Lehmann et al. Journal of Medical Case Reports 2011, 5:47 http://www.jmedicalcasereports.com/content/5/1/47 Page 2 of 3 Figure 1 High-resolution computed tomographic (CT) scan showing a left stapes prosthesis. There appears to be an otospongiotic focus by the anterior lip of the stapes footplate. The platinum-Teflon prostheses appear to be extending deep into the vestibule. Auditory manifestations include hyperacusis to bone- conducted sounds and conductive hearing loss with normal acoustic reflexes. A directed patient history, documentation of upward and torsional nystagmus evoked by sound and/or pressure and radiologic findings are helpful in the diagnosis of SCD. Acoustic reflexes and vestibular evoked myogenic potentials (VEMPs) aid in the identification of patients with an apparent conductive hearing loss with normal acoustic reflexes or those patients who are found to have an asymptomatic dehiscence on radiology [4]. The treat- ment involves avoidance of the precipitating stimuli [5]. Figure 2 High-resolution CT scan showing a left superior semicircular canal dehiscence (arrow). The typical audiometric findings are of an air-bone gap in the low and middle frequencies (≤2,000 Hz) with no gap or only a small gap at higher frequencies. The low- frequency (<2,000 Hz) bone conduction thresholds are sometimes at supranormal levels, 0 to -20 dB or better. The lack of middle ear pathologic findings as a cause of the conductive hearing loss (CHL) in SCD has been well documented by a variety of diagnostic tests, such as tym- panometry, acoustic reflexes, laser Doppler vibrometry, air-conducted VEMP testing, otoacoustic emission test- ing and exploration of the middle ear [6-13]. Definitive evidence that the SCD can cause CHL is demonstrated by resolution of the air-bone gap upon patching or plug- ging the dehiscence, as reported by various investigators [10,14]. The mechanism of CHL in a patient with SCD is a combination of an increase in air conduction thresholds combined with an improvement in bone conduction thresholds [15,16] as described above. Conclusion In choosing treatment options, the severity of symptoms in each individual patient should be considered. Patients with minimal or minor symptoms should avoid provocative sti- muli and undergo supportive measures such as vestibular rehabilitation or vestibular suppressants. These patients may require longer follow-up to ensure symptom resolution. Patients with disabling sound- or pressure-induced vertigo, imbalance or oscillopsia may require surgical treatment. The standard surgical options include middle fossa craniot- omy for superior canal occlusion or resurfacing and trans- mastoid superior semicircular canal occlusion [6]. The aim of all of these surgical options is to occlude the superior semicircular canal to eliminate the third mobile inner ear window. The short- and long-term results depend on the approach and procedure. Another new surgical technique has been described recently by Silverstein and Van Ess [17], who occluded the round window niche using a transcanal approach and reported resolution or improvement of symp- toms associated with SCD [17,18]. Consent Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Acknowledgements TU is a visiting fellow from the Department of Otorhinolaryngology, Head and Neck Surgery, Barnet and Chase Farm NHS Hospitals, Enfield and Barnet, United Kingdom. Authors’ contributions ML and JE analyzed and interpreted the patient data regarding the otorhinolaryngological disease. TU and HS were major contributors in writing the manuscript. All authors read and approved the final manuscript.