Anterior Cerebral Artery Velocity Research Articles

Effects of butylphthalide on cerebral vascular circulation, coagulation function, and neurological function in patients with acute severe ischemic stroke following intravenous thrombolysis: a preliminary study

Objective To analyze the effects of Butylphthalide on cerebral vascular circulation, coagulation function, and neurological function in patients with acute severe ischemic stroke following intravenous thrombolysis. Methods Clinical efficacy, cerebral vascular circulation indicators [anterior cerebral artery (ACA), middle cerebral artery (MCA), vertebral artery (VA) blood flow velocity], coagulation function indicators [prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (FIB)], neurological function indicators [Activities of Daily Living (ADL) score. Results The total effective rate of treatment in the control group was 76.47%, while in the observation group, it was 96.08%, with the observation group showing a significantly higher total effective rate than the control group (p < 0.05). Before treatment, there was no significant difference in ACA, MCA, and VA blood flow velocity between the two groups (p > 0.05). However, after treatment, the ACA, MCA, and VA blood flow velocity in the observation group were significantly higher than those in the control group (p < 0.05). Before treatment, there was no significant difference in PT, APTT, TT, and FIB levels between the two groups (p > 0.05). Conclusion In patients with acute severe ischemic stroke undergoing intravenous thrombolysis, the addition of Butylphthalide to the treatment regimen yields favorable clinical outcomes. Compared to Alteplase alone, the addition of Butylphthalide further improves cerebral vascular circulation and coagulation function, promoting the recovery and reconstruction of neurological function in patients. Importantly, the addition of Butylphthalide does not increase the risk of adverse reactions, making it a safe and ideal option for clinical application.

The influence of contralateral circulation on computational fluid dynamics of intracranial arteries: simulated versus measured flow velocities

BackgroundThis study aimed to retrospectively evaluate the influence of contralateral anterior circulation on computational fluid dynamics (CFD) of intracranial arteries, by comparing the CFD values of flow velocities in unilateral anterior circulation with the measured values from phase-contrast magnetic resonance angiography (PC-MRA).MethodsWe analyzed 21 unilateral anterior circulation models without proximal stenosis from 15 patients who performed both time-of-flight MRA (TOF-MRA) and PC-MRA. CFD was performed with the inflow boundary condition of a pulsatile flow of the internal carotid artery (ICA) obtained from PC-MRA. The outflow boundary condition was given as atmospheric pressure. Simulated flow velocities of the middle cerebral artery (MCA) and anterior cerebral artery (ACA) from CFD were compared with the measured values from PC-MRA.ResultsThe velocities of MCA were shown to be more accurately simulated on CFD than those of ACA (Spearman correlation coefficient 0.773 and 0.282, respectively). In four models with severe stenosis or occlusion of the contralateral ICA, the CFD values of ACA velocities were significantly lower (< 50%) than those measured with PC-MRA. ACA velocities were relatively accurately simulated in the models including similar diameters of both ACAs.ConclusionIt may be necessary to consider the flow condition of the contralateral anterior circulation in CFD of intracranial arteries, especially in the ACA.Relevance statementIncorporating the flow conditions of the contralateral circulation is of clinical importance for an accurate prediction of a rupture risk in Acom aneurysms as the bidirectional flow and accurate velocity of both ACAs can significantly impact the CFD results.Key points• CFD simulations using unilateral vascular models were relatively accurate for MCA.• Contralateral ICA steno-occlusion resulted in an underestimation of CFD velocity in ACA.• Contralateral flow may need to be considered in CFD simulations of ACA.Graphical

Relationship of cerebral blood volume with arterial and venous flow velocities in extremely low-birth-weight infants.

