Middle Cerebral Artery Flow Research Articles

PS-096 Feasibility And Safety Of Ductal Closure Using Amplatzer Pda Occluder Ado Iias In Newborn Less Than 2500 Grams

<h3>Objective</h3> To evaluate feasibility and safety of patent ductus arteriosus (PDA) occlusion in very low birth weight newborns &lt; 2500 g when surgery was indicated by PDA occluder under X ray and ultrasounds <h3>Methods</h3> After ultrasound evaluation and Ibuprofen treatment when required, significant haemodynamic PDA were defined by high flow in pulmonary artery branch &gt;45 cm/sec, absence or reverse flow in middle cerebral artery, renal and mesenteric arteries, left to right shunt, and DA diameter. Interventional catheterism was proposed as first option. Babies were anaesthetised with ketamine and sufenta. Femoral vein access by 4F Desilets. A catheter was positionned in descending thoracic aorta and the PDA II AS occluder positionned under horizontal X ray and ultrasound. Temperature was kept between 35.5 and 36°C along the procedure. <h3>Results</h3> Twelve newborns had a PDA closure. Mean weight was 1740 g (850–2480). The series started at the highest weight. Mean diameter of the duct was 3,3 mm (2,2–4) and length 6 (2–11). PDA ADO IISA used were 3 × 4(2) 4 × 2(1), 4 × 4(4), 4 × 6(2), 5 × 2(2) and 5 × 6(1). Two were repositioned. Mean duration of the entire procedure was 32 min (10–90). X ray exposure was 12 min (3–24) and dose 1,5 grey/cm2 (0.2–4). Two transitional paraprothetic shunts closed spontaneously after few days. One premature infant already in renal failure, died ten days later despite ductal closure. In the others the follow up showed improvement in cerebral and pulmonary blood flows without any haemodynamic problems such as observed after surgical procedures. <h3>Conclusion</h3> This preliminary series showed feasibility and safety when combining X-ray and US to close a PDA with PDA ADO IIAS.

Transcranial Doppler-based assessment of cerebral autoregulation in critically ill children during diabetic ketoacidosis treatment.

Impaired cerebral autoregulation may be associated with poor outcome in diabetic ketoacidosis. We examined change in cerebral autoregulation during diabetic ketoacidosis treatment. Prospective observational cohort study. Tertiary care children's hospital. Children admitted to the ICU with diabetic ketoacidosis (venous pH < 7.3, glucose > 300 mg/dL, HCO3 < 15 mEq/L, and ketonuria) constituted cases, and children with type I diabetes without diabetic ketoacidosis constituted controls. None. Between 2005 and 2009, 32 cases and 50 controls were enrolled. Transcranial Doppler ultrasonography was used to measure middle cerebral artery flow velocities, and cerebral autoregulation testing was achieved via tilt-table testing. Cases underwent two and controls underwent one cerebral autoregulation test. Cerebral autoregulation was quantified by the autoregulatory index (autoregulatory index < 0.4 = impaired and autoregulatory index 0.4-1.0 = intact autoregulation). The first autoregulation test was obtained early (time 1, 12-24 hr; median [interquartile range], 8 hr [5-18 hr]) during diabetic ketoacidosis treatment, and a second autoregulation test was obtained during recovery (time 2, 36-72 hr; median [ interquartile range], 46 hr [40-59 hr]) from time 0 (defined as time of insulin start). Cases had lower autoregulatory index at time 1 than time 2 (p < 0.001) as well lower autoregulatory index than control subjects (p < 0.001). Cerebral autoregulation was impaired in 40% (n = 13) of cases at time 1 and in 6% (n = 2) of cases at time 2. Five cases (17%) showed persistent impairment of cerebral autoregulation between times 1 and 2 of treatment. All control subjects had intact cerebral autoregulation. Impaired cerebral autoregulation was common early during diabetic ketoacidosis treatment. Although the majority improved during diabetic ketoacidosis treatment, 17% of subjects had impairment between 36 and 72 hours after start of insulin therapy. The observed impaired cerebral autoregulation appears specific to the diabetic ketoacidosis process in patients with type I diabetes.

