脑血管反应性的临床应用及其评估价值

脑血管反应性(cerebrovascular reactivity，CVR)是指脑血管在各种使其扩张的因素作用下能够舒张的能力。CVR可以充分提供关于脑血管自动调节能力和侧支循环状态的信息。目前有3种测试方法用于检测脑血管反应性：屏息法、CO2吸入法，乙酰唑胺法。3种方法均基于脑血管在高碳酸血症时反应性扩张的机制。经颅多普勒超声(TCD)，磁共振血管成像(MRA)，单光子发射计算机断层扫描(SPECT)，正电子发射计算机断层扫描(PET)等影像学技术结合这些测试方法可以检测脑血管反应性。CVR已经在临床广泛应用，尤其是缺血性脑卒中如：①评价颈动脉狭窄或闭塞患的脑血流动力学变化，预测发生缺血性脑卒中的危险性。②评价颈动脉内膜切除术前后脑血流动力学变化。③血管手术再通后的预后评估及其他。脑血管反应性可以充分评价脑血管的调节能力，对缺血性脑卒中的早期诊断、治疗、预后评价及康复干预均有重要意义。     

脑血管反应性的临床应用及其评估价值

脑血管反应性(cerebrovascularreactivity,CVR)是指脑血管在各种使其扩张的因素作用下能够舒张的能力。CVR可以充分提供关于脑血管自动调节能力和侧支循环状态的信息。目前有3种测试方法用于检测脑血管反应性:屏息法、CO2吸入法,乙酰唑胺法。3种方法均基于脑血管在高碳酸血症时反应性扩张的机制。经颅多普勒超声(TCD),磁共振血管成像(MRA),单光子发射计算机断层扫描(SPECT),正电子发射计算机断层扫描(PET)等影像学技术结合这些测试方法可以检测脑血管反应性。CVR已经在临床广泛应用,尤其是缺血性脑卒中如:①评价颈动脉狭窄或闭塞患者的脑血流动力学变化,预测发生缺血性脑卒中的危险性。②评价颈动脉内膜切除术前后脑血流动力学变化。③血管手术再通后的预后评估及其他。脑血管反应性可以充分评价脑血管的调节能力,对缺血性脑卒中的早期诊断、治疗、预后评价及康复干预均有重要意义。     

糖尿病患者脑血流动力学及血管运动反应性观测

早期发现糖尿病患脑血管功能异常，是预防脑卒中的关键。应用经历多普勒(TCD)技术，对糟尿病患的脑血流动力学进行检测，同时通过过度换气(HV)前后脑血流速变化，评价脑血管的运动反应性及脑血管储备力，可以发现脑血管功能损害的早期指征并做出较推确的判断。     

脑血流自动调节测定的应用

目的：总结并分析脑血流自动调节的生理机制及其在脑卒中后的病理生理变化，探讨脑血流自动调节的测定原理及其在神经科的应用。 资料来源：应用计算机检索Medline1959-01／2004-12关于脑血流自动调节的文章。检索词“cerebral autoregulation”并限定文章的语种类为English。同时利用计算机检索中国期刊全文数据库1994-01／2004-12的相关文章，限定文章语言种类为中文，检索词“脑血流自动调节”。 资料选择：对资料进行初审，纳入标准：①关于脑血流自动调节的定义、生理机制、影响因素和测定。②对具体事件的回顾调查研究。排除标准：排除重复性研究。 资料提炼：共收集到符合上述要求的文献49篇，排除2l篇重复性研究。28篇符合纳入标准：其中16篇关于脑血流自动调节的定义及生理机制，5篇关于卒中后脑血流自动调节变化，7篇关于脑血流自动调节的具体案例。 资料综合：脑血流自动调节是指当血压在一定范围内变动时，脑血管能维持脑血流量相对恒定的能力。脑血流自动调节受多种生理因素影响，卒中后可以观察到脑动脉的自动调节功能下降。 结论：脑血流自动调节对于维持脑血流恒定是至关重要的，它受多种因素影响，对脑血流自动调节的测定可能有助于卒中的风险研究。     