Unstable cerebral blood flow is theorised to contribute to the occurrence of intraventricular haemorrhage (IVH) in extremely low-birth-weight infants (ELBWIs), which can be caused by increased arterial flow, increased venous pressure, and impaired autoregulation of brain vasculature. As a preliminary step to investigate such instability, we aimed to check for correlations of cerebral blood volume (CBV), as measured using near-infrared spectroscopy, with the flow velocities of the anterior cerebral artery (ACA) and internal cerebral vein (ICV), as measured using Doppler ultrasonography.Data were retrospectively analysed from 30 ELBWIs uncomplicated by symptomatic patent ductus arteriosus, which can influence ACA velocity, and severe IVH (grade ≥ 3), which can influence ICV velocity and CBV. The correlation between tissue oxygen saturation (StO2) and mean blood pressure was also analysed as an index of autoregulation.CBV was not associated with ACA velocity; however, it was significantly correlated with ICV velocity (Pearson R = 0.59 [95% confidence interval: 0.29-0.78], P = 0.00061). No correlation between StO2 and mean blood pressure was observed, implying that autoregulation was not impaired. Conclusion:Although our findings are based on the premise that cerebral autoregulation was unimpaired in the ELBWIs without complications, the same result cannot be directly applied to severe IVH cases. However, our results may aid future research on IVH prediction by investigating the changes in CBV when severe IVH occurs during ICV velocity fluctuation. What is Known: • The pathogenesis of IVH includes unstable cerebral blood flow affected by increased arterial flow, increased venous pressure, and impaired cerebral autoregulation. • The approaches that can predict IVH are under discussion. What is New: • ACA velocity is not associated with CBV, but ICV velocity is significantly correlated with CBV. • CBV measured using NIRS may be useful in future research on IVH prediction.

The Frontal Bone Window for Transcranial Doppler Ultrasonography in Critically Ill Patients: Validation of a New Approach in the ICU

Background and ObjectiveThe temporal bone window (TBW) for transcranial Doppler (TCD) often fails to insonate the anterior cerebral artery (ACA). The frontal bone window (FBW) has never been evaluated in intensive care units (ICU). The main objective was to determine the ability of the FBW to assess ACA velocities in critically ill patients.MethodsA prospective study was conducted in two ICUs of the Montpellier University Hospital (France), between November 2014 and September 2016. Adult patients admitted to ICU for brain injury, with a Glasgow Coma Scale score ≤ 13, were enrolled within 3 days after admission. A first TCD examination was carried out bilaterally through the TBW and FBW by an intensivist expert in TCD, repeated by the same examiner, and 15 min later by an intensivist certified in TCD, designated as non-expert, blinded. The success of the FBW examinations was defined by the ability to measure the ACA velocities. Intra- and interobserver agreements were analyzed according to the Bland and Altman method.ResultsA total of 147 patients were analyzed. The FBW succeeded in insonating the ACA in 66 patients [45%, CI (37–53)], 45 bilaterally and 21 unilaterally. For 16 patients (11%), the FBW was the only way to measure ACA velocities. By combining the two techniques, the ACA success rate increased from 62% CI (54–70) to 73% CI (65–79) (P = 0.05). Intra- and interobserver mean biases and 95% limits of agreement for ACA systolic velocity measurements through the FBW were 1 (− 33 to 35) and 2 (− 34 to 38) cm s−1, respectively. For paired TBW and FBW measures of ACA velocities, mean biases (± SD) for ACA systolic, and mean and diastolic velocities were relatively close to zero, but negatives (− 7 ± 33, − 2 ± 19, − 1 ± 15 cm s−1, respectively), highlighting that ACA velocities were lower with the FBW (A2 segment) than TBW (A1 segment). The correlation coefficient for ACA systolic velocities measured by the FBW and TBW was R = 0.47, CI (0.28–0.62). No risk factors for failure of the FBW were identified.ConclusionsIn ICU, the FBW was able to insonate the ACA in 45% of patients admitted for brain injury, without the use of contrast agents. The FBW could improve the detection of ACA vasospasms.

A comprehensive analysis of the relationship between ACA velocities and ACA infarction following aneurysmal subarachnoid hemorrhage

PurposeTo evaluate the relationship between anterior cerebral artery (ACA) velocities (and ancillary parameters) and ACA infarction following aneurysmal subarachnoid hemorrhage (aSAH), and to examine the factors that influence velocities. MethodsRetrospective investigation of 500 consecutive aSAH patients. ACA mean velocities (Vm) were evaluated by daily transcranial ultrasound during the early (days 1–4) and late (days 5–20) periods posthemorrhage. Presence and timing of acute ACA infarctions were identified by serial retrospective review of cerebral computerized tomography (CT) scans. Predictors of ACA velocities were identified and compared to predictors of vasospasm and infarction from the literature. ResultsDecreased velocities on the day of infarction were observed in infarct-positive vessels when compared to infarct-negative vessels. ACA velocity increases, ipsilateral/contralateral ACA velocity ratios, and ACA velocity ranges, were inaccurate in anticipating infarction.Decreased ACA index velocities were moderately accurate in anticipating ACA infarction during the early [Vm<60cms/s], late [Vm<70cms/s] and overall [Vm<70cms/s] time periods. Decreased index velocities also independently predicted infarction during all time periods.ACA velocities were most consistently predicted by age, race, hemorrhage quantity on CT, and ACA/ACom (anterior communicating artery) aneurysm location. ConclusionsACA velocity increases and ancillary parameters do not relate to the development of infarction, whereas velocity decreases are moderately accurate in anticipating infarction. Predictors of velocity increases generally coincide with those of vasospasm, whereas predictors of velocity decreases coincide more with those of infarction following aSAH.

