J Neurol Surg B Skull Base 2018; 79(S 01): S1-S188
DOI: 10.1055/s-0038-1633660
Poster Presentations
Georg Thieme Verlag KG Stuttgart · New York

Delayed Ipsilateral Facial Paresis after Operative Repair of Superior Semicircular Canal Dehiscence

Ryan Stephenson
1   UCLA Head and Neck Surgery, Los Angeles, California, United States
,
John J. Arsenault
2   The Warren Alpert Medical School of Brown University, Providence, Rhode Island, United States
,
Isaac Yang
3   UCLA Neurological Surgery, Los Angeles, California, United States
,
Quinton Gopen
1   UCLA Head and Neck Surgery, Los Angeles, California, United States
› Author Affiliations
Further Information

Publication History

Publication Date:
02 February 2018 (online)

 

Background Superior semicircular canal dehiscence (SSCD) is the result of a bony defect in the middle cranial fossa floor that is associated with symptoms of sound-induced vertigo, oscillopsia, hearing loss, pulsatile tinnitus, aural fullness, and autophony. This is thought to be secondary to a third-window effect from the dehiscence. Patients with symptoms not controlled by nonsurgical therapy may be treated by resurfacing the superior semicircular canal to eliminate the third-window effect. This report describes a previously undescribed complication of the surgical repair of this condition.

Methods A review of a patient database of SSCD at the UCLA revealed three cases of delayed facial nerve paresis. Patient characteristics were gathered from an electronic medical record including age, gender, side of surgery, time to onset of facial paresis, therapy received for paresis, and outcome. Thickness of the bone was measured using imaging software and measuring tools.

Results Three patients demonstrated delayed facial nerve paresis 4 to 21 days after surgery. All three cases had undergone left SSCD repair and experienced ipsilateral facial paresis. The age ranged from 38 to 70 years. Two patients were female and one was male. The severity of the paresis ranged from mild (House–Brackmann 2/6) to complete (House–Brackmann 6/6) and improved in each patient with oral corticosteroids. The thickness of bone overlying the geniculate ganglion was completely dehiscent in two patients and measured 0.9 mm in one patient.

Discussion This is the first report, to our knowledge, of delayed facial nerve paresis after repair of SSCD. Corticosteroids may be considered for initial therapy and improved symptoms in this small sample of patients. These patients each had radiographic findings of thin bone or dehiscence overlying the geniculate ganglion suggesting a possible relation of this dehiscence to manipulation of the middle cranial fossa floor.