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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.

Adult↗

The effect of adrenergic blockade on blushing and facial flushing.

The effect of adrenergic blockade on vascular responses in the forehead was assessed during stressful mental arithmetic, singing, and moderate exercise in 21 frequent blushers and 21 infrequent blushers. Adrenergic antagonists were introduced into a small site on the forehead by iontophoresis, and vascular responses were monitored bilaterally with laser Doppler flowmetry. Beta blockade prevented increases in blood flow in infrequent blushers during mental arithmetic and partially inhibited vasodilatation during singing, indicating minor participation of beta-adrenoceptors in blushing. Alpha blockade did not affect blushing but augmented vasodilatation during exercise. Despite higher ratings of self-consciousness in frequent than in infrequent blushers, vascular responses were similar in both groups. Thus, blushing propensity does not appear to be related to the density of alpha- or beta-adrenoceptors in facial vessels and may have a psychological basis.

Adolescent↗

Naloxone, ethanol, and the chlorpropamide alcohol flush.

The effects of ethanol and subsequent administration of intravenous naloxone were studied in double-blind, placebo-controlled fashion with a group of six male chlorpropamide alcohol flushers (CPAF) and a group of 13 nonflushing males. The effect of ethanol intoxication on fine motor control was measured by a typing test. When sober, the two groups performed in comparable fashion. When intoxicated, the CPAF group displayed significantly greater impairment than the nonflushing group as measured by typing errors committed in 3 min (CPAF: 55.4 +/- 10.1 errors, n = 12; vs. nonflushing: 15.6 +/- 2.3, n = 32; p = 0.0000015 by Student's unpaired t test). Chlorpropamide alcohol flushers appeared to be more sensitive to ethanol. Naloxone reversed this effect for individuals in the CPAF group (saline treatment: 51.0 +/- 11.7 errors per minute; vs. naloxone treatment: 23.7 +/- 4.2; p = 0.034 by Student's paired t test, n = 6). Naloxone had no effect in the nonflushing group. Unlike the normal, nonflushing group, the CPAF group demonstrated an increased sensitivity to ethanol that was partially antagonized by naloxone.

Adult↗