Horner's syndrome was first recognized in a funeral portrait painted somewhere between 190 and 210 AD. The patient who was depicted was most likely alive since the painter also painted the patient's conjunctiva which would not be found in a dead person with this syndrome.
Claude Bernard reported this syndrome in his rabbit experiments in 1852. Horner described the triad of ptosis, miosis and enophthalmous in 1869. However, Weir Mitchell gave the first full account 5 years before in a 24 year old soldier with a gunshot wound to his neck.
Sympathetic Anatomy
Miosis can be influenced by completeness of injury, alertness, ambient lighting, degree of denervation, supersensitivity, and focusing at near or far. The anisocoria is greatest during the first 10 seconds after redilation in the dark. Pontine miosis is not a Horner's, but represents increased parasympathetic activity.
Palumbo noted that the sympathetics do not pass through the entire stellate ganglion. If he removed only the lower half of the ganglion as a treatment for hyperhydrosis, he procured the desired clinical effect without the development of a Horner's syndrome.
Ptosis may go unnoticed if the patient uses his frontalis muscle and the examiner is not aware. The sympathetics also innervate the muscle of Riolan in the lower lid. This muscle pulls the lower lid down and against the globe. If you have a patient in whom Horner's is suspected, have the patient follow a hand light. Do this until the lower lid on the side suspected of a Horner's is made to line up with the lower limbus of that eye. You will note an area of sclera showing between the lower lid and lower limbus of the other side.
Sometimes a reverse situation occurs. In an effort to raise a slightly ptotic lid, equal innervation to a yoke muscle (the other levator) can cause retraction of the other normal lid and this raised lid and widened palpebral fissure may be what the patient complains about.
Anhidrosis occurs with lesions below the stellate ganglion. The sweat fibers come off the stellate ganglion and go out by way of the external carotid artery. Therefore, patients with lesions above the stellate ganglion retain sweating.
Enophthalmous is not seen in human cases. It just looks like enophthalmos because of the narrow fissure.
Causes
35% of all cases of Horner's are due to tumors such as thyroid, Hodgkin's and Pancoast tumors of lung. If we count all cases, then 60% are vascular, mostly involving the 3rd neuron. Most of the tumor cases are 2nd neuron according to Giles and Henderson. Also see: Younge AJO 90:419, 1980.
Raeder's Syndrome
This has the same signs as a Horner's except severe pain over the first division of the fifth cranial nerve. The first case described by Raeder was caused by a meningioma of the Gasserian ganglion. All other cases were non-tumors. If other cranial nerves are involved, this rule does not apply and is not a true Raeder's syndrome.
Raeder's syndrome occurs 7 to 1 in males with average age of 46. It is usually self-limited but also highly responsive to steroids. The lesion is supposed to be in carotid sheath where the first division of the fifth nerve and sympathetic run together in the sheath.
Tests for Horner's Syndrome
Cocaine 4%: The original application by Gagel and Forster is not useful. Thompson and others have reviewed the use of cocaine. They found that the difference between the pupils was more important than how much each pupil dilated to cocaine. If the pupil difference between the two pupils after instillation of cocaine is one mm minimum, then that is good evidence of a Horner's. That is, if the pupil fails to dilate or dilates less (at least 1 mm) than the normal, Horner's syndrome is present.
Hydroxyamphetamine paradrine: One drop of solution in each eye. If it is a third neuron Horner's, then the smaller pupil does not dilate and the other does. If it is a first or second neuron Horner's, then both dilate.
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Tests for Horner's
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Thomas J. Walsh, M.D.
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