糖尿病患者脑血流动力学及血管运动反应性观测

早期发现糖尿病患者脑血管功能异常,是预防脑卒中的关键。应用经颅多普勒(TCD)技术,对糖尿病患者的脑血流动力学进行检测,同时通过过度换气(HV)前后脑血流速变化,评价脑血管的运动反应性及脑血管储备力,可以发现脑血管功能损害的早期指征并做出较准确的判断。     

长期居住海平藏族急性低氧时脑循环动力学的动态观察

动态观察长期居住海平藏族急性低氧时脑循环动力学变化。方法：采用脑循环动力学检测仪在不同氧时间进行循环动力参数检测。结果：低氧３０分钟组，脑平衡血流速度明显增加，增幅９％，低氧３０分钟、６０分钟时，脑血管调节功能明显增强。结论：藏族在急性低氧的早期，脑血流速度及脑血管调节功能明显增加。     

脑血流自动调节测定的应用

目的:总结并分析脑血流自动调节的生理机制及其在脑卒中后的病理生理变化,探讨脑血流自动调节的测定原理及其在神经科的应用。资料来源:应用计算机检索Medline1959-01/2004-12关于脑血流自动调节的文章。检索词“cerebralautoregulation”并限定文章的语种类为English。同时利用计算机检索中国期刊全文数据库1994-01/2004-12的相关文章,限定文章语言种类为中文,检索词“脑血流自动调节”。资料选择:对资料进行初审,纳入标准:①关于脑血流自动调节的定义、生理机制、影响因素和测定。②对具体事件的回顾调查研究。排除标准:排除重复性研究。资料提炼:共收集到符合上述要求的文献49篇,排除21篇重复性研究。28篇符合纳入标准:其中16篇关于脑血流自动调节的定义及生理机制,5篇关于卒中后脑血流自动调节变化,7篇关于脑血流自动调节的具体案例。资料综合:脑血流自动调节是指当血压在一定范围内变动时,脑血管能维持脑血流量相对恒定的能力。脑血流自动调节受多种生理因素影响,卒中后可以观察到脑动脉的自动调节功能下降。结论:脑血流自动调节对于维持脑血流恒定是至关重要的,它受多种因素影响,对脑血流自动调节的测定可能有助于卒中的风险研究。     

脑血管对CO2的反应在经颅多普勒超声中的应用

脑组织的代谢水平很高.血流量较多。脑血流量受脑动、静脉之间压差和脑血管对血流的阻力两个条件的影响。脑血流的阻力又受许多复杂的因素所调节,其中血液中的CO_2对脑血管舒缩功能的调节占有重要地位。近几年来国外对CO_2对脑血管的调节在经颅多普勒超声(TCD)中的表现研究较多,特综述如下。 1.血液中CO_2对脑血管舒缩功能的调节机制 已经证明CO_2对脑血管的平滑肌有松弛作用,当     

电刺激小脑顶核对脑血流动力学的影响

目的 探讨电刺激小脑顶核对患者脑血流动力学的影响，为用脑循环功能治疗仪治疗脑梗塞等病人提供理论及实践依据。方法 对50例脑梗塞患者用脑循环功能治疗仪治疗，并在治疗前后进行脑血流动力学检测，测定脑血流动力学有关指标。如平均脑血流量（Qmean),特性阻抗（Zc)，脑血管阻力（R）和平均脑血流速度（Vmean)等参数。结果 治疗后脑血管阻力（R）减小，平均脑血流量增加，经统计学处理有显著差异。结论 电刺激小脑顶核治疗后，脑血管阻力减小，脑血流量增加，说明使用该治疗仪可以改善脑部血液循环。     

脑血流自动调节功能与最佳脑灌注压

正常人脑的血流量占全身的15％～20％,消耗25％的氧.而脑组织自身无能量储备,需要稳定且持续的脑血流供应,维持结构和功能.脑血管本身具有自动调节功能(cerebral auto regulation,CAR),并通过复杂的代谢性、化学性、神经源性及血管压力系统自身进行调节,以保证稳定的脑血流量[1].当脑外伤(traumatic brain injury,TBI)或卒中等病理状态下,脑血管自动调节功能的完整性受到影响,导致脑缺血或过度充血.损害性脑灌注伴随的细胞氧供不足和代谢障碍,是导致中枢神经疾病恶化的重要病理生理因素[2].因此脑外伤及卒中后,予以严密神经监测及治疗,防止继发性缺血性损害.     

