Development Of Cerebral Hyperperfusion Research Articles

Delayed development of cerebral atrophy after cerebral hyperperfusion following arterial bypass for adult patients with ischemic moyamoya disease: supplementary analysis of a 5-year prospective cohort.

Adult patients with moyamoya disease (MMD) occasionally exhibit cerebral hyperperfusion after arterial bypass surgery, leading to persistent cognitive decline. The present supplementary analysis of a prospective 5-year cohort study aimed to determine whether cerebral hyperperfusion after arterial bypass surgery for adult patients with misery perfusion due to ischemic MMD causes cerebral atrophy, and whether the development of cerebral atrophy is related to persistent cognitive decline. In total, 31 patients who underwent arterial bypass surgery also underwent fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) and neuropsychological testing before surgery and at the end of a 5-year follow-up. The development of cerebral hyperperfusion and hyperperfusion syndrome after surgery was defined based on brain perfusion single-photon emission computed tomography (SPECT) findings and clinical symptoms. Univariate and multivariate logistic regression analyses of factors related to the development of cerebral atrophy on FLAIR MRI or cognitive decline on neuropsychological testing at the end of the 5-year follow-up were performed. Eleven patients (35%) developed cerebral atrophy in the frontal lobe where the superficial temporal artery was anastomosed. Cerebral hyperperfusion on brain perfusion SPECT (odds ratio [OR], 50.6; p = 0.0008) or cerebral hyperperfusion syndrome (OR, 41.8; p = 0.0026) was independently associated with the development of cerebral atrophy, and cerebral atrophy development was significantly associated with cognitive decline (OR, 47.7; p = 0.0010). Cerebral hyperperfusion after arterial bypass surgery for adult patients with misery perfusion due to ischemic MMD can cause cerebral atrophy related to persistent cognitive decline.

De Novo Cerebral Microbleeds and Cognitive Decline in Cerebral Hyperperfusion After Direct Revascularization for Adult Moyamoya Disease

ObjectivesAdult patients with moyamoya disease (MMD) occasionally develop cognitive decline due to cerebral hyperperfusion following direct revascularization surgery. However, how the hyperperfusion phenomenon contributes to declines in cognitive function remains unclear. The present supplementary analysis of a prospective study aimed to determine whether cerebral hyperperfusion following direct revascularization surgery for adult MMD with ischemic presentation and misery perfusion leads to development of de novo cerebral microbleeds (CMBs) and whether postoperative cognitive decline is related to these CMBs. Materials and MethodsIn total, 32 patients who underwent direct revascularization surgery also underwent T2*-weighted magnetic resonance imaging (T2*WI) and neuropsychological testing before and 2 months after surgery. Development of cerebral hyperperfusion and hyperperfusion syndrome following surgery was defined based on brain perfusion single-photon emission computed tomography (SPECT) findings and clinical symptoms. ResultsCerebral hyperperfusion on brain perfusion SPECT (95% confidence interval [CI], 1.1–10.8; p = 0.0175) or cerebral hyperperfusion syndrome (95%CI, 1.3–15.3; p = 0.0029) was significantly associated with postoperatively increased CMBs on T2*WI. Postoperatively increased CMBs were significantly associated with postoperative cognitive decline (95%CI, 1.8–20.4, p = 0.0041). For patients with cerebral hyperperfusion on brain perfusion SPECT, the incidence of postoperative cognitive decline was significantly greater in patients with than in those without postoperatively increased CMBs (p = 0.0294). ConclusionsCerebral hyperperfusion following direct revascularization surgery for adult MMD with ischemic presentation and misery perfusion contributes to the development of de novo CMBs and postoperative cognitive decline is related to these CMBs.

Prediction of Cerebral Hyperperfusion after Superficial Temporal Artery-Middle Cerebral Artery Anastomosis by Three-Dimensional-Time-of-Flight Magnetic Resonance Angiography in Adult Patients with Moyamoya Disease

Introduction: Superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis is an effective surgical procedure for adult patients with moyamoya disease (MMD) and is known to have the potential to prevent cerebral ischemia and/or hemorrhagic stroke. Cerebral hyperperfusion (CHP) syndrome is one of the serious complications of this procedure that can result in deleterious outcomes, such as delayed intracerebral hemorrhage, but the prediction of CHP before revascularization surgery remains challenging. The present study evaluated the diagnostic value of preoperative three-dimensional (3D)-time-of-flight (TOF) magnetic resonance angiography (MRA) for predicting CHP after STA-MCA anastomosis for MMD. Materials and Methods: The signal intensity of the peripheral portion of the intracranial major arteries, such as the anterior cerebral artery (ACA), MCA, and posterior cerebral artery (PCA) ipsilateral to STA-MCA anastomosis, on preoperative MRA was graded (0–2 in each vessel) according to the ability to visualize each vessel on 97 affected hemispheres in 83 adult MMD patients. Local cerebral blood flow (CBF) at the site of anastomosis was quantitatively measured by N-isopropyl-p-[¹²³I]-iodoamphetamine single-photon emission computed tomography 1 and 7 days after surgery, in addition to the preoperative CBF value at the corresponding area. Then, we investigated the correlation between the preoperative MRA score and the development of CHP. Results: The CHP phenomenon 1 day after STA-MCA anastomosis (local CBF increase over 150% compared with the preoperative value) was evident in 27 patients (27/97 hemispheres; 28%). Among them, 8 (8 hemispheres) developed CHP syndrome. Multivariate analysis revealed that the hemispheric MRA score (0–6), the summed ACA, MCA, and PCA scores for the affected hemisphere, was significantly associated with the development of CHP syndrome (p = 0.011). The hemispheric MRA score was also significantly correlated with the CHP phenomenon, either symptomatic or asymptomatic (p < 0.001). Conclusion: The signal intensity of the intracranial major arteries, including the ACA, MCA, and PCA, on preoperative 3D-TOF MRA may identify adult MMD patients at higher risk for CHP after direct revascularization surgery.

