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Endovascular management of labyrintho-vascular otic capsule dehiscence (type II): A different therapeutical approach
P Reynard1, M Hitier2, R Moreno-Gomez3
1Department of Audiology and Otoneurological Explorations, Civil Hospitals of Lyon, 69003 Lyon, France; Laboratoire Vibrations Acoustique, Insa Lyon, Villeurbanne, France.
Introduction:
Otic capsule dehiscence (OCD) encompasses a spectrum of third mobile window disorders, including type II variants characterized by a direct interface between the membranous labyrinth and adjacent vascular structures. These labyrinthine-vascular dehiscences (type IIa: superior semicircular canal-superior petrosal sinus (SPS); type IIb: internal jugular vein-vestibular structures) may induce pulsatile tinnitus, vertigo, and hearing loss. Endovascular treatment has emerged as a minimally invasive alternative to conventional surgery, aiming to reduce vascular pulsatility transmission to the inner ear. This study evaluates the interest, clinical outcomes and limitations of such approaches.
Methods:
We conducted a retrospective case series including patients with unilateral type II OCD confirmed by high-resolution imaging and presenting with disabling symptoms as assessed by the DHI and the THI. All patients underwent comprehensive audio-vestibular assessment and multimodal imaging. Endovascular treatment strategies included stenting of the SPS (type IIa) or stent-assisted coiling of the jugular bulb/internal jugular vein (type IIb). Outcomes were assessed clinically, audiometrically, and radiologically at follow-up.
Results:
Eight patients were included (4 type IIa, 4 type IIb). Endovascular treatment was feasible in most cases, with one technical failure and one conversion to surgery due to unfavorable venous anatomy. At 6 months, 7/7 evaluable patients showed marked clinical improvement, with significant reductions in THI and DHI scores. Pulsatile tinnitus and vertigo improved in the majority of cases. Audiometric outcomes were variable, with closure of the air-bone gap in 4 patients. Vestibular function remained largely preserved, with only transient postoperative impairment in one case. No major complications or venous thrombosis were observed on follow-up imaging.
Conclusion:
Endovascular management of type II OCD appears to be a safe and effective minimally invasive alternative in selected patients, particularly for vascular-related symptoms. The outcomes depend heavily on venous anatomy and meticulous preoperative imaging. While clinical outcomes are encouraging, limitations include technical feasibility and variable auditory results. Endovascular approaches may be considered a first-line option when anatomically suitable, with surgery reserved for selected or failed cases.
