## 4 Discussion
were more frequently observed on the side with higher VAS and PI values, suggesting a possible hemodynamic mismatch and localized perfusion deficit. Furthermore, the side-specific findings in our study may indicate localized vascular involvement. Although not all parameters showed statistically significant differences, we observed a trend toward higher vascular indices, such as vertebral artery stiffness and PI, on the same side as the reported tinnitus symptoms. For instance, right-sided stiffness and PI values were significantly higher in patients with right-sided tinnitus. [PERSON] et al. observed that abnormal cervical vascular findings were associated with worse outcomes in patients with idiopathic sudden sensorineural hearing loss, underscoring the relevance of vertebral artery function in auditory disorders [19]. These findings suggested a possible lateralized vascular contribution, although the interpretation should remain cautious given the limited sample size and the lack of statistical significance for some comparisons. Larger studies are needed to confirm these trends and clarify the clinical implications of such lateralization. The vascular hypothesis of tinnitus is further supported by studies such as [PERSON] et al. who linked vascular risk factors with sensorineural hearing loss and cognitive decline, highlighting the broader systemic implications of vascular dysfunction on the auditory system [18]. Likewise, [PERSON] et al. emphasized that cerebral and cochlear perfusion are closely linked, with vascular stiffness contributing to hypoperfusion in both central and peripheral auditory pathways [21]. Compared to previously published studies, our investigation differed in several important aspects. Earlier research examining arterial stiffness in tinnitus patients focused primarily on large central arteries, particularly the carotid artery, and utilized systemic parameters such as pulse wave velocity (PWV) or carotid intima-media thickness (CIMT) [16; 17; 22]. While these metrics are well-established markers of cardiovascular risk, they do not offer region-specific insight into the vertebbasilar system, which directly supplies the cochlear and brainstem auditory pathways [18; 21]. Unlike studies employing Young's Elastic Modulus (YEM), which assumes homogeneity in arterial wall composition [31], our approach utilized a localized Doppler-derived stiffness index based on real-time arterial diameter and blood pressure measurements [15]. Compared to earlier studies evaluating CIMT or systemic arterial stiffness indices such as YEM, our Doppler-based methodology allows for dynamic, segmental assessment of the vertebral arteries, reflecting real-time systolic-diastolic diameter changes under physiological pressure conditions. This localized approach may offer better clinical relevance in disorders such as tinnitus where regional microvascular health is critical [30; 31; 32]. Additionally, we were the first to demonstrate a side-specific relationship between vertebral artery stiffness and the reported side of tinnitus, suggesting that focal hemodynamic alterations may be clinically relevant. These methodological innovations and anatomical focus allowed us to contribute new evidence supporting a vascular component in tinnitus pathophysiology. Overall, our findings suggest that vertebral artery stiffness is an important vascular biomarker in tinnitus patients, and its assessment using Doppler ultrasonography may offer a valuable, non-invasive diagnostic tool for clinical practice. Although the differences in VAS and PI between tinnitus patients and controls were statistically significant, their clinical implications warrant further consideration. Elevated VAS and PI may reflect reduced vascular compliance and impaired microcirc regulation, which could contribute to cochlear hypoperfusion and inner ear dysfunction.