Reduction of carotid artery blood flow in pediatric patients with syncope: evaluation with head-up tilt test

We investigated the effect of postural changes on cerebral circulation by measuring carotid artery blood flow (CABF) in the supine position and during head-up tilt (HUT) test using a Doppler flow meter. Subjects included 10 patients with neurally mediated syncope, 10 patients with orthostatic intolerance, 8 with epilepsy, aged between 8 to 24 years (mean +/- SD, 13.9 +/- 4.1 years). The test caused pallor and dizziness in 16 patients (symptomatic), while no symptoms were recognized in the other 12 patients (asymptomatic). Significant reductions in the mean CABF (Fm), maximum CABF (Fs) and minimum CABF (Fd), components of the CABF waveform, were noticed during HUT compared to before HUT (supine), and these reductions in symptomatic patients were more severe than those in asymptomatic patients (Fm: - 2.8 +/- 2.0 SD vs - 0.7 +/- 1.4 SD; Fs: - 2.7 +/- 1.5 SD vs - 0.9 +/- 1.3 SD; Fd: - 4.5 +/- 2.8 SD vs - 2.2 +/- 2.1 SD). Reductions in Fm, Fs and Fd in the symptomatic patients during HUT lasted longer than those of the asymptomatic patients, being statistically significant for Fm and Fs (Fm: p < 0.01; Fs: p < 0.05). The criteria during HUT for distinguishing neurally mediated syncope (NMS) from others was Fs: < - 4 SD and Fd: < - 5 SD. Our data suggest that reduction of CABF should be carefully evaluated for the diagnosis of neurally mediated syncope in pediatric patients. Such a reduction might be an essential mechanism of syncopal attacks.     

Midodrine in neurally mediated syncope: a double-blind,randomized, crossover study

Neurally mediated syncope is the most frequent cause of syncope in patients without structural heart disease. Its most common trigger is a reduction in venous return to the heart due to excessive venous pooling in the legs. We conducted a double-blind, randomized, crossover trial to investigate the efficacy of midodrine, a selective alpha-1 adrenergic agonist that decreases venous capacitance, in preventing neurally mediated syncope triggered by passive head-up tilt. Twelve patients with history of recurrent neurally mediated syncope, which was reproduced during head-up tilt, were randomized to receive a nonpressor dose of midodrine (5mg) or placebo on day 1 and the opposite on day 3. One hour after drug or placebo administration, patients underwent 60-degree head-up tilt lasting 40 minutes (unless hypotension or bradycardia developed first). In the supine position, midodrine produced no significant change in blood pressure or heart rate. The responses to head-up tilt were significantly different on the midodrine and the placebo day: on the placebo day, 67% (8/12) of the subjects suffered neurally mediated syncope, whereas only 17% (2/12) of the subjects developed neurally mediated syncope on the midodrine day (p < 0.02). These results indicate that midodrine significantly improves orthostatic tolerance during head-up tilt in patients with recurrent neurally mediated syncope.     

Combined transcranial Doppler and EEG recording in vasovagal syncope

BACKGROUND: In neurally mediated syncope a 'typical' EEG pattern during hyperventilation (HV) may be observed. This study aimed to investigate transcranial Doppler (TCD) and EEG variations in response to hyper- and hypocapnia using simultaneous recording. METHODS: Syncope patients with a typical EEG pattern during HV (SEEG+, n = 15) and those without abnormalities (SEEG-, n = 16) were compared with healthy controls (n = 20). Simultaneous TCD and EEG recordings were performed at rest (baseline), during 2 apnea tests and during HV. Cerebrovascular vasoreactivity, index for hypocapnia, total vasomotor reserve and time to flow velocity normalization after HV (t-norm) were recorded. RESULTS: With TCD, a reduction in Vasomotor reserve was observed in SEEG+ compared with the other 2 groups (control: 67 +/- 8%; SEEG-: 67 +/- 10%; SEEG+: 57 +/- 8%; p < 0.0001). t-norm was longer in all syncopal patients and in particular in SEEG+ (control: 20.2 +/- 3 s; SEEG-: 40 +/- 7 s; SEEG+: 123 +/- 45s; p < 0.0001). Quantitative EEG showed an increase in slow bands in all subjects during HV, small and nonsignificant in controls and SEEG-, higher and significant in SEEG+, related with flow reduction. CONCLUSIONS: Changes in the sympathetic modulation of cerebral vasoconstriction may explain both the pathophysiology of vasovagal syncope and the typical paroxysmal EEG findings.     

