静息状态的动态脑血流自动调节：检查方法及临床应用

CA是维持脑血流恒定的生理机制。测量CA的方法很多。本文要介绍的是在静息状态下， 利用传递函数计算外围动脉血压和脑血流间的低频相位差，即可测量CA。CA和脑血管疾病的预后有 关，因此它有潜力成为有用的临床诊疗工具。     

Reduced cerebral blood flow velocity and impaired cerebral autoregulation in patients with Fabry disease

Abstract. In Fabry disease, there is glycosphingolipid storage in vascular endothelial and smooth muscle cells and neurons of the autonomic nervous system. Vascular or autonomic dysfunction is likely to compromise cerebral blood flow velocities and cerebral autoregulation. This study was performed to evaluate cerebral blood flow velocities and cerebral autoregulation in Fabry patients. In 22 Fabry patients and 24 controls, we monitored resting respiratory frequency, electrocardiographic RR-intervals, blood pressure, and cerebral blood flow velocities (CBFV) in the middle cerebral artery using transcranial Doppler sonography. We assessed the Resistance Index, Pulsatility Index, Cerebrovascular Resistance, and spectral powers of oscillations in RR-intervals, mean blood pressure and mean CBFV in the high (0.15–0.5 Hz) and sympathetically mediated low frequency (0.04–0.15 Hz) ranges using autoregressive analysis. Cerebral autoregulation was determined from the transfer function gain between the low frequency oscillations in mean blood pressure and mean CBFV. Mean CBFV (P < 0.05) and the powers of mean blood pressure (P < 0.01) and mean CBFV oscillations (P < 0.05) in the low frequency range were lower,while RR-intervals, Resistance Index (P < 0.01), Pulsatility Index, Cerebrovascular Resistance (P < 0.05), and the transfer function gain between low frequency oscillations in mean blood pressure and mean CBFV (P < 0.01) were higher in patients than in controls. Mean blood pressure, respiratory frequency and spectral powers of RR-intervals did not differ between the two groups (P > 0.05). The decrease of CBFV might result from downstream stenoses of resistance vessels and dilatation of the insonated segment of the middle cerebral artery due to reduced sympathetic tone and vessel wall pathology with decreased elasticity. The augmented gain between blood pressure and CBFV oscillations indicates inability to dampen blood pressure fluctuations by cerebral autoregulation. Both, reduced CBFV and impaired cerebral autoregulation, are likely to be involved in the increased risk of stroke in patients with Fabry disease.     

Continuous monitoring of cerebrovascular autoregulation: a validation study

BACKGROUND: Continuous monitoring of dynamic cerebral autoregulation, using a moving correlation index of cerebral perfusion pressure and mean middle cerebral artery flow velocity, may be useful in patients with severe traumatic brain injury to guide treatment, and has been shown to be of prognostic value. OBJECTIVE: To compare an index of dynamic cerebral autoregulation (Mx) with an index of static cerebral autoregulation (sRoR). METHODS: Mx was validated in a prospective comparative study against sRoR, using 83 testing sessions in 17 patients with traumatic brain injury. sRoR and Mx were calculated simultaneously during pharmacologically induced blood pressure variations. RESULTS: Mx was significantly correlated with sRoR (R = -0.78, p < 0.05). Nine patients were found to have failure of cerebral autoregulation, with an sRoR value < 50%. If an Mx value of 0.3 was used as the cut off point for failure of cerebral autoregulation, this index had 100% sensitivity and 90% specificity for demonstrating failure of autoregulation compared with the sRoR. An increase in cerebral blood flow velocity correlated significantly with Mx (R = 0.73, p < 0.05) but not with cerebral perfusion pressure (R = 0.41). CONCLUSIONS: Dynamic and static cerebral autoregulation are significantly correlated in traumatic brain injury. Cerebral autoregulation can be monitored continuously, graded, and reliably assessed using a moving correlation analysis of cerebral perfusion pressure and cerebral blood flow velocity (Mx). The Mx index can be used to monitor cerebral blood flow regulation. It is useful in traumatic brain injury because it does not require any external stimulus.     

