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Figure 1: Cluster headache pathophysiology. Pain afferents from the trigeminovascular system traverse the ophthalmic division of the trigeminal nerve, taking signals from the cranial vessels and dura mater (shown by purple fibers). These inputs synapse in the TCC and project to higher brain structures such as the thalamus (T) and cortex resulting in pain perception (shown in blue fibers). Activation of the trigeminovascular system by stimulation of dural structures also causes neuronal activation in the SSN within the pons, which is the origin of cells for the cranial parasympathetic autonomic vasodilator pathway. There is subsequent activation of this parasympathetic reflex through the outflow from the SSN and is relayed through the SPG (shown by pink fibres), but also through the facial (VIIth cranial) nerve (not shown). Activation of both trigeminal and autonomic nerves defines the trigeminal autonomic reflex arc, which is integral to the pathophysiology of cluster headache and the other TACs. The HT is functionally connected to the ipsilateral trigeminal system and other brain areas of the pain matrix. Red dashed lines indicate the pathways by which the HT controls or triggers pain. A third-order sympathetic nerve lesion thought to be caused by vascular changes to the ICA in the cavernous sinus with subsequent irritation of the local plexus of nerve fibers, can give rise to sympathetic symptoms (incomplete Horner syndrome) (shown by yellow fibers). IML = Intermediolateral tract of spinal cord, SCG = Superior cervical ganglion, SN = Suprachiasmatic nucleus, TCC = Trigeminocervical complex, SSN = Superior salivatory nucleus, SPG = Sphenopalatine ganglion, HT = Hypothalamus, ICA = Internal carotid artery

Figure 1: Cluster headache pathophysiology. Pain afferents from the trigeminovascular system traverse the ophthalmic division of the trigeminal nerve, taking signals from the cranial vessels and dura mater (shown by purple fibers). These inputs synapse in the TCC and project to higher brain structures such as the thalamus (T) and cortex resulting in pain perception (shown in blue fibers). Activation of the trigeminovascular system by stimulation of dural structures also causes neuronal activation in the SSN within the pons, which is the origin of cells for the cranial parasympathetic autonomic vasodilator pathway. There is subsequent activation of this parasympathetic reflex through the outflow from the SSN and is relayed through the SPG (shown by pink fibres), but also through the facial (VII<sup>th</sup> cranial) nerve (not shown). Activation of both trigeminal and autonomic nerves defines the trigeminal autonomic reflex arc, which is integral to the pathophysiology of cluster headache and the other TACs. The HT is functionally connected to the ipsilateral trigeminal system and other brain areas of the pain matrix. Red dashed lines indicate the pathways by which the HT controls or triggers pain. A third-order sympathetic nerve lesion thought to be caused by vascular changes to the ICA in the cavernous sinus with subsequent irritation of the local plexus of nerve fibers, can give rise to sympathetic symptoms (incomplete Horner syndrome) (shown by yellow fibers). IML = Intermediolateral tract of spinal cord, SCG = Superior cervical ganglion, SN = Suprachiasmatic nucleus, TCC = Trigeminocervical complex, SSN = Superior salivatory nucleus, SPG = Sphenopalatine ganglion, HT = Hypothalamus, ICA = Internal carotid artery