Symptom: Dizziness with Ear Pressure

What's Your Diagnosis? Symptoms: Middle Ear Mass and Unilateral Hearing Loss

Symptom: Conductive Hearing Loss after Cholesteatoma Surgery

Symptom: Deafness After Stapedectomy

Symptom: Unilateral Facial Paralysis

Journal Club

Symptom: Unilateral Hearing Loss

To investigate posterior external ear canal wall reconstruction with a composite cartilage titanium mesh graft in canal wall down tympanoplasty and revision surgery for open mastoids. Retrospective case review. Tertiary referral centre. As a preliminary study, 15 selected patients underwent reconstruction of a posterior ear canal wall defect with titanium mesh. Large defects of the posterior external auditory canal wall, resulting from canal wall down tympanoplasty or present in revision surgery, were eliminated by reconstruction using a titanium mesh. The mesh was covered with conchal cartilage and attached to the cortical mastoid bone using 3-mm titanium screws. All patients maintained a normal contour of the external ear canal, without depression, extrusion or infection. There were no failures, based on short-term post-operative controls. However, two procedures had to be revised due to incomplete coverage of the titanium mesh. This study shows that reconstruction of the posterior ear canal wall with a composite cartilage titanium mesh is a valuable method for preserving the morphology of the external auditory canal in selected cases. Problems occurring in canal wall down tympanomastoidectomy and radical cavities may therefore be avoided. However, long-term results have yet to be evaluated.

Perioperative vestibular assessment and testing

Temporary removal of the posterior external ear canal wall allows excellent exposure of the middle ear and epitympanum without the negative sequelae of a cavity as can occur after canal-wall down procedures. Safe fixation of the bony canal wall, however, has not always been possible with a risk for prolonged healing and bone necrosis. A new technique permits rigid internal fixation of the posterior canal wall. A titanium miniplate of 10 holes length commonly used for orbital rim surgery is adapted to the cortical surface of the mastoid just posterior to the external ear canal. Six holes for 1.3 mm screws are drilled into the cortical bone: two screws behind the ear canal, two screws on the temporal line, and two on the mastoid tip. All fixation material is then removed and a mastoidectomy is carried out with preservation of the cortical bone for the screws. The external ear canal skin, which has been incised previously near the fibrous annulus with lateral extensions, is mobilized laterally using a newly designed retroflected microraspatory. This creates a vital skin flap that might be essential to avoid bone necrosis. No other skin incisions are needed in the canal. The posterior bony canal wall is cut using an oscillating saw Osseoscalpel, secured by facial nerve monitoring. After middle ear surgery and tympanoplasty have been completed, the canal wall is repositioned and fastened precisely in its place with rigid internal fixation allowing a secure stabilization. This new technique has proven to be safe and reliable on the first five patients. There has been no bone necrosis within an observation period of 18 months. Rigid internal fixation is an alternative technique to safely readapt the posterior auditory canal wall.

The superior canal dehiscence (SCD) syndrome consists of sound- or pressure-induced nystagmus and vertigo caused by a defect in bone overlying the superior semicircular canal. The SCD syndrome is diagnosed based upon characteristic symptoms, signs, and findings on CT imaging of the temoral bones. However, SCD syndrome is often misdiagnosed as perilymphatic fistula (PLF), and the symptoms of sound- and pressure-induced vertigo are more commonly attributed to the vestibular utricle, rather than to the superior semicircular canal. This study explored the role of the superior canal and the utricle in the pathophysiology of SCD syndrome. Three-dimensional scleral search coils were used to record eye movements in 11 patients with SCD syndrome. Ten patients developed nystagmus with upward torsional slow phases characteristic of superior canal activation when loud tones were presented to the affected ear or when the patients performed a Valsalva maneuver. Visual fixation led to a suppression of the nystagmus and the appearance of a sustained torsional deviation of the eyes. Two patients also had sound-evoked head movements in the same direction as the ocular slow phases. The response of the affected superior canal to rapid head rotations was tested in nine patients. The response was diminished in those with large (>/=5 mm) defects in the bone overlying the superior canal. The evoked eye movements in patients with SCD syndrome arise from the superior canal, not the utricle. The syndrome is recognized by the characteristic nystagmus evoked by tones or maneuvers that change middle ear or intracranial pressure. Examination for this nystagmus should be performed under conditions that prevent visual fixation.