Cerebral blood flow and dynamic cerebral autoregulation during ethanol intoxication and hypercapnia.

More than one-third of patients diagnosed with head injury are intoxicated with ethanol. Most clinical and animal studies have shown alcohol to have a deleterious impact in the setting of cerebrovascular trauma; however, there are also data showing neuroprotective effects in low ethanol doses. Human studies using imaging modalities suggest that small doses of alcohol produce cerebral vasodilatation and higher doses cerebral vasoconstriction. The aim of this study was to investigate the effect of ethanol intake on dynamic cerebral autoregulation and velocities in the middle cerebral arteries, and compare these changes with the effects of hypercapnia. Dynamic cerebral autoregulation and cerebral blood flow velocities were analysed before and after alcohol intake (1.1 g/kg of body weight) in six adult volunteers. Cerebral blood flow velocities in both middle cerebral arteries were monitored continuously by transcranial Doppler. A value for dynamic cerebral autoregulation was calculated from the rate of increase in middle cerebral artery velocities after a rapid-step decrease in arterial blood pressure. A sudden decrease in blood pressure was achieved by the release of previously inflated large blood pressure cuffs around the subject's thighs. Three volunteers were also tested before alcohol intake with CO(2) challenge (breathing 6% CO(2)) during the autoregulation procedure. Blood alcohol level reached 90 mg/dl approximately 60 min after ethanol ingestion. Cerebral blood velocities increased by 8% from baseline for uncorrected end-tidal (et) CO(2) and by 24% for correction to et CO(2)=40. Dynamic cerebral autoregulation measured as an autoregulation index decreased from 4.3+/-1.3 to 2.9+/-1.1 (p=0.089), which did not reach statistical significance. During hypercapnic conditions, dynamic cerebral autoregulation dropped from 4+/-0.8 to 0.9+/-0.9. In conclusion, mild alcohol intoxication caused cerebral vasodilatation with a subsequent increase in cerebral blood flow of 8-24%. Dynamic cerebral autoregulation was not found to be significantly impaired by ethanol. Hypercapnia almost completely destroys the physiological autoregulatory mechanism. A mild hyper-ventilation to etCO(2)=34-36 may be a compensatory contra-measure for ethanol-induced vasodilatation in the setting of head trauma.     

Neurovascular Coupling and Cerebral Autoregulation in Patients with Stenosis of the Posterior Cerebral Artery

Neurovascular coupling and cerebral autoregulation are two brain intrinsic vasoregulative mechanisms that rapidly adjust local cerebral blood flow. This study examined if stenotic disease affects both mechanisms in the posterior cerebral artery. Ten patients with altogether 13 stenosed (≥50%) posterior cerebral artery (PCA) sides were studied. In addition, 6 control persons without a PCA stenosis were examined. Cerebral blood flow velocity was assessed from both PCAs with transcranial Doppler sonography; blood pressure was measured noninvasively via fingerplethysmography. Neurovascular coupling was assessed by a control system approach using a standard visual stimulation paradigm. Cerebral autoregulation dynamics were measured from spontaneous oscillations of blood pressure and cerebral blood flow velocity by transfer function analysis (phase and gain). The parameters of neurovascular coupling and cerebral autoregulation did not show relevant differences between controls, nonstenosed sides, and stenosed sides. The 3 severely stenosed PCA sides showed a trend to a minor functional flow velocity change and attenuation of the neurovascular coupling mechanism in relation to sides with moderate stenosis. Phase and gain were not altered on sides with PCA stenosis. We conclude that in a group of patients with mainly moderate stenosis of the PCA neurovascular coupling and dynamic autoregulation dynamics seem to be unaltered.     