Cool head, hot brain: cerebral blood flow distribution during exercise

Cool head, hot brain: cerebral blood flow distribution during exercise

Transcranial Doppler Ultrasound Velocity, Cerebral Vasculopathy, and Silent Infarcts In Sickle Cell Disease

AbstractAbstract 269 Background:Approximately one-fourth of children with sickle cell disease (SCD), type SS, show evidence of cerebral ischemia on magnetic resonance imaging (MRI) without overt neurologic symptoms. Children with these silent infarcts have an increased risk of neuropsychological abnormalities and overt stroke. The pathophysiology of silent infarcts is unclear. Elevated transcranial Doppler ultrasound (TCD) velocities in the internal cerebral artery (ICA) and middle cerebral artery (MCA) are associated with an increased risk of overt stroke, but have not been associated previously with silent infarct. However, prior studies of silent infarcts failed to examine the association with anterior cerebral artery (ACA) vessel abnormalities, despite a predominantly frontal distribution of these infarcts. In addition, the relationship of magnetic resonance angiography (MRA) abnormalities to silent infarcts has not been extensively studied, although children with abnormal TCD velocity who also have stenosis or occlusion of vessels by MRA have the highest risk of overt stroke. We hypothesized that elevated ACA velocity and/or significant vasculopathy of the cerebral vessels demonstrated by MRA would be associated with a higher risk of silent stroke. Methods:A retrospective analysis of children followed at our Sickle Cell Center with SCD, type SS or Sb0-thalassemia was performed. Children with TCD (with ACA velocity) and brain MRI/A performed within a year of each other were included. TCD studies performed while on chronic transfusions were excluded. The last eligible MRI/TCD combination was used for patients who had multiple studies. Laboratory values obtained within a year of the MRI also were analyzed. Results:Of the 254 eligible subjects, 54% were male and the mean age was 10.6 ± 5.2 years. Silent infarcts were present in 78/254 (30.7%); the location was frontoparietal in 68%. The mean time-averaged mean of the maximal velocity (TAMMvel) of qualifying STOP vessels (MCA, bifurcation, and ICA) was 139±35cm/s, while the mean TAMMvel of the ACA was 117±34cm/s, which is 84% of the velocity of the other anterior vessels. As previously reported, TAMMvel inversely correlated with age (r=-0.40, p<0.0001) and hemoglobin concentration (r=-0.30, p<0.0001). There was no significant difference in TAMMvel in STOP qualifying vessels (MCA, bifurcation, DICA; 137cm/s vs. 145cm/s, p=0.08) among those with and without silent infarct. However, silent infarcts were associated with abnormal TAMMvel (≥200cm/s, 69/239 with normal/conditional vs. 9/15 with abnormal TAMMvel p=0.01) in these vessels. TAMMvel in the ACA was significantly higher (125 cm/s vs. 113 cm/s, p=0.004) in children with silent infarcts, and elevated ACA TAMMvel (≥170cm/s) was associated with silent infarcts (70/242 with normal vs. 8/12 with elevated velocity, p=0.006). No other single vessel velocity was significantly associated with silent infarct. Abnormal ICA/MCA TAMMvel was associated with stenosis of these vessels by MRA (p<0.001), and abnormal ACA velocities were associated with ACA stenosis by MRA (p<0.001). Further, stenosis by MRA in the ICA/MCA was associated with silent infarct (p<0.006) as were abnormalities of the ACA vessels (p=0.001). Conclusions:Unlike prior studies, we demonstrate a significant association between abnormal ICA/MCA velocity and silent infarcts. We also show an association between ACA velocity and silent infarct, which may in part be due to the predominantly frontoparietal distribution of these lesions. This, together with the association of MRA abnormalities of all three anterior vessels (ICA, MCA, ACA) with silent infarcts suggests a possible role of larger cerebral vessel vasculopathy in the pathophysiology of silent infarcts. This could be due to decreased distal blood flow related to the larger vessel narrowing, embolization of thrombus in larger vessels, or small vessel vasculopathy associated with larger vessel disease. However, mechanisms other than larger vessel vasculopathy are also likely to be involved given that silent infarcts occur in a substantial number of children without elevated TCD velocity or vasculopathy by MRA. Nonetheless, assessment of TCD velocity and MRA abnormalities may help provide information on risk assessment for CNS disease in children with SCD. Disclosures:No relevant conflicts of interest to declare.

