Kader A, Young W L
Department of Neurological Surgery, Albert Einstein College of Medicine, New York, USA.
Neurosurg Clin N Am. 1996 Oct;7(4):767-81.
Significantly decreased perfusion pressure is common in vascular territories irrigating neuronal tissue in patients with AVMs. Without an adaptive mechanism, many of these patients would suffer from ischemic symptoms because their perfusion pressure would fall well below the lower limit of the "normal" autoregulation curve. There is evidence that an "adaptive autoregulatory displacement" occurs in these patients which maintains CBF above ischemic levels in spite of sometimes severe arterial hypotension. This "adaptive autoregulatory displacement" may explain why only a minority of patients appear to suffer from ischemic neurologic deficits attributed to "steal." Although CBF may be mildly reduced in hypotensive regions, function is maintained and there is no increase in CBV which would be expected as a result of ischemic arteriolar vasodilatation. The mechanism for the coupled reduction in CBF, CBV, and cerebral metabolic rate in AVM patients remains to be determined, but diaschisis and decreased neuronal mass may play a role. Adaptive changes in autoregulation may also explain, in part, why NPPB is only rarely encountered after AVM resection, despite the presence of significant arterial hypotension in the majority of patients. Chronic arteriolar vasodilation does not usually lead to vasomotor paralysis because most patients maintain a constant CBF in spite of increase in systemic arterial pressure. Our studies revealed bihemispheric changes in CBF after AVM removal which do not correlate with pre-resection arterial hypotension. Therefore, arterial hypotension may be a necessary but not sufficient condition for the development of "steal" and NPPB. Other nonhemodynamic mechanisms such as abnormal sensory and autonomic innervation of the cerebral vasculature may play a role in the pathogenesis of cerebral hyperemia. Finally, AVM hemodynamics appear to play an important role in the etiology of spontaneous ICH. There is accumulating evidence that lesions with severe arterial hypotension (and greatest "buffering effect") are least likely to hemorrhage. This is important in clinical practice because these lesions are usually large, high-flow AVMs, that is, those with the highest risk from treatment. Hemodynamic and anatomic characteristics of the venous drainage as well as interactions of AVM flow dynamics with the coagulation system also appear to play an important role in determining the natural history of what is probably a heterogeneous disease process with distinct prognostic risk groups.
在患有动静脉畸形（AVM）的患者中，灌注压显著降低在为神经组织供血的血管区域很常见。如果没有适应性机制，这些患者中的许多人会出现缺血症状，因为他们的灌注压会远低于“正常”自动调节曲线的下限。有证据表明，这些患者会发生“适应性自动调节移位”，尽管有时会出现严重的动脉低血压，但仍能将脑血流量（CBF）维持在缺血水平以上。这种“适应性自动调节移位”可能解释了为什么只有少数患者似乎患有归因于“盗血”的缺血性神经功能缺损。尽管低血压区域的CBF可能会轻度降低，但功能仍能维持，并且不会出现因缺血性小动脉血管舒张而预期的脑血容量（CBV）增加。AVM患者中CBF、CBV和脑代谢率的联合降低机制仍有待确定，但远隔性脑功能障碍和神经元数量减少可能起了作用。自动调节的适应性变化也可能部分解释了为什么尽管大多数患者存在明显的动脉低血压，但在AVM切除术后很少遇到术后正常灌注压突破（NPPB）。慢性小动脉血管舒张通常不会导致血管运动麻痹，因为大多数患者尽管全身动脉压升高，但仍能维持恒定的CBF。我们的研究显示，AVM切除术后CBF出现双侧半球变化，这与切除术前的动脉低血压无关。因此，动脉低血压可能是发生“盗血”和NPPB的必要但不充分条件。其他非血流动力学机制，如脑血管异常的感觉和自主神经支配，可能在脑充血的发病机制中起作用。最后，AVM血流动力学似乎在自发性脑出血（ICH）的病因中起重要作用。越来越多的证据表明，动脉低血压严重（“缓冲效应”最大）的病变出血的可能性最小。这在临床实践中很重要，因为这些病变通常是大型高流量AVM，即治疗风险最高的那些。静脉引流的血流动力学和解剖学特征以及AVM血流动力学与凝血系统的相互作用，在确定这一可能是具有不同预后风险组的异质性疾病过程的自然史中似乎也起重要作用。
