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

• Published in: Cephalalgia 2006-06, Vol.26 (6), p.633-641
• Main Author: Drummond, PD
• Format: Article
• Language: English
• Subjects: Animals; Autonomic Nervous System Diseases - complications; Autonomic Nervous System Diseases - diagnosis; Autonomic Nervous System Diseases - physiopathology; Cluster headache; Cluster Headache - complications; Cluster Headache - diagnosis; Cluster Headache - physiopathology; Face - innervation; Face - physiopathology; Humans; Models, Neurological; parasympathetic; sympathetic; vasoactive intestinal polypeptide
• ISSN: 0333-1024; 1468-2982
• DOI: 10.1111/j.1468-2982.2006.01106.x

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.