Effects of extracranial carotid stenosis on intracranial blood flow.

The hemodynamic effects of extracranial carotid stenosis on intracranial blood flow are not well characterized. We sought to determine the impact of degree of stenosis, stenosis length, and residual lumen on intracranial blood flow in patients with extracranial carotid stenosis. Carotid stenosis patients who had undergone both vessel flow rate measurements using quantitative magnetic resonance angiography and digital subtraction angiography were examined. The impact of the anatomic measurements of the stenosis relative to ipsilateral internal carotid artery (ICA) flow and ipsilateral-to-contralateral middle cerebral artery (MCA) flow ratio were assessed. Forty-four patients (mean age, 67 years; 64% symptomatic) were included. Higher percentage stenosis and smaller residual lumen were associated with a significant decrease in ICA flow (P<0.01 and 0.04, respectively). On multivariate analysis, percentage stenosis remained as the primary predictor of ICA flow (P<0.001). MCA flow ratio was not significantly associated with percentage stenosis, stenosis length, or residual lumen. However, mean MCA flow ratio was significantly lower in symptomatic compared with asymptomatic patients (0.92 versus 1.22; P=0.001). In contrast, mean ICA flow ratio was similar among these 2 groups (0.55 versus 0.55; P=0.99). Percentage stenosis and residual lumen are significantly associated with ICA but not MCA flow, suggesting that local hemodynamic effects of carotid stenosis do not translate directly to distal vasculature, because intracranial flows can be maintained through collaterals. The lower MCA flow ratio in symptomatic patients highlights the potential importance of distal hemodynamics in symptomatic presentation.

Optimal dose of landiolol for preventing abrupt changes in both cardiac output and middle cerebral artery flow velocity after electroconvulsive therapy.

The purpose of this study was to examine the dose-dependent effects of landiolol on systemic hemodynamics, cardiac output, and cerebral artery blood flow. Eight patients undergoing electroconvulsive therapy (ECT) received 1 of the 3 drugs/doses (saline, 0.125 mg/kg of landiolol, 0.25 mg/kg of landiolol), in turn, for 3 ECT sessions, immediately after the administration of succinylcholine. In the case of 0.25 mg/kg of landiolol, heart rate, mean arterial pressure, and cardiac output remained unchanged throughout the study period.We believe that 0.25 mg/kg of landiolol may be suitable for preventing the increase in systemic hemodynamics, including cardiac output after ECT.

P05.15: Massive fetal subdural hemorrhage presented with elevated middle cerebral artery flow velocity and reverse end‐diastolic flow

<scp>P</scp>05.15: Massive fetal subdural hemorrhage presented with elevated middle cerebral artery flow velocity and reverse end‐diastolic flow

Influence of α-Stat and pH-Stat Blood Gas Management Strategies on Cerebral Blood Flow and Oxygenation in Patients Treated With Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrest

In patients treated with therapeutic hypothermia after out-of-hospital cardiac arrest, two blood gas management strategies are used regarding the PaCO2 target: α-stat or pH-stat. We aimed to compare the effects of these strategies on cerebral blood flow and oxygenation. Prospective observational single-center crossover study. ICU of University hospital. Twenty-one therapeutic hypothermia-treated patients after out-of-hospital cardiac arrest more than 18 years old without history of cerebrovascular disease were included. Cerebral perfusion and oxygenation variables were compared in α-stat (PaCO2 measured at 37 °C) versus pH-stat (PaCO2 measured at 32-34 °C), both strategies maintaining physiological PaCO2 values: 4.8-5.6 kPa (36-42 torr). Bilateral transcranial middle cerebral artery flow velocities using Doppler and jugular vein oxygen saturation were measured in both strategies 18 hours (14-23 hr) after the return of spontaneous circulation. Pulsatility and resistance indexes and cerebral oxygen extraction were calculated. Data are expressed as median (interquartile range 25-75) in α-stat versus pH-stat. No differences were found in temperature, arterial blood pressure, and oxygenation between α-stat and pH-stat. Significant differences were found in minute ventilation (p = 0.006), temperature-corrected PaCO2 (4.4 kPa [4.1-4.6 kPa] vs. 5.1 kPa [5.0-5.3 kPa], p = 0.0001), and temperature-uncorrected PaCO2 (p = 0.0001). No differences were found in cerebral blood velocities and pulsatility and resistance indexes in the overall population. Significant differences were found in jugular vein oxygen saturation (83.2% [79.2-87.6%] vs. 86.7% [83.2-88.2%], p = 0.009) and cerebral oxygen extraction (15% [11-20%] vs. 12% [10-16%], p = 0.01), respectively. In survivors, diastolic blood velocities were 25 cm/s (19-30 cm/s) versus 29 cm/s (23-35 cm/s) (p = 0.004), pulsatility index was 1.10 (0.97-1.18) versus 0.94 (0.89-1.05) (p = 0.027), jugular vein oxygen saturation was 79.2 (71.1-81.8) versus 83.3% (76.6-87.8) (p = 0.033), respectively. However, similar results were not found in nonsurvivors. In therapeutic hypothermia-treated patients after out-of-hospital cardiac arrest at physiological PaCO2, α-stat strategy increases jugular vein blood desaturation and cerebral oxygen extraction compared with pH-stat strategy and decreases cerebral blood flow velocities in survivors.

Decreased placental thickness and impaired Doppler indices in idiopathic polyhydramnios: a prospective case–control study

Objective: To evaluate placental thickness, Doppler velocimetry, biophysical profile and perinatal outcomes in pregnancies complicated by idiopathic polyhydramnios.Materials and methods: This prospective case–control study was conducted on 139 pregnant women, of these 70 patients with idiopathic polyhydramnios comprised the study group and 60 pregnant women comprised the control group. Risk factors recorded were; age, parity, body mass index (BMI), gestational weeks, amniotic fluid index (AFI), biophysical profiles (BPP), placental thickness, middle cerebral artery pulsatility index (MCA PI), umbilical artery Doppler velocimetry (Umb A S/D) values and perinatal outcomes.Results: Sixty-nine of the cases had mild-moderate (AFI: 250–450 mm) polyhydramnios (%98.5) and one of the cases had severe polyhydramnios (>450 mm) in study group. There was no statistically significant difference between the groups in terms of age, parity, BMI, gestational weeks, fetal birth weights and BPP (p > 0.05). Placental thickness, MCA PI and UA S/D values showed statistically significant difference between the groups (p < 0.05). The fetuses with lower placental thickness had lower scores of biophysical profile. There were negative correlations between placental thickness and AFI (r = −0.265), umbilical artery S/D and placental thickness (r = −0.212), MCA PI and AFI (r = −171, p = 0.44). However there was a positive correlation between AFI and umbilical artery Doppler values (r = 0.450).Conclusion: Idiopathic polyhydramnios is associated with decreased placental thickness, impaired uterine, umbilical and middle cerebral artery flow.

A computational model of the fetal circulation to quantify blood redistribution in intrauterine growth restriction.

Intrauterine growth restriction (IUGR) due to placental insufficiency is associated with blood flow redistribution in order to maintain delivery of oxygenated blood to the brain. Given that, in the fetus the aortic isthmus (AoI) is a key arterial connection between the cerebral and placental circulations, quantifying AoI blood flow has been proposed to assess this brain sparing effect in clinical practice. While numerous clinical studies have studied this parameter, fundamental understanding of its determinant factors and its quantitative relation with other aspects of haemodynamic remodeling has been limited. Computational models of the cardiovascular circulation have been proposed for exactly this purpose since they allow both for studying the contributions from isolated parameters as well as estimating properties that cannot be directly assessed from clinical measurements. Therefore, a computational model of the fetal circulation was developed, including the key elements related to fetal blood redistribution and using measured cardiac outflow profiles to allow personalization. The model was first calibrated using patient-specific Doppler data from a healthy fetus. Next, in order to understand the contributions of the main parameters determining blood redistribution, AoI and middle cerebral artery (MCA) flow changes were studied by variation of cerebral and peripheral-placental resistances. Finally, to study how this affects an individual fetus, the model was fitted to three IUGR cases with different degrees of severity. In conclusion, the proposed computational model provides a good approximation to assess blood flow changes in the fetal circulation. The results support that while MCA flow is mainly determined by a fall in brain resistance, the AoI is influenced by a balance between increased peripheral-placental and decreased cerebral resistances. Personalizing the model allows for quantifying the balance between cerebral and peripheral-placental remodeling, thus providing potentially novel information to aid clinical follow up.

