Ipsilateral Cerebral Blood Flow Research Articles

Metabolic Diaschisis in Mild Traumatic Brain Injury.

Neurophysiological diaschisis presents in traumatic brain injury (TBI) as functional impairment distant to the lesion site caused by axonal neuroexcitation and deafferentation. Diaschisis studies in TBI models have evaluated acute phase functional and microstructural changes. Here, in vivo biochemical changes and cerebral blood flow (CBF) dynamics following TBI are studied with magnetic resonance. Behavioral assessments, magnetic resonance spectroscopy (MRS), and CBF measurements on rats followed cortical impact TBI. Data were acquired pre-TBI and 1-3 h, 2-days, 7-days, and 14-days post-TBI. MRS was performed on the ipsilateral and contralateral sides in the cortex, striatum, and thalamus. Metabolites measured by MRS included N-acetyl aspartate (NAA), aspartate (Asp), lactate (Lac), glutathione (GSH), and glutamate (Glu). Lesion volume expanded for 2 days post-TBI and then decreased. Ipsilateral CBF dropped acutely versus baseline on both sides (-62% ipsilateral, -48% contralateral, p < 0.05) but then recovered in cortex, with similar changes in ipsilateral striatum. Metabolic changes versus baseline included increased Asp (+640% by Day 7 post-TBI, p < 0.05) and Lac (+140% on Day 2 post-TBI, p < 0.05) in ipsilateral cortex, while GSH (-67% acutely, p < 0.05) and NAA decreased (-50% on Day 2, p < 0.05). In contralateral cortex Lac decreased (-73% acutely, p < 0.05). Analysis of variance showed significance for Side (p < 0.05), Time after TBI (p < 0.05), and interactions (p < 0.005) for Asp, GSH, Lac, and NAA. Transient decreases of GSH (-30%, p < 0.05, acutely) and NAA (-23% on Day 2, p < 0.05) occurred in ipsilateral striatum with reduced GSH (-42%, p < 0.005, acutely) in the contralateral striatum. GSH was decreased in ipsilateral thalamus (-59% ipsilateral on Day 2, p < 0.05). Delayed increases of total choline were seen in the contralateral thalamus were noted as well (+21% on Day 7 post-TBI, p < 0.05). Both CBF and neurometabolite concentration changes occurred remotely from the TBI site, both ipsilaterally and contralaterally. Decreased Lac levels on the contralateral cortex following TBI may be indicative of reduced anaerobic metabolism during the acute phase. The timing and locations of the changes suggest excitatory and inhibitory signaling processes are affecting post-TBI metabolic fluctuations.

Characteristics of donor vessels and cerebral blood flow in the chronic phase after combined revascularization surgery for moyamoya disease

ObjectiveThis study aimed to analyze whether the development of donor vessels after combined revascularization surgery for moyamoya disease (MMD) is related to cerebral blood flow (CBF) changes. MethodsWe retrospectively reviewed the charts of 11 adult (12 hemispheres) and 13 pediatric (19 hemispheres) patients who underwent combined revascularization in our department. The total vessel cross-sectional area (TVA) was the sum of the cross-sectional areas of the superficial temporal, middle meningeal, and deep temporal arteries imaged using time-of-flight magnetic resonance angiography. The ipsilateral relative CBF (RCBF) on the brain surface in the craniotomy area was calculated by single-photon emission computed tomography. ΔTVA and ΔRCBF were defined as the preoperative and postoperative ratios of TVA and RCBF, and their correlations were analyzed in adult and pediatric patients. ResultsThe TVA and RCBF showed a significant increase after surgery, regardless of the age group. However, there was no significant correlation between ΔTVA and ΔRCBF in either the adult or pediatric groups. While the adult group exhibited significantly higher ΔRCBF values compared to the pediatric group (p < 0.01, r = −0.44), the ΔTVA values were higher in the pediatric group compared to the adult group (p = 0.06). ConclusionsIn the chronic phase after combined revascularization surgery for MMD, the development of measurable TVA of donor vessels does not necessarily correlate with an increase in CBF around the craniotomy area.

The Nociceptin/Orphanin FQ peptide receptor antagonist, SB-612111, improves cerebral blood flow in a rat model of traumatic brain injury.