Doppler CO2-test in patients with vertebrobasilar isehemia

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.     

脑出血患者脑血流速度的观察

目的 观察脑出血后脑主要动脉的血流速度变化,进而研究脑血流动力学变化的临床价值。方法 采用经颅超声多普勒(transcranial Doppler,TCD)分别对216例脑出血患者和80名健康对照者的大脑中动脉、大脑前动脉、大脑后动脉、颈内动脉、基底动脉和椎动脉等颅内主要动脉的血流速度进行检测分析,记录包括收缩期峰速(Vs)、舒张期末流速(Vd)及搏动指数(PI)等血流参数及频谱形态。结果 脑出血组患者收缩期峰速与舒张末期流速与对照组比较均降低,差异有显著性意义(P<0.001)。脑出血组有164例患者(7.93％)颅内动脉血流速度降低,其中51例(23.61％)发生于脑出血早期,以舒张期末流速降低为主,113例(52.31％)发生于脑出血的中、后期,表现为普遍性流速降低。另有52例(24.07％)脑血流速度基本正常。结论 多数脑出血患者脑组织处于低循环状态,其程度与病情相关,因此对脑出血患者进行血流动力学监测有助于指导治疗及判断预后。     

Cerebral autoregulation during orthostatic stress in healthy controls and in patients with posturally related syncope

Abstract. Posturally related syncope (PRS) is a common and distressing problem, which frequently occurs in people with no apparent clinical disorder and is ultimately caused by a reduction in blood supply to the brain. The aim of this study was to compare cerebrovascular responses to orthostatic stress in otherwise healthy patients suffering from PRS, and who were shown to have a poor orthostatic tolerance (n=28), with those in healthy control subjects with good orthostatic tolerance (n=11). Responses of heart rate, arterial blood pressure, end tidal carbon dioxide and middle cerebral artery (MCA) blood flow velocity were determined during a progressive orthostatic stress test of combined head-up tilting and lower body suction, which was continued until presyncope. We assessed the efficiency of autoregulation of cerebral blood flow from the relationship between values of MCA velocity and pressure obtained over the expected range for autoregulation (> 55mmHg). All patients with PRS had a significant correlation between MCA velocity and pressure, but this was seen in only two of the controls. Furthermore, the values of the correlation coefficients were significantly higher in patients than controls, (p<0.001). We interpret these data as indicating that autoregulation in patients with PRS is less effective than in controls and suggest that this provides evidence for a link between abnormalities of regulation of the cerebral circulation and predisposition to syncope.     

Cerebrovascular CO2 reactivity during delayed vasospasm in a canine model of subarachnoid hemorrhage

While the in vitro reactivity of cerebral conducting vessels following subarachnoid hemorrhage has been extensively studied, in vivo cerebrovascular CO2 reactivity has not been systematically investigated. We tested the hypothesis that, in the canine model of subarachnoid hemorrhage, the rise in cerebral blood flow normally seen with hypercapnia is blunted during delayed vasospasm. Four groups of animals were studied: one received two 4-ml subarachnoid injections of nonheparinized arterial blood into the cisterna magna (n = 8), one received three subarachnoid injections of 5 ml blood (n = 5), one received two subarachnoid injections of 4 ml saline (n = 5), and a control group (n = 5) had no subarachnoid injections or angiography. Basilar artery diameter was measured from baseline and follow-up angiography. We determined CO2 reactivity by randomly varying the concentration of inspired CO2 and measuring regional cerebral blood flow with radiolabeled microspheres. Basilar artery diameter was not affected by saline injection and was reduced by 26 +/- 2.9% in the two-hemorrhage group and 55 +/- 1.9% in the three-hemorrhage group. Baseline cerebral blood flow and CO2 reactivity were similar in all four groups. We conclude that, in this model of delayed vasospasm, regional cerebral vascular CO2 reactivity is intact and extrapolation of in vitro data regarding basilar artery diameter and reactivity to cerebral blood flow must be done cautiously.     

