Objective: Tinnitus is described as the perception of sound without any external acoustic stimulation. Any pathology of auditory pathways or any system of the human body may result with tinnitus. The pathophysiology of tinnitus accompanying the disorders of auditory system is not fully understood and there is not any particular effective treatment method has been specified. Tinnitus masking therapy has been reported as an effective treatment modality in the treatment of tinnitus. In this study, the results of tinnitus masking treatment on the parameters were evaluated prospectively. Patients and methods: Patients with normal physical examination was enrolled in the study. Blood tests (complete blood count, biochemical analysis of lipid profile, and thyroid hormones), pure tone audiometry, tympanometric measurement of the middle ear pressure and stapedial reflexes were performed, Sixty six patients with normal results of blood tests and normal hearing thresholds with type A tympanogram were included. Tinnitus sufferers questionnaires (socio-demographics, clinical information, Tinnitus Handicap Inventory (THI), Beck Depression Inventory (BDI) was filled, audiological tests were performed, tinnitus parameters (frequency, intensity, minimal masking levels, residual inhibition) were measured. After four weeks of the treatment the questionnaires were repeated. Results: Masking treatment for tinnitus patients resulted with significant decrease in Tinnitus Handicap Inventory and VAS scores. After four weeks of the masking treatment the questionnaire was repeated. Twenty patients did not respond to treatment. Conclusion: Masking therapy is one of the most effective methods of treatment for tinnitus patients. Masking therapy, that is not invasive and cost-effective has an important place in the treatment of tinnitus. Especially in a short time provides a significant reduction in tinnitus parameters.

Objectives: Otosclerosis is a disease involving abnormal bone turnover in the human otic capsule that results in hearing loss. Several hypotheses have been suggested for the etiopathogenesis of otosclerosis; however, its etiology remains unclear. Methods: This study evaluated the correlation between otosclerosis and levels of paraoxonase-1 (PON1), arylesterase, total antioxidant status, total oxidant status (TOS), oxidative stress index (OSI), total sulfhydryl (-SH) groups, lipid hydroperoxide, and ceruloplasmin in the serum of otosclerosis patients and healthy subjects with respect to oxidative stress. Results: In our study, TOS and OSI levels were higher in the otosclerosis patients than in the controls. The PON1 levels showed that oxidative stress was severe, and as a result, antioxidants were consumed and depleted. Discussion: When an imbalance between oxygen free radical production and antioxidative defense mechanisms occurs, reactive oxygen species levels may increase, which in turn may damage cells and tissues through the peroxidation of phospholipid membrane structures. The body initially responds with increased antioxidant production, but if the oxidative stress is severe, decreased antioxidant levels may result. This study reports expression levels of oxidative stress species in otosclerosis patients.

Objective: Our objective was to evaluate whether there was a subclinical change in the functions of the facial nerve after parotidectomy. Methods: Facial nerve functions of 21 patients who had parotidectomy between January 1999 and December 2003 were assessed using electromyography (EMG) at least 5 years after the surgery. Results: There was no significant difference between both sides of the face in the EMG amplitudes (P > 0.05) except for the amplitudes obtained from the site of nasolabial sulcus (P < 0.05). In the patients who underwent total parotidectomy, the EMG amplitudes were significantly different for both sides of the face (P < 0.05). No significant difference was found in the comparison of other measurements performed by EMG. Conclusions: Tumor histopathologic type (benign or malignant) and type of parotidectomy (superficial or total) do not cause a subclinical dysfunction of the facial nerve after parotidectomy in the patients who also have clinically normal facial functions. The only exception to this contention is the subclinical dysfunction in nasal branches of the facial nerve in total parotidectomy cases.