Preoperative prediction of cerebral hyperperfusion after carotid endarterectomy using middle cerebral artery signal intensity in 1.5-tesla magnetic resonance angiography followed by cerebrovascular reactivity to acetazolamide using brain perfusion single-photon emission computed tomography

Objective: The purpose of the present study was to determine whether the signal intensity of the middle cerebral artery (MCA) on preoperative 1.5-T magnetic resonance angiography (MRA) could identify patients at risk for hyperperfusion following carotid endarterectomy (CEA) as a clinical screening test and whether an additional measurement of preoperative cerebrovascular reactivity (CVR) to acetazolamide on brain perfusion single-photon emission computed tomography (SPECT) could increase the predictive accuracy for the development of hyperperfusion.Methods: In 301 patients, the signal intensity of the MCA ipsilateral to CEA on MRA was preoperatively graded according to the ability to visualize the MCA. For patients with reduced MCA signal intensity on the MRA study, CVR to acetazolamide was subsequently assessed using brain perfusion SPECT. Cerebral hyperperfusion was determined intraoperatively using transcranial regional cerebral oxygen saturation monitoring with near-infrared spectroscopy.Results: Preoperative reduced MCA signal intensity was significantly associated with the development of cerebral hyperperfusion (95% CI, 1.188-3.965; p = 0.0352). While the sensitivity and negative predictive value were 100% both for the preoperative MCA signal intensity alone and in combination with subsequent preoperative CVR to acetazolamide, the specificity and positive predictive value were significantly greater for the latter than for the former (p < 0.05).Conclusions: Signal intensity of the MCA on preoperative 1.5-T MRA identifies patients at risk for hyperperfusion following CEA as a clinical screening test. An additional measurement of preoperative CVR to acetazolamide increases the predictive accuracy for the development of hyperperfusion.

Preoperative Cerebral Hemodynamic Impairment and Reactive Oxygen Species Produced During Carotid Endarterectomy Correlate With Development of Postoperative Cerebral Hyperperfusion

The purpose of the present study was to determine whether preoperative cerebral hemodynamic impairment and reactive oxygen species produced during carotid endarterectomy (CEA) correlate with development of postoperative cerebral hyperperfusion. Concentrations of malondialdehyde-modified low-density lipoprotein (MDA-LDL), a biochemical marker of oxidative damage, were measured in serum samples obtained from 90 patients undergoing CEA for ipsilateral ICA stenosis (>70%). Serum samples were obtained from a venous catheter inserted into the ipsilateral jugular bulb before clamping of the internal carotid artery (ICA), 10 minutes after clamping of the ICA, and 5 and 20 minutes after declamping of the ICA. Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were also measured using single-photon emission computed-tomography before CEA. In addition, CBF was measured postoperatively. Hyperperfusion (CBF increase >100% compared with preoperative values) was observed immediately after CEA in 12 patients (13%). Logistic regression analysis demonstrated that reduced preoperative CVR (95% CIs, 1.053 to 1.453; P=0.0097) and an increase in MDA-LDL (calculated as a percentage of the preclamp values) after ICA declamping (95% CIs, 0.862 to 0.980; P=0.0098) were significantly associated with development of postoperative cerebral hyperperfusion among the variables tested. Ten of 11 patients with reduced preoperative CVR and increased MDA-LDL after ICA declamping developed post-CEA hyperperfusion, and 2 of these patients developed cerebral hyperperfusion syndrome. Both preoperative cerebral hemodynamic impairment and reactive oxygen species produced during surgery correlate with development of cerebral hyperperfusion after CEA.

Cerebral Hyperperfusion after Carotid Endarterectomy is Associated with Preoperative Hemodynamic Impairment and Intraoperative Cerebral Ischemia

The aim of this study was to investigate whether postoperative hyperperfusion is associated with preoperative cerebral hemodynamic impairment due to chronic ischemia and with acute cerebral ischemia during clamping of the internal carotid artery (ICA) during carotid endarterectomy (CEA). Transcranial cerebral oxygen saturation (SO2) was monitored intraoperatively using near-infrared spectroscopy in 89 patients undergoing CEA for ipsilateral ICA stenosis (>70%). Cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were also measured using single photon emission computed tomography (SPECT) before CEA. In addition, CBF was measured immediately after CEA and on the third postoperative day. Hyperperfusion (CBF increase>100% compared with preoperative values) was observed immediately after CEA in 10 of 18 patients (56%) with reduced preoperative CVR. Also, post-CEA hyperperfusion was observed in nine of 16 patients (56%) whose SO2 during clamping of the ICA decreased to less than 90% of the preclamping value. Logistic regression analysis showed that reduced preoperative CVR and reduced SO2 during ICA clamping were significant independent predictors of the development of hyperperfusion immediately after CEA. In fact, all patients with reduced preoperative CVR and reduced SO2 during ICA clamping developed post-CEA hyperperfusion, and two of these patients developed cerebral hyperperfusion syndrome. These data suggest that development of cerebral hyperperfusion after CEA is associated with preoperative hemodynamic impairment and intraoperative cerebral ischemia.