## 1 Introduction  
Tinnitus is a complex and often debilitating auditory condition defined by the perception of sound in the absence of external auditory stimuli. Globally, it affects approximately 10-15% of the adult population, with a significant proportion experiencing chronic and distressing symptoms that negatively impact their quality of life, sleep, emotional well-being, and cognitive performance [1; 2; 3; 4]. Despite its high prevalence, the underlying pathophysiological mechanisms of tinnitus remain incompletely understood and are believed to be multifactorial, involving both peripheral and central auditory pathways as well as non-auditory brain networks [5; 6; 7]. Several theoretical models have been proposed to explain the onset and persistence of tinnitus. One prevailing hypothesis suggests that cochlear damage due to noise exposure, ototoxic drugs, or age-related degeneration leads to diminished peripheral input, which triggers maladaptive neuroplastic changes in the central auditory cortex. This maladaptive cortical reorganization may result in aberrant spontaneous neural activity, perceived as phantom sounds [8]. In addition, growing evidence has pointed to the involvement of oxidative stress, neuroinflammation, and impaired vascular regulation in the pathogenesis of tinnitus [9; 10; 11; 12]. Vascular dysfunction, particularly microvascular insufficiency, has received increasing attention as a potential contributing factor in tinnitus development. Microvascular impairment may lead to hypoxia and ischemia in cochlear structures, notably affecting the stria vascularis, outer hair cells, and spiral ganglion neurons, which are critical for normal auditory function [13]. Among the systemic vascular contributors, arterial stiffness has emerged as a promising biomarker due to its association with endothelial dysfunction, oxidative stress, and atherosclerosis, all of which may compromise cochlear perfusion [14]. Arterial stiffness, typically characterized by reduced vascular compliance and elasticity, leads to elevated pulse pressure and increased pulsatile flow, which may exacerbate microvascular injury [15]. Most previous studies evaluating arterial stiffness in tinnitus patients have focused on central elastic arteries such as the carotid artery or assessed systemic parameters using pulse wave velocity (PWV) and carotid intima-media thickness (CIMT) [16; 17]. While informative, these measurements do not provide direct information on the vertebobasilar system, which plays a crucial role in posterior cerebral and inner ear perfusion. The vertebral arteries, which supply blood to the posterior circulation including the cochlea, brainstem, and cerebellum, represent a highly relevant but understudied vascular region in tinnitus research. Recent studies have suggested that vertebral insufficiency may contribute to both auditory and vestibular symptoms, including tinnitus, vertigo, and sensorineural hearing loss [18; 19]. Furthermore, abnormalities in vertebral artery hemodynamics, including elevated pulsatility index (PI), resistive index (RI), and stiffness index (SI), may reflect microvascular compromise relevant to tinnitus pathophysiology [20; 21]. Doppler ultrasonography has become an increasingly utilized non-invasive technique for the assessment of arterial stiffness, as it allows real-time measurement of vessel diameter changes in relation to systolic and diastolic blood pressure, thus providing localized vascular parameters [22]. Unlike systemic indices, Doppler-derived stiffness measurements offer a region-specific evaluation that may better correlate with organ-specific microvascular dysfunction, such as cochlear ischemia in tinnitus patients. Given these considerations, the current study aimed to investigate the potential relationship between vertebral artery stiffness and idiopathic subjective tinnitus by utilizing Doppler ultrasonography to obtain detailed vascular parameters.