Abstract
BACKGROUND: Vestibular disorders, particularly Ménière's disease, represent significant neurological conditions affecting balance, spatial orientation, and quality of life. While endolymphatic hydrops is recognized as the pathological hallmark of Ménière's disease, the relationship between thyroid dysfunction and vestibular pathology remains incompletely understood. Clinical observations suggest associations between hypothyroidism and vestibular symptoms, yet experimental evidence demonstrating causality is lacking. OBJECTIVE: To investigate whether surgically-induced hypothyroidism causes endolymphatic hydrops development in an experimental rat model and to characterize the histopathological changes in vestibular structures. METHODS: Twelve male Wistar albino rats were randomly allocated to total thyroidectomy (n = 4), sham surgery (n = 4), and control (n = 4) groups. Thyroid function was assessed via serum thyroid-stimulating hormone (TSH) and thyroxine (T4) measurements at baseline and postoperative day 15. Animals were euthanized at 28 days post-surgery for comprehensive histopathological examination of temporal bones. Endolymphatic hydrops was evaluated using standardized semiquantitative scoring systems for Reissner's membrane, vestibular structures, stria vascularis, and utricular macula. RESULTS: Thyroidectomized rats developed significant biochemical hypothyroidism with elevated TSH (mean difference: 0.378 μIU/mL, 95% CI: 0.183-0.573, p = 0.021) and decreased T4 levels (mean difference: -2.357 pmol/L, 95% CI: -3.521 to -1.193, p = 0.021). Histopathological examination revealed universal development of endolymphatic hydrops in all thyroidectomized animals (100% vs. 0% in controls, p < 0.001), affecting Reissner's membrane, vestibular apparatus, stria vascularis, and utricular macula with varying severity. CONCLUSION: This study provides the first direct experimental evidence that thyroid hormone deficiency induces endolymphatic hydrops in all examined vestibular structures. These findings establish a mechanistic link between hypothyroidism and vestibular pathology, with important implications for the neurological evaluation and management of patients presenting with vestibular symptoms and comorbid thyroid dysfunction.