PDF(Pubmed)
Abstract：
BACKGROUND: Idiopathic intracranial hypertension is a disease characterized by increased intracranial cerebrospinal fluid volume and pressure without evidence of other intracranial pathology. Dural sinuses are rigid structures representing a privileged low-pressure intracranial compartment. Rigidity of dural sinus ensures that the large physiologic fluctuations of cerebrospinal fluid pressure associated with postural changes or to Valsalva effect cannot be transmitted to the sinus. An abnormal dural sinus collapsibility, especially when associated with various anatomical sinus narrowing, has been proposed as a key factor in the pathogenesis of idiopathic intracranial hypertension. This pathogenetic model is based on an excessive collapsibility of the dural sinuses that leads to the triggering of a self-limiting venous collapse positive feedback-loop between the cerebrospinal fluid pressure, that compresses the sinus, and the increased dural sinus pressure upstream, that reduces the cerebrospinal fluid reabsorption rate, increasing cerebrospinal fluid volume and pressure at the expense of intracranial compliance and promoting further sinus compression. Intracranial compliance is the ability of the craniospinal space to accept small volumetric increases of one of its compartments without appreciable intracranial pressure rise. In idiopathic intracranial hypertension, a condition associated with a reduced rate of CSF reabsorption leading to its volumetric expansion, a pathologically reduced IC precedes and accompanies the rise of ICP. Syncope is defined as a transient loss of consciousness due to a transient cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. A transient global cerebral hypoperfusion represents the final mechanism of syncope determined by cardiac output and/or total peripheral resistance decrease. There are many causes determining low cardiac output including reflex bradycardia, arrhythmias, cardiac structural disease, inadequate venous return, and chronotropic and inotropic incompetence. Typically, syncopal transient loss of consciousness is mainly referred to an extracranial mechanism triggering a decrease in cardiac output and/or total peripheral resistance. Conversely, the association of syncope with a deranged control of intracranial compliance related to cerebral venous outflow disorders has been only anecdotally reported.
METHODS: We report on a 57-year-old woman with daily recurrent orthostatic hypotension syncope and idiopathic intracranial hypertension-related headaches, which resolved after lumbar puncture with cerebrospinal fluid subtraction.
CONCLUSIONS: A novel mechanism underlying the triggering of orthostatic syncope in the presence of intracranial hypertension-dependent reduced intracranial compliance is discussed.
METHODS: We report on a 57-year-old woman with daily recurrent orthostatic hypotension syncope and idiopathic intracranial hypertension-related headaches, which resolved after lumbar puncture with cerebrospinal fluid subtraction.
CONCLUSIONS: A novel mechanism underlying the triggering of orthostatic syncope in the presence of intracranial hypertension-dependent reduced intracranial compliance is discussed.
摘要：
背景：特发性颅内高压是一种以颅内脑脊液容量和压力增加为特征的疾病，没有其他颅内病理的证据。硬脑膜窦是刚性结构，代表特权低压颅内室。硬脑膜窦的刚性确保与姿势变化或Valsalva效应相关的脑脊液压力的巨大生理波动不能传递到窦。硬膜窦异常塌陷，特别是当与各种解剖窦狭窄相关时，已被认为是特发性颅内高压发病的关键因素。此发病模型基于硬脑膜窦的过度塌陷，导致触发脑脊液压力之间的自限静脉塌陷正反馈回路，压缩鼻窦，上游硬脑膜窦压力升高，降低脑脊液重吸收率，以颅内顺应性和促进鼻窦进一步压迫为代价增加脑脊液容量和压力。颅内顺应性是颅脊髓间隙接受其一个隔室的小体积增加而没有明显颅内压升高的能力。在特发性颅内高压中，与CSF重吸收速率降低相关的条件，导致其体积膨胀，病理性降低的IC先于并伴随着ICP的兴起。晕厥被定义为由于以快速发作为特征的短暂性脑灌注不足而导致的短暂性意识丧失。持续时间短,自发完全恢复。短暂性全脑灌注不足代表由心输出量和/或总外周阻力降低决定的晕厥的最终机制。有许多原因可以确定低心输出量，包括反射性心动过缓，心律失常,心脏结构疾病,静脉回流不足,以及变时性和肌力能力不足。通常,晕厥短暂的意识丧失主要是指引起心输出量和/或总外周阻力减少的颅外机制。相反，仅有轶事报道了晕厥与脑静脉流出障碍相关的颅内顺应性控制紊乱的关系。
方法：我们报告了一名57岁女性，每天反复出现体位性低血压晕厥和特发性颅内高压相关头痛，经腰穿脑脊液减量后解决。
结论：讨论了在存在颅内高压依赖性颅内顺应性降低的情况下引发直立性晕厥的新机制。
方法：我们报告了一名57岁女性，每天反复出现体位性低血压晕厥和特发性颅内高压相关头痛，经腰穿脑脊液减量后解决。
结论：讨论了在存在颅内高压依赖性颅内顺应性降低的情况下引发直立性晕厥的新机制。
