The JB is a dynamic structure that forms after 2 years, and its size stabilizes in adulthood. The determinants in its exact position and size are multifactorial and may be related to blood flow. Improved understanding of this structure's development may help to better understand the cause of the high-riding JB and JB diverticulum, both of which may cause clinical symptoms.

Jugular bulb abnormalities can erode into the vestibular aqueduct, facial nerve, and the posterior semicircular canal. While symptoms may include pulsatile tinnitus, vertigo, or conductive hearing loss, in contrast to earlier reports, half of the patients were asymptomatic. Dehiscence of vestibular aqueduct rarely leads to clinical or histologic hydrops. The VEMP testing was useful in confirming the presence of inner ear dehiscence due to JBAs. Because the natural history of JBAs is unknown, these patients should be followed closely to evaluate for progression of the JBA or development of symptoms.

Objective Jugular bulb abnormalities (JBA), including high-riding jugular bulb (HRJB) and jugular bulb diverticulum (JBD), can erode into the inner ear. In this study, the authors investigate the prevalence and consequences of JBA and their erosion into inner ear structures using temporal bone histopathology and computed tomography (CT). Study Design Cross-sectional study of temporal bone histopathology and radiology. Setting Academic medical center. Subjects and Methods In total, 1579 temporal bone specimens and 100 CT of the temporal bones (200 ears) were examined for JBA and any associated dehiscence of inner ear structures. Temporal bone specimens were examined for histological consequences of inner ear erosion. Jugular bulb dimensions were measured on axial CT scans and compared across groups. Accompanying demographic and clinical information were reviewed. Results High jugular bulbs were noted in 8.2% (130/1579) of temporal bone specimens and in 8.5% (17/200) of temporal bone CT. The prevalence of JBA increases during the first 4 decades of life and stabilizes thereafter. High-riding jugular bulbs eroded inner ear structures such as the vestibular aqueduct, vertical facial nerve, or posterior semicircular canal in 2.8% (44/1579) of cases histologically and 1.5% (3/200) radiologically. In most, jugular bulb–mediated inner ear dehiscence was clinically and radiologically silent. Conclusion Jugular bulb abnormalities are common. They are present in 10% to 15% individuals and are primarily acquired by the fourth decade of life. In 1% to 3% of cases, the HRJB erodes into the inner ear and most frequently involves the vestibular aqueduct.

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JBME abnormalities are rare, present across age groups, and may demonstrate serial growth over time. They are usually associated with multiple other diverticula within the same JB. Our clinical series suggests that JBME's development and uniquely aggressive behavior results from contralateral transverse sinus outflow obstruction.

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