Wagshul Mark E, Kelly Erin J, Yu Hui Jing, Garlick Barbara, Zimmerman Tom, Egnor Michael R
Department of Radiology, Stony Brook University, Stony Brook, New York 11794, USA.
J Neurosurg Pediatr. 2009 May;3(5):354-64. doi: 10.3171/2009.1.PEDS08109.
The intracranial pulse pressure is often increased when neuropathology is present, particularly in cases of increased intracranial pressure (ICP) such as occurs in hydrocephalus. This pulse pressure is assumed to originate from arterial blood pressure oscillations entering the cranium; the fact that there is a coupling between the arterial blood pressure and the ICP is undisputed. In this study, the nature of this coupling and how it changes under conditions of increased ICP are investigated.
In 12 normal dogs, intracarotid and parenchymal pulse pressure were measured and their coupling was characterized using amplitude and phase transfer function analysis. Mean intracranial ICP was manipulated via infusions of isotonic saline into the spinal subarachnoid space, and changes in transfer function were monitored.
Under normal conditions, the ICP wave led the arterial wave, and there was a minimum in the pulse pressure amplitude near the frequency of the heart rate. Under conditions of decreased intracranial compliance, the ICP wave began to lag behind the arterial wave and increased significantly in amplitude. Most interestingly, in many animals the pulse pressure exhibited a minimum in amplitude at a mean pressure that coincided with the transition from a leading to lagging ICP wave.
This transfer function behavior is characteristic of a resonant notch system. This may represent a component of the intracranial Windkessel mechanism, which protects the microvasculature from arterial pulsatility. The impairment of this resonant notch system may play a role in the altered pulse pressure in conditions such as hydrocephalus and traumatic brain swelling. New models of intracranial dynamics are needed for understanding the frequency-sensitive behavior elucidated in these studies and could open a path for development of new therapies that are geared toward addressing the pulsation dysfunction in pathological conditions, such as hydrocephalus and traumatic brain injury, affecting ICP and flow dynamics.
当存在神经病理学情况时,尤其是在颅内压(ICP)升高的情况下,如脑积水时,颅内脉压通常会升高。这种脉压被认为源于进入颅骨的动脉血压波动;动脉血压与颅内压之间存在耦合这一事实是无可争议的。在本研究中,研究了这种耦合的性质以及在颅内压升高的情况下它是如何变化的。
在12只正常犬中,测量颈内动脉和实质脉压,并使用幅度和相位传递函数分析来表征它们之间的耦合。通过向脊髓蛛网膜下腔输注等渗盐水来控制平均颅内压,并监测传递函数的变化。
在正常情况下,颅内压波领先于动脉波,并且在心率频率附近脉压幅度存在最小值。在颅内顺应性降低的情况下,颅内压波开始滞后于动脉波,并且幅度显著增加。最有趣的是,在许多动物中,脉压在平均压力处幅度出现最小值,该平均压力与颅内压波从领先变为滞后的转变相吻合。
这种传递函数行为是共振陷波系统的特征。这可能代表颅内风箱机制的一个组成部分,该机制可保护微血管免受动脉搏动的影响。这种共振陷波系统的损害可能在脑积水和创伤性脑肿胀等情况下脉压改变中起作用。需要新的颅内动力学模型来理解这些研究中阐明的频率敏感行为,并可能为开发新的治疗方法开辟道路,这些治疗方法旨在解决影响颅内压和血流动力学的病理状况(如脑积水和创伤性脑损伤)中的搏动功能障碍。