Traumatic brain injury (TBI) affects more than 2.5 million people in the U.S. each year and is the leading cause of death and disability in children and adults ages 1 to 44. Approximately 90% of TBI cases are classified as mild but may still lead to acute detrimental effects such as impaired cerebral blood flow (CBF) that result in prolonged impacts on brain function and quality of life in up to 15% of patients. We previously reported that nociceptin/orphanin FQ (N/OFQ) peptide (NOP) receptor antagonism reversed mild blast TBI-induced vestibulomotor deficits and prevented hypoxia. To explore mechanisms by which the NOP receptor-N/OFQ pathway modulates hypoxia and other TBI sequelae, the ability of the NOP antagonist, SB-612111 (SB), to reverse TBI-induced CBF and associated injury marker changes were tested in this study. Male Wistar rats randomly received sham craniotomy or craniotomy + TBI via controlled cortical impact. Injury severity was assessed after 1h (modified neurological severity score (mNSS). Changes in CBF were assessed 2h post-injury above the exposed cortex using laser speckle contrast imaging in response to the direct application of increasing concentrations of vehicle or SB (1, 10, and 100µM) to the brain surface. TBI increased mNSS scores compared to baseline and confirmed mild TBI (mTBI) severity. CBF was significantly impaired on the ipsilateral side of the brain following mTBI, compared to contralateral side and to sham rats. SB dose-dependently improved CBF on the ipsilateral side after mTBI compared to SB effects on the respective ipsilateral side of sham rats but had no effect on contralateral CBF or in uninjured rats. N/OFQ levels increased in the cerebral spinal fluid (CSF) following mTBI, which correlated with the percent decrease in ipsilateral CBF. TBI also activated ERK and cofilin within 3h post-TBI; ERK activation correlated with increased CSF N/OFQ. In conclusion, this study reveals a significant contribution of the N/OFQ-NOP receptor system to TBI-induced dysregulation of cerebral vasculature and suggests that the NOP receptor should be considered as a potential therapeutic target for TBI.

3D doppler ultrasound imaging of cerebral blood flow for assessment of neonatal hypoxic-ischemic brain injury in mice.

Cerebral blood flow (CBF) acutely reduces in neonatal hypoxic-ischemic encephalopathy (HIE). Clinic studies have reported that severe CBF impairment can predict HIE outcomes in neonates. Herein, the present study uses a non-invasive 3D ultrasound imaging approach to evaluate the changes of CBF after HI insult, and explores the correlation between CBF alterations and HI-induced brain infarct in mouse pups. The neonatal HI brain injury was induced in postnatal day 7 mouse pups using the Rice-Vannucci model. Non-invasive 3D ultrasound imaging was conducted to image CBF changes with multiple frequencies on mouse pups before common carotid artery (CCA) ligation, immediately after ligation, and 0 or 24 hours after HI. Vascularity ratio of the ipsilateral hemisphere was acutely reduced after unilateral ligation of the CCA alone or in combination with hypoxia, and partially restored at 24 hours after HI. Moreover, regression analysis showed that the vascularity ratio of ipsilateral hemisphere was moderately correlated with brain infarct size 24 hours after HI, indicating that CBF reduction contributes to of HI brain injury. To further verify the association between CBF and HI-induced brain injury, a neuropeptide C-type natriuretic peptide (CNP) or PBS was intranasally administrated to the brain of mouse pups one hour after HI insult. Brain infarction, CBF imaging and long-term neurobehavioral tests were conducted. The result showed that intranasal administration of CNP preserved ipsilateral CBF, reduced the infarct size, and improved neurological function after HI brain injury. Our findings suggest that CBF alteration is an indicator for neonatal HI brain injury, and 3D ultrasound imaging is a useful non-invasive approach for assessment of HI brain injury in mouse model.

The preoperative focal cerebral blood flow status may be associated with slow flow in the bypass graft after combined surgery for moyamoya disease.

The aim of this study was to investigate the association between early postoperative slow flow in bypass grafts and preoperative focal cerebral blood flow (CBF) in patients who underwent combined surgery for moyamoya disease (MMD). The subjects were 18 patients (22 surgeries) who underwent single photon emission computed tomography (SPECT) before surgery. The CBF value of the middle cerebral artery territory was extracted from the SPECT data, and the value relative to the ipsilateral cerebellar CBF (relative CBF, or RCBF) was calculated. The association between RCBF and early postoperative slow flow in the bypass graft was investigated. In addition, the correlation between the revascularization effect and preoperative RCBF was analyzed. In four of 22 surgeries (18.2%), slow flow in the bypass graft was identified in the early postoperative period. Preoperative RCBF in the slow flow and patent groups was 0.86 ± 0.15 and 0.87 ± 0.15, respectively, with no significant difference (P = 0.72). The signal intensity of four slow-flowed bypasses was improved in all cases on magnetic resonance angiography images captured during the chronic phase (mean of 3.3 months postoperatively). The revascularization scores were 2 ± 0.82 and 2.1 ± 0.68 in the slow flow and patent groups, respectively, and did not differ significantly (P = 0.78). A significant correlation was not observed between preoperative RCBF and the revascularization effect. No significant association was observed between preoperative RCBF and early postoperative slow flow in bypass grafts in patients with MMD undergoing combined surgery. Given the high rate of improved depiction of slow-flowed bypass in the chronic postoperative phase, the conceptual significance of an opportune surgical intervention is to maintain CBF by supporting the patient's own intracranial-extracranial conversion function.

