Mechanisms of Autonomic Disturbance in the Face During and Between Attacks of Cluster Headache

Abstract

Drummond PD. Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache. Cephalalgia 2006; 26:633-641. London. ISSN 0333-1024 Lacrimation and nasal secretion during attacks of cluster headache appear to be due to massive trigeminal-parasympathetic discharge. In addition, the presence of oculo-sympathetic deficit and loss of thermoregulatory sweating and flushing on the symptomatic side of the forehead indicate that the cervical sympathetic pathway to the face is injured in a subgroup of cluster headache patients. In this review, it is argued that a peripheral rather than a central lesion produces signs of cervical sympathetic deficit, probably resulting from compression of the sympathetic plexus around the internal carotid artery. Although trigeminal-parasympathetic discharge appears to be the main trigger for vasodilation during attacks, supersensitivity to neurotransmitters such as vasoactive intestinal polypeptide, together with release of sympathetic vasoconstrictor tone, may boost facial blood flow in patients with cervical sympathetic deficit. In addition, parasympathetic neural discharge may provoke aberrant facial sweating during attacks in patients with cervical sympathetic deficit. Although neither trigeminal-parasympathetic discharge nor cervical sympathetic deficit appears to be the primary trigger for attacks of cluster headache, these autonomic disturbances could contribute to the rapid escalation of pain once the attack begins. For example, a pericarotid inflammatory process that excites trigeminal nociceptors might initiate neurogenic inflammation and trigeminal-parasympathetic vasodilation. To complete the loop, neurogenic inflammation and trigeminal-parasympathetic vasodilation could provoke the release of mast cell products, which aggravate inflammation and intensify trigeminal discharge. ᮀ Cluster headache, parasympathetic, sympathetic, vasoactive intestinal polypeptide

Immersing the foot in painfully-cold water evokes ipsilateral extracranial vasodilatation

“…Noxious stimulation of the eyes, nose, lips, mouth or face triggers trigeminalparasympathetic vasodilator reflexes in orofacial tissues and the forehead microvasculature, and also initiates antidromic vasodilatation in the terminal distribution of stimulated trigeminal nerve fibres (Izumi, 1999;Drummond, 2006b). In addition, increases in body temperature (Drummond & Finch, 1989) and emotions that provoke blushing (Drummond & Lance, 1987;Licht & Pilegaard, 2008) generate active sympathetic vasodilatation of facial vessels, whereas sympathetic vasoconstrictor tone limits blood flow through exposed parts of 7 the face in cold environments, particularly the nose, lips and ears (Blair et al, 1961;Fox et al, 1962;Drummond & Finch, 1989).…”

“…The functional significance of this nociceptive vasodilator response is uncertain but could be worth exploring, as loss of sympathetic vasoconstrictor tone may aggravate the extracranial vascular component of pain in disorders such as cluster headache and migraine (Drummond, 1991;Drummond, 2006b). …”

Trigeminal autonomic cephalalgia sine headache

“…Pathological sweating and flushing in sympathetically denervated parts is mediated by parasympathetic functional connections. Release of calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) during trigeminal-parasympathetic discharge could release mast cell products, which further increase trigeminal neurogenic inflammation and pain, and subsequent autonomic disturbances, until mast cells are depleted [17]. Dependency of autonomic activation on nociceptive activation of the trigeminal nerve has always been assumed, but this was questioned by the report of cases with CH-H.…”

“…Pure autonomic symptoms have been described of a 44-year-old woman with hemicrania continua who underwent occipital nerve stimulation and subsequently experienced six episodes of ipsilateral lacrimation, nasal stuffiness and a feeling of sand in the eye without the development of head pain [9]. Instead of a central/diencephalic stimulus, it is also suggested that episodic painless autonomic disturbances could be caused by a peripheral stimulus like allergy or infection [17]. However, we can not explain the absence of parasympathetic stimulation of peripheral nociceptors [17], nor awareness of such, in theories of both central and peripheral generation of pure autonomic attacks.…”

Klasehodepine

“…Postganglionaere fibre går til blant annet tårekjertelen, hjernehinner og kraniale blodkar. Man antar at sterk aktivitet i den trigeminale kjernen (smertesignaler) reflektorisk aktiverer disse fibrene (14). Under anfall er dilatasjon av ulike intrakraniale kar påvist med ulike teknikker, og temperaturen i ansiktet på den affiserte siden øker.…”