Postoperative Cerebral White Matter Damage Associated with Cerebral Hyperperfusion and Cognitive Impairment after Carotid Endarterectomy: A Diffusion Tensor Magnetic Resonance Imaging Study

Abstract

Background: Cerebral hyperperfusion after carotid endarterectomy (CEA), even when asymptomatic, often impairs cognitive function. However, conventional magnetic resonance (MR) imaging rarely demonstrates structural brain damage associated with postoperative cognitive impairment. MR diffusion tensor imaging (DTI) is potentially more sensitive for detection of white matter damage. Among the common parameters derived by DTI, fractional anisotropy (FA) is a marker of tract integrity, and mechanical disruption of axonal cylinders and loss of continuity of myelin sheaths may be responsible for reduced FA in white matter. The purpose of the present study was to determine whether postoperative cerebral white matter damage that can be detected by FA derived by DTI is associated with cerebral hyperperfusion after CEA and correlates with postoperative cognitive impairment. Methods: In 70 patients undergoing CEA for ipsilateral internal carotid artery stenosis (≥70%), cerebral blood flow (CBF) was measured using single-photon emission computed tomography (SPECT) before and immediately after CEA and on postoperative day 3. FA values in cerebral white matter were assessed using DTI before and 1 month after surgery. These values were normalized and analyzed using statistical parametric mapping 5. In each corresponding voxel in the pre- and postoperative normalized FA maps of each patient, a postoperative FA value minus a preoperative FA value was calculated, and a voxel with postoperatively reduced FA was defined based on data obtained from healthy volunteers. The number of voxels with postoperatively reduced FA was calculated and defined as the volume with postoperatively reduced FA. Neuropsychological testing, consisting of the Wechsler Adult Intelligence Scale Revised, the Wechsler Memory Scale and the Rey-Osterreith Complex Figure test, was also performed preoperatively and after the first postoperative month. Postoperative cognitive impairment on neuropsychological testing in each patient was defined based on data obtained from patients with asymptomatic unruptured cerebral aneurysms. Results: Post-CEA hyperperfusion on brain perfusion SPECT (CBF increase ≥100% compared with preoperative values) and postoperative cognitive impairment on neuropsychological testing were observed in 11 (16%) and 9 patients (13%), respectively. The volume with postoperatively reduced FA in cerebral white matter ipsilateral to surgery was significantly greater in patients with post-CEA hyperperfusion than in those without (p < 0.0001). This volume in cerebral white matter ipsilateral to surgery was also significantly associated with postoperative cognitive impairment (95% confidence interval, 1.559–8.853; p = 0.0085). Conclusions: Cerebral hyperperfusion after CEA results in postoperative cerebral white matter damage that correlates with postoperative cognitive impairment.

Preoperative Cerebral Oxygen Extraction Fraction Imaging Generated from 7T MR Quantitative Susceptibility Mapping Predicts Development of Cerebral Hyperperfusion following Carotid Endarterectomy

“…5 Moreover, several studies have found that post-CEA hyperperfusion, even when asymptomatic, causes slight but diffuse damage to the ipsilateral cerebral cortex and white matter. 3,6,7 This damage that occurs after CEA hyperperfusion is a principal cause of the postoperative cognitive impairment observed in 10% of patients following CEA. 3,6,7 Cerebrovascular autoregulatory mechanisms operate through dilation of precapillary resistance vessels that maintain CBF when reductions in cerebral perfusion pressure occur, and this is referred to as stage 1 ischemia.…”

Postoperative neurocognitive and psycho-emotional disorders in patients with internal carotid arteries atherosclerosis after carotid endarterectomy

“…Важной причиной послеоперационного снижения нейрокогнитивных функций считается синдром цере-бральной гиперперфузии, который может иметь место по-сле реконструкции брахицефальных артерий [2,47]. Ча-стота его развития, по данным разных авторов, составляет от 0,2 до 18% [2].…”

“…Ча-стота его развития, по данным разных авторов, составляет от 0,2 до 18% [2]. Синдром церебральной гиперперфузии обусловлен значительным повышением кровотока в бас-сейне стенозированной артерии, развивающимся после КЭ и превышающим метаболические потребности мозга [2,47]. T. Nanba и соавт.…”

“…T. Nanba и соавт. [47] при помощи МРТ фиксиро-вали структурные изменения белого вещества головного мозга в виде зон лейкоареоза, а с помощью пред-и после-операционного тестирования -нарушения когнитивных функций. Они отметили особую роль синдрома гиперпер-фузии головного мозга как причины нарушений когни-тивных функций у больных после операций на сонных артериях.…”

Changes of neurocognitive cerebral functions in patients after aortic arch and brachiocephalic arteries surgery (review)

“…T. Nanba и соавт. [27] при помощи МРТ фиксировали структурные изменения белого вещества ГМ в виде зон лейкоареоза, а с помощью пред-и послеоперационного тестирования -нарушения КФ. Они уделяли особое внимание синдрому гиперпер-фузии как причине нарушений КФ у пациентов сразу по-сле операции на сонных артериях.…”