Sympathetic nervous system hyperactivity results in potent cerebral hypoperfusion in swine.

Cerebral vasospasm is a complex disease resulting in reversible narrowing of blood vessels, stroke, and poor patient outcomes. Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm. We sought to demonstrate that stimulation of SCG in swine can cause ipsilateral cerebral perfusion deficit similar to that of significant human cerebral vasospasm. Furthermore, we aimed to show that inhibition of SCG can block the effects of sympathetic-mediated cerebral hypoperfusion. SCG were surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT) and time-to-maximum (TMax). Syngo.via software was used to determine regions of interest and quantify perfusion measures. SCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p<0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p>0.05). In swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic mediated cerebral hypoperfusion.

Confirming subarachnoid hemorrhage induction in the endovascular puncture mouse model

Background and purposeExperimental studies of subarachnoid hemorrhage (SAH) using the endovascular perforation model routinely use either cerebral blood flow (CBF) or intracranial pressure (ICP) monitoring to confirm SAH induction. We designed this study to test the hypothesis that contralateral CBF is a better marker of SAH induction than ipsilateral CBF. MethodsSixty-eight adult C57BL/6J mice were subjected to endovascular perforation. Mice were monitored using laser Doppler (for relative CBF) or ICP probes. ResultsThe ipsilateral CBF significantly decreased prior to ICP rising. However, reduction of the CBF in the contralateral hemisphere occurred at the same time as the rise in ICP. When CBF is monitored on both hemispheres simultaneously, the drop in ipsilateral CBF precedes the drop in the contralateral CBF. ConclusionsThe most suitable method for confirming puncture and induction of SAH in the endovascular mouse model is by ICP. Monitoring the CBF of the contralateral hemisphere is also able to detect the moment of SAH induction, but is not able to distinguish SAH severity. However, monitoring the ipsilateral CBF is not satisfactory for determining induction of SAH.

Higher Cerebral Blood Flow Predicts Early Hematoma Expansion in Patients With Intracerebral Hemorrhage: A Clinical Study.

The early hematoma expansion of intracerebral hemorrhage (ICH) indicates a poor prognosis. This paper studies the relationship between cerebral blood flow (CBF) around the hematoma and hematoma expansion (HE) in the acute stage of intracerebral hemorrhage. A total of 50 patients with supratentorial cerebral hemorrhage were enrolled in this study. They underwent baseline whole-brain CTP within 6 h after intracerebral hemorrhage, and non-contrast CT within 24 h. Absolute hematoma growth and relative hematoma growth were calculated, respectively. A relative growth of Hematoma volume >33% was considered to be hematoma expansion. The Ipsilateral peri-edema CBF and Ipsilateral edema CBF were calculated by CTP maps in patients with and without hematoma expansion, respectively. In this study the incidence of hematoma expansion in the early stage of supratentorial cerebral hemorrhage was 32%; The CBF of the hematoma expansion group was higher than that of the patients without hematoma expansion (23.5 ± 12.5 vs. 15.1 ± 7.4, P = 0.004). After adjusting for age, gender, Symptom onset to NCCT and Baseline hematoma volume, ipsilateral peri-edema CBF was still an independent risk factor for early HE (or = 1.095, 95% CI = 1.01–1.19, P = 0.024). Here, we concluded that higher cerebral blood flow predicts early hematoma expansion in patients with intracerebral hemorrhage.

Relationship between cerebral hyperperfusion syndrome and the immediate change of cerebral blood flow after carotid artery stenting evaluated by single-photon emission computed tomography.

