Abstract

Idiopathic intracranial hypertension (IIH) is a debilitating condition that has traditionally been difficult to treat. In recent years, there has been increasing focus on the role of intracranial venous hypertension in the pathophysiology of IIH. Based on increased understanding of this pathophysiology, venous sinus stenting (VSS) has emerged as a safe and reliable treatment for a certain population of patients with IIH. Stratifying patients with IIH based on the status of their venous outflow can provide insight into which patients may enjoy reduction in their symptoms after VSS and provides information regarding why some patients may have symptom recurrence. The traditional view of IIH as a disease due to obesity in young women has been cast into doubt as the understanding of the role of intracranial venous hypertension has improved.

Highlights

  • Idiopathic intracranial hypertension (IIH), previously referred to as pseudotumor cerebri, or more recently chronic intracranial venous hypertension syndrome (CIVHS) [1], is a condition characterized by a combination of intractable headaches, papilledema, visual symptoms, tinnitus, and elevated cerebrospinal fluid (CSF) opening pressure (OP) on lumbar puncture (LP) in the absence of an intracranial mass

  • This has led to the development of venous sinus stenting (VSS) as a safe and effective treatment option for patients with IIH and a documented trans-stenosis pressure gradient (TSPG) [2]

  • While VSS was first reported as a successful treatment for IIH in 2002 [3], only recently have we begun to piece together the pathophysiology of intracranial venous hypertension and how it relates to the clinical syndrome of IIH

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Summary

Introduction

Idiopathic intracranial hypertension (IIH), previously referred to as pseudotumor cerebri, or more recently chronic intracranial venous hypertension syndrome (CIVHS) [1], is a condition characterized by a combination of intractable headaches, papilledema, visual symptoms, tinnitus, and elevated cerebrospinal fluid (CSF) opening pressure (OP) on lumbar puncture (LP) in the absence of an intracranial mass. This is a debilitating condition that has traditionally been managed relatively unsuccessfully with a variety of treatments, including high doses of carbonic anhydrase inhibitors, weight loss, CSF shunting procedures, and optic nerve sheath fenestration surgeries. The pathophysiologic mechanisms leading to these elevated pressures continue to play a role after VSS, and our improved understanding of these mechanisms continues to influence post-operative management strategies

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