Cerebral syncope: insights from Valsalva maneuver

BACKGROUND AND PURPOSE: Cerebral syncope refers to a loss of consciousness associated with cerebral vasoconstriction in the absence of systemic hypotension. The diagnosis of cerebral syncope could be established by the head-up tilt test (HUT) and transcranial Doppler ultrasonography. Valsalva maneuver (VM) permitted assessment of cerebral autoregulatory function by provoking blood pressure (BP) changes. To develop a path-physiological approach for vasomotor reactivity of cerebral syncope, the authors combined these maneuvers (HUT/transcranial Doppler/VM). METHODS: Using transcranial Doppler ultrasonography, we simultaneously recorded systemic arterial BP in the radial artery and flow velocities in both middle cerebral arteries (MCAFV) in 10 cerebral syncope patients (4 males and 6 females, 35.24 +/- 4.5 years old) during the Valsalva maneuver. RESULTS: The characteristic changes in BP (phases I-IV) were seen in all subjects, accompanying distinct changes in cerebral blood flow velocity. The BP/heart rate responding to VM was within normal limit in all subjects. There was no orthostatic hypotension. Instead, BP increased during the tilting test in 2 subjects (20.00%). The MCAFV dropped 25.4 +/- 2.3% from baseline. Abnormal flattening of MCAFV during late phase II (IIb), the paradoxical drop of flow velocity despite restoration of BP, was noted in 9 subjects (90.00%). CONCLUSION: During VM there are complex changes in relevant cardiovascular and cerebrovascular variables within a short time span. The paradoxical drop of MCAFV during phase IIb was the result of complex parameters. Among them, a failure in cerebrovascular resistance reduction and even paradoxical vasoconstriction might further compromise cerebral perfusion pressure and lead to syncope.     

Cerebral blood flow abnormalities in patients with neurally mediated syncope

The aim of this study is to investigate regional cerebral blood flow (rCBF) in patients with syncope. We compared brain single photon emission computed tomography (SPECT) images of neurally mediated syncope patients with those of age/sex matched healthy volunteers. ^99mTc-ethylcysteinate dimer (ECD) brain SPECT was performed in 35 patients (M/F = 17/18, mean 36.6 years) with syncope during the asymptomatic period, and in 35 healthy volunteers. For statistical parametric mapping (SPM) analysis, all SPECT images were spatially normalized to the standard SPECT template and then smoothed using a 14-mm full width at half maximum Gaussian kernel. The mean duration of syncope history was 4.9 years and the mean number of syncope episodes was 6.3. In all patients, syncope or presyncope episodes occurred during head-up tilt tests, and all were the vasodepressive type. SPM analysis of brain SPECT images showed significantly decreased rCBF in the right anterior insular cortex, left parahippocampal gyrus, bilateral fusiform gyri, bilateral middle and inferior temporal gyri, left lingual gyrus, bilateral precuneus and bilateral posterior lobes of the cerebellum in syncope patients at a false discovery rate corrected p < 0.05. There were no brain regions that showed increased rCBF in syncope patients. Furthermore, we found a negative correlation between the total number of syncopal episodes and the rCBF of the right prefrontal cortex, and between the duration of syncope history and the rCBF of the right cingulate gyrus at uncorrected p < 0.001. Decreases of rCBF in multiple brain regions may be responsible for autonomic dysregulation and improper processing of emotional stress in neurally mediated syncope patients, and frequent syncope episodes may lead to frontal dysfuction.     

发作期抑郁症患者脑动脉血流速度与注意力、执行功能关系

目的探讨发作期抑郁症患者脑动脉血流速度及其与注意力、执行功能的关系。方法 70例发作期抑郁症患者及65名健康对照纳入研究。采用24项汉密尔顿抑郁量表(24 items Hamilton depression scale,HAMD-24)评估抑郁症患者抑郁情绪,划销测验(cancellation test,CT)、威斯康星卡片分类测验(Wisconsin card sorting test,WCST)评估的认知功能,采用经颅多普勒超声(transcranial Doppler,TCD)检测脑动脉血流速度。结果与对照组比较,发作期抑郁症患者基底动脉、左侧大脑中动脉、右侧大脑中动脉、左大脑前动脉与右大脑前动脉平均血流速度均减慢,差异具有统计学意义(P0.05)。患者组CT各阶段净分及总净分低于对照组,而WCST总应答数、错误应答数、持续性错误数、完成第一个分类所需应答数均高于对照组,差异具有统计学意义(P0.01)。发作期抑郁症患者大脑基底动脉(r=0.25)、左中动脉(r=0.46)、右中动脉(r=0.25)、右后动脉(r=0.26)平均血流速度与CT总净分呈正相关(P0.05),各大脑动脉平均血流速度与WCST总应答数、持续性错误数呈负相关(P0.05),基底动脉、左右后动脉与错误应答数、完成第一个分类所需应答数呈负相关(P0.05)。结论发作期抑郁症患者大脑动脉平均血流速度普遍降低,注意力与执行功能受损。认知功能受损可能与脑动脉平均血流速度的改变有关。     