Efficacy and dose-dependent safety of intra-arterial delivery of mesenchymal stem cells in a rodent stroke model.

Intra-arterial (IA) delivery of mesenchymal stem cells (MSCs) for acute ischemic stroke is attractive for clinical translation. However, studies using rat model of stroke have demonstrated that IA MSCs delivery can decrease middle cerebral artery (MCA) flow, which may limit its clinical translation. The goal of this study is to identify a dose of IA MSCs (maximum tolerated dose; MTD) that does not compromise MCA flow and evaluate its efficacy and optimal timing in a rat model of reversible middle cerebral artery occlusion (rMCAo). We sought to determine if there is a difference in efficacy of acute (1 h) versus sub-acute (24 h) IA MSCs treatment after rMCAo. Adult female Sprague-Dawley rats underwent rMCAo (90 min) and an hour later a single dose of MSCs (at de-escalating doses 1×106, 5×105, 2×105, 1×105 and 5×104) was given using IA route. MSCs were suspended in phosphate buffered saline (PBS) and PBS alone was used for control experiments. We measured the percent change in mean laser Doppler flow signal over the ipsilateral MCA in de-escalating doses groups to determine MTD. The results demonstrated that the lowering of IA MSC dose to 1×105 and below did not compromise MCA flow and hence an IA MSC dose of 1×105 considered as MTD. Subsequently, 1 h and 24 h after rMCAo, rats were treated with IA MSCs or PBS. The 24 h delivery of IA MSCs significantly improved neurodeficit score and reduced the mean infarct volume at one month as compared to control, but not the 1 h delivery. Overall, this study suggests that the IA delivery of MSCs can be performed safely and efficaciously at the MTD of 1×105 delivered at 24 hours in rodent model of stroke.

Interindividual relationships between blood pressure and cerebral blood flow variability (1184.11)

The relationships between blood pressure variability (BPV) and cerebral blood flow variability (CFV) are poorly understood. This study sought to characterize the interindividual characteristics between spontaneous BPV and CFV across individuals with intact cerebrovascular control. We analyzed blood pressure and flow velocity data from 105 healthy subjects. Spontaneously occurring fluctuations in mean arterial blood pressure (MAP) and middle cerebral artery flow velocity (MCAvmean; Transcranial Doppler ultrasound) were characterized using power spectral and transfer function analysis in the very low‐ (0.02‐0.07 Hz), low‐ (0.07‐0.20 Hz), and high‐frequency (0.20‐0.40 Hz) ranges. Across our study sample, MAP was a positive predictor of MCAvmean to varying degrees in all three frequency ranges (Very Low Frequency (R2= 0.088, P&lt; 0.01) Low Frequency (R2= 0.47, P&lt; 0.01), High Frequency (R2 = 0.55, P&lt; 0.01)). The increased predictive power of MAP for MCAvmean in higher frequencies demonstrates that BPV is a determinant of CFV. However, factors other than BPV are influential, especially in the very low frequencies. These results demonstrate that intermittent blood pressure, a clinical measurement predominantly representative of very low frequency BPV content, is an inadequate surrogate of cerebral perfusion variability.