Cerebral hyperperfusion syndrome (CHS) is a critical complication after carotid artery stenting (CAS). However, few CAS studies have evaluated immediate and temporary changes in ipsilateral cerebral blood flow (CBF) quantitatively. The study was performed to evaluate immediate changes in CBF after CAS and subsequent CBF changes in patients with cerebral hyperperfusion (HP) using 123I-IMP SPECT. The subjects were 223 patients with chronic extracranial carotid artery stenosis who underwent CAS in our department between March 2010 and March 2020. Quantitative CBF and cerebrovascular reactivity to acetazolamide in the middle cerebral artery were assessed before CAS by 123I-IMP SPECT. CBF was also measured immediately after CAS by 123I-IMP SPECT. When HP was detected, CBF was measured again 3 and 7days after CAS. The median (interquartile range) ipsilateral quantitative CBF change after CAS was - 0.1% (- 9.5-8.2%), and the upper value of the 95% CI of the quantitative CBF change was 48.2%. Thus, we defined HP after CAS as an increase in quantitative CBF of > 48.2% compared with the preoperative value. Of 223 patients, 5 (2.2%) had HP, and 4 of these patients (80%) developed CHS. In the CHS patients, HP was maintained for about 3days and improved after about 7days. An immediate CBF increase of > 48.2% after CAS may lead to development of CHS. In CHS after CAS, HP persisted for about 1week and postoperative management may be required for at least 1week.

Non-invasive assessment of cerebral microvascular changes for predicting postoperative cerebral hyperperfusion after surgical revascularisation for moyamoya disease: an arterial spin labelling MRI study

Cerebral hyperperfusion syndrome (CHPS) can result after anastomotic surgery as the reperfusion is established in chronically ischemic cerebral territories in patients of moyamoya disease (MMD). In this study, we have evaluated the feasibility of arterial spin labelling (ASL) perfusion MRI to predict cerebral hyperperfusion syndrome based on changes of cerebral blood flow (CBF) after revascularisation surgery in patients of MMD. Our prospective study included 25 patients with MMD who underwent superficial temporal artery-middle cerebral artery (STA-MCA) bypass with or without dural/muscle synangiosis. ASL MRI was performed before and 1-7days after surgery. On the side planned for operation, 5-mm ROI circle was drawn on the predetermined regions in frontal lobe, temporal lobe, parietal lobe and basal ganglia in proximal and distal territories of MCA to calculate ipsilateral CBF values (CBFi). An attempt was made to select the same location on contralateral side (non-operative) (CBFc) for each measurement for calculation of hemispheric normalised CBF (nCBFh) ratios. To adjust for inter individual variation among MR imagers and CBF, additional regions of interest were drawn within the cerebellum (CBFcbl) for cerebellar CBF normalised ratios (nCBFCbl). Of the 25 patients (26 operated hemispheres), 5 patients showed significant immediate postoperative symptoms suggestive of CHPS. Based on our findings, sensitivity and specificity of ASL perfusion to detect CHPS were evaluated. ASL was found to have 47-100% sensitivity and 45-88% specificity to detect CHPS. We have tried to calculate the prevalence of CHPS in postoperative patients of moyamoya disease, which in our study ranged from 6.83 to 40.70%. Based on our results, we concluded that ASL perfusion is an appropriate alternative to standard nuclear medicine studies to monitor the changes in perfusion after STA-MCA bypass surgery in moyamoya patients. ASL MR perfusion can be used to identify changes in cerebral blood flow (CBF) for early detection of cerebral hyperperfusion syndrome in patients with otherwise normal conventional MRI sequences with very high sensitivity but moderate specificity.

Which repetitive transcranial magnetic stimulation modality affects vasomotor reactivity in healthy subjects and how long does it last?

Objectives The aim of our study was to evaluate the effects of low and high-frequency repetitive transcranial magnetic stimulation (rTMS) on hypoxia-induced changes in bilateral cerebrovascular reserve up to 24 h in the same individuals. Methods Right-handed ten healthy male individuals participated in the study. All participants had neither drug therapy nor a concomitant disease and none of them had a variation in the circle of Willis, intracranial stenosis, arteriovenous malformation, or aneurysm which may have an impact on transcranial doppler ultrasound (TCD) examination and transcranial magnetic stimulation (TMS) recording. Results There was a statistically significant difference in the breath‐holding index (BHI) between before and after 0, 15, 30 min after 1 Hz repetitive stimulation (p < 0.05). When applying 5 Hz repetitive stimulation there was no difference before and after BHI values (p > 0.05). There were no differences in bilateral, ipsilateral, or contralateral middle cerebral artery (MCA) mean cerebral blood flow velocity (CBFV) after low or high-frequency rTMS application (p > 0.05). Conclusion The main result of the study was that low-frequency rTMS reduced vasomotor reactivity (VMR) for the very first 30 min and then this effect disappears. And the high-frequency rTMS did not affect VMR at all. Significance The effect of rTMS on VMR may continue up to 30 min but then return to the baseline and can be used safely.

