Page 15 - The clinical aspects and management of chronic migraine Judith Anne Pijpers

(Figure 1). Upon activation, Calcitonin gene-related peptide (CGRP) is released, causing vasodilation of the meningeal arteries and signal transmission from the trigeminal afferents to the TNC.1,14 The activation of the trigeminovascular system corresponds to the intracranial hypersensitivity experienced by patients (i.e. pulsating or throbbing type of pain, aggravated by pressure or physical activity).1,15 The cause of activation, and thereby the origin of a migraine attack remains largely unknown, but changes in the brainstem and hypothalamus seem important factors.1,10,16 Furthermore, the meninges can be stimulated by cortical events, such as ‘cortical spreading depression’, a depolarisation wave spreading over the cortex, which is regarded as the neurophysiological substrate of migraine aura.2
meningeal blood vessels
Figure 1. Migraine pathophysiology
Migraine headache is caused by activation of the trigeminovascular system, resulting in activation of the trigeminal afferents, trigeminal ganglion (TG) and trigeminal nucleus caudalis (TNC). Subsequently, sensory input is transmitted to the thalamus. This ascending nociceptive system is influenced by the descending pain modulation network, including the hypothalamus, periaqueductal grey (PAG) and locus coeruleus (LC).
LC = locus coeruleus; PAG = periaqueductal grey; TG = Trigeminal Ganglion; TNC = Trigeminal Nucleus Caudalis.
Image from Nervus Nascholing June 2017
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General introduction
trigeminal afferents
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