[Show abstract][Hide abstract] ABSTRACT: To present symptoms, patterns of nystagmus, and computed tomographic scan identification of patients with sound- and/or pressure-induced vertigo due to dehiscence of bone overlying the superior semicircular canal. To describe anatomical findings and outcome in 2 patients undergoing plugging of the superior semicircular canal for treatment of these symptoms.
Prospective study of a case series in a tertiary care referral center.
Eight patients with vertigo, oscillopsia, and/or disequilibrium related to sound, changes in middle ear pressure, and/or changes in intracranial pressure were identified in a 2-year period. Seven of these patients also had vertical-torsional eye movements induced by these sound and/or pressure stimuli. The direction of the evoked eye movements could be explained by excitation or inhibition of the superior semicircular canal in the affected ear. Computed tomographic scans of the temporal bones identified dehiscence of bone overlying the affected superior semicircular canal in each case. Disabling disequilibrium in 2 patients prompted plugging of the dehiscent superior canal through a middle cranial fossa approach. Symptoms were improved in each case. One patient developed recurrent symptoms requiring an additional plugging procedure and developed sensorineural hearing loss several days after this second procedure.
We have identified patients with a syndrome of vestibular symptoms induced by sound in an ear or by changes in middle ear or intracranial pressure. These patients can also experience chronic disequilibrium. Eye movements in the plane parallel to that of the superior semicircular canal were evoked by stimuli that have the potential to cause ampullofugal or ampullopetal deflection of this canal's cupula in the presence of a dehiscence of bone overlying the canal. The existence of such deshiscences was confirmed with computed tomographic scans of the temporal bones. Surgical plugging of the affected canal may be beneficial in patients with disabling symptoms.
Archives of Otolaryngology - Head and Neck Surgery 03/1998; 124(3):249-58. DOI:10.1001/archotol.124.3.249 · 2.33 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To determine the incidence and etiology of dehiscences of bone overlying the superior semicircular canal in a temporal bone archive.
A microscopic study was performed of 1000 temporal bones from 596 adults in a university hospital registry. Specimens were sectioned vertically in the plane of the superior semicircular canal. Measurements of minimum bone thickness over the superior canal were made in a subset of 108 randomly chosen specimens. All bones were examined for thinning or dehiscence relative to these norms. Clinical histories, when available, were reviewed.
Complete dehiscence of the superior canal was identified in 5 specimens (0.5%), at the middle fossa floor (n = 1) and where the superior petrosal sinus was in contact with the canal (n = 4). In 14 other specimens (1.4%), the bone at the middle fossa floor (n = 8) or superior petrosal sinus (n = 6) was no thicker than 0.1 mm, significantly less than values measured in the control specimens (P<.001). Abnormalities were typically bilateral. Specimens from infants demonstrated uniformly thin bone over the superior canal in the middle fossa at birth, with gradual thickening until 3 years of age.
Dehiscence of bone overlying the superior canal occurred in approximately 0.5% of temporal bone specimens (0.7% of individuals). In an additional 1.4% of specimens (1.3% of individuals), the bone was markedly thin (< or =0.1 mm), such that it might appear dehiscent even on ultra-high-resolution computed tomography of the temporal bone. Sites affected were in the middle fossa floor or a deep groove for the superior petrosal sinus, often bilaterally. These abnormalities may arise from failure of postnatal bone development. Thin areas of bone over the superior canal may be predisposed to disruption by trauma.
Archives of Otolaryngology - Head and Neck Surgery 02/2000; 126(2):137-47. DOI:10.1001/archotol.126.2.137 · 2.33 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Air is commonly trapped within the skull in patients who have been treated for trauma or intracranial hemorrhage. In Sweden, when such a patient is transported by air ambulance it is standard procedure to maintain sea-level pressure in the cabin to prevent increased intracranial pressure (ICP). However, this type of flight operation is more difficult and expensive. Maintenance of sea-level cabin pressure is not common practice all over the world, and the criteria supporting the choice of pressurization during transport are inadequate and in need of evaluation. The purpose of this study was to develop and evaluate a model to simulate the influence of intracranial air on ICP during air transport.
We identified an existing nonlinear model of the cerebral spinal fluid and intracranial pressure dynamics, then added intracranial air as a new component and evaluated the model through simulations.
The model behaved as expected, and the simulations indicated that under normal flying conditions with decreased cabin pressure the initial intracranial air volume will increase by approximately 30% at normal maximum cabin altitude, 8000 ft. The increase in ICP depends upon both the initial air volume and the rate of change in cabin altitude. For an intracranial air volume of 30 ml the estimated worst-case increments of ICP from sea level to maximum altitude would be from 10 mm Hg to 21.0 mm Hg, or from 20 mm Hg to 31.8 mm Hg.
Our results support the need for maintenance of sea-level pressure during air transport of patients with suspected intracranial air, since an ICP increment could potentially impair the patient's clinical condition.
Aviation Space and Environmental Medicine 03/2003; 74(2):138-44. · 0.88 Impact Factor
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