特发性高颅压患者脑血流自动调节研究

目的 分析特发性颅内压增高（idiopathic intracranial hypertension，IIH）患者脑血流自动调节机能。
方法 连续入组2018年12月-2019年3月在首都医科大学附属北京天坛医院就诊的IIH患者，并选取年
龄匹配的健康志愿者作为对照组。应用传递函数的算法分析TCD显示的大脑中动脉血流速度及动脉
血压的自然波动以评估脑血流自动调节机能。
结果 入组IIH组10例，对照组13例。所有入组者均完成了双侧大脑半球的脑血流自动调节检测，共
检测了20个高颅压半球及26个正常对照半球。与对照组相比，IIH组大脑中动脉脑血流增益显著降
低[（0.64±0.35）%/% vs（0.37%±0.20）%/%，P =0.004]；相位也显著降低（58.80±20.86°vs
39.16±23.79°，P =0.005），差异有统计学意义。IIH组每秒钟脑血流速度的恢复率较对照更低，但差
异尚未达到统计学意义（[ 26.34±43.29）%/s vs（38.81±20.16）%/s，P=0.240]。
结论 IIH患者脑血流自动调节机能显著受损。     

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.     

Cerebral autoregulation in the microvasculature measured with near-infrared spectroscopy

Cerebral autoregulation (CA) is the mechanism that allows the brain to maintain a stable blood flow despite changes in blood pressure. Dynamic CA can be quantified based on continuous measurements of systemic mean arterial pressure (MAP) and global cerebral blood flow. Here, we show that dynamic CA can be quantified also from local measurements that are sensitive to the microvasculature. We used near-infrared spectroscopy (NIRS) to measure temporal changes in oxy- and deoxy-hemoglobin concentrations in the prefrontal cortex of 11 human subjects. A novel hemodynamic model translates those changes into changes of cerebral blood volume and blood flow. The interplay between them is described by transfer function analysis, specifically by a high-pass filter whose cutoff frequency describes the autoregulation efficiency. We have used pneumatic thigh cuffs to induce MAP perturbation by a fast release during rest and during hyperventilation, which is known to enhance autoregulation. Based on our model, we found that the autoregulation cutoff frequency increased during hyperventilation in comparison to normal breathing in 10 out of 11 subjects, indicating a greater autoregulation efficiency. We have shown that autoregulation can reliably be measured noninvasively in the microvasculature, opening up the possibility of localized CA monitoring with NIRS.     

Cerebral autoregulation in Alzheimer's disease

Cerebral autoregulation aims to stabilize blood flow to the brain during variations in perfusion pressure, thus protecting the brain against the risks of low or high systemic blood pressure. This vital mechanism is severely impaired in the transgenic mouse model of Alzheimer''s disease (AD) that abundantly produces amyloid-β peptide β₁₋₄₂. These observations have been extrapolated to human AD, wherein impairment of autoregulation could have important implications for the clinical management and prevention of AD. Research on cerebral autoregulation in human AD, however, has only recently become available. Contrary to the animal models, preliminary studies suggest that cerebral autoregulation is preserved in patients with AD. Further research is urgently needed to elucidate this discrepancy in the current literature, given the accumulating evidence that implicates cerebrovascular pathology in AD.     

One-Minute Dynamic Cerebral Autoregulation in Severe Head Injury Patients and its Comparison with Static Autoregulation. A Transcranial Doppler Study

Objective  To compare dynamic and static responses of cerebral blood flow to sudden or slow changes in arterial pressure in severe traumatic brain injury (TBI) patients. Design  Prospective study. Patients and Methods  We studied 12 severe TBI patients, age 16–63 years, and median GCS 6. We determined the dynamic cerebral autoregulation: response of cerebral blood flow velocity to a step blood pressure drop, and the static cerebral autoregulation: change in cerebral blood flow velocity after a slow hypertensive challenge. Results  During the dynamic response, the median drop in arterial pressure was 21 mm Hg. Dynamic response was graded between 9 (best) and 0 (worst). The median value was 5; four patients showed high values, (8–9), five patients showed intermediate values (4–6). In three patients (value = 0), the CBFV drop was greater than the cerebral perfusion pressure drop, and maintained through 60 s. The static cerebral autoregulation was preserved in 6/11 patients. The comparison between the two showed four different combinations. The five patients with impaired static cerebral autoregulation showed unfavorable outcome. Conclusions  A sharp dynamic vasodilator response could not be sustained, and a slow or absent reaction to a sudden hypotensive challenge could show an acceptable cerebral autoregulation in the steady state. We found that patients with impaired static cerebral autoregulation had a poor outcome, whereas those with preserved static cerebral autoregulation experience favorable outcomes.     

