Daffertshofer M, Hennerici M
Department of Neurology, University of Heidelberg--Klinikum Mannheim, Germany.
J Clin Ultrasound. 1995 Feb;23(2):125-38. doi: 10.1002/jcu.1870230207.
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 dysintegration 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.
维持脑灌注压是预防脑缺血的前提条件。全身灌注压的生理波动可通过脑血管自动调节得到补偿。脑灌注不足可能由以下原因导致：(1) 全身血流动力学衰竭（如严重动脉狭窄远端），使血管调节能力过度负荷；(2) 脑血管自动调节功能障碍和耗竭；或 (3) 两者皆有。超声具有出色的时间分辨率，是非侵入性的，并且易于用于后续检查。尽管经颅多普勒超声的空间分辨率较差，但它已被用于测定脑灌注储备研究，即在高碳酸血症期间或应用血管活性药物（如乙酰唑胺）时测量脑血流速度（CBFV）。这种方法评估了在脑供血动脉严重狭窄或闭塞远端存在血流动力学损害的患者的血管舒缩调节。在倾斜试验期间监测CBFV可直接测量脑自动调节。在患有全身性直立性低血压的患者中，尽管全身血压调节正常，但可能会显示脑血管补偿的维持或失败，甚至更重要的是脑血管调节异常。在适当的神经元刺激期间，CBFV变化反映了血管神经元耦合。神经元功能障碍与CBFV异常有关，例如有先兆偏头痛患者大脑后动脉（PCA）局灶性脑功能障碍的情况，在扩散性抑制期间，血管神经元耦合和缺血的大量改变具有威胁性。在发作间期，血管神经元耦合的高度显著不对称增强可能是这些患者的触发机制。由于各种神经元刺激（如运动感觉或认知范式）的空间分辨率较差，仅能引发大脑中动脉（MCA）CBFV全局变化中代表性不足的局部神经元区域，因此在MCA区域内测试血管神经元耦合更为困难。然而，运动刺激诱发的CBFV可用于指示急性脑缺血伴感觉运动性偏瘫过程中血管神经元耦合的解体，而且似乎对运动功能缺损具有预后价值。