Endothelium-Targeted Deletion of microRNA-15a/16-1 Promotes Poststroke Angiogenesis and Improves Long-Term Neurological Recovery.

Angiogenesis promotes neurological recovery after stroke and is associated with longer survival of stroke patients. Cerebral angiogenesis is tightly controlled by certain microRNAs (miRs), such as the miR-15a/16-1 cluster, among others. However, the function of the miR-15a/16-1 cluster in endothelium on postischemic cerebral angiogenesis is not known. To investigate the functional significance and molecular mechanism of endothelial miR-15a/16-1 cluster on angiogenesis in the ischemic brain. Endothelial cell-selective miR-15a/16-1 conditional knockout (EC-miR-15a/16-1 cKO) mice and wild-type littermate controls were subjected to 1 hour middle cerebral artery occlusion followed by 28-day reperfusion. Deletion of miR-15a/16-1 cluster in endothelium attenuates post-stroke brain infarction and atrophy and improves the long-term sensorimotor and cognitive recovery against ischemic stroke. Endothelium-targeted deletion of the miR-15a/16-1 cluster also enhances post-stroke angiogenesis by promoting vascular remodeling and stimulating the generation of newly formed functional vessels, and increases the ipsilateral cerebral blood flow. Endothelial cell-selective deletion of the miR-15a/16-1 cluster up-regulated the protein expression of pro-angiogenic factors VEGFA (vascular endothelial growth factor), FGF2 (fibroblast growth factor 2), and their receptors VEGFR2 (vascular endothelial growth factor receptor 2) and FGFR1 (fibroblast growth factor receptor 1) after ischemic stroke. Consistently, lentiviral knockdown of the miR-15a/16-1 cluster in primary mouse or human brain microvascular endothelial cell cultures enhanced in vitro angiogenesis and up-regulated pro-angiogenic proteins expression after oxygen-glucose deprivation, whereas lentiviral overexpression of the miR-15a/16-1 cluster suppressed in vitro angiogenesis and down-regulated pro-angiogenic proteins expression. Mechanistically, miR-15a/16-1 translationally represses pro-angiogenic factors VEGFA, FGF2, and their receptors VEGFR2 and FGFR1, respectively, by directly binding to the complementary sequences within 3'-untranslated regions of those messenger RNAs. Endothelial miR-15a/16-1 cluster is a negative regulator for postischemic cerebral angiogenesis and long-term neurological recovery. Inhibition of miR-15a/16-1 function in cerebrovascular endothelium may be a legitimate therapeutic approach for stroke recovery.

Impact of cerebral blood flow changes due to arterial bypass surgery on cognitive function in adult patients with symptomatic ischemic moyamoya disease.

Some adult patients with moyamoya disease (MMD) undergoing revascularization surgery show an improvement or decline in cognition postoperatively. Revascularization surgery for ischemic MMD augments cerebral blood flow (CBF) and improves cerebral oxygen metabolism. However, cerebral hyperperfusion, which is a short-term, major increase in ipsilateral CBF that is much greater than the metabolic needs of the brain, sometimes occurs as a complication. Cerebral hyperperfusion produces widespread, minimal injury to the ipsilateral white matter and cortical regions. The aim of the present prospective study was to determine how changes in CBF due to arterial bypass surgery affect cognitive function in adult patients with symptomatic ischemic MMD and misery perfusion. Thirty-two patients with cerebral misery perfusion, as determined on the basis of 15O gas positron emission tomography, underwent single superficial temporal artery-middle cerebral artery (M4 in the precentral region) anastomosis. Brain perfusion single-photon emission computed tomography (SPECT) studies were performed preoperatively, on the 1st postoperative day, and 2 months after surgery. Neuropsychological tests were also performed preoperatively and 2 months after surgery. Postoperative neuropsychological assessments demonstrated cognitive improvement in 10 cases (31%), no change in 8 cases (25%), and decline in 14 cases (44%). Based on brain perfusion SPECT and symptoms, 10 patients were considered to have cerebral hyperperfusion syndrome, and all of these patients exhibited a postoperative decline in cognition. Relative precentral CBF on the 1st postoperative day was significantly greater in patients with postoperative cognitive decline (167.3% ± 15.3%) than in those with improved (105.3% ± 18.2%; p < 0.0001) or unchanged (131.4% ± 32.1%; p = 0.0029) cognition. The difference between relative precentral CBF 2 months after surgery and that before surgery was significantly greater in patients with postoperative cognitive improvement (17.2% ± 3.8%) than in those with no postoperative change (10.1% ± 2.4%; p = 0.0003) or with postoperative decline (11.5% ± 3.2%; p = 0.0009) in cognition. Cerebral hyperperfusion in the acute stage after arterial bypass surgery impairs cognitive function. An increase in CBF in the chronic stage without acute-stage cerebral hyperperfusion improves cognitive function in adult patients with symptomatic ischemic MMD and misery perfusion.