Mechanisms of cerebral autoregulation, assessment and interpretation by means of transcranial doppler sonography

Cerebrovascular autoregulation assures constancy of cerebral perfusion despite blood pressure changes, as long as mean blood pressure remains in a range between 50-170 mmHg. Static and dynamic myogenic mechanisms dampen sudden blood pressure changes. Neurogenic influences of sympathetic, noradrenergic fibers modulate primarily proximal, large diameter segments of cerebral arteries, but also small 15-20 microns diameter vessels. Parasympathetic, vasodilating impulses are of less influence. Monoaminergic brainstem centers such as the dorsal raphe nucleus, locus coeruleus or nucleus reticularis pontis oralis also influence vessel tone. Metabolic, local parenchymal and endothelial substances have major impact on cerebral vessel tone. Particularly important are nitric oxide, calcitonin gene related peptide, substance P, endothelin, potassium channels and autocoids such as histamine, bradykinin, arachidonic acid, prostanoids, leucotrienes, free radicals or serotonin. The clinical examination of autoregulation is mostly based on brief blood pressure changes induced by drugs such as angiotensin, phenylephrine or sodium nitroprusside, or by challenge maneuvers. Frequently, blood pressure is challenged by a tilt-table maneuver, the "leg-cuff"-method according to Aaslid, or a Valsalva maneuver. The analysis of coherence and phase relation between spontaneous or metronomic breathing modulation of blood pressure and brain perfusion also assesses autoregulatory function. Cerebral blood flow is determined by means of transcranial Doppler sonography, mostly of the proximal segment of the mid-cerebral artery. There is some controversy whether a decrease of cerebral blood flow velocity measured at this segment indicates vasodilatation at the insonated segment or reflects blood flow reduction due to decreased perfusion of down-stream vessel segments. Various clinical and animal studies are presented demonstrating diameter constancy of the insonated mid-cerebral artery segment and thus indicating that slowing of mid cerebral artery blood flow velocity as assessed by transcranial Doppler sonography is due to a decrease of down-stream perfusion. Direct, intraoperative measurements of vessel diameter confirm this conclusion.     

Autonomic dysfunction and impaired cerebral autoregulation in cirrhosis

Cerebral blood flow autoregulation is lost in patients with severe liver cirrhosis. The cause of this is unknown. We determined whether autonomic dysfunction was related to impaired cerebral autoregulation in patients with cirrhosis. Fourteen patients with liver cirrhosis and 11 healthy volunteers were recruited. Autonomic function was assessed in response to deep breathing, head-up tilt and during 24-h Holter monitoring. Cerebral autoregulation was assessed by determining the change in mean cerebral blood flow velocity (MCAVm, transcranial Doppler) during an increase in blood pressure induced by norepinephrine infusion (NE). The severity of liver disease was assessed using the Child–Pugh scale (class A, mild; class B, moderate; class C, severe liver dysfunction). NE increased blood pressure similarly in the controls (27 (24–32) mmHg) and patients with the most severe liver cirrhosis (Child–Pugh C, 31 (26–44) mmHg, p=0.405 Mann–Whitney). However, the increase in MCAVm was greater in cirrhosis patients compared to the controls (Child–Pugh C, 26 (24–39) %; controls, 3 (−1.3 to 3) %; respectively, p=0.016, Mann–Whitney). HRV during deep breathing was reduced in the cirrhosis patients (Child–Pugh C, 6.0±2.0 bpm) compared to the controls (21.7±2.2 bpm, p=0.001, Tukey’ test). Systolic blood pressure fell during head-up tilt only in patients with severe cirrhosis. Our results imply that cerebral autoregulation was impaired in the most severe cases of liver cirrhosis, and that those with impaired cerebral autoregulation also had severe parasympathetic and sympathetic autonomic dysfunction. Furthermore, the degree of liver dysfunction was associated with increasing severity of autonomic dysfunction. Although this association is not necessarily causal, we postulate that the loss of sympathetic innervation to the cerebral resistance vessels may contribute to the impairment of cerebral autoregulation in patients with end-stage liver disease. Financial support The study was funded by: Danish Medical Research Council. The Danish Hospital Foundation for Medical Research, Region of Copenhagen, the Faroe Islands and Greenland. Rigshospitalet. University of Copenhagen. The Laerdal Foundation for Acute Medicine. Sawmill owner Jeppe Juhl and Wife Ovita Juhls Foundation. The Novo Nordisk Foundation. The King Christian the 10th Foundation. The AP-Moeller Foundation. The Beckett Foundation.     