Diltiazem and autoregulation of canine cerebral blood flow

Recent in vitro evidence suggests the existence of stretch-activated calcium channels in cerebrovascular smooth muscle. These channels, which may play a role in cerebral autoregulation, also appear resistant to antagonism by the benzothiazepine calcium antagonist diltiazem, an agent known to block potential-sensitive and receptor-operated calcium channels. If cerebral autoregulation involves stretch-sensitive diltiazem-resistant calcium channels, then autoregulation should remain intact during vasodilatation produced by diltiazem. The present study was conducted to test this hypothesis. Using a canine cerebral venous outflow preparation, experiments were first performed to determine the optimum dose and route of administration for diltiazem. Although continuous i.v. diltiazem (1-100 micrograms/kg/min) did not increase cerebral perfusion at any normotensive dose, i.a. (lingual artery) diltiazem at 10.0 micrograms/kg/min increased cerebral blood flow by 36% and decreased cerebrovascular resistance by 31% without significant effects on blood gas levels, cerebral oxygen uptake, cardiac output or mean arterial pressure. In autoregulation experiments, 10.0 micrograms/kg/min of diltiazem significantly attenuated but did not eliminate autoregulatory responses to increases (inflation of an aortic balloon) and decreases (hemorrhage) in cerebral perfusion pressure. Autoregulatory responses to increases and decreases in perfusion pressure were equally affected by diltiazem, but both were unaffected by i.a. saline. These data support the view that cerebral autoregulation involves both diltiazem-sensitive and diltiazem-resistant mechanisms. The diltiazem-resistant mechanisms, which may include the proposed population of stretch-sensitive calcium channels appear to account for up to one-half of the autoregulatory capacity in the cerebral circulation.     

Cerebrovascular regulation and vasoneuronal coupling

Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegation of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit. © 1995 John Wiley & Sons, Inc.     

Transcranial Doppler Assessment of Cerebral Autoregulation

Cerebral autoregulation describes the process by which cerebral blood flow is maintained despite fluctuations in cerebral perfusion pressure. The assessment of cerebral autoregulation is a key to the optimisation of cerebral perfusion pressure in patients with brain injury. This review evaluates the current evidence for transcranial Doppler in the assessment of cerebral autoregulation. The study of cerebral autoregulation classically assesses changes in cerebral perfusion pressure secondary to changes in systemic blood pressure. It is defined static autoregulation if blood pressure changes are progressive, thereby allowing a steady-state autoregulatory response to be completed. For sudden changes in blood pressure, the autoregulatory response is defined as dynamic. The static and dynamic components of cerebral autoregulation have been approached using linear mathematical models (models based in direct correlations). Over the past decade, demonstration of the nonstationary (the property of changing over time or space) behaviour of cerebral autoregulation has emphasised the benefit obtained in using nonlinear statistical models (models based on changeable functions), suggesting that these methods may improve the mathematical representation of cerebral autoregulation. Despite the multiple determinants involved in cerebral autoregulation, it appears feasible to reliably assess cerebral autoregulation through the combination of linear and nonlinear methods. Nonlinear methods appear attractive in the research setting, but the challenge is how to adopt these methods to the clinical setting. (E-mail: 30489jbr@comb.es)     