The effect of remote ischemic conditioning on blood coagulation function and cerebral blood flow in patients with aneurysmal subarachnoid hemorrhage.

To explore the effect of remote ischemic conditioning (RIC) on blood coagulation function and cerebral blood flow in patients with aneurysmal subarachnoid hemorrhage. According to inclusion and exclusion standards, from October 2017 to June 2018, 30 consecutive patients of aneurysmal subarachnoid hemorrhage admitted to Intensive Care Unit, Department of Neurosurgery at Xuanwu Hospital, were given remote ischemic conditioning 5 times intervention to each patient within 7days, and blood coagulation function testing, including prothrombin activity (PTA), prothrombin time (PT), activated partial prothrombin time (APTT), fibrinogen (Fib), D-dimer, and thromboelastogram (TEG, including R, K, Angle, MA, EPL, LY30, A, CI, G, and A30) were performed for each patient before and after the RIC intervention, as well as venous ultrasound monitoring before and after the RIC intervention for detection of deep vein thrombosis (DVT). Transcranial Doppler evaluation (TCD), including cerebral blood flow of bilateral ACA, MCA, PCA and intracranial segments of VA, as well as BA and the ratios of MCA cerebral blood flow/terminal segment of ipsilateral ICA cerebral blood flow, was performed before and after RIC intervention; and fresh infarction was evaluated by head CT or MRI recheck after RIC intervention. Thirty cases without RIC intervention of matched age, gender, and Hunt Hess grade with aneurysmal subarachnoid hemorrhage were selected to compare coagulation function and cerebral blood flow using TCD with RIC group. (1) Comparing the data before and after the RIC intervention, there was no significant difference for APTT, Fib, and D-dimer (P > 0.05), while PTA decreased and PT increased slightly after intervention as well as INR (P < 0.05) but all still in normal reference values. (2) Comparing the data before and after the RIC intervention, within TEG parameters, only the R value increased with significant difference (P< 0.05) but still in normal reference value, while K, Angle, MA, EPL, LY30, A, CI, G, and A30 had no significant difference (P > 0.05). (3) Comparing the data before and after the RIC intervention, DVT was not detected on the pressurized limbs of patients. (4) Comparing the data before and after the RIC intervention, the cerebral blood flow of bilateral MCA, L-ACA, L-VA, and BA increased (P < 0.05), while the elevation ranges were all in 25%, and the other parameters showed no significant difference. (5) Head CT or MRI showed no fresh cerebral infarction after the RIC intervention. (6) Compared with the group without RIC intervention, the coagulation function and the cerebral blood flow evaluated by TCD of the RIC group showed no statistical difference (P > 0.05) except APTT and D-dimer decreased after RIC but still in normal reference values. RIC showed no obvious effect on blood coagulation function and cerebral blood flow in patients with aneurysmal subarachnoid hemorrhage both after the intervention and compared with the non-intervention group. DVT was not detected on the pressurized limbs of patients and no fresh cerebral infarction was detected. This preliminary study confirmed the safety of RIC on blood coagulation function and cerebral blood flow in patients with aneurysmal subarachnoid hemorrhage, and the application of RIC on patients with aneurysmal subarachnoid hemorrhage needs further study to confirm and validate the safety and effectiveness.

Wide-area measurement-based supervision of the cerebral venous hemodynamic in a novel rat model

BackgroundTraumatic brain injury (TBI) includes primary and secondary injuries, while monitoring intracranial pressure (ICP) and cerebral blood flow (CBF) is conducive to improve the prognosis of patients. However, the function of cerebral venous in this process is still unclear. New methodAn acute epidural hematoma (AEDH) model was developed by placing a controllable micro balloon in the right epidural space of a rat. The laser speckle contrast imaging (LSCI) system was used to observe CBF in real time, while ICP was monitored simultaneously. And the stability of this model was examined by magnetic resonance imaging (MRI). ResultsThe blood perfusion rate (BPR) of venous was significantly negatively correlated with ICP. In the 100 μ L group, the ipsilateral cerebral venous and microcirculation blood flow significantly decreased. According to the gross observations and pathological results, ischemic brain injury was the most serious on this condition. Comparison with existing method(s)Modeling method is relatively simple, which effectively reduces the cost. The volume of the micro balloon is adjusted to simulate the volume of different size of hematomas. In addition, LSCI, as an advanced blood flow monitoring technology, has high sensitivity to detect subtle changes in CBF. ConclusionThis study successfully developed a stable and reproducible AEDH rat model. Based on this model, it is preliminarily demonstrated that local intracranial hypertension can cause cerebral venous return restriction, which is an indispensable factor leading to the aggravation of secondary brain injury.

