What is the role of vascular compromise in the pathophysiology of sudden hearing loss?

Updated: Aug 28, 2019
  • Author: Neeraj N Mathur, MBBS, MS, DNB(ENT), MNAMS, FAMS; Chief Editor: Arlen D Meyers, MD, MBA  more...
  • Print

The cochlea is an end organ with respect to its blood supply, with no collateral vasculature. Cochlear function is exquisitely sensitive to changes in blood supply. Vascular compromise of the cochlea due to thrombosis, embolus, reduced blood flow, or vasospasm seems to be a likely etiology for ISSHL. The time course correlates well with a vascular event, a sudden or abrupt loss. A reduction in oxygenation of the cochlea is the likely consequence of alterations in cochlear blood flow. Alterations in perilymph oxygen tension have been measured in response to changes in systemic blood pressure or intravascular carbon dioxide partial pressure (pCO2).

Histologic evidence of cochlear damage following occlusion of the labyrinthine vessels was documented in temporal bone studies in animals and humans. Intracochlear hemorrhage was noted as an early development; subsequently, fibrosis and ossification of the cochlea evolved.

In one study, a partial overlap was found between classical coronary risk factors and risk factors for sudden hearing loss. Hypercholesterolemia and hypoalphalipoproteinemia (low HDL cholesterol levels) were not found to be apparent major risk factors for sudden hearing loss, whereas the GPIa C807T polymorphism, elevated fibrinogen levels, and smoking were associated with an increased risk for ISSHL.

In contrast to the above study, a historical prospective cohort study by Chang et al indicated that hypercholesterolemia is associated with an increased risk for idiopathic sudden sensorineural hearing loss (ISSNHL). Comparing nearly 74,000 patients with hypercholesterolemia with the same number of age-matched controls, the investigators found the incidence of ISSNHL to be 1.62 times greater in the hypercholesterolemia group. [2]

Altogether, the various study findings suggest a vascular involvement in the pathogenesis of ISSHL. This may have important implications for the development of therapeutic and preventive strategies for ISSHL. [3]

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!