Age‐related differences in carotid and cerebral blood flow regulation (1069.4)

Common carotid artery (CA) and middle cerebral artery (MCA) blood flow are controlled by multiple factors to ensure that the brain receives adequate blood supply. Additionally, CA arterial stiffness may affect blood flow regulation. The purpose of this study was to investigate the effect of cyclooxygenase (COX) inhibition on arterial stiffness and the relationship between CA and MCA blood flow in young (26±5y) and older (66±7y) adults to determine if aging modifies this relationship. While baseline CA flow and flow velocity were similar between groups, baseline MCA flow velocity was greater in young (59±6 cm/s) compared to older (40±4 cm/s) adults (p&lt;0.05). During COX inhibition, CA flow, CA flow velocity and MCA flow velocity decreased from baseline in young (∆: ‐116±35 mL/min, ‐6±1 cm/s, ‐23±5 cm/s; respectively) and older adults (∆: ‐153±40 mL/min, ‐5±1 cm/s, ‐11±2 cm/s; respectively). The association between CA flow velocity and MCA flow velocity was altered by COX inhibition (r=0.60 vs. r=0.15). β‐stiffness was higher in older compared to young adults (13±2 vs. 5±1 AU; p&lt;0.05). Among older adults, there was a trend for COX inhibition to increase β‐stiffness. Our results suggest that CA and MCA blood flow are regulated differently and that COX inhibition alters the correlation between CA and MCA blood flow. Therefore, it may be incorrect to assume that CA flow is a surrogate measurement for cerebral blood flow.

Effect of acute resistance exercise on carotid artery stiffness and cerebral blood flow pulsatility

Arterial stiffness is associated with cerebral flow pulsatility. Arterial stiffness increases following acute resistance exercise (RE). Whether this acute RE-induced vascular stiffening affects cerebral pulsatility remains unknown. Purpose: To investigate the effects of acute RE on common carotid artery (CCA) stiffness and cerebral blood flow velocity (CBFv) pulsatility. Methods: Eighteen healthy men (22 ± 1 yr; 23.7 ± 0.5 kg·m−2) underwent acute RE (5 sets, 5-RM bench press, 5 sets 10-RM bicep curls with 90 s rest intervals) or a time control condition (seated rest) in a randomized order. CCA stiffness (β-stiffness, Elastic Modulus (Ep)) and hemodynamics (pulsatility index, forward wave intensity, and reflected wave intensity) were assessed using a combination of Doppler ultrasound, wave intensity analysis and applanation tonometry at baseline and 3 times post-RE. CBFv pulsatility index was measured with transcranial Doppler at the middle cerebral artery (MCA). Results: CCA β-stiffness, Ep and CCA pulse pressure significantly increased post-RE and remained elevated throughout post-testing (p < 0.05). No changes in MCA or CCA pulsatility index were observed (p > 0.05). There were significant increases in forward wave intensity post-RE (p < 0.05) but not reflected wave intensity (p > 0.05). Conclusion: Although acute RE increases CCA stiffness and pressure pulsatility, it does not affect CCA or MCA flow pulsatility. Increases in pressure pulsatility may be due to increased forward wave intensity and not pressure from wave reflections.

RBC volume deficiency in patients with excessive orthostatic decrease in cerebral blood flow velocity

BackgroundOrthostatic intolerance (OI) is common but heterogeneous. There is a subgroup of OI patients who have excessive decrease in cerebral blood flow velocity (CBFV) of bilateral middle cerebral arteries (MCAs) during head-up tilt without systemic blood pressure change. This study evaluated the role of blood volume reduction in such patients. MethodsPatients with idiopathic OI who had excessive orthostatic decrease (>20% of the supine level) in mean CBFV of bilateral MCAs and who also received blood volume determination were collected. The chromium (51Cr) dilution method was used for red blood cell (RBC) volume determination in these patients. The blood volume was expressed as a percentage of the expected volume. These patients were further divided into two groups, those with postural tachycardia syndrome (POTS group) and those without (non-POTS group). The data of RBC volume were compared between the two groups. Besides, we used multivariate linear regression to evaluate the factors that predict RBC volume. ResultsTwenty-five patients (13 females, median age = 28 years) were enrolled in this study. Nine of these patients had POTS (5 females, median age = 26 years) and 16 did not (8 females, median age = 29.5 years). Compared with the expected volume, the RBC volume was significantly reduced in all patients (median = 82% of the expected volume). Moreover, the RBC volume was significantly lower in the POTS group than that in the non-POTS group (78% vs. 85% of the expected volume, p = 0.013). The orthostatic decrease of MCA flow velocity was 28.3% in the POTS group and 32.5% in the non-POTS group (p = 0.140). The orthostatic pulsatility index increment was 15.4% in the POTS group and 20.5% in the non-POTS group (p = 0.438). Moreover, basic demography and hemoglobin levels were not different between the two groups. After multivariate linear regression (dependent variables including age, sex, body surface, and groups), only the presence of POTS significantly predicted the RBC volume (p = 0.006). ConclusionThe results of our study indicated that low RBC volume may play an important role in the pathophysiology of OI in this group of patients. Moreover, its role seems even more relevant in patients with POTS than in those without. Further studies for mechanistic evaluation are needed in the future.