Transcranial Optical Monitoring of Cerebral Hemodynamics in Acute Stroke Patients during Mechanical Thrombectomy

Introduction: Mechanical thrombectomy is revolutionizing treatment of acute stroke due to large vessel occlusion (LVO). Unfortunately, use of the modified Thrombolysis in Cerebral Infarction score (mTICI) to characterize recanalization of the cerebral vasculature does not address microvascular perfusion of the distal parenchyma, nor provide more than a vascular “snapshot.” Thus, little is known about tissue-level hemodynamic consequences of LVO recanalization. Diffuse correlation spectroscopy (DCS) and diffuse optical spectroscopy (DOS) are promising methods for continuous, noninvasive, contrast-free transcranial monitoring of cerebral microvasculature. Methods: Here, we use a combined DCS/DOS system to monitor frontal lobe hemodynamic changes during endovascular treatment of 2 patients with ischemic stroke due to internal carotid artery (ICA) occlusions. Results and Discussion: The monitoring instrument identified a recanalization-induced increase in ipsilateral cerebral blood flow (CBF) with little or no concurrent change in contralateral CBF and extracerebral blood flow. The results suggest that diffuse optical monitoring is sensitive to intracerebral hemodynamics in patients with ICA occlusion and can measure microvascular responses to mechanical thrombectomy.

Short-term external counterpulsation augments cerebral blood flow and tissue oxygenation in chronic cerebrovascular occlusive disease.

Background and purposeExternal counterpulsation improves cerebral perfusion velocity in acute stroke and may stimulate collateral artery growth. However, whether (non‐acute) at‐risk patients with high‐grade carotid artery disease may benefit from counterpulsation needs to be validated.MethodsTwenty‐eight patients (71 ± 6.5 years, five women) with asymptomatic unilateral chronic severe internal carotid artery stenosis (>70%) or occlusion were randomized to receive 20 min active counterpulsation followed by sham treatment or vice versa. Cerebral blood flow velocity (CBFV) (measured bilaterally by transcranial middle cerebral artery Doppler), tissue oxygenation index (TOI) (measured over the bilateral prefrontal cortex by near‐infrared spectroscopy) and cerebral hemodynamic parameters, such as relative pulse slope index (RPSI), were monitored.ResultsIpsilateral mean CBFV (ΔV mean +3.5 ± 1.2 cm/s) and tissue oxygenation (ΔTOI +2.86 ± 0.8) increased significantly during active counterpulsation compared to baseline, whilst the sham had little effect (ΔV mean +1.13 ± 1.1 cm/s; ΔTOI +1.25 ± 0.65). On contralateral sides, neither counterpulsation nor sham control had any effect on either parameter. During counterpulsation, early dynamic changes in ΔRPSI of the ipsilateral CBFV signal predicted improved tissue oxygenation during counterpulsation (odds ratio 1.179, 95% confidence interval 1.01–1.51), whilst baseline cerebrovascular reactivity to hypercapnia failed to show an association.ConclusionsIn patients with high‐grade carotid disease, ipsilateral cerebral oxygenation and blood flow velocity are increased by counterpulsation. This is a necessary condition for the stimulation of regenerative collateral artery growth and thus a therapeutic concept for the prevention of cerebral ischaemia. This study provides a rationale for further clinical investigations on the long‐term effects of counterpulsation on cerebral hemodynamics and collateral growth.

Carotid stenting for unilateral stenosis can increase contralateral hemispheric cerebral blood flow

BackgroundThe revascularization of carotid stenosis can increase ipsilateral cerebral blood flow (CBF). Occasionally, elevated CBF is also evident on the contralateral side, but this phenomenon is poorly understood.ObjectiveTo analyze retrospectively...

