SUMMARY Prolactin (PRL) has been associated with the pathogenesis of migraine, and various approaches have been used to investigate its role. In the present study, the PRL response to thyrotropin-releasing hormone (TRH) was evaluated in eight women migraineurs during an attackfree state and during a migraine attack. PRL baseline values were not different in the two states, and the same was true for the TSH responses to TRH. The PRL responses to TRH were, however, significantly higher during the attack, a finding that indicates a latent disturbance of the PRLregulating systems in migraine, with a higher responsiveness during migraine attacks.Increased levels of plasma prolactin (PRL) found in some conditions associated with migraine attacks (stress, exercise, use of oral contraceptives), and the PRL suppressing effect of some anti-migraine drugs (ergot alkaloids, clonidine), are observations that support the notion that PRL is involved in the mechanism of migraine pathogenesis.1 2 Certain studies, however, failed to demonstrate a PRL involvement,3`6 while others, using the levodopa inhibiting test, showed some abnormalities in the PRL secretion mechanisms in migraine.7-9 In the present study, we investigated the PRL response to thyrotropin-releasing-hormone (TRH) injury within the last year or evidence of endocrine abnormalities were excluded. All patients were free of drugs during the 2 weeks before testing, and were found normal in a systematic physical and neurological examination. Their EEGs and CTs of the head were also normal. They all had a formal psychiatric examination, and the Hamilton Depression Scale'" was completed. No evidence of depression or other significant psychiatric disturbance was found.The first TRH test was performed during an attack free interval. The patient was then instructed to come during an attack to have the test repeated, if the attack occurred during the morning hours. The TRH test was thus always performed between 0800 and 1200 hours, with the patient recumbent. Blood samples were drawn throtigh an indwelling catheter that was kept patent with slow infusion of normal saline. After the first blood sample was obtained (time 0) 0 4 mg TRH were given IV as a bolus and samples were further obtained at 20, 40 and 60 minutes. Plasma was separated by centrifugation and kept at -30°C until estimation. PRL levels were assayed by radioimmunoassay techniques (Biodata kit) and the results expressed in ng/ml.