The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

Abstract

Hydrocephalus is a common complication of aneurysmal subarachnoid hemorrhage (aSAH) and reportedly contributes to poor neurological outcomes. In this review, we summarize the molecular and cellular mechanisms involved in the pathogenesis of hydrocephalus following aSAH and summarize its treatment strategies. Various mechanisms have been implicated for the development of chronic hydrocephalus following aSAH, including alterations in cerebral spinal fluid (CSF) dynamics, obstruction of the arachnoid granulations by blood products, and adhesions within the ventricular system. Regarding molecular mechanisms that cause chronic hydrocephalus following aSAH, we carried out an extensive review of animal studies and clinical trials about the transforming growth factor-β/SMAD signaling pathway, upregulation of tenascin-C, inflammation-dependent hypersecretion of CSF, systemic inflammatory response syndrome, and immune dysregulation. To identify the ideal treatment strategy, we discuss the predictive factors of shunt-dependent hydrocephalus between surgical clipping and endovascular coiling groups. The efficacy and safety of other surgical interventions including the endoscopic removal of an intraventricular hemorrhage, placement of an external ventricular drain, the use of intraventricular or cisternal fibrinolysis, and an endoscopic third ventriculostomy on shunt dependency following aSAH were also assessed. However, the optimal treatment is still controversial, and it necessitates further investigations. A better understanding of the pathogenesis of acute and chronic hydrocephalus following aSAH would facilitate the development of treatments and improve the outcome.

Admission Lower Serum Phosphate Ion Levels Predict Acute Hydrocephalus of Aneurysmal Subarachnoid Hemorrhage

“…Emerging data have established that inflammatory pathways are likely to play an essential role in the pathogenesis of aHCP. Inflammatory markers in CSF and peripheral blood are associated with the possibility of developing aHCP ( 9 , 10 , 12 , 39 ). Lower sPi levels are negatively correlated with the levels of inflammatory cytokines ( 19 ).…”

“…Aneurysmal subarachnoid hemorrhage (aSAH) is a fast developing, devastating, and life-threatening hemorrhagic stroke with high mortality and disability ( 1 – 3 ). Hydrocephalus (HCP) is a frequent complication of aSAH, with a reported incidence ranging from 6.5 to 85% ( 4 – 7 ), which is classified as acute (0–3 days post-hemorrhage), subacute (4–13 days post-hemorrhage), or chronic (14 days post-hemorrhage) ( 8 , 9 ). Acute hydrocephalus (aHCP) is a potentially treatable cause of early neurological deterioration, and 20% of aSAH patients develop aHCP within 72 h ( 6 , 8 ).…”

Disturbances of cerebrospinal fluid dynamics as a complication of aneurysmal subarachnoid hemorrhage: predictors of development and influence of aneurysm occlusion method on the development of shunt-dependent hydrocephalus

“…ризм ВББ -серед прооперованих ендоваскулярно (9 (40,9 %) Чинниками, що призводять до розвитку хронічної гідроцефалії після аневризматичного САК, вважають різні механізми (зміну ліквородинаміки, обструкцію пахіонових грануляцій продуктами розпаду крові та розвиток спайкового процесу в шлуночковій системі) [5].…”

Prediction of Adult Post-hemorrhagic Hydrocephalus: A Risk Score Based on Clinical Data

“…Attention has been paid to the change in osmotic pressure caused by a large amount of protein accumulation in the CSF, which disrupts the osmotic balance of CSF circulation causing hydrocephalus [36]. Several studies have shown that early CSF drainage plus EVD can reduce the content of erythrocyte degradation products and CSF-TP, thereby reducing the incidence of CSF obstruction and hydrocephalus [37][38][39]. Given that the correlation between CSF-TP and hydrocephalus has been con rmed [40], the present study included CSF-TP as the research object.…”