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Approximately 15 million Americans have a severe form of tinnitus, the perceived sensation of a ringing, roaring or humming sound without actual acoustic stimulation. Although several theories have been proposed to explain the mechanism of tinnitus, the exact cause for this condition remains unknown; suggested treatments for the condition have not worked well in alleviating the symptoms.
A number of patients with this disorder find the condition debilitating, interfering with work, socialization and sleep. A new study asserts that melatonin use is associated with improvement of tinnitus and sleep. Melatonin is a hormone produced by the pineal gland, known to be involved in regulating the sleep-wake cycle.
The authors of "The Effects of Melatonin on Tinnitus and Sleep," are Jay F. Piccirillo, MD, Uchechukwu C. Megwalu, and Joshua E. Finnell, all with the Department of Otolaryngology-Head and Neck Surgery, at the Washington University School of Medicine, in St. Louis, MO. Their findings appear in the February 2006, edition of Otolaryngology-Head and Neck Surgery, the medical and scientific journal of the American Academy of Otolaryngology-Head and Neck Surgery.
Methodology
This prospective open-label study involved 18 patients between the ages of 18 and 70 who had idiopathic, troublesome, unilateral or bilateral, nonpulsatile tinnitus of six month's duration or greater who sought treatment at the Washington University Department of Otolaryngology-Head and Neck Surgery. The average age of the study subjects was 61 years and the average duration of tinnitus was 11.3 years.
Patients with tinnitus related to cochlear implantation, retrocochlear lesion, or other known anatomic and structural lesions of the ear and temporal bone were excluded from the study. The Tinnitus Handicap Inventory (THI) and the Pittsburgh Sleep Quality Index (PSQI) questionnaires were administered at the beginning of the study. The patients took 3mg of melatonin, one pill, one to two hours before bedtime for four weeks. This was followed by an additional four weeks of observation during which time the patients received no melatonin.
The THI and PSQI were administered at weeks 2, 4, 6, and 8. The independent variable was the administration of melatonin; the dependent variables included the scores on the THI and the PSQI. Primary outcome measures were the changes in THI and PSQI between weeks 0 and 4 and between weeks 0 and 8. The secondary outcome measure was the association between the change in THI and the change in PSQI.
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