Modification to the Rice-Vannucci perinatal hypoxic-ischaemic encephalopathy model in the P7 rat improves the reliability of cerebral infarct development after 48 hours

BackgroundThe Rice-Vannucci model of hypoxic-ischaemic encephalopathy (HIE) has been associated with a high degree of variability with respect to the development of cerebral infarction and infarct lesion volume. For this reason, we examined the occurrence of communicational blood flow within the common carotid (CCA), internal (ICA), and external (ECA) carotid arteries following CCA occlusion as a source of variability in the model. New methodWe propose a novel modification to the Rice-Vannucci model, whereby both the CCA and ECA are permanently ligated; mitigating communicational blood flow. ResultsUsing magnetic resonance angiography, phase-contrast velocity encoding, and pulsed arterial spin labelling, the modified Rice-Vannucci model (CCA/ECA occlusion) was demonstrated to mitigate communicational blood flow, whilst significantly reducing ipsilateral hemispherical cerebral blood flow (CBF). Comparatively, the original Rice-Vannucci model (CCA occlusion) demonstrated anterograde and retrograde blood flow within the ICA and CCA, respectively, with a non-significant reduction in ipsilateral CBF. Furthermore, CCA/ECA occlusion plus hypoxia (8% O2/92% N2; 2.5h) resulted in 100% of animals presenting with an infarct (vs 87%), significantly larger infarct volume at 48h (18.5% versus 10.0%; p<0.01), reduced standard deviation (±10% versus ±15%), and significantly worsened functional outcomes when compared to CCA occlusion plus hypoxia. Comparison with existing methodWe compared a modified Rice-Vannucci model (CCA/ECA occlusion±hypoxia) to the commonly used Rice-Vannucci model (CCA occlusion±hypoxia). ConclusionThis study demonstrates that CCA/ECA occlusion in the Rice-Vannucci model of HIE reduces infarct volume variability by limiting communicational blood flow.

Rationale for graft selection in patients with complex internal carotid artery aneurysms treated with extracranial to intracranial high-flow bypass and therapeutic internal carotid artery occlusion.

OBJECTIVE After internal carotid artery (ICA) sacrifice without revascularization for complex aneurysms, ischemic complications can occur. In addition, hemodynamic alterations in the circle of Willis create conditions conducive to the formation of de novo aneurysms or the enlargement of existing untreated aneurysms. Therefore, the revascularization technique remains indispensable. Because vessel sizes and the development of collateral circulation are different in each patient, the ideal graft size to prevent low flow-related ischemic complications (LRICs) in external carotid artery (ECA)-middle cerebral artery (MCA) bypass with therapeutic ICA occlusion (ICAO) has not been well established. Authors of this study hypothesized that the adequate graft size could be calculated from the size of the sacrificed ICA and the values of MCA pressure (MCAP) and undertook an investigation in patients with complex ICA aneurysms treated with ECA-graft-MCA bypass and therapeutic ICAO. METHODS In the period between July 2006 and January 2016, 80 patients with complex ICA aneurysms were treated with ECA-MCA bypass and therapeutic ICAO. Preoperative balloon test occlusion (BTO) was performed, and the BTO pressure ratio was defined as the mean stump pressure/mean preocclusion pressure. Low flow-related ischemic complications were defined as new postoperative neurological deficits and ipsilateral cerebral blood flow reduction. Initial MCAP (iMCAP), MCAP after clamping the ICA (cMCAP), and MCAP after releasing the graft (gMCAP) were intraoperatively monitored. The MCAP ratio was defined as gMCAP/iMCAP. Based on the Hagen-Poiseuille law, the expected MCAP ratio ([expected gMCAP]/iMCAP) was hypothesized as follows: (1 - cMCAP/iMCAP)(graft radius/ICA radius)2 + (cMCAP/iMCAP). Correlations between the BTO pressure ratio and cMCAP/iMCAP, and between the actual and expected MCAP ratios, were evaluated. Risk factors for LRICs were also evaluated. RESULTS The mean BTO pressure ratio was significantly correlated with the mean cMCAP/iMCAP (r = 0.68, p < 0.0001). The actual MCAP ratio correlated with the expected MCAP ratio (r = 0.43, p < 0.0001). If the expected MCAP ratio was set up using the BTO pressure ratio instead of cMCAP/iMCAP (BTO-expected MCAP ratio), the mean BTO-expected MCAP ratio significantly correlated with the expected MCAP ratio (r = 0.95, p < 0.0001). During a median follow-up period of 26.1 months, LRICs were observed in 9 patients (11%). An actual MCAP ratio < 0.80 (p = 0.003), expected MCAP ratio < 0.80 (p = 0.001), and (M2 radius/graft radius)2 < 0.49 (p = 0.002) were related to LRICs according to the Cox proportional-hazards model. CONCLUSIONS Data in the present study indicated that it was important to use an adequate graft to achieve a sufficient MCAP ratio in order to avoid LRICs and that the adequate graft size could be evaluated based on a formula in patients with complex ICA aneurysms treated with ICAO.