The anatomy of the adult human cochlear aqueduct and its surrounding structures, and their normal variations at tomography, microdissection and plastic molding are described. The mean length of the aqueduct is 12.9 mm and the mean width of its funnel-shaped external aperture 4.2 mm. The mean width of the narrowest portion is 0.14 mm. No difference in aqueductal width was found between the youngest and oldest age groups. Complete bony obstruction was revealed at microdissection in 3 out of 82 specimens. In the remaining 79 the entire aqueduct was patent. The aqueduct usually runs parallel to the internal auditory canal when seen from above, and the AP projection is therefore most suitable for tomography. At tomography the entire aqueduct was visualized in 60% of the specimens. The isthmic portion was not visible in 40%. Major reasons for nonvisualization of the entire aqueduct are: 1) a luminal width less than 0.1 mm, 2) a high jugular fossa, 3) a posteriorly directed aqueductal convexity (10%), and 4) bony obliteration (4%). Accessory canals close to and often wider than the aqueduct may complicate tomographic evaluation of the aqueductal patency. Nonvisualization of the aqueduct at tomography does not necessarily indicate nonpatency.

From a series of patients undergoing routine radiographic examination, 112 temporal bones with a high jugular fossa were selected. Among these, 43 jugular bulb diverticula were found. The structures affected by a high fossa or diverticulum were recorded and correlated to the clinical symptoms of the patient. The vestibule was suspected to be affected in five patients. Two of these patients had tinnitus and vertigo, and three had hearing loss. In one of the latter the hearing loss was most marked in the supine position. The cochlea was close to the fossa in three patients, all of whom had tinnitus. Four patients had a defect of the posterior semicircular canal. One of them lost his hearing after a severe fit of coughing, became unsteady and showed signs of a fistula. The internal acoustic meatus and the mastoid portion of the facial canal were affected in two and four patients, respectively, who had no recorded symptoms. Twelve of 34 patients with Menière's disease and a high jugular fossa on the side of the diseased ear had a dehiscence of the vestibular aqueduct caused by the fossa or diverticulum, compared with nine of 58 patients in the unselected material. For comparison and demonstration of topographic relationships, 58 casts of unselected radiographed temporal bone specimens with high jugular fossae or diverticula were investigated. In patients with a high jugular fossa or jugular bulb diverticulum, tomographic assessment may be of value.

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The radioanatomy of high jugular fossae and their topographic relations to the inner ear structures were investigated in 245 unselected temporal bones. One hundred and fifty specimens were submitted to multidirectional and 10 to computed tomography. After careful chemical and fermentative maceration plastic casts were made, using polyester resin and silicone rubber. With the use of vacuum, even minute structures became filled with the casting material. The specimens offered a three-dimensional view of the jugular fossae and surrounding structures. Fifty-eight (24%) of the total 245 specimens had high jugular fossae at a level above the lower border of the round window. Five casts showed a dehiscence of the peripheral portion of the vestibular aqueduct caused by the high jugular fossa. In 2 casts the proximal portion of the cochlear aqueduct was affected. In some casts the posterior semicircular canal, the facial canal, the stapedial muscle and the round window lay so close to the fossa that a dehiscence could not be excluded. In a clinical material of 102 high fossae the radiographic findings were in accordance with the experimental results. High jugular fossae were predominantly found in pyramids with low-grade mastoid bone pneumatization and sparse or no perilabyrinthine air cells.

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