Pomeranz S, Beni L, Shalit M N
Neurosurgery Department, Hadassah University Hospital, Jerusalem, Israel.
Acta Neurochir (Wien). 1993;122(1-2):113-7. doi: 10.1007/BF01446996.
Intracranial hypotension is a known clinical entity but its pathophysiology has been meagerly studied. Any setting with cerebrospinal fluid leakage or drainage can cause intracranial hypotension. A feline model of kaolin induced chronic hydrocephalus with controlled cerebrospinal fluid drainage from a lateral ventricle yields reproducible intracranial hypotension of up to -15 torr for several hours to -80 torr of about 10 minutes. The magnitude of this hypotension is significantly greater than can be attained by cisterna magna drainage. This new model allows multiple cerebral parameters to be studied during intracranial hypotension. In 11 cats with stable blood pressure and intracranial hypotension of at least -15 torr, regional blood flow utilizing the hydrogen clearance method in the cerebral cortex and subcortical nuclei was unchanged relative to the baseline. These results imply that: 1) cerebral vascular autoregulation is maintained during significantly increased perfusion pressure due to negative intracranial pressure, 2) the symptomatology of clinical intracranial hypotension is not due to decreased cerebral perfusion.
颅内低压是一种已知的临床病症,但其病理生理学研究甚少。任何伴有脑脊液漏出或引流的情况都可导致颅内低压。一种高岭土诱导的慢性脑积水猫模型,通过侧脑室进行可控脑脊液引流,可产生数小时内高达 -15 托、约 10 分钟内达 -80 托的可重复性颅内低压。这种低血压的程度明显大于通过枕大池引流所能达到的程度。这个新模型允许在颅内低压期间研究多个脑参数。在 11 只血压稳定且颅内低压至少为 -15 托的猫中,利用氢清除法测得的大脑皮质和皮质下核的区域血流量相对于基线没有变化。这些结果表明:1)由于颅内负压导致灌注压显著升高时,脑血管自动调节功能得以维持;2)临床颅内低压的症状并非由脑灌注减少所致。