The study of the association between superior semicircular canal and other dehiscences in the temporal bone. We have studied computed tomography of radiologically diagnosed people with superior or posterior semicircular canal dehiscences, in four health centres. In addition, we have studied one isolated human temporal bone, one skull and one cadaver head belonging to the collection of the Department of Human Anatomy and Histology of the University of Zaragoza that had dehiscence in the superior semicircular canal. The most frequent association that we observed was between superior semicircular canal dehiscence and tegmen tympani dehiscence (37.33%). Three cases (two clinical cases and one isolated temporal bone) showed multiple associated dehiscences (tegmen tympani, mastoid antrum, posterior semicircular canal, internal auditory canal, glenoid cavity, tympanum bone and geniculate ganglion) associated with superior semicircular canal dehiscence. When the superior semicircular canal dehiscence is associated to other in the petrous bone (tegmen tympani, mastoid antrum, posterior semicircular canal, internal auditory canal) could be grouped into the same syndrome called "otic capsule syndrome", since they have the same origin and common aetiology (otic capsule).

Patient: Male, 52-year-oldFinal Diagnosis: Superior semicircular canal dehiscence • tegmen tympani dehiscenceSymptoms: Dizziness • hearing loss • vertigo • vomitingClinical Procedure: —Specialty: RadiologyObjective:Rare diseaseBackground:Superior semicircular canal dehiscence is an inner-ear pathology which presents with vertigo, disequilibrium, and hearing loss. Although the exact etiology of superior semicircular canal dehiscence is unknown, it is thought that an increase in middle-ear pressure disrupts a thin overlying temporal bone. Superior semicircular canal dehiscence is frequently seen in association with dehiscence of the tegmen tympani, which overlies the middle ear. Here, we present a case report of a 52-year-old Puerto Rican man with vertigo, dizziness, vomiting, and mild hearing loss associated with superior semicircular canal and tegmen tympani dehiscence after performing improper scuba diving techniques.Case Report:A 52-year-old Puerto Rican man presented to the emergency department with vertigo, dizziness, vomiting, and mild hearing loss in the right ear. The symptoms began shortly after scuba diving with inadequate decompression techniques on ascent. He was treated with recompression therapy with mild but incomplete improvement in symptoms. Bilateral temporal magnetic resonance imaging was suggestive of segmental dehiscence of the right superior semicircular canal and tegmen tympani. High-resolution computed tomography of the temporal bone confirmed right superior semicircular canal and tegmen tympani dehiscence with an intact left inner ear.Conclusions:The increased inner-ear pressure that occurs during scuba diving can lead to dehiscence of the superior semi-circular canal and tegmen tympani, causing vertigo and hearing loss. Performance of improper diving techniques can further increase the risk of dehiscence. Therefore, appropriate radiologic evaluation of the inner ear should be performed in such patients.

