• DOI:10.1212/01.wnl.0000299894.30700.d2
• Corpus ID: 30729677

Endovascular treatment of idiopathic intracranial hypertension

@article{Donnet2008EndovascularTO,
  title={Endovascular treatment of idiopathic intracranial hypertension},
  author={Anne Donnet and Philippe Metellus and Olivier L{\'e}vrier and Choukri Mekkaoui and S Fuentes and Henri Dufour and John Conrath and François Grisoli},
  journal={Neurology},
  year={2008},
  volume={70},
  pages={641 - 647}
}

• A. Donnet, P. Metellus, +5 authors F. Grisoli
• Published 19 February 2008
• Medicine
• Neurology

Objective: To explore the relation between venous disease and idiopathic intracranial hypertension. Background: Optic nerve sheath fenestration and ventricular shunting are the classic methods when medical treatment has failed. Idiopathic intracranial hypertension is caused by venous sinus obstruction in an unknown percentage of cases. Recently, endoluminal venous sinus stenting was proposed as an alternative treatment. Methods: Ten consecutive patients with refractory idiopathic intracranial hypertension underwent examination with direct retrograde cerebral venography and manometry to characterize the morphologic features and venous pressures in their cerebral venous sinus. All patients demonstrated morphologic obstruction of the venous lateral sinuses. The CSF pressure was measured in all patients. The CSF pressure on lumbar puncture ranged from 27 to 45 mm Hg with normal composition. All patients had headache, and visual acuity loss was noted in eight patients. Funduscopic examination demonstrated papilledema for all patients. All patients had stenting of the venous sinuses. Intrasinus pressures were recorded before and after the procedure and correlated with clinical outcome. Results: Intrasinus pressures were invariably reduced by stenting. For headache, six patients were rendered asymptomatic, two were improved, and two were unchanged after venous sinus stenting for a mean (± SD) follow-up of 17 ± 10.1 months (range 6 to 36 months). Papilledema disappeared in all patients. In all cases, CSF pressure was normalized at 3-month follow-up. In all patients, direct retrograde cerebral venography or multidetector row CT angiography was performed at 6-month follow-up and demonstrated the absence of stent thrombosis. Conclusion: The importance of venous sinus disease in the etiology of idiopathic intracranial hypertension is probably underestimated. Patients with idiopathic intracranial hypertension in whom a venous sinus stenosis is demonstrated by a noninvasive radiologic workup should be evaluated with direct retrograde cerebral venography and manometry. In patients with a lesion of the venous sinuses who experienced medical treatment failure, endovascular stent placement seems to be an interesting alternative to classic surgical approaches.