John P Carey1, Americo A Migliaccio, Lloyd B Minor. 1. Department of Otolaryngology-Head & Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. jcarey@jhmi.edu
Abstract
OBJECTIVE: To characterize semicircular canal function before and after surgery for superior semicircular canal dehiscence (SCD) syndrome. STUDY DESIGN: Prospective unblinded study of physiologic effect of intervention. SETTING: Tertiary referral center. PATIENTS: Patients with SCD syndrome documented by history, sound- or pressure-evoked eye movements, vestibular-evoked myogenic potential testing, and high-resolution multiplanar computed tomographic scans. INTERVENTION: Nineteen subjects with SCD had quantitative measurements of their angular vestibulo-ocular reflexes (AVOR) in response to rapid rotary head thrusts measured by magnetic search coil technique before and after middle fossa approach and repair of the dehiscence. In 18 subjects, the dehiscence was plugged; and in 1, it was resurfaced. MAIN OUTCOME MEASURES: The AVOR gains (eye velocity/head velocity) for excitation of each of the semicircular canals. RESULTS: Vertigo resulting from pressure or loud sounds resolved in each case. Before surgery, mean AVOR gains were normal for the ipsilateral horizontal (0.94 +/- 0.07) and posterior (0.84 +/- 0.09) canals. For the superior canal to be operated on, AVOR gain was 0.75 +/- 0.13; but this was not significantly lower than the gain for the contralateral superior canal (0.82 +/- 0.11, p = 0.08). Mean AVOR gain decreased by 44% for the operated superior canals (to 0.42 +/- 0.11, p < 0.0001). There was a 13% decrease in gain for the ipsilateral posterior canal (p = 0.02), perhaps because plugging affected the common crus in some cases. There was a 10% decrease in gain for excitation of the contralateral posterior canal (p < 0.0001), which likely reflects the loss of the inhibitory contribution of the plugged superior canal during head thrusts exciting the contralateral posterior canal. Mean AVOR gain did not change for any of the other canals, but two subjects did develop hypofunction of all three ipsilateral canals postoperatively. CONCLUSION: Middle fossa craniotomy and repair of SCD reduce the function of the operated superior canal but typically preserve the function of the other ipsilateral semicircular canals.
OBJECTIVE: To characterize semicircular canal function before and after surgery for superior semicircular canal dehiscence (SCD) syndrome. STUDY DESIGN: Prospective unblinded study of physiologic effect of intervention. SETTING: Tertiary referral center. PATIENTS: Patients with SCD syndrome documented by history, sound- or pressure-evoked eye movements, vestibular-evoked myogenic potential testing, and high-resolution multiplanar computed tomographic scans. INTERVENTION: Nineteen subjects with SCD had quantitative measurements of their angular vestibulo-ocular reflexes (AVOR) in response to rapid rotary head thrusts measured by magnetic search coil technique before and after middle fossa approach and repair of the dehiscence. In 18 subjects, the dehiscence was plugged; and in 1, it was resurfaced. MAIN OUTCOME MEASURES: The AVOR gains (eye velocity/head velocity) for excitation of each of the semicircular canals. RESULTS: Vertigo resulting from pressure or loud sounds resolved in each case. Before surgery, mean AVOR gains were normal for the ipsilateral horizontal (0.94 +/- 0.07) and posterior (0.84 +/- 0.09) canals. For the superior canal to be operated on, AVOR gain was 0.75 +/- 0.13; but this was not significantly lower than the gain for the contralateral superior canal (0.82 +/- 0.11, p = 0.08). Mean AVOR gain decreased by 44% for the operated superior canals (to 0.42 +/- 0.11, p < 0.0001). There was a 13% decrease in gain for the ipsilateral posterior canal (p = 0.02), perhaps because plugging affected the common crus in some cases. There was a 10% decrease in gain for excitation of the contralateral posterior canal (p < 0.0001), which likely reflects the loss of the inhibitory contribution of the plugged superior canal during head thrusts exciting the contralateral posterior canal. Mean AVOR gain did not change for any of the other canals, but two subjects did develop hypofunction of all three ipsilateral canals postoperatively. CONCLUSION: Middle fossa craniotomy and repair of SCD reduce the function of the operated superior canal but typically preserve the function of the other ipsilateral semicircular canals.