Dexamethasone suppression test, melatonin and TRH-test in cluster headache

Abstract

The origin of Cluster Headache (CH) is still unknown. The periodicty and presence of symptoms due to both sympathetic and parasympathetic activity suggest the involvement of central nervous system structures, particularly the hypothalamus. To investigate hypothalamic involvement in CH, we employed a neuroendocrinological approach. We observed a normal dexamethasone suppression test (DST) in all patients, increased cortisol plasma levels in remission patients at 8.00am before and at the end of the DST, while only in CH patients during cluster period did we find a reduced TSH response to TRH and a reduced night-time melatonin peak. The neuroendocrinological derangements found in CH may be consistent with hypothalamic involvement.

The Role of Melatonin in the Treatment of Primary Headache Disorders

“…Notably, there are melatonin receptors (MT1 and MT2) in the suprachiasmatic nucleus of the hypothalamus, so direct action of exogenous melatonin at the hypothalamus is possible. During cluster periods, the timing and peak of endogenous melatonin release can become blunted or even absent—exogenous melatonin supplementation may help by restoring these rhythms.…”

Corticosteroid treatment in cluster headache: Evidence, rationale, and practice

“…Further elevations in plasma cortisol levels have been associated with specific CH attacks [34]. Dexamethasone suppression testing in CH patients has been found to be normal [38][39][40]; however, ovine corticotrophin-releasing hormone testing and insulin tolerance testing produced blunted plasma ACTH and cortisol elevations in patients with CH compared with control subjects [37,41]. Leone et al [37,41] have interpreted these collective findings as indicative of a primary dysfunction in the hypothalamic-pituitary-adrenal axis in CH.…”

The Role of Melatonin in the Treatment of Chronic Headache

“…У пациентов с эпизодической кластерной головной болью уровень ночной выработки мелатонина снижается во время периода обострения [8,10,28] или может совсем отсутствовать суточная ритмика выработки мела-тонина [9,10]. В ряде исследований у пациентов, страда-ющих кластерной головной болью, во время ремиссии определяется более низкий уровень мелатонина по срав-нению со здоровыми людьми [29,30].…”

“…Примечательно, что в супрахиазматическом ядре гипоталамуса [5,6] определя-ются мелатониновые рецепторы MT1 и MT2, что делает возможным прямое воздействие экзогенного мелатонина на гипоталамус. Во время периода кластеров ночной пик выделения эндогенного мелатонина может снижаться или даже отсутствовать [7][8][9][10][11], при этом экзогенное вве-дение мелатонина может восстановить этот ритм.…”