Cerebral autoregulation in middle cerebral artery territory precedes that of posterior cerebral artery in human cortex.

OBJECTIVE: Cerebral autoregulation tends to compensate changes in arterial blood pressure. This mechanism of cerebral blood flow regulation appears to be insufficient in orthostatic dysregulation in which mainly vertebrobasilar symptoms occur. To investigate this hypothesis, we compared cerebral autoregulation in the vascular territory of the carotic and vertebrobasilar vessel system using a leg cuff test to induce a drop in cerebral perfusion pressure. METHODS: We measured blood flow velocity in 10 healthy young volunteers (aged 26.7 +/- 0.3 years, 7 male) simultaneously in the middle and posterior cerebral artery with transcranial Doppler sonography. A leg cuff test was used to induce a sudden decrease in arterial blood pressure. Arterial blood pressure was measured with a non-invasive photoplethysmographic method. The averaged relative blood flow velocity changes due to the pressure step were compared between both vessel territories. RESULTS: After cuff release systolic (diastolic) blood flow velocity increased with a latency of 1.1 +/- 0.3 s (1.8 +/- 0.4 s). Due to a smaller decrease and identical time courses cerebral blood flow velocity recovery in the posterior cerebral artery precedes blood flow recovery in the middle cerebral artery by 0.9 +/- 0.3 s. DISCUSSION: Cerebral autoregulation in the carotid and vertebrobasilar system does not differ in the time course of the blood flow velocity recovery. Due to a smaller decrease in blood flow velocity recovery in the posterior cerebral artery precedes recovery in the middle cerebral artery by nearly 1 s.     

Ischemic Conditioning Is Safe and Effective for Octo- and Nonagenarians in Stroke Prevention and Treatment