Abstract W P171: Intracranial Blood Flow Changes After Extracranial Carotid Stenting

Objectives: To determine the effects of extracranial carotid stenting on intracranial blood flow. Methods: Records of patients who underwent stenting for extracranial carotid stenosis at our institution between 2004-2012 and had flow rates obtained pre and post stenting using quantitative magnetic resonance angiography were retrospectively reviewed. Measurements of degree of stenosis, stenosis length, and residual lumen were made from cerebral angiography images. Results: 18 patients with complete anatomic and flow data were included. Mean age was 66 years with 61% presenting with symptomatic stenosis. Degree of stenosis ranged from 60% to 90%. Internal carotid artery (ICA) mean flow improved significantly post stenting from 174.9 +/- 83.6 mL/min to 250.7 +/- 91.2 mL/min ( P =0.011). Ipsilateral middle cerebral artery (MCA) flow, however, was not significantly altered post stenting (101.8 +/- 47.7 mL/min vs. 111.3 +/- 37.4 mL/min; P =0.15). Multiple regression analysis revealed that improvement in residual lumen, but not percentage stenosis (p=0.45) or stenosis length (p=0.992), is an independent predictor of increased change in ipsilateral ICA flow ( P =0.005). Degree of stenosis, stenosis length, residual lumen, and ICA flow post-stenting were not predictive of ipsilateral MCA flow ( P =0.65,0.37,0.25,0.79). The ratio of ipsilateral to contralateral ICA flow improved from 0.67 +/- 0.36 at baseline to 0.94 +/- 0.34 after stenting ( P =0.007). The ratio of ipsilateral to contralateral MCA flow was 1.08 +/- 0.59 at baseline, and was unchanged at 1.09 +/- 0.46 after stenting ( P =0.91). Conclusions: ICA flow compromise was evident in the setting of carotid stenosis, which improved by 43% on average post stenting. Improvement in residual lumen at the site of stenosis was the strongest predictor of increased flow, indicating that this parameter is the best indicator of a hemodynamically successful intervention. Unlike ICA flow, intracranial flow measured in the MCA was not significantly compromised at baseline compared to the contralateral hemisphere, nor significantly altered after stenting. This reflects compensatory intracranial collateral supply pre-stenting, which redistributes once the ipsilateral ICA is revascularized.

Abstract T P100: Effect of Carotid Endarterectomy on Cerebral Hemodynamics Using Quantitative Magnetic Resonant Angiography

