Cluster headache and TACs: state of the art
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MIGRAINE AND PRIMARY HEADACHES
Cluster headache and TACs: state of the art Luca Giani 1 & Alberto Proietti Cecchini 1 & Massimo Leone 1,2
# Fondazione Società Italiana di Neurologia 2020
Abstract Cluster headache (CH), paroxysmal hemicrania (PH), short-lasting unilateral neuralgiform headache attacks (including SUNCT and SUNA), and hemicrania continua (HC) compose the group of trigeminal autonomic cephalalgias (TACs). Here, we review the recent advances in the field and summarize the current knowledge about the origin of these headaches. Similar to the other primary headaches, the pathogenesis is still much obscure. However, advances are being made in both animal models and humans studies. Three structures clearly appear to be crucial in the pathophysiology of TACs: the trigeminal nerve, the facial parasympathetic system, and the hypothalamus. The physiologic and pathologic functioning of each of these elements and their interactions is being progressively clarified, but critical questions are still open. Keywords Trigeminal autonomic cephalalgias . Cluster headache . Headache . CGRP . PACAP
Introduction
Trigeminal autonomic cephalalgias
Trigeminal autonomic cephalalgias (TACs) share the presentation of unilateral head pain associated with ipsilateral autonomic cranial phenomena [1]. Different syndromes are recognized, mainly differentiated by the duration and frequency of the headaches: cluster headache (CH), paroxysmal hemicrania (PH), short-lasting unilateral neuralgiform headache attacks (including the subtypes with both conjunctival injection and tearing (SUNCT), or not (SUNA)), and hemicrania continua (HC) [1]. Components from both the central and the peripheral nervous systems are involved in the generation of headache attacks in TACs. Because of the usual distribution of pain in the periorbital area, the trigeminal nerve, which provides sensory innervation to most of the head, is logically considered at its origin. The pathognomonic autonomic phenomena are attributed to an activation of the facial parasympathetic system. Finally, the peculiar periodicity of attacks first called for a regulatory role of the hypothalamus [2].
CH is the most frequent trigeminal autonomic cephalalgia (TAC) with an estimated lifetime prevalence of 0.1% [3]. The other TACs, namely PH, SUNCT/SUNA, and HC, are rarer than CH, and proper epidemiological investigations are lacking. SUNCT/SUNA has an estimated prevalence of around 6.6 per 100,000 [4]. PH may account for about 4% of all the TACs [4] or about 1 in 50,000 [5]. HC seems to be even rarer [6]. From a taxonomic and diagnostic point of view, the essential difference between TACs lies in the attack duration (SUNCT/SUNA < PH < CH < HC) and frequency (SUNCT/SUNA > PH > CH > HC) [1]; in some cases, the response to therapy is a diagnostic criteria (HC and PH) (Table 1) [1]. CH attacks have the longest duration, up to 3 h, and a lower frequency compared with SUNCT/SUNA and PH. CH attacks improve markedly with oxygen and sumatriptan but such improvement is not a diagnostic cri
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