Dural Venous Sinus Stent in Idiopathic Intracranial Hypertension

Idiopathic intracranial hypertension (IIH) has long been associated with the hallmark clinical triad of headaches, papilledema, and visual loss in the absence of neurologic signs (except possible CN VI palsy), Hydrocephalus or intracranial masses on CT or MRI. findings without evidence of thrombosis; lumbar puncture opening pressure of >25 cmH2O; normal biochemical and cytological composition of the CSF. The overall age-adjusted and gender-adjusted annual incidence is increasing and was reported to be 2.4 per 100 000 within the last decade (2002-2014).A variety of aetiologies have been suggested to explain the pathophysiology behind IIH, including meningeal inflammation, metabolic disturbances (e.g., hyper- or hypoadrenalism and hypoparathyroidism), medication effects (e.g., excess vitamin A, corticosteroids, and tetracycline), and cerebral venous hypertension.Imaging of patients with IIH is traditionally performed to exclude lesions that produce intracranial hypertension. MR imaging features of IIH include posterior globe flattening, a protrusion of the subarachnoid space in the cavum sellae (Empty Sella), distension of the preoptic subarachnoid space, enhancement of the prelaminar optic nerve, vertical tortuosity of the orbital optic nerve, and intraocular protrusion of the prelaminar optic nerve. Although these findings support the presence of elevated ICP and, thus, the diagnosis of IIH, they are not predictive of the severity of visual loss, and their absence does not exclude the diagnosis. It should not guide a specific management of patients with IIH .

The first line of treatment for IIH consists of weight loss and/or medical therapy including diuretics such as acetazolamide. When medical treatment fails, surgical options include cerebrospinal fluid (CSF) diversion via ventriculoperitoneal (VP) or lumboperitoneal (LP) shunting or optic nerve sheath fenestration. Recently, another etiology of cerebral venous hypertension has garnered increasing attention as a putative cause of IIH, cerebral venous Dural sinus stenosis. In medically refractory IIH patients with a physiologic pressure gradient across venous stenosis, cerebral venous stenting has emerged as an alternative treatment to traditional surgical approaches.

Transverse sinus stenosis can be seen in 2 morphologic forms: an extrinsic smooth gradually narrowing tapered stenosis and intrinsic discrete obstructions, presumably due to arachnoid granulations or fibrous septae. While intrinsic transverse sinus stenosis might cause IIH by completely occluding the transverse sinus, the extrinsic compression resolves with CSF drainage. might be secondary to intracranial hypertension. Venous sinus stenting (VSS) reduces intracranial venous pressures and improves idiopathic intracranial hypertension (IIH) symptoms.

Inclusion criteria

• 40 Patients of idiopathic intracranial hypertension subjected to Dural venous sinus stenting met the modified Dandy criteria for (IIH).

• Signs and symptoms of increased intracranial pressure: Headaches, nausea, vomiting, visual changes, and papilledema.
• No localizing or focal neurologic signs: Except for possible unilateral or bilateral VI nerve paresis.
• Elevated cerebrospinal fluid (CSF) pressure: Without cytologic or chemical abnormalities.
• No etiology for increased intracranial pressure: On neuroimaging findings.

• Age: 18-60 years
• Gender: Male or Female Inclusion Criteria.

Exclusion criteria

• Age less than or equal to 18 years.
• severe allergic reaction to iodine contrast or chronic Kidney disease.
• contraindication to general anesthesia or antiplatelet anticoagulants, Hemorrhagic Diathesis
• patients with secondary causes of intracranial hypertension: Dural arteriovenous fistula or other arteriovenous lesion affecting cortical venous flow.
• pregnancy.