Objective: To examine the effect of carotid endarterectomy (CEA) on cerebral hemodynamics using quantitative magnetic resonance angiography (QMRA). Methods: A total of 42 patients with severe carotid artery stenosis were studied (6 patients had asymptomatic stenosis). 6 of 42 patients had contralateral carotid artery occlusion. Pre- and post-op blood flow measurements of major cerebral arteries were performed using QMRA (NOVA,Vasol, Inc.). Results: Patients ranged from 39 to 85 (mean 66) years old, 17 female. Ipsilateral carotid artery flow was significantly increased after CEA, 253 ± 110 ml/min compare to 159 ± 79 ml/min (p&lt;0.001). Middle cerebral artery (MCA) flow was not significantly increased (p=0.11), 127 ± 39 ml/min versus pre-op 115 ± 33 ml/min after CEA. Ipsilateral anterior cerebral artery (ACA) flow direction of 6 patients changed to anterograde, 5 patients’ ipsilatral posterior communicating artery (PCOM) flow direction changed to posterior, 1 patient had both flow direction of Ipilateral ACA and PCOM changed after CEA. Post-op Ipsilateral hemisphere flow (IHF), defined as the sum of MCA, ACA2, and PCA flows, was increased (p=0.05) from 220 ± 45 ml/min to 251 ± 83 ml/min. Conclusions: Carotid stenosis can result in ICA flow compromise, and CEA can increase the flow rate of the ipsilateral carotid artery significantly. However, the collateral capacity of the circle of Willis appears to be the more important determinant of Intracranial ipsilateral MCA flow.

Abstract W P217: The Impaired Leptomeningeal Collateral Flow Recruitment in the Type II Diabetic Mice is Independent of Hyperglycemia

Introduction: Previously we found that type II diabetic mice db/db strain exhibited impaired collateral flow recruitment between the middle cerebral artery (MCA) and anterior cerebral artery (ACA) vascular networks during MCA occlusion (MCAO)contributed to the worse stroke outcome when compared to their normoglycemic strain. However, it is unclear whether the underlying etiology in the diabetic stroke mice is attributed to hyperglycemia or other vascular pathology. Methods: Adult male db/+ received intraperitoneal injection of dextrose (HG) or normal saline (NG) (n=5-6/group), respectively, 60 minutes prior to distal MCAO. Doppler optical coherence tomography (DOCT) was used to quantify the MCA flow direction and velocity at baseline and 30 min after MCAO. The chosen regions of interest of MCA network were classified according to branching order as segment 1 (seg1), seg2 and seg3, with seg1 most proximal to ACA while most distal to MCA. 5-10 points corresponding to the same location of each segment were selected for quantification. Results: Blood glucose level was maintained at approximately 382± 83.8 mg/dl in the HG group during blood flow imaging, compared to 166± 60.1 mg/ml in the NG group. It fell to 141± 36.3 mg/dl and 142± 46.3 mg/dl at 24h after stroke in both groups. Hyperglycemia didn't change baseline flow velocity (NG: 6.8±0.8/9.2±0.7/12.5±0.5mm in seg1/seg2/seg3; HG: 5.7±0.7/8.2±0.5/12.6±0.9 mm/s, NS in all segments). At 30 min after MCAO, collateral flow was induced in both groups and there was no significant difference in flow velocity between groups (NG: -3.8±0.3/-2.7±0.1/-2.7±0.3mm/s; HG: -4.1±0.2/-3.1±0.3/2.2±0.4mm/s, NS in all segments). There was also no significant difference in vessel diameter between the groups both at baseline (NG: 48.9±3.5/55.1±1.6/61.5±2.7μm; HG: 45.6±1.7/48.8±2.7/59.2±2.7μm, NS in all segments) and 30 min after MCAO (NG: 48.4±2.0/50.8±2.6/55.5±2.6μm, HG: 42.6±2.3/49.9±2.0/52.5±2.6 μm in HG, NS in all segments). Conclusions: Temporary induction of hyperglycemia doesn't affect collateral flow in normoglycemic mice during acute stroke, suggesting that the observed impairment of collateral flow recruitment in the type II diabetic mice is likely attributed to chronic vascular pathology.

Trapping of Endovascular Microguidewire: A Rare and Serious Complication During Therapeutic Microcatheterization for Cerebrovascular Disease

