CorrespondencePathophysiology of Acute Hydrocephalus After Subarachnoid Hemorrhage
Section snippets
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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Cited by (26)
Safety and Clinical Outcome of Good-Grade Aneurysmal Subarachnoid Hemorrhage in Non-Intensive Care Units
2020, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :Aneurysmal subarachnoid hemorrhage (SAH) is associated with both neurologic and systemic complications.1–7
High-Grade Aneurysmal Subarachnoid Hemorrhage: Predictors of Functional Outcome
2019, World NeurosurgeryCitation Excerpt :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
2017, World NeurosurgeryCitation Excerpt :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
A New Determinant of Poor Outcome After Spontaneous Subarachnoid Hemorrhage: Blood pH and the Disruption of Glossopharyngeal Nerve–Carotid Body Network: First Experimental Study
2017, World NeurosurgeryCitation Excerpt :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
2016, World NeurosurgeryCitation Excerpt :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