Purpose : In order to determine specific differences, we compared the temporal bone CT findings of chronic otitis media(COM) with and without cholesteatoma, focusing on bone change. Materials and Methods : Between 1997 and 1998, 82 patients(84 cases) underwent temporal bone CT and were shown to have COM, with or without cholesteatoma after mastoidectomy and tympanoplasty. There were 36cases of COM with cholesteatoma(26 patients, M:F=11:15; age range, 16-61 [mean, 36.2] years), and 58 cases without cholesteatoma(56 patients, M:F=25:31, age range, 15-61 [mean, 36.2]years). The findings of temporal bone CT were analyzed at the point of bony changes including erosion and medial displacement of ossicles(malleus, incus, and stapes), erosion or destruction of the scutum, tegmen, facial canal, and lateral semicircular canal, and ballooning of the tympanic cavity and mastoid antrum. In addition, the soft tissue changes seen on temporal bone CT were analyzed at the site of lateral bulging of soft tissue in Prussak’ s space, perforation of the pars flaccida, tympanic membrane retraction, and tympanosclerosis. We retrospectively compared the findings of temporal bone CT with the surgical findings, and to assess statistical significance, the Chi-square test was used. Results : Bone erosion or destruction was seen in 36.2 % of COM cases without cholesteatoma, and in 96.2% of cases with cholesteatoma. Comparing COM with and without cholesteatoma, the erosion of ossicles includ-ing the malleus(81%, 24%), incus(88%, 14%), stapes(58%, 10%), scutum(88%, 10%), facial canal(8%, 0%), and lateral semicircular canal(8%, 0%), was more common in COM with cholesteatoma(p-value 0.05), with the exception of erosion of the tegmen(8%, 3%). Other bony changes including medial displacement of ossi-cles (27%, 3%), ballooning of tympanic cavity and mastoid antrum(96%, 16%), and the soft tissue changes including lateral bulging of soft tissue in Prussak’ s space(58%, 14%) and perforation of the pars flaccida(35%, 9%) were more common in COM with cholesteatoma (p-alue 0.05). Soft tissue in Prussak’ s space(58%, 72%), retraction of the tympanic membrane(19 %, 9%), and tympanosclerosis(8%, 10%) were not however,important findings(p-value 0.05). Conclusion : Bone erosion or destruction was seen in COM without cholesteatoma, but expansile bone erosion or destruction with mass effect suggested COM with cholesteatoma. These findings of temporal bone CT in COM demonstrate the existence and extent of combined cholesteatoma, and are therefore valuable.

Conclusion: Superior semicircular canal dehiscence (SSCD) syndrome may present with various symptoms. CT scans previously interpreted as normal may show SSCD, especially if special reconstructions tailored for superior canal evaluation are added. Objectives: The purpose of this study was to investigate prevalence of SSCD, its length and its correlation with symptoms in patients who had previously undergone temporal bone CT examination that was reported normal and to demonstrate the importance of reformatted images in the diagnosis of SSCD. Methods: We retrospectively reviewed 108 patients who had undergone temporal bone CT examination for various symptoms and were reported as normal. High-resolution temporal bone CT imaging was performed with 1 mm slice thickness in the transverse plane. Each of the superior semicircular canals was evaluated in the plane of Pöschl and Stenver reformatted images together with axial images. Results: Ninety-three patients were included in the study. Nineteen patients with semicircular canal dehiscence were detected. The mean age of the study group was 45 years. Radiologic evidence of SSCD occurred in 23 of 186 temporal bones with a radiologic prevalence of 12%. The most common symptoms in dehiscent patients were vertigo, hearing loss and tinnitus. Defect lengths varied between 1 mm and 6.5 mm.

Objective--Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia with loud sounds and/or stimuli that result in changes in middle ear or intracranial pressure. Findings on temporal bone CT were analyzed to determine if a developmental abnormality is associated with the syndrome. Material and methods--Temporal bone CT scans [0.5 mm collimation and projections into the superior semicircular canal (SC) plane] were used to compare the bone overlying the SC in patients with SCD syndrome (20 unilateral, 7 bilateral) and in 88 patients without SCD syndrome who had undergone temporal bone CT for evaluation of other otologic disorders (controls). Results--The thickness of bone overlying the SC in the controls measured 0.67±0.38 mm (mean±SD). For individual control subjects, the thickness of bone on one side was correlated with that on the other side (r=0.43; p<0.0001). The thickness of bone overlying the SC on the intact side in patients with unilateral dehiscence measured 0.31±0.23 mm, and was thinner than that noted in the controls (p<0.0001). Conclusions--These findings support the notion that there is a developmental abnormality underlying SCD syndrome. When dehiscence is found on one side, the contralateral side is likely to be thin.