Several types of assessments are typically recommended to diagnose CRSD, ie, sleep logs and diaries, questionnaires, actigraphy, polysomnography, and circadian phase (timing) markers. The 24-hour endogenous melatonin rhythm is a rhythm driven by the central circadian pacemaker, and the timing of the onset of melatonin secretion in the evening (dim light melatonin onset [DLMO]) is strongly associated with the timing

of sleep in normal individuals,5-7 making evaluation of DLMO a useful marker of the timing of the circadian system[8] and thus a useful diagnostic tool for diagnosing CRSD. DLMO is used to determine whether abnormal sleep timing is associated with abnormal circadian rhythm timing (and thus DLMO can confirm the presence of a CRSD). For example, in ASPD, sleep timing is advanced to an earlier than desired time, and DLMO would Torin 1 research buy be expected to also be advanced, while in DSPS, sleep timing is delayed to a later than desired time. DLMO is also a potentially valuable tool in the differential diagnosis of sleep disorders that are typically thought to have a noncircadian

origin, eg, psychophysiological insomnia,3,9-12 SCH772984 mouse because clinical symptoms can sometimes mimic CRSD symptoms. The headache centre of the Gelderse Vallei Hospital works closely together with the sleep center of that hospital and is the Dutch national referral center for headache patients with insomnia. As part of routine examination, DLMO in these patients is measured from saliva samples collected by the patients in MCE their home, as described elsewhere.[13] Headache patients with late DLMO are typically treated with melatonin, 1-5 mg, administered 5 hours before DLMO, but not earlier than 19:00 hours. Patients

complete an internet questionnaire just before their first visit to the headache clinic and again 6 weeks after starting the melatonin treatment. This questionnaire evaluates headache symptoms and other potential side effects from the melatonin. The same questionnaire is also completed by patients presenting to our sleep clinic with insomnia symptoms (but without headache) who are treated with melatonin. We found that headache disappeared or considerably diminished during melatonin treatment in 78.6% of 328 patients with headache and CRSD. However, headache occurred during melatonin treatment in 13.8% of 676 patients with CRSD without prior headache (see the Table). The high percentage of patients with decreases of their headache during melatonin treatment supports a hypothesized causative relationship with melatonin treatment.