area with decreased postoperative glucose metabolism in these 2 patients was greater than that in other patients.

CONCLUSIONS

Postoperative changes in cerebral glucose metabolism, as measured using FDG-PET, are associated with cognitive improvement and impairment after CEA.