Intraventricular and periventricular lesions often result in obstructive hydrocephalus and can be effectively managed by ventriculoscopy. This avoids the significant risk of injury to vascular and neural structures that are encountered during open craniotomy and exposure of these deep lesions. It is important to consider endoscopic third ventriculostomy (ETV) in any adult patient with obstructive hydrocephalus given the significantly higher long-term success rate of primary ETV compared with VP shunts.
View Article and Find Full Text PDFThis article provides an in-depth review of cerebrospinal fluid (CSF) shunts for managing hydrocephalus and idiopathic intracranial hypertension, with a focus on advanced surgical techniques and strategies to prevent complications. It examines the placement of ventricular, lumbar, peritoneal, atrial, and pleural catheters, highlighting the benefits of neuro-navigation, endoscopic visualization, and laparoscopic-assisted approaches. Evidence-based methods to reduce shunt infections, malfunctions, and overdrainage are discussed, along with a comparative analysis of shunt types tailored to individual patient needs.
View Article and Find Full Text PDFIn 1965, Hakim and Adams described 3 patients with normal pressure hydrocephalus who responded to treatment with a ventriculoatrial shunt. Afterward the adoption of shunt treatment without clear diagnostic criteria and surgical techniques resulted in poor outcomes with significant complications. The clinical practice guidelines for the diagnosis and treatment of idiopathic normal pressure hydrocephalus were first published by the Japanese Neurosurgical Society in 2004 and the international guidelines were published in 2005.
View Article and Find Full Text PDFAdult hydrocephalus is a common neurologic condition with an estimated prevalence of 85 per 100,000 globally, caused by abnormal cerebrospinal fluid (CSF) accumulation within the cerebral ventricles. Subtypes include idiopathic normal pressure hydrocephalus, posthemorrhagic, postinfectious, posttraumatic, and tumor-associated forms. Its pathophysiology involves glymphatic dysfunction, neuroinflammation, vascular compromise, and impaired CSF absorption.
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