{'fraction_non_alphanumeric': 0.02631578947368421, 'fraction_numerical': 0.0, 'mean_word_length': 6.059880239520958, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Migraine homocysteine‐related: Old and new mechanisms

In this review, we discussed how homocysteinemia can induce migraine. Vascular and neurogenic mechanisms of migraine‐onset, such as the classical “triggers”, were examined. Favourable effects induced on the syndrome by folate supplementation were also illustrated. However, it was recently shown that hyper‐homocysteinemia can favor migraine by the production of homocysteic acid.This acts as an agonist of the N‐acetyl‐aspartame‐D receptor, and is a potent neurotoxic stimulus causing migraine. Its detrimental effects seem to be antagonized by N‐acetyl‐cysteine, calcium chelators, a naturally‐occurring dipeptide widely distribuited in the muscular and nervous systems. This compound showed positive results in animal models. Elevated homocysteic acid levels secondary to hyper‐homocysteinemia could sensitize the dura mater and cerebral arteries and favor the activation of the trigeminovascular system, predisposing to migraine attacks. However, other experimental and human studies are requested to ratify the negative effect of homocysteic acid on migraine and the positive results obtaining with of its antagonists.