Lolansen Sara Diana, Rostgaard Nina, Capion Tenna, Norager Nicolas H, Olsen Markus Harboe, Juhler Marianne, Mathiesen Tiit Illimar, MacAulay Nanna
Department of Neuroscience, University of Copenhagen, DK-2200 Copenhagen, Denmark.
Department of Neurosurgery, University Hospital of Copenhagen-Rigshospitalet, DK-2100 Copenhagen, Denmark.
Int J Mol Sci. 2023 Jul 14;24(14):11476. doi: 10.3390/ijms241411476.
The molecular mechanisms underlying the development of posthemorrhagic hydrocephalus (PHH) remain incompletely understood. As the disease pathogenesis often cannot be attributed to visible cerebrospinal fluid (CSF) drainage obstructions, we here aimed to elucidate whether elevated CSF osmolality following subarachnoid hemorrhage (SAH) could potentiate the formation of ventricular fluid, and thereby contribute to the pathological CSF accumulation observed in PHH. The CSF osmolality was determined in 32 patients with acute SAH after external ventricular drainage (EVD) placement and again upon EVD removal and compared with the CSF osmolality from 14 healthy control subjects undergoing vascular clipping of an unruptured aneurism. However, we found no evidence of elevated CSF osmolality or electrolyte concentration in patients with SAH when compared to that of healthy control subjects. We detected no difference in CSF osmolality and electrolyte content in patients with successful EVD weaning versus those that were shunted due to PHH. Taken together, elevated CSF osmolality does not appear to underlie the development of PHH following SAH. The pathological CSF accumulation observed in this patient group must thus instead be attributed to other pathological alterations associated with the abnormal presence of blood within the CSF compartments following SAH.
出血后脑积水(PHH)发展的分子机制仍未完全明确。由于该疾病的发病机制往往不能归因于可见的脑脊液(CSF)引流梗阻,我们在此旨在阐明蛛网膜下腔出血(SAH)后CSF渗透压升高是否会促进脑室液的形成,从而导致PHH中观察到的病理性CSF积聚。在32例急性SAH患者进行脑室外引流(EVD)时测定CSF渗透压,并在拔除EVD时再次测定,同时与14例接受未破裂动脉瘤血管夹闭术的健康对照受试者的CSF渗透压进行比较。然而,与健康对照受试者相比,我们没有发现SAH患者CSF渗透压或电解质浓度升高的证据。我们未检测到成功撤掉EVD的患者与因PHH而接受分流的患者在CSF渗透压和电解质含量方面存在差异。综上所述,CSF渗透压升高似乎并非SAH后PHH发展的基础。因此,该患者组中观察到的病理性CSF积聚必定归因于SAH后CSF腔室内血液异常存在相关的其他病理改变。