Vascular Tinnitus in General Practice: Hemodynamic Mechanisms and Differential Diagnosis

Abstract

This report examines the phenomenon of tinnitus through the lens of foundational medical textbooks and manuals on propedeutics of internal diseases (N. A. Mukhin, V. S. Moiseev), as well as contemporary international scientific publications. Hemodynamic, vascular, neurological, and neuroendocrine mechanisms responsible for the formation of acoustic symptoms in arterial hypertension, atherosclerosis, anemic syndrome, and psychosocial stress are thoroughly analyzed. Despite the extensive literature on tinnitus-induced stress, the role of stress as a primary etiological factor in tinnitus genesis remained under-researched for a long time. The hypothalamic-pituitaryadrenal (HPA) axis—one of the main neuroendocrine systems involved in the stress response— consistently demonstrates dysregulation in patients with tinnitus. Patients with chronic tinnitus display abnormal responses to psychosocial stress characterized by blunted and delayed HPA axis reactivity, indicating a substantial contribution of chronic stress to the pathogenesis of this condition. The sympathetic branch of the autonomic nervous system and its hyperactivation also play a pivotal role in initiating and perpetuating tinnitus. Psychosocial stress has been proven to carry an equal probability of inducing tinnitus as occupational noise exposure, while their combined effect doubles this risk. Whereas short-term stress exerts a protective effect on the cochlear apparatus, chronic stress leads to structural neurosensory damage and aggravates symptom severity.