Postoperative Cortical Neural Loss Associated With Cerebral Hyperperfusion and Cognitive Impairment After Carotid Endarterectomy

Abstract

Background and Purpose-Although cerebral hyperperfusion after carotid endarterectomy (CEA) often impairs cognitive function, MRI does not always demonstrate structural brain damage associated with postoperative cognitive impairment. The purpose of the present study was to determine whether postoperative cortical neural loss, which can be detected by 123 I-iomazenil single-photon emission CT, is associated with cerebral hyperperfusion after CEA and whether it correlates with postoperative cognitive impairment. Methods-In 60 patients undergoing CEA for ipsilateral internal carotid artery stenosis (Ͼ70%), cerebral blood flow was measured using N-isopropyl-p-[ 123 I]-iodoamphetamine single-photon emission CT before and immediately after CEA and on the third postoperative day. The distribution of benzodiazepine receptor binding potential in the cerebral cortex was assessed using 123 I-iomazenil single-photon emission CT before and 1 month after surgery and was analyzed using 3-dimensional stereotactic surface projection. Neuropsychological testing was also performed preoperatively and at the first postoperative month. Results-Post-CEA hyperperfusion and postoperative cognitive impairment were observed in 9 patients (15%) and 8 patients (13%), respectively. Post-CEA hyperperfusion was significantly associated with postoperative hemispheric reduction of benzodiazepine receptor binding potential (95%

Selective Neuronal Loss in Ischemic Stroke and Cerebrovascular Disease

“…171 Therefore, in addition to the co-existing subcortical infarcts, SNL may contribute to the development of subtle poststroke cognitive impairment, depending on the degree of neuronal damage.…”

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.…”

“…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. 3,[8][9][10] However, the autoregulatory mechanism provides insufficient compensation for severe decreases in cerebral perfusion pressure, which then leads to decreased CBF, referred to as misery perfusion or stage 2 ischemia.…”

Changes in Cognitive Function After Carotid Endarterectomy in Older Patients: Comparison With Younger Patients

“…A recent study suggested that normalization of cerebral metabolism via improvements in cerebral hemodynamics after CEA may result in cognitive improvement as well as functional recovery of the neurotransmitter system. 5) Other investigators have hypothesized that cognitive impairment after CEA may result from three possible mechanisms 2,[6][7][8][9][11][12][13]18) : cerebral hemispheric hypoperfusion during ICA clamping, intraoperative gaseous and particulate emboli from the surgical site, and postoperative cerebral hyperperfusion. The present study showed no relationship between duration of ICA clamping or new ischemic lesions on postoperative diffusion-weighted imaging and postoperative cognitive change.…”