Low superior vena cava flow on day 1 and adverse outcome in the very low birthweight infant

Background:Superior vena cava (SVC) flow assesses blood flow from the upper body, and may provide a reliable assessment of systemic blood flow.Aim:(i) To assess the relationship between SVC flow in...

Elevated blood flow velocity in the anterior cerebral artery and stroke risk in sickle cell disease: extended analysis from the STOP trial

Elevated velocity in the internal carotid artery (ICA) or middle cerebral artery (MCA), detected by transcranial Doppler (TCD) ultrasonography, predicts an increased risk of stroke in children with sickle cell disease (SCD). Although strokes also occur in an anterior cerebral artery (ACA) distribution, the significance of elevated velocity in this vessel has not been determined previously. We assessed the effect of elevated ACA velocity on stroke risk using the results of the first adequate TCD study performed on 1975 children as part of The Stroke Prevention Trial in Sickle Cell Anemia (STOP). Elevated ACA velocity (> or =170 cm/s) was associated with an increased risk of stroke (P = 0.0013) after adjusting for the ICA/MCA classification. Among subjects with normal ICA/MCA velocity, the risk of stroke was more than 10-fold greater in those with elevated compared with normal ACA velocity (2.13 and 0.20 per 100 patient-years, respectively, P < 0.001); risk more than doubled with elevated compared with normal ACA velocity in those already at high risk due to abnormal ICA/MCA findings (7.56 vs. 3.22 per 100 patient-years, P = 0.042). Few of the strokes in those with elevated ACA velocity occurred in an ACA distribution, suggesting changes in blood flow velocity in anterior vessels may be associated with diffuse arterial disease or, alternatively, manifest collateral flow from compromised middle cerebral vessels.

Transcranial Doppler sonography in chronic paroxysmal hemicrania.

Three patients with chronic paroxysmal hemicrania (CPH) (1 M, 2 F) and 9 healthy controls (8 M 1 F) were studied with transcranial Doppler (TCD) sonography. One patient who was studied during the spontaneous attacks hyperventilated markedly. Middle cerebral artery velocity (VMCA) was measured in the first attack, and anterior cerebral artery velocity (VACA) in the second attack, respectively. VMCA and VACA decreased bilaterally during attack. VMCA started to decrease at an early stage of the attack, i.e. prior to the major hyperventilation that was observed during the attack. VACA on the symptomatic side decreased less than that on the other side (P < 0.05). Cerebral vasomotor reactivity (VMR) was expressed as the percentage change in mean blood flow velocity as a function of end-tidal PCO2 (PETCO2) reduction induced by voluntary hyperventilation (delta V/delta PETCO2). In the 3 patients, a slightly lowered VMR was observed in the MCA and posterior cerebral artery on both sides, and in the ACA on the symptomatic side (P > 0.05) in comparison with controls. These observations may imply an abnormal vascular reactivity in CPH.

Cluster headache: transcranial Doppler assessment of dynamic cerebral circulatory changes during hypocapnia and attack.

