It results in ptosis (drooping upper eyelid), miosis (constricted pupil), and occasionally enophthalmos (the impression that the eye is sunk in) and anhidrosis (decreased sweating) on one side of the face.

In children Horner's syndrome sometimes leads to a difference in eye color between the two eyes (heterochromia). This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.

History

It is named after Dr Johann Friedrich Horner (1831-1886), the Swiss ophthalmologist who first described the syndrome in 1869. Several others had previously described cases, but "Horner's syndrome" is most prevalent. In France, Claude Bernard is also eponymised with the condition being called "syndrome Bernard-Horner".

Causes

Horner's syndrome is usually acquired but may also be congenital. Although most causes are relatively benign, Horner's syndrome may reflect serious pathology in the neck or chest (such as a Pancoast tumor) and hence requires workup.

Horner's Syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side that the symptoms are on. The following are examples of conditions that cause the clinical appearance of Horner's Syndrome:

First-order neuron disorder: Central lesions that involve the hypothalamospinal pathway (e.g. transection of the cervical spinal cord).
Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor).
Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus).

Diagnosis

Three tests are useful in confirming the presence and severity of Horner's syndrome:

Cocaine test - Cocaine blocks the reuptake of norepinephrine resulting in the dilation of a normal pupil. The pupil will fail to dilate in Horner's syndrome.
Paredrine test
Dilation lag test

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No compensatory sweating after botulinum toxin treatment of palmar hyperhidrosis
From Journal of Drugs in Dermatology, 5/1/05

No Compensatory Sweating after Botulinum Toxin Treatment of Palmar Hyperhidrosis

Krogstad AL, et al. British Journal of Dermatology. 2005;152:329-333.

Summary

The authors present a trial to determine if treating palmar hyperhidrosis with botulinum A toxin results in compensatory sweating in other body areas. Compensatory sweating has been observed in patients with hyperhidrosis treated with transthoracic endoscopic sympathectomy. Seventeen patients with palmar hyperhidrosis were enrolled and underwent botulinum A toxin injections in their palms. Injections were standardized using a plastic sheet with perforations through which black ink dots were placed, forming a grid. There were 75 to 80 injections per hand. On average, 230 units of toxin were used for the right hand and 237 units were used for the left hand. All patients were treated by the same physician. The degree of sweating was evaluated by measuring water evaporation using a handheld dual probe system. The hands, feet, forehead, breast, abdomen, legs, axillae, and forearms were evaluated. Six measurements were made, 2 before treatment and the remaining 4 at various time points from treatment to 6 months afterward. Patients also subjectively evaluated sweating of the palms and feet using a 10-point scale. All patients reached a statistically significant reduction in water evaporation of their palms. Sweating gradually increased after treatment; however, at 6 months time, a significant difference was still noted compared to pretreatment values. This was also true for the subjective evaluation of sweating by the patients. None of the untreated body locations measured a statistically significant increase in water evaporation after treatment with botulinum A toxin.

Comment

This was a relatively small study, but provided good data regarding the efficacy of botulinum A toxin for palmar hyperhidrosis. Statistically significant differences between pre- and post-treatment values of water evaporation were noted up to 6 months after treatment. This was reinforced by the patients' subjective evaluations of sweating. As noted above, patients with palmar hyperhidrosis have been treated with transthoracic endoscopic sympathectomy. During this procedure, a pneumothorax is created in the patient and then a thoracoscope is inserted into the pleural space. (1) The sympathetic trunk is then electrically resected as the scope contains a suction coagulation probe, grasping forceps, and a wire electrode. (1) Patients treated with this procedure have experienced sweating in new body areas, a phenomenon known as compensatory hyperhidrosis. In a systematic review of the literature, Furlan et al found that roughly 50% of patients undergoing either open or transthoracic sympathectomy experienced compensatory hyperhidrosis and that 25% of these patients considered it to be worse than their initial disease or disabling. (2) This treatment also has associated complications relating to the disruption of sympathetic nerves such as transient or permanent Horner's syndrome and neuralgic pains, not to mention the complications related to the surgical procedure. (2) This study demonstrates the safety, efficacy, and lack of side effects when treating palmar hyperhidrosis with botulinum A toxin and establishes a role for dermatologists in treating this condition.

References

1. Kux M. Thoracic endoscopic sympathectomy in palmar and axillary hyperhidrosis. Arch Surg. 1978; 113(3):264-6.

2. Furlan AD, et al. Are We Paying a High Price for Surgical Sympathectomy? A Systematic Literature Review of Late Complications. The Journal of Pain. 2000;1(4):245-257.

Return to Horner's syndrome

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