The patient is a 69-year-old woman. She was infected with pneumonia at the age of three and had a high fever for a long period. After the fever abated, she became aware of hearing loss. Because she lived in a mountain village, she rarely visited medical facilities. Since then, she had never worn a hearing aid, had gone to a school for the deaf from elementary school to high school, and communicated with people in sign language. Her husband also used sign language, so she had not used oral communication from elementary school to the present. In 2011, family stress triggered the onset of tinnitus. Because around the same time, she began suffering from sleep onset disorder (it took about one hour until sleep onset), nocturnal awakening, and palpitations, she went to a nearby psychosomatic medicine clinic. She received medication at the clinic but her tinnitus did not improve, so she was referred to our department in 2014.
Various questionnaires were given at her consultation. The result of THI (Tinnitus Handicap Inventory), which is used to evaluate the severity of tinnitus, was a high of 94, which indicates the most severe form of tinnitus. Also, an SDS (Self-rating Depression Scale) score, which is used to measure depression tendency, was as high as 61, showing that she had a tendency toward depression. The STAI (State-Trait Anxiety Inventory), which is used to measure anxiety tendency, returned a State Anxiety (STAIs) score of 69 and a Trait Anxiety (STAIt) score of 67, indicating that she had an extremely high anxiety tendency. As one of the personal features of her tinnitus, she had no concept of the "loudness of tinnitus" because she had been deaf since childhood.
In imaging tests, there were no abnormal findings except for a slight enlargement of the inner ear canals observed by temporal bone CT scan. Head MRI showed no abnormal findings within the skull or in the internal auditory canals.
For treatment, we started oral administration of a serotonin reuptake inhibitor (SSRI) (paroxetine hydrochloride, Paxil , 12.5 mg, started as one tablet a day, increased to three tablets a day) and a sleep-inducing agent (suvorexant, Belsomra , 15 mg, one tablet a day). One and a half months later, the sleep onset disorder and nocturnal awakening improved, but early morning arousal persisted. Then, a benzodiazepine anxiolytic was added (etizolam, Depas , 0.5 mg, one tablet a day). At four months after the initial visit, THI was 84, SDS 43, STAIs 50, and STAIt 48, which showed that her psychological condition had improved, although the tinnitus distress level did not change.
At this time, there was no improvement in perceived palpitations, and "pulsatile tinnitus" that seemed to synchronize with the heartbeat became the chief complaint concerning tinnitus, which led us to suspect that she had autonomic disorders. Six months after the initial visit, she started to receive psychotherapy (autogenic training). After the start of the treatment, we treated the patient with psychotherapy once a month, which continued until the 7th therapy session was completed. At the end of psychotherapy, our test results showed THI at 60, SDS 45, STAIs 32, and STAIt 43, showing a further improvement trend. The THI score was still high at 60, but the subjective tinnitus distress became "not so annoying," and the "echoing tinnitus" that was the cause of the patient's discomfort at the time of the initial visit disappeared. Only the pulsatile tinnitus, which seemed to be related to palpitations, remained.
One year and seven months after the initial visit, palpitations and pulsatile tinnitus, as well as anxiety and insomnia, were aggravated due to work stress. She restarted psychotherapy. At the same time, SSRIs were replaced by noradrenergic and specific serotonergic antidepressants (NaSSAs) (mirtazapine, Reflex , 15 mg, started as one tablet a day, increased to two tablets a day). As a result, improvement of the palpitations and insomnia gradually occurred, and two years and one month after the initial visit, our test results showed THI at 40, SDS 47, STAIs 40, and STAIt 46.
By three years after the initial visit, the symptoms had stabilized and the anxiolytic drug was discontinued, but oral administration of the NaSSA and sleep induction drugs continued. The subjective tinnitus and palpitations at the time of sleep almost disappeared, and the sleep onset disorder and nocturnal awakening rarely occurred.
Now 4.5 years have passed and she is taking only a low dose NaSSA (mirtazapine, Reflex , 15 mg, 0.5 Tablets a day). The latest test results were THI 0, SDS 43, STAIt 47, and STAIs 50, indicating that the tinnitus distress had disappeared completely.