Abstract
Objectives:
Idiopathic unilateral sudden sensorineural hearing loss (ISSNHL) has been debated to arise from either a vascular or viral etiology. Recent studies citing evidence of a vascular etiology have been correlational in design without examination of histopathological data. It has been well established that vascular compromise results in fibrosis and/or neo-osteogenesis within the scala tympani of the cochlea. Conversely, sudden hearing loss due to viral infections, such as measles and mumps, has been demonstrated to lead to degeneration of the stria vascularis, organ of Corti, and tectorial membrane. Abundant other research has indicated a probable viral etiology, including cochlear nerve enhancement on magnetic resonance imaging, suggesting an inflammatory process.
Methods:
A retrospective case review including clinical history, audiometry, and temporal bone histopathology of 7 temporal bones with known vascular impairment due to surgical intervention was compared to that of 11 bones with a history of ISSNHL with attention to the spiral ligament, stria vascularis, organ of Corti hair cells, tectorial membrane, ganglion cell population, and degree of perilymph fibrosis and/or neo-osteogenesis.
Results:
Compared to 6 out of 7 vascular cases (86%) with fibrosis (P ≤ .001), ISSNHL cases exhibited more widespread tectorial membrane abnormalities, no perilymph fibrosis, less loss of ganglion cells (P ≤ .035), greater survival of spiral ligament (P ≤ .029), and twice the survival of hair cells on average.
Conclusions:
Analysis of human temporal bones from patients with sudden sensorineural hearing loss does not support a vascular insufficiency but rather suggests a viral etiology.
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