Symptomatic intracranial arterial stenosis (SIAS) is very common in octo- and nonagenarians, especially in the Chinese population, and is likely the most common cause of stroke recurrence worldwide. Clinical trials demonstrate that endovascular treatment, such as stenting, may not be suitable for octogenarians with systemic diseases. Hence, less invasive methods for the octogenarian patients are urgently needed. Our previous study (unique identifier: {"type":"clinical-trial","attrs":{"text":"NCT01321749","term_id":"NCT01321749"}}NCT01321749) showed that repetitive bilateral arm ischemic preconditioning (BAIPC) reduced the incidence of stroke recurrence by improving cerebral perfusion (confirmed by single photon emission computed tomography and transcranial Doppler sonography) in patients younger than 80 years of age; however, the safety and effectiveness of BAIPC on stroke prevention in octo- and nonagenarians with SIAS are still unclear. The objective of this study was to evaluate the safety and effectiveness of BAIPC in reducing stroke recurrence in octo- and nonagenarian patients with SIAS. Fifty-eight patients with SIAS were enrolled in this randomized controlled prospective study for 180 consecutive days. All patients enrolled in the study received standard medical management. Patients in the BAIPC group (n = 30) underwent 5 cycles consisting of bilateral arm ischemia followed by reperfusion for 5 min each twice daily. Those in the control group (n = 28) underwent sham-BAIPC twice daily. Blood pressure, heart rate, local skin status, plasma myoglobin, and plasma levels of thrombotic and inflammatory markers were documented in both groups before beginning the study and for the first 30 days. Finally, the incidences of stroke recurrence and magnetic resonance imaging during the 180 days of treatment were compared. Compared with the control, BAIPC had no adverse effects on blood pressure, heart rate, local skin integrity, or plasma myoglobin, and did not induce cerebral hemorrhage in the studied cohort. BAIPC reduced plasma high sensitive C-reactive protein, interleukin-6, plasminogen activator inhibitor-1, leukocyte count, and platelet aggregation rate and elevated plasma tissue plasminogen activator (all p < 0.01). In 180 days, 2 infarctions and 7 transient ischemic attacks were observed in the BAIPC group compared with 8 infarctions and 11 transient ischemic attacks in the sham BAIPC group (p < 0.05). BAIPC may safely inhibit stroke recurrence, protect against brain ischemia, and ameliorate plasma biomarkers of inflammation and coagulation in octo- and nonagenarians with SIAS. A multicenter trial is ongoing.Clinical Trial Registration: www.clinicaltrials.gov, unique identifier: {"type":"clinical-trial","attrs":{"text":"NCT01570231","term_id":"NCT01570231"}}NCT01570231.

Electronic supplementary material

The online version of this article (doi:10.1007/s13311-015-0358-6) contains supplementary material, which is available to authorized users.Key Words: Remote ischemic preconditioning, octogenarian, nonagenarians, intracranial arterial stenosis, stroke, recurrence     

Impaired cerebrovascular hemodynamics are associated with cerebral white matter damage

White matter hyperintensities (WMH) in elderly individuals with vascular diseases are presumed to be due to ischemic small vessel diseases; however, their etiology is unknown. We examined the cross-sectional relationship between cerebrovascular hemodynamics and white matter structural integrity in elderly individuals with vascular risk factors. White matter hyperintensity volumes, fractional anisotropy (FA), and mean diffusivity (MD) were obtained from MRI in 48 subjects (75±7years). Pulsatility index (PI) and dynamic cerebral autoregulation (dCA) was assessed using transcranial Doppler ultrasound of the middle cerebral artery. Dynamic cerebral autoregulation was calculated from transfer function analysis (phase and gain) of spontaneous blood pressure and flow velocity oscillations in the low (LF, 0.03 to 0.15 Hz) and high (HF, 0.16 to 0.5 Hz) frequency ranges. Higher PI was associated with greater WMH (P<0.005). Higher phase across all frequency ranges was associated with greater FA and lower MD (P<0.005). Lower gain was associated with higher FA in the LF range (P=0.001). These relationships between phase and FA were significant in the territories limited to the middle cerebral artery as well as across the entire brain. Our results show a strong relationship between impaired cerebrovascular hemodynamics (PI and dCA) and loss of cerebral white matter structural integrity (WMH and DTI metrics) in elderly individuals.     

Cerebral circulatory and metabolic effects of hypotension produced by deep halothane anaesthesia

Hypotension to a mean blood pressure of 33 mmHg for periods of 70 to 187 minutes was induced by increasing the inspired halothane concentration in 11 baboons which were already anaesthetized with 0·5% halothane, nitrous oxide, and oxygen. During hypotension, cerebral blood flow, measured by Xenon clearance and by a carotid electromagnetic flowmeter, decreased by more than half, and sagittal sinus oxygen saturation was 46%. Cerebral oxygen uptake fell from 5·15 to 3·56 ml./100 g/min at this deeper level of halothane anaesthesia. Cerebral hyperaemia developed after hypotension in those animals which regained a mean blood pressure greater than 70 mmHg. Acidbase measurements on CSF from the cisterna magna revealed no metabolic acidosis during or after hypotension. In all four animals with intact autoregulation before hypotension, this was absent or impaired afterwards.     