A 71-year-old woman was admitted for endovascular treatment of a small but wide-necked aneurysm at the right middle cerebral artery (MCA) bifurcation. Our plan was to first apply a microcatheter protective technique, reserving stent protection as a fall-back strategy. Under general anesthesia, a 6F guiding catheter was thus advanced to the cervical segment of right internal carotid artery, followed by passage of an Excelsior SL-10 microcatheter (Boston Scientific, Natick, MA) into the superior division of MCA. At this point, a microcatheter of larger caliber (Prowler Select Plus, Codman, Miami Lakes, FL) was to replace the Excelsior SL-10, relying on a long microguidewire (Transend 300 Floppy, Boston Scientific) to effect the exchange. Unfortunately, the microwire became trapped during the exchange process and was impossible to readily advance or retrieve. Attempts at forcible withdrawal retracted the entire right cerebral artery, without releasing the wire. Furthermore, the M1 trunk was not visualized on angiography, and all tension on the microwire was released. This maneuver restored main MCA flow, but the superior division of MCA was still not visualized. We assumed that hyperacute vasospasm had intervened due to arterial perforation by the microguidewire. Introduction

Cerebral blood flow change during volatile induction in large-dose sevoflurane versus intravenous propofol induction: transcranial Doppler study.

BackgroundThe impact of volatile induction using large-dose sevoflurane (VI-S) on cerebral blood flow has not been well investigated. The present study compared the changes in cerebral blood flow of middle cerebral artery using transcranial Doppler (TCD) during VI-S and conventional induction using propofol.MethodsPatients undergoing elective lumbar discectomy were randomly allocated to receive either sevoflurane (8%, Group VI-S, n = 11) or target-controlled infusion of propofol (effect site concentration, 3.0 µg/ml; Group P, n = 11) for induction of anesthesia. The following data were recorded before and at 1, 2, and 3 min after commencement of anesthetic induction (T0, T1, T2, and T3, respectively): mean velocity of the middle cerebral artery (VMCA) by TCD, mean blood pressure (MBP), heart rate, bispectral index score (BIS) and end-tidal CO2 (ETCO2). Changes in VMCA and MBP from their values at T0 (ΔVMCA and ΔMBP) at T1, T2, and T3 were also determined.ResultsBISs at T1, T2 and T3 were significantly less than that at T0 in both groups (P < 0.05). ΔVMCA in Group VI-S at T2 and T3 (18.1% and 12.4%, respectively) were significantly greater than those in Group P (-7.6% and -19.8%, P = 0.006 and P < 0.001, respectively), whereas ETCO2 and ΔMBP showed no significant intergroup difference.ConclusionsVI-S using large-dose sevoflurane increases cerebral blood flow resulting in luxury cerebral flow-metabolism mismatch, while conventional propofol induction maintains cerebral flow-metabolism coupling. This mismatch in VI-S may have to be considered in clinical application of VI-S.

Hidden Dense Middle Cerebral Artery Sign in a 4-Year-Old Boy With Traumatic Subarachnoid Hemorrhage

A 4-year-old boy was admitted with acute onset of hemiplegia of the right side that was secondary to a traffic accident. Initial computed tomography revealed a traumatic subarachnoid hemorrhage, and follow-up computed tomography showed a more localized hematoma of the left sylvian cistern. After a few days of conservative treatment, magnetic resonance imaging (MRI) revealed a cerebral infarction of the left lenticulostriate territory, even though magnetic resonance angiography showed preserved middle cerebral artery flow. Thus, we realized that the hematoma of the sylvian cistern was the so-called dense middle cerebral artery sign. This case of posttraumatic infarction suggested the importance of meticulous investigations and clinical correlations of imaging studies in pediatric patients with head injuries.

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after subarachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypothermia on Doppler blood flow velocity after SAH. In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFV(MCA)) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFV(MCA) was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming. Hypothermia was induced on average 5 days after SAH (range 1-12) and maintained for 144 h (range 29-270). After hypothermia induction, MFV(MCA) decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFV(MCA) further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypothermia, MFV(MCA) remained unchanged after rewarming (65.6 ± 32.1 vs 70.3 ± 36.8 cm/s; p = 0.219). However, patients treated with hypothermia alone showed an increase in MFV(MCA) after rewarming (p = 0.016). Therapeutic hypothermia after SAH decreases Doppler blood flow velocity in both intracranial hypertension and DCI cases. The results can be the effect of hypothermia-related mechanisms or resolving cerebral vasospasm during prolonged hypothermia.