Types of tinnitus (literature overview)

Tinnitus affects up to 40 % of the population in Western countries. One to three percent of the general populations report a significant reduction in their quality of life due to tinnitus through its effect on sleep and mood. Tinnitus presents a burden to the health care system that has been rising in recent years. Population-based studies provide crucial underpinning evidence, highlighting the need for further research to address issues around effective diagnosis and clinical management of this heterogeneous condition. The discussion is done on the basis of Claussen and Shulman classification of the four main groups of tinnitus types: type I — bruit (objective), type II — endogenous tinnitus (subjective maskable), type III — exogenous tinnitus (subjective non-maskable), type IV — slow brainstem degeneration syndrome. Type I: a) pulsatile tinnitus. It can have many causes; aneurism is the most dangerous condition. Mitral insufficiency, temporomandibular joint sounds may be associated with pulsatile tinnitus; b) non-pulsatile (or periodical): vessel sclerosis. Non-pulsatile, or periodical, otosclerosis (otospongiosis) is an idiopathic infiltrative process of the petrous temporal bone that may present with tinnitus. The most common type is fenestral otosclerosis (85 %), which is associated with conductive hearing loss. In a preliminary study, etidronate appeared to be an effective treatment for the neurootologic symptoms of otosclerosis. Type II, subjective maskable. Sensory neural hearing decrease (peripheral) might have several causes: disorder of the inner hair cells, outer hair cells (OHCs), acoustic neuritis, acoustic neurinoma. Discovering the roles of inner hair cells, OHCs, and auditory neurons in speech understanding in quiet and in the presence of background noise is currently a hot topic in the scientific community. Previous studies have suggested that the auditory nerve (AN) may play a role in speech understanding in the presence of background noise. S.G. Kujawa, M.C. Liberman (2009) have shown that noise exposure causes temporary damage to OHCs (as measured by distortion product otoacoustic emissions) and permanent damage to the AN (measured by a decrease in the wave I amplitude of the auditory brainstem response). These preliminary results suggest that both OHCs and the AN contribute to speech recognition in the presence of background noise. However, OHC damage may play a primary role in hearing difficulties in this complex listening situation. Type III, subjective non-maskable (with hyperacusis), mostly central. Many people with tinnitus also suffer from hyperacusis. Both clinical and basic scientific data indicate an overlap in pathophysiologic mechanisms. In a study, 935 (55 %) out of 1713 people were characterized as hyperacusis patients. Hyperacusis in tinnitus was associated with younger age, higher tinnitus-related, mental and general distress, and higher rates of pain disorders and vertigo. Blockers of H1 histaminic receptors, Ca channels and muscarinic blockers seem to be effective. Type IV, slow brainstem degeneration syndrome. Etiology: old age, severe head trauma, poisoning, neural infections. Manifestations: dizziness, emotional disturbances, cognitive impairment, tinnitus and headaches.