Cerebral autoregulation and outcome in acute brain injury

The purpose of this study was to examine the relationship between Czosnyka and others' Pressure Reactivity Index (PRx) and neurologic outcome in patients with acute brain injury, including traumatic brain injury (TBI) and cerebrovascular pathology. PRx measures the correlation between arterial blood pressure and intracranial pressure waves and may reflect cerebral autoregulation in response to blood pressure changes. A negative PRx reflects intact cerebrovascular response, whereas a positive PRx reflects impaired response. Positive PRx has been shown to correlate with poorer outcome in individuals with TBI, but these findings have not been confirmed by replication in other studies, nor have PRx values been reported for individuals with cerebrovascular pathology. In this study, PRx was determined in 52 patients with TBI (n = 27) or cerebrovascular pathology (n = 25). Hierarchical linear regression was used to evaluate the contribution of PRx to outcome, controlling for age and Glasgow Coma Scale score. Analysis of all subjects together did not support the previously reported relationship between PRx and outcome. However, for those with TBI, positive PRx was a significant predictor of negative outcome (P = 0.03). For those with cerebrovascular pathology, the effect was not significant (P = 0.10) and was in the opposite direction. For individuals with TBI, PRx may provide useful information related to cerebral autoregulation that is predictive of outcome. The meaning of PRx in individuals with cerebrovascular pathology is unclear, and further study is needed to examine the paradoxical findings observed.     

Loss of cerebrovascular autoregulation in experimental meningitis in rabbits.

The present study was designed to determine whether cerebrovascular autoregulation is intact in experimental meningitis and to examine the relationship between fluctuations in cerebral blood flow (CBF) and increased intracranial pressure (ICP). Measurements of CBF were determined by the radionuclide microsphere technique in rabbits with experimental Streptococcus pneumoniae meningitis with simultaneous ICP monitoring via an implanted epidural catheter. CBF and ICP measurements were determined at baseline and when mean arterial blood pressure (MABP) was artificially manipulated by either pharmacologic or mechanical means. CBF was pressure passive with MABP through a range of 30-120 torr, and ICP directly correlated with CBF. These findings indicate that autoregulation of the cerebral circulation is lost during bacterial meningitis, resulting in a critical dependency of cerebral perfusion on systemic blood pressure, and that the parallel changes in ICP and in CBF suggest that fluctuations in CBF may influence intracranial hypertension in this disease.     

Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity

OBJECTIVE: To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Neurosurgical intensive care unit of a university hospital. PATIENTS: Twenty-seven patients suffering from severe traumatic brain injury. INTERVENTIONS: Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale). MEASUREMENTS AND MAIN RESULTS: Both ORx and bPtio2 correlated significantly with PRx (r=.55 for ORx, r=.52 for bPtio2, p<.01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r=-.42 for PRx, r=-.41 for ORx, p<.05) and outcome (r=-.52 for PRx, r=-.62 for ORx, p<.01), whereas bPtio2 did not. CONCLUSIONS: ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.     

Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation

OBJECTIVE: Acute respiratory dysfunction frequently occurs following severe aneurysmal subarachnoid hemorrhage requiring positive end-expiratory pressure (PEEP) ventilation to maintain adequate oxygenation. High PEEP levels, however, may negatively affect cerebral perfusion. The goal of this study was, to examine the influence of various PEEP levels on intracranial pressure, brain tissue oxygen tension, regional cerebral blood flow, and systemic hemodynamic variables. DESIGN: Animal research and clinical intervention study. SETTING: Surgical intensive care unit of a university hospital. SUBJECTS AND PATIENTS: Experiments were carried out in five healthy pigs, followed by a clinical investigation of ten patients suffering subarachnoid hemorrhage. INTERVENTIONS: Under continuous monitoring of intracranial pressure, brain tissue oxygen tension, regional cerebral blood flow, mean arterial pressure, and cardiac output, PEEP was applied in increments of 5 cm H2O from 5 to 25 cm H2O in the experimental part and from baseline to 20 cm H2O in the clinical part. MEASUREMENTS AND MAIN RESULTS: In animals, high PEEP levels had no adverse effect on intracranial pressure, brain tissue oxygen tension, or regional cerebral blood flow. In patients with severe subarachnoid hemorrhage, stepwise elevation of PEEP resulted in a significant decrease of mean arterial pressure and regional cerebral blood flow. Analyses of covariance revealed that these changes of regional cerebral blood flow depended on mean arterial pressure changes as a result of a disturbed cerebrovascular autoregulation. Consequently, normalization of mean arterial pressure restored regional cerebral blood flow to baseline values. CONCLUSIONS: Application of high PEEP does not impair intracranial pressure or regional cerebral blood flow per se but may indirectly affect cerebral perfusion via its negative effect on macrohemodynamic variables in case of a disturbed cerebrovascular autoregulation. Therefore, following severe subarachnoid hemorrhage, a PEEP-induced decrease of mean arterial pressure should be reversed to maintain cerebral perfusion.     

Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury

BACKGROUND: Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. OBJECTIVE: This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. DESIGN: Prospective study. SETTING: Neurosurgical intensive care unit PATIENTS: A total of 42 patients with severe head injuries. INTERVENTIONS: Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. MEASUREMENTS AND MAIN RESULTS: Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 +/- 0.32 to 0.71 +/- 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (> or =5 mm Hg) in the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. CONCLUSION: Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.     

Dynamic cerebral autoregulatory capacity is affected early in Type 2 diabetes

Type 2 diabetes is associated with an increased risk of endothelial dysfunction and microvascular complications with impaired autoregulation of tissue perfusion. Both microvascular disease and cardiovascular autonomic neuropathy may affect cerebral autoregulation. In the present study, we tested the hypothesis that, in the absence of cardiovascular autonomic neuropathy, cerebral autoregulation is impaired in subjects with DM+ (Type 2 diabetes with microvascular complications) but intact in subjects with DM- (Type 2 diabetes without microvascular complications). Dynamic cerebral autoregulation and the steady-state cerebrovascular response to postural change were studied in subjects with DM+ and DM-, in the absence of cardiovascular autonomic neuropathy, and in CTRL (healthy control) subjects. The relationship between spontaneous changes in MCA V(mean) (middle cerebral artery mean blood velocity) and MAP (mean arterial pressure) was evaluated using frequency domain analysis. In the low-frequency region (0.07-0.15 Hz), the phase lead of the MAP-to-MCA V(mean) transfer function was 52+/-10 degrees in CTRL subjects, reduced in subjects with DM- (40+/-6 degrees ; P<0.01 compared with CTRL subjects) and impaired in subjects with DM+ (30+/-5 degrees ; P<0.01 compared with subjects with DM-), indicating less dampening of blood pressure oscillations by affected dynamic cerebral autoregulation. The steady-state response of MCA V(mean) to postural change was comparable for all groups (-12+/-6% in CTRL subjects, -15+/-6% in subjects with DM- and -15+/-7% in subjects with DM+). HbA(1c) (glycated haemoglobin) and the duration of diabetes, but not blood pressure, were determinants of transfer function phase. In conclusion, dysfunction of dynamic cerebral autoregulation in subjects with Type 2 diabetes appears to be an early manifestation of microvascular disease prior to the clinical expression of diabetic nephropathy, retinopathy or cardiovascular autonomic neuropathy.     

Reactivity of cerebral vessels in patients with circulatory encephalopathy, arterial hypertension and cerebral hypoperfusion risk

AIM: To study cerebral vasomotor reactivity (CVR) in patients with chronic cerebrovascular disturbances caused by arterial hypertension (AH) and to determine criteria of cerebral hypoperfusion risk during antihypertensive therapy. MATERIAL AND METHODS: 80 patients with chronic cerebrovascular disturbances because of AH and 15 normotensive subjects without any neurological pathology (control group) were examined using CT of the brain, duplex scanning of extra- and intracranial arteries, echocardiography. CVR was assessed with transcranial dollperography of the blood flow velocity in both middle cerebral arteries before and after nitroglycerine provoked test. RESULTS: CVR in the patients significantly differed from that of the controls. Main factors responsible for changes in CVR ara the age, form and duration of arterial hypertension, circadian rhythm of blood pressure, occlusive extra- or intracranial arteries disease. CT signs of focal (lacunes) or diffuse (leukoaraiosis) ischemic brain damage, deformations of the neck vessels, left ventricular hypertrophy may be leading markers of severe disturbances in CVR. CONCLUSION: In patients with chronic cerebrovascular disease disturbances of CVR arise due to arterio/arteriolopathy as a result of AH. Limitation of the vasodilatation potential demonstrates cerebral autoregulation dysfunction. Thus, factors and markers of CVR impairment can be considered as risk criteria of cerebral hypoperfusion during inadequate antihypertensive treatment.