A transcranial Doppler study of basilar hemodynamics in progressive carotid artery disease

Abstract

In carotid artery disease (CAD) the basilar artery (BA) may act as an important intracranial collateral to supply hypoperfused middle cerebral artery (MCA) territories. Transcranial Doppler studies were performed to study the dependency between BA hemodynamics in relation to the MCA perfusion status. BA and MCA blood flow velocities (BFV), pulsatility indices (API) and cerebrovascular reactivity (CVR) were assessed in 40 patients with a progressive MCA hypoperfusion due to progressive CAD. All patients had patent cervical segments of their vertebral arteries with an antegrade vertebral flow profile. Duplex studies were performed to diagnose the severi~ of CAD. Hypoperfusion of the MCA was diagnosed by the degree of vasoparalysi assessed by a Diamox procedure. Analysis showed that the basilar BFV significantly increased in cases of progressive CAD; the basilar PI decreased but the basilar CVR remained unchanged. However, in cases of bilateral hemodynamic significant CAD and bilateral exhausted CVR in the MCA territory, the basilar artery did not exhibit an increase of BFVs or a decrease of the basilar PI, but the basilar CVR showed a significant decrease. Basilar artery CVR is not impaired if this artery has a function as intracranial collateral in CAD. However in cases of bilateral hypoperfused MeA territories the basilar artery does not function as a collateral pathway. The basilar CVR declines under these circumstances which merely reflects the exhausted hemodynamics in the anterior/posterior borderzones. This situation might lead to an increased stroke risk in the distal basilar supply zones. [Neural Res 1998; 20: 493-498]     

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

BACKGROUND: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity in patients with head injury. OBJECTIVES: To validate this index and study its relation with cerebral blood flow velocity and cerebral autoregulation; and to identify variables associated with impairment or preservation of cerebral vasomotor reactivity. METHODS: The PRx was validated in a prospective study of 40 head injured patients. A PRx value of less than 0.3 indicates intact cerebral vasomotor reactivity, and a value of more than 0.3, impaired reactivity. Arterial blood pressure, intracranial pressure, mean cerebral perfusion pressure, and cerebral blood flow velocity, measured bilaterally with transcranial Doppler ultrasound, were recorded. Dynamic cerebrovascular autoregulation was measured using a moving correlation coefficient between arterial blood pressure and cerebral blood flow velocity, the Mx, for each cerebral hemisphere. All variables were compared in patients with intact and impaired cerebral vasomotor reactivity. RESULTS: No correlation between arterial blood pressure or cerebral perfusion pressure and cerebral blood flow velocity was seen in 19 patients with intact cerebral vasomotor reactivity. In contrast, the correlation between these variables was significant in 21 patients with impaired cerebral vasomotor reactivity, whose cerebral autoregulation was reduced. There was no correlation with intracranial pressure, arterial blood pressure, cerebral perfusion pressure, or interhemispheric cerebral autoregulation differences, but the values for these indices were largely within normal limits. CONCLUSIONS: The PRx is valid for monitoring and quantifying cerebral vasomotor reactivity in patients with head injury. This intracranial pressure based index reflects changes in cerebral blood flow and cerebral autoregulatory capacity, suggesting a close link between blood flow and intracranial pressure in head injured patients. This explains why increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected head injured patients (those with intact cerebral vasomotor reactivity).     

Effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery

We noninvasively evaluated the effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery of 10 patients aged 17-60 (mean +/- SD 46.1 +/- 11.8) years. During fentanyl/diazepam/nitrous oxide anesthesia, mean blood flow velocity in the middle cerebral artery was measured and cerebral vascular reactivity to hypocapnia induced by hyperventilation was assessed before and during the administration of nicardipine. Mean blood flow velocity was measured using transcranial Doppler ultrasonography, and the cerebral vascular reactivity was expressed as the percentage change in mean blood flow velocity per unit change in end-tidal PCO2. During the administration of 5.1 +/- 1.3 micrograms/kg/min nicardipine, which caused a 26% reduction in mean arterial blood pressure, mean blood flow velocity increased significantly from 57.2 +/- 19.2 to 64.2 +/- 21.6 cm/sec (p less than 0.01, paired t test), whereas cerebral vascular reactivity showed no significant change (4.0 +/- 1.2% and 4.9 +/- 2.5%, respectively). In conclusion, during fentanyl/diazepam/nitrous oxide anesthesia in patients, cerebral vascular reactivity to hypocapnia was maintained and nicardipine-induced hypotension resulted in increased middle cerebral artery blood flow velocity with maintenance of carbon dioxide reactivity to hypocapnia.     

Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.     

Changes in mean cerebral blood flow velocity during cognitive task-induced cerebral fatigue in high performance fighter pilots*★

BACKGROUND： Several studies have demonstrated that sustained cognitive tasks can induce cognitive fatigue and that the mean cerebral blood flow velocity changes in some cerebral regions during cerebral fatigue. OBJECTIVE： To dynamically monitor the changes in mean cerebral blood flow velocity in different brain regions of high performance fighter pilots during mental arithmetic tasks and consecutive performance tasks. DESIGN, TIME AND SETTING： The present neurophysiological trial, based on controlled observation, was performed at the Laboratory of Neurophysiology, Institute of Aviation Medicine, Air Force of China between January 2003 and December 2005. PARTICIPANTS： Forty-five males, high performance fighter pilots, averaging （27.6±2.5） years, were recruited for this study. METHODS： The mean cerebral blood flow velocity in the anterior cerebral artery, middle cerebral artery, and posterior cerebral artery of subjects was dynamically tested using transcranial Doppler during 5- hour mental arithmetic tasks and during 5- hour consecutive performance tasks. The neurobehavioral ability index was analyzed throughout each trial according to the number of correct responses, false responses, and lost responses. Simultaneously, cerebral cognitive fatigue-induced lethargy was assessed by the Stanford Sleepiness Scale. MAIN OUTCOME MEASURES： Changes in mean cerebral blood flow velocity in the anterior cerebral artery, middle cerebral artery, and posterior cerebral artery; neurobehavioral ability index of mental arithmetic and consecutive performance tasks; Stanford Sleepiness Scale scores. RESULTS： During mental arithmetic tasks, the mean cerebral blood flow velocity in the anterior cerebral artery increased during hour 2 and decreased after hour 4. There was no significant change in mean cerebral blood flow velocity in the middle cerebral artery and posterior cerebral artery. During hour 4, cerebral cognitive fatigue was observed and, simultaneously, Stanford Sleepiness Scale scores demonstrated the pres     

Early changes in rabbit cerebral artery reactivity after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage frequently leads to long-term cerebral artery narrowing called vasospasm. Very early changes in cerebral arteries have not been studied extensively and may be critical for the later pathological developments. We therefore determined what changes in the reactivity of cerebral arteries could be observed after 10 minutes' or 24 hours' contact with subarachnoid blood. METHODS: Ten minutes or 24 hours after the injection of blood or physiological solution (sham hemorrhage) into the cisterna magna of anesthetized rabbits or no injection (control rabbits), segments of the middle cerebral, basilar, and vertebral arteries were removed for conventional in vitro tension measurements. Concentration-response curves to four endogenous constrictors likely to be released after hemorrhage were obtained, and the maximum relaxation to acetylcholine was determined. RESULTS: There were no significant differences between the sham hemorrhage and control groups. Compared with control rabbits, treated animals showed increased reactivity to uridine triphosphate in the basilar and vertebral arteries at 10 minutes but not at 24 hours, whereas reactivity was increased in the middle cerebral artery only at 24 hours. Reactivity to serotonin was greatly increased in all arteries at both latencies (up to 2.7 times). Reactivity to noradrenaline was unchanged in the basilar and vertebral arteries at 10 minutes; reactivity in both the basilar and middle cerebral arteries was increased at 24 hours, which is compatible with denervation supersensitivity. There were only minor changes in the reactivity to histamine, and only at 10 minutes. Relaxation to acetylcholine was increased for the middle cerebral artery at 10 minutes but otherwise was not significantly changed. CONCLUSIONS: Reactivity to uridine triphosphate, serotonin, and noradrenaline greatly increases by 10 minutes to 24 hours after subarachnoid hemorrhage, and this increase is not owing to the mechanical effects of intracranial hypertension, nor is it related to impaired endothelium-dependent relaxation. It is suggested that these and other spasmogens cause excessive muscular calcium loading with a very rapid onset after subarachnoid hemorrhage.     