Tissue oxygenation indices of cerebrovascular autoregulation in healthy volunteers: a comparison of two NIRS devices

ABSTRACT

Background

Correlation coefficients between blood pressure and cerebral oxygen saturation measured using near-infrared spectrometry may be used to derive the tissue oximetry index of cerebral autoregulation. Cerebral oxygen saturations demonstrate poor agreement between near-infrared spectrometers however it is unclear if measurements of autoregulation are similarly specific to the equipment used.     

Compromised cerebrovascular modulation in chronic anxiety: evidence from cerebral blood flow velocity measured by transcranial Doppler sonography

Objective Cerebral autoregulation(CA) is the mechanism by which constant cerebral blood flow is maintained despite changes in cerebral perfusion pressure.CA can be evaluated by dynamic monitoring of cerebral blood flow velocity(CBFV) with transcranial Doppler sonography(TCD).The present study aimed to explore CA in chronic anxiety.Methods Subjects with Hamilton anxiety scale scores≥14 were enrolled and the dynamic changes of CBFV in response to an orthostatic challenge were investigated using TCD.Results In both the anxious and the healthy subjects,the mean CBFV was significantly lower in the upright position than when supine.However,the CBFV changes from supine to upright differed between the anxious and the healthy groups.Anxious subjects showed more pronounced decreases in CBFV with abrupt standing.Conclusion Our results indicate that cerebrovascular modulation is compromised in chronic anxiety;anxious subjects have some insufficiency in maintaining cerebral perfusion after postural change.Given the fact that anxiety and impaired CA are associated with cardiovascular disease,early ascertainment of compromised cerebrovascular modulation using TCD might suggest interventional therapies in the anxious population, and improve the primary prevention of cardiovascular disease.     

血压波动对脑梗死后脑灌注的影响

本文主要从脑血管的自动调节与自动调节受损、脑小血管病变可导致脑血管反应性受损、脑梗死患者脑血流速度、脑血流量与血压的相关性,脑梗死侧大脑半球脑灌注降低、低血压对脑主要动脉狭窄者可导致狭窄远端脑组织局部低灌注等几个方面来讨论脑梗死后血压的变化对脑血流速度、脑血流量的影响。给临床医生提出一个思考问题,在脑梗死的急性期把血压控制在多少才是最合适的水平,对患者的功能恢复最有益。     

Contribution of mathematical modelling to the interpretation of bedside tests of cerebrovascular autoregulation

OBJECTIVES—Cerebral haemodynamic responses toshort and longlasting episodes of decreased cerebral perfusion pressurecontain information about the state of autoregulation of cerebral bloodflow. Mathematical simulation may help to elucidate which of theindices, that can be derived using transcranial Doppler ultrasonographyand trends of intracranial pressure and blood pressure, are useful inclinical tests of autoregulatory reserve.
METHODS—Time dependent interactions betweenpressure, flow, and volume of cerebral blood and CSF were modelledusing a set of non-linear differential equations. The model simulateschanges in arterial blood inflow and storage, arteriolar and capillaryblood flow controlled by cerebral autoregulation, venous blood storageand venous outflow modulated by changes in ICP, and CSF storage and reabsorption. The model was used to simulate patterns of blood flowduring either short or longlasting decreases in cerebral perfusionpressure. These simulations can be considered as clinically equivalentto a short compression of the common carotid artery, systemichypotension, and intracranial hypertension. Simulations were performedin autoregulating and non-autoregulating systems and compared withrecordings obtained in patients.
RESULTS—After brief compression of the commoncarotid artery, a subsequent transient hyperaemia can be interpreted asevidence of intact autoregulation. During longlasting sustainedhypoperfusion, a gradual increase in the systolic value of the bloodflow velocity waveform along with a decrease in the diastolic value isspecific for an autoregulating cerebrovascular system.
CONCLUSION—Modelling studies help to interpretboth clinical and experimental cerebral haemodynamic phenomena andtheir dependence on the state of autoregulation.