This study aims to identify clinical determinants and factors that predict outcome including primary outcome and secondary outcome depending on factors in individual patients with Idiopathic intracranial hypertension treated by Dural venous sinus stenting.
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.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
40
40 patients with idiopathic intracranial hypertension according to Modified Dandy Criteria will subjected to Dural venous stenting
Faculty of Medicine
Asyut, Egypt
change in headache impact scale(HIT-6)
The Headache Impact Test (HIT) is a tool used to measure the impact headaches have on your ability to function on the job, at school, at home and in social situations. Your score shows you the effect that headaches have on normal daily life and your ability to function. minimum score 36 and maximum score 78
Time frame: 3, 6 months
Papilledema Friesen grading scale
The Frisen grading system is an objective criteria used to describe the degree of papilledema, which is swelling of the optic disc from increased ICP grading from zero to 5
Time frame: 3 months and 6 months
Visual filed Assessment Perimetry
Perimetry is the systematic measurement of visual field function (the total area where objects can be seen in the peripheral vision while the eye is focused on a central point).
Time frame: 3,6 months
Changes in other symptoms tinnitus, abducent nerve palsy and Transient visual Obsecuration
changes in other symptomology including tinnitus ,abducent nerve palsyand TVO
Time frame: 3,6 months
Stent Patency and pressure change
Diagnostic DSA follow up and measuring pressure gradient changes pre and post stenting
Time frame: 6 months
stent Patency
in stent stenosis and Adjacent stent stenosis
Time frame: 6 months
Safety outcome measures
Safety outcomes of occurrences of complication: Subdural Hematoma, Subarachnoid Hemorrhage, Intracerebral hematoma puncture site complication (retroperitoneal hematoma or femoral artery aneurysm)
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Time frame: 10 days
Quality of life improvement
Quality of life measure: SF-36 for fatigue.
Time frame: 3,6 months