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Neurogenic: Horner Syndrome

Neurogenic: Horner Syndrome

Anisocoria and partial eyelid ptosis were detected during the routine eye examination of a 66-year-old woman. These findings had not been present during an examination 2 years earlier. Because the patient had no symptoms, she could not recall when these signs began. Her general health was unremarkable; she had smoked 1 pack of cigarettes per day for 40 years. The margin reflex distance test, which demonstrates the distance from the light reflex on the cornea to the central upper eyelid in straight gaze, showed a mild ptosis limited to 1 or 2 mm that resulted from weakness of the Mueller muscle. The involved pupil was smaller than the unaffected pupil, and the anisocoria increased in dim illumination. Anisocoria is greatest after about 5 seconds of darkness, when the normal pupil is as large as it can become1; the affected pupil then dilates slowly. This dilation lag is characteristic and virtually diagnostic of Horner syndrome. When the lesion is below the superior cervical ganglion, reduced ipsilateral sweating or anhidrosis of the face may be present. Horner syndrome involves the fibers that compose the oculosympathetic pathway. These fibers have a long and tortuous course from the hypothalamus to the eye. A variety of vascular, traumatic, