Pathological sweating and flushing accompanying the trigeminal lacrimal reflex in patients with cluster headache and in patients with a confirmed site of cervical sympathetic deficit. Evidence for parasympathetic cross-innervation.

Electrodermal responses (as a measure of sweating) and vascular responses to irritation of the eye were investigated in 11 cluster headache patients and, for comparison, in another 24 patients with a confirmed site of lesion in the cervical sympathetic pathway. Seven of the cluster headache patients had ocular and thermoregulatory signs of a postganglionic sympathetic lesion. In these patients, and in six of seven patients with a postganglionic sympathetic lesion from some other cause, the electrodermal response to ocular stimulation was far greater on the denervated side of the forehead than on the sympathetically intact side. This pathological response can be explained by lacrimotor fibres branching into vacant sympathetic sudomotor pathways. The response could account for excessive forehead sweating during attacks of cluster headache, in spite of the presence of Horner's syndrome, because parasympathetic outflow to the lacrimal glands increases during attacks. In patients with diminished sympathetic vasomotor outflow, the vascular response to ocular irritation was also greater on the denervated side of the forehead than on the sympathetically intact side, irrespective of the site of the lesion. The excessive vascular response in sympathetically denervated skin could be caused by adaptive supersensitivity to peptides such as vasoactive intestinal polypeptide, which is known to be released from parasympathetic terminals. The same mechanism might augment vasodilatation during attacks of cluster headache.