Transcranial Doppler ultrasound (TCD) investigations have been carried out in cluster headache patients (8 during remission and 6 during bout) and 14 healthy subjects, to assess cerebral vasomotor reactivity (VMR) to hypocapnia induced by voluntary hyperventilation. VMR was expressed as the relative change in blood flow velocity (V) (%) as a function of the reduction in end-tidal PCO2 (PETCO2) (kPa), i.e. V/P ETCO2. TCD with simultaneous PETCO2 monitoring, was also performed in 5 patients during spontaneous attacks. Prior to hyperventilation, there was bilaterally lower anterior cerebral artery velocity (VACA) during the bout than during remission (P < 0.05 on the symptomatic side), and also lower than in the controls. During remission, VACA was higher on the symptomatic side than on the other side (P < 0.05). ACA also showed a lower VMR during the bout than during remission, and it was also lower than in controls (bout vs. remission on the non-symptomatic side, P < 0.01; on the symptomatic side, P > 0.1). Approximately 30 minutes after the onset of attack, PETCO2 started to decrease gradually from 4.65 to 4.10 kPa in one patient with severe attack. The VACA decreased markedly and bilaterally already at an early stage of the attack, i.e. prior to the hyperventilation. Middle cerebral artery velocity tended to decrease 30 minutes after the onset of attack on the symptomatic side, and 50 minutes after onset on the non-symptomatic side. It is concluded that the vascular changes observed most likely are secondary phenomena during the cluster headache attack.

Angiographic and Doppler diagnosis of cerebral artery vasospasm following subarachnoid haemorrhage

Angiographic middle and anterior cerebral artery diameter and transcranial ultrasound flow velocity measurements were performed within 24 h of each other in 102 patients with recent aneurysmal subarachnoid haemorrhage. There was a significant inverse correlation between middle cerebral artery diameter and flow velocity (r = -0.54, p < 0.001). No such correlation was seen for anterior cerebral arteries (r = -0.25). The ratio of middle cerebral artery to extracranial internal carotid artery velocities, which is an index of vasospasm, did not show improved correlation with arteriographic diameters, compared with uncorrected middle cerebral artery readings. Middle and anterior cerebral artery velocities and diameters both began to show significant changes indicative of vasospasm from day 4-5 onwards, suggesting that an increase in Doppler velocity is a good indicator of middle cerebral artery diameter, as shown by angiography. These studies indicate that transcranial Doppler is a useful non-invasive monitor for the development of delayed vasospasm following subarachnoid haemorrhage.

Cerebral arterial and venous flow-velocity measurements in post-haemorrhagic ventricular dilatation and hydrocephalus.

Simultaneous anterior cerebral artery (ACA) and internal cerebral vein (ICV) flow-velocities were measured in 18 babies with post-haemorrhagic ventricular dilatation (PHVD) and hydrocephalus (PHH). Compared with a control group matched for post-conceptional age, the resistance index of the ACA was increased. This was shown to occur at an early stage of PHVD in a longitudinal study of seven of the babies. There were no significant changes in ACA or ICV time-averaged velocities. Eight babies with PHH had ventricular taps on 18 occasions to relieve raised intracranial pressure. There was a significant decrease in the resistance index of the ACA, accompanied by an increase in the ACA time-averaged velocity, but no change in the ICV time-averaged velocity.

Anterior cerebral artery velocity changes in disease of the middle cerebral artery stem.

Transcranial Doppler ultrasonography can map the changes in blood velocity that result from stenosis or occlusion of the middle cerebral artery. To evaluate patterns of collateral blood flow in disease of the middle cerebral artery stem, we used both cerebral angiography and transcranial Doppler ultrasonography to study the systolic blood velocities in both anterior cerebral arteries in 10 consecutive patients with middle cerebral artery stenosis or occlusion. Five patients had no evidence of hemodynamically significant carotid disease and good-quality measurements of systolic velocity in each anterior cerebral artery. Two of the five patients had middle cerebral artery stem stenosis and the other three had occlusion. The ratios of mean blood velocity in the normal compared with the abnormal side for the five patients (mean 1.34 +/- 0.23, range 1.15-1.74) were significantly higher than ratios for 10 controls (mean 1.04 +/- 0.12, range 0.76 +/- 1.19) using an unpaired t test (t = 3.492, 0.0005 less than p less than 0.005). Our results suggest that transcranial Doppler ultrasound measurements of anterior cerebral artery blood velocity may be a useful index of collateral blood flow from the anterior cerebral artery territory into the middle cerebral artery territory. Changes in mean velocity ratio may document the evolution and adequacy of collateral blood flow over the cerebral convexity in middle cerebral artery stem disease. In addition, the changes in anterior cerebral artery blood velocity appear to be an important corroborative finding for middle cerebral artery stem occlusion.