Supine-to-standing transcranial Doppler test in patients with multiple system atrophy

BackgroundSupine-to-standing test, a transcranial Doppler (TCD) based technique, has been recently developed to evaluate cardiovascular dysautonomia. We explored the value of supine-to-standing TCD test in predicting the course of multiple system atrophy (MSA) with orthostatic hypotension (OH).MethodsBy monitoring the signals of middle cerebral artery during supine-to-standing posture changes, the trend curves of cerebral blood flow velocities, pulsatility index and resistance index were obtained from 38 MSA patients with OH and 31 healthy subjects. The correlation between TCD findings and the clinical outcome of the patients, which was determined by follow-up structured phone interview, was analyzed. Adverse outcome was defined if a patient died, was in bed-ridden state or had recurrent syncope (>1 per month).ResultsTwo characteristic TCD findings were revealed in the MSA patients but not in the controls, i.e. a blunted cerebral blood flow velocity rebound after standing and/or sustained higher pulsatility index upon standing than supine baseline. Structured phone interview was completed in 31 of the 38 patients (mean follow-up time, 20 ± 11 months). While no subject had recurrent syncope before enrollment, 12 patients developed an adverse outcome during follow-up. The coexistence of two characteristic TCD findings predicted adverse outcomes with positive predictive value 66.7% and negative predictive value 87.5%.ConclusionsSupine-to-standing TCD test is valuable in predicting the course of MSA with OH at early stage. We hypothesize baroreflex failure effects and paradoxical cerebral vasoconstriction in response to OH may account for the TCD findings in MSA patients.     

Combined electroencephalography and measurements of transcranial blood flow velocity during orthostatic testing—a new approach to assess syncope of unknown origin?

Differential diagnosis of syncope and seizures frequently imposes a major problem, particularly if interictal examinations are normal. We performed orthostatic testing combined with surface electroencephalography (EEG) and non-invasive measurements of cerebral blood flow velocity. Ten healthy controls, ten patients with confirmed diagnosis of epilepsy and 25 patients with history of syncope of unknown origin were examined. The following parameters were evaluated continuously and simultaneously during orthostatic challenge: computerized EEG with synchronous video-monitoring, transcranial Doppler sonography (TCD), heart rate and blood pressure. Isolated cerebrovascular dysregulation (i.e. a drop in cerebral perfusion despite the absence of a significant drop in peripheral blood pressure) occurred in 2/10 controls, 3/10 patients with epilepsy and 11/25 patients with syncope of unknown origin. The combined EEG and TCD measurements represent a new approach to the work-up of patients with otherwise unexplained syncope, helping us to understand the interdependence of neuronal activity and peripheral/cerebrovascular autoregulation under postural stress.     

尼麦角林对偏头痛患者脑血流动力学与血浆5-羟色胺的影响

目的探讨尼麦角林对偏头痛患者脑血流动力学与血浆5-羟色胺(5-HT)水平的影响。方法选择67例偏头痛患者随机分为尼麦角林治疗组(35例)和对照组(32例),同时选择30例健康体检者为健康对照组,治疗组应用尼麦角林治疗,对照组应用双氯芬酸钠治疗,应用经颅多普勒超声(TCD)技术检测治疗组和对照组治疗前后及健康对照组双侧大脑中动脉、大脑前动脉、椎动脉和基底动脉的(mean velocity,Vm)变化。采用高效液相色谱紫外光法测定3组血浆5-HT浓度,比较3组颅内动脉血流动力学的改变与血浆5-HT水平。结果 67例服药前大脑前动脉、大脑中动脉、椎动脉和基底动脉的平均血流速度与健康对照组比较增快。治疗后对照组变化不明显,治疗组大脑前动脉、大脑中动脉、椎动脉和基底动脉的平均血流速度降低,且与健康对照组比较差异无统计学意义(P0.05)。与健康对照组比较,偏头痛患者(治疗组和对照组)发作期血浆5-HT水平降低,发作间期血浆5-HT水平升高,差异有统计学意义(P0.05)。治疗后治疗组血浆5-HT水平发作期较治疗前和对照组显著升高,发作间期较治疗前和对照组明显下降(P0.05)。结论尼麦角林可明显预防和减轻偏头痛患者的发作,改善偏头痛患者的脑血流,调节偏头痛患者发作期和发作间期的血浆5-HT水平可能是其作用机制之一。     

Changes in mean cerebral blood flow velocity during cognitive task-induced cerebral fatigue in high performance fighter pilots

BACKGROUND:Several studies have demonstrated that sustained cognitive tasks can induce cognitive fatigue and that the mean cerebral blood flow velocity changes in some cerebral regions during cerebral fatigue. OBJECTIVE: To dynamically monitor the changes in mean cerebral blood flow velocity in different brain regions of high performance fighter pilots during mental arithmetic tasks and consecutive performance tasks. DESIGN,TIME AND SETTING: The present neurophysiological trial,based on controlled observati...