Elsevier

World Neurosurgery

Volume 82, Issues 1–2, July–August 2014, Pages e386-e387
World Neurosurgery

Correspondence
Pathophysiology of Acute Hydrocephalus After Subarachnoid Hemorrhage

https://doi.org/10.1016/j.wneu.2013.08.007Get rights and content

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Letter:

I read the article written by Shah et al. (14). As noted by Niemelä and Marbacher (13), the etiology of hydrocephalus after subarachnoid hemorrhage (SAH) is not yet fully understood. A better understanding of the pathophysiology of hydrocephalus after SAH would lead to better patient outcomes. In our study, we stated increased cerebrospinal fluid secretion may be triggered by hemorrhage at the early phase via stimulation of the irritant receptors at glossopharyngeal and vagal nerve endings,

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    Aneurysmal subarachnoid hemorrhage (SAH) is associated with both neurologic and systemic complications.1–7

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    Therefore, in addition to early aggressive resuscitation and definitive treatment of the aneurysm, targeting modifiable predictors of perioperative cerebral infarction, including the duration of intraoperative arterial occlusion and admission plasma glucose, may improve outcomes in patients with high-grade aSAH.37-39 Acute hydrocephalus in aSAH, resulting from an abrupt impairment of CSF flow at the ictus of aneurysm rupture, has been established as an important risk factor for shunt-dependent hydrocephalus.40-42 However, the mechanisms that underlie the transition between the acute obstructive and chronic communicating phases of post-aSAH hydrocephalus have yet to be fully elucidated.43

  • New Evidence for Causal Central Mechanism of Hyperglycemia in Subarachnoid Hemorrhage Secondary to Ischemic Degenerative Disruption of Circuitry Among Insular Cortex, Nodose Ganglion, and Pancreas: Experimental Study

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    Despite major improvements in surgical techniques for aneurysmal SAH, 30-day mortality from SAH has been shown to have changed little from what it was 40 years ago.16 A better understanding of the pathophysiology of hydrocephalus after SAH would lead to better patient outcomes.17 Understanding of the pathology after SAH continues to evolve.18

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    In SAH, brain damage is attributable to compromised cerebral metabolism, ischemia, tissue hypoxia, and the consequence of these events.27 Better understanding, identification, and management of modifiable risk factors for SAH are pivotal to reducing its incidence.28,29 It would undoubtedly lead to better patient outcome.29

  • Uncovering a New Cause of Obstructive Hydrocephalus Following Subarachnoid Hemorrhage: Choroidal Artery Vasospasm-Related Ependymal Cell Degeneration and Aqueductal Stenosis - First Experimental Study

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    This study has some limitations. This is an experimental, observational study in a rabbit SAH model, and our experimental rabbit model of SAH may not accurately mimic the human disease process.16,23,24,28 Perhaps the most important limitation of the study is that it is difficult to evaluate these changes in vivo or through autopsy, particularly in humans with SAH.34

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