[The pathogenetic bases of hemicrania]

Migraine remains a complex neurological condition with unclear pathophysiological mechanisms. Prior research has shown that migraine with aura involves hypoperfusion in cortical regions corresponding to clinical symptoms, followed by hyperperfusion. However, the link between these hemodynamic changes and headache remains uncertain. Studies have not found focal cerebral blood flow abnormalities in migraine without aura. Vasodilation of extracranial and intracranial arteries occurs during headache phases, but the role of vasodilation in pain generation is debated. Biochemical evidence suggests that pain may arise from sensitized blood vessels and circulating substances like bradykinin and serotonin. The trigeminovascular system has been implicated in migraine through the release of sensory peptides such as substance P and calcitonin gene-related peptide. These peptides can cause vasodilation and plasma extravasation, suggesting a role in neurogenic inflammation. Despite these findings, the precise relationship between vasodilation and headache remains unresolved.

This review aims to clarify the pathophysiological mechanisms underlying migraine headaches, focusing on cerebral blood flow dynamics and the role of the trigeminovascular system. The study seeks to evaluate how hypoperfusion and hyperperfusion patterns correlate with clinical symptoms and headache onset. It also investigates the role of vasodilation and neurogenic inflammation in pain generation. The purpose is to assess the evidence supporting serotonin's involvement in linking vasodilation to headache. The review examines the contribution of perivascular trigeminal fibers in migraine pathogenesis. It also explores the role of endorphinergic brain tonus in central nociceptive dysfunction. The study aims to evaluate the effectiveness of sumatriptan in modulating serotonin receptors to alleviate migraine symptoms. The goal is to synthesize findings to better understand the interplay between vascular changes, neuroinflammation, and pain perception in migraine.

The review approach includes a synthesis of existing literature on cerebral blood flow in migraine with and without aura. The authors analyze studies using neuroimaging techniques to track hypoperfusion and hyperperfusion patterns. They examine biochemical evidence related to pain-producing substances such as bradykinin and serotonin. The review incorporates findings on the trigeminovascular system and its role in neurogenic inflammation. The authors assess the evidence for perivascular trigeminal fibers releasing sensory peptides like substance P and calcitonin gene-related peptide. They evaluate the role of serotonin receptors in modulating vasodilation and headache. The review includes data on endorphinergic brain tonus and its potential impact on nociception. The authors synthesize findings from clinical trials on sumatriptan's effectiveness in treating migraine.

Key findings from the literature indicate that hypoperfusion in cortical regions is associated with migraine aura, followed by hyperperfusion. However, hyperperfusion does not strictly correlate with headache onset. Experimental cortical spreading depression is a proposed mechanism for hypoperfusion propagation. No focal blood flow abnormalities are observed in migraine without aura. Vasodilation of extracranial and intracranial arteries occurs during headache phases. Biochemical evidence suggests that pain may result from sensitized blood vessels and circulating substances like bradykinin and serotonin. Perivascular trigeminal fibers release sensory peptides that cause vasodilation and plasma extravasation. Activation of the trigeminovascular system is implicated in migraine pain mechanisms.

Synthesis and implications suggest that hypoperfusion and hyperperfusion patterns in migraine with aura are topographically linked to clinical symptoms. However, hyperperfusion does not necessarily lead to headache. Vasodilation of extracranial and intracranial arteries is a consistent feature of migraine headaches. The trigeminovascular system's activation is likely involved in both vasodilation and pain perception. Sensory peptides such as substance P and calcitonin gene-related peptide contribute to neurogenic inflammation. Reduced endorphinergic brain tonus supports the hypothesis of central nociceptive dysfunction in migraine. The effectiveness of sumatriptan in alleviating migraine symptoms underscores serotonin's role in linking vasodilation to headache. Further research is needed to clarify the exact relationship between vasodilation and headache mechanisms.