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Fig. 3 | The Journal of Headache and Pain

Fig. 3

From: Debate: Are cluster headache and migraine distinct headache disorders?

Fig. 3

Trigeminovascular system (TVS). Generation of Cluster headache (CH) involves the trigeminocervical complex (TCC), the parasympathetic nerve fibers (trigeminal autonomic reflex (TAR)), and the hypothalamus [21,22,23,24,25,26,27,28,29]. Peripheral fibers of neurons in the trigeminal ganglions (TG) transmit nociceptive information from dura mater and cranial vessels to the TCC in the brainstem. Fibers from the TCC project to thalamic neurons (via the trigemino-thalamic tract) and to hypothalamic neurons (via the trigemino-hypothalamic tract). Neurons within the TCC are connected to parasympathetic neurons in the superior salivatory nucleus, and the activation of the parasympathetic system by the trigeminal neurons comprises the TAR. The parasympathetic fibers from the superior salivatory nucleus pass through the facial nerve and the sphenopalatine ganglion (SPG) on the way to the periphery. Release of neuropeptides upon activation of the parasympathetic system causes autonomic symptoms such as cephalic vasodilation, conjunctival injection, lacrimation and rhinorrhea. Clinical experience indicates involvement of TAR in CH more than migraine. This notion is further strengthened by the finding that low frequency SPG stimulation induced CH attacks with autonomic features, which could subsequently be treated by high frequency SPG stimulation [30]. Low frequency stimulation of the SPG did not induce migraine attacks or autonomic symptoms in migraine patients. These data suggest that increased parasympathetic outflow by (SPG) neurostimulator does not initiate migraine attacks [31]. However, a recent study demonstrated that low frequency SPG stimulation induced autonomic features but no CH attacks [32]. The clinical manifestation of CH attacks, including circadian rhythm dependence, relapsing– remitting presentations and ipsilateral cranial autonomic symptoms indicate hypothalamic involvement. While the anterior hypothalamus might contribute to the circadian rhythm of CH attacks, the lateral and posterior part might generate the restlessness experienced by CH patients during the attack. Neuroimaging investigations report a role of the hypothalamus during the prodrome symptoms and dorsolateral pons during the ictal phase of attacks in individuals with migraine patients. CH and migraine seem to share anatomical structure with distinct biology

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