Innervation of sweat glands in the forehead. A study in patients with Horner's syndrome.

The amount of sweating in lateral and medial sites in the forehead was investigated with quantitative evaporimetry in 18 patients with Horner's syndrome: eight cases with a central (1st), five with a preganglionic (2nd), and five with a postganglionic (3rd) neurone lesion. The amount of sweating was measured after body heating, and, at another occasion, after intracutaneous injection of the cholinergic drug pilocarpine. The two sites were at the root of the nose (medial position) and at the lateral angle of the eye (lateral position). Generally, there was a reduced level of sweating on the symptomatic versus the non-symptomatic side in both positions during body heating, except in the lateral part of the forehead in the 3rd neurone lesions, where sweating was greater on the symptomatic than on the non-symptomatic side. There was a nearly symmetrical sweating response after pilocarpine injection at all sites. There was one exception to this rule; the lateral position in the preganglionic neurone lesion group where pilocarpine induced more sweating on the non-symptomatic side. Thus, the results suggest a relative supersensitivity to pilocarpine in the medial position for all patients and in the lateral position for the central neurone lesion group. The findings suggest that the innervation of sweat glands in the medial and lateral parts of the forehead is different, the medial part being supplied by nerve fibres from the sympathetic plexus of the internal carotid artery, while the sweat glands in the lateral part is furnished from the plexus surrounding the external carotid artery.

Iatrogenic Horner's syndrome secondary to chest tube thoracostomy.

We report a 22-year-old male who underwent a left thoracostomy and left lower lobectomy for a shotgun wound of the left anterior chest. During surgery, two chest tubes were placed in the left hemithorax at the level of the first and second intervertebral spaces. On the 10th postoperative day, the patient developed a left-sided miosis and ptosis. The diagnosis of a left preganglionic Horner's syndrome was confirmed by pharmacologic testing. The Horner's syndrome was unchanged 3 months after discharge. We conclude that the chest tubes damaged the preganglionic sympathetic fibers of the left orbit resulting in this patient's Horner's syndrome.