SYNOPSIS Endogenous opioids and 5‐hydroxytryptamine are the main neurotransmitters that regulate nociception, hedonia and autonomia. These functions are simultaneously impaired in idiopathic headaches. Enkephalins, beta‐endorphin, and tryptophan (5‐HT precursor) were evaluated in CSF and plasma of migraine and cluster headache sufferers. The following results were obtained:(a) decreased levels of CSF enkephalins in migraine attack and cluster headache,(b) increased CSF Tryptophan (TP) in migraine,(c) increased free plasma TP in migraine attack,(d) increased serum beta‐endorphin‐like‐immunore‐activity at the end of attack.A possible link between these findings and the impairment of nociception, hedonia and vegetative balance in headache sufferers is here discussed.

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Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.

SYNOPSIS Free and total plasma tryptophan (TRY) was evaluated in migraine and daily headache sufferers. In migraineurs, free plasma TRY was significantly higher on the day of the attack, the day preceding and subsequent to the attack in comparison with controls. The possibility that in migraineurs a lowering of brain 5‐HT may displace TRY from its binding to plasma albumin through an unknown feedback mechanism is suggested. In daily headache sufferers total plasma TRY levels were statistically significantly lower compared with controls. This may reflect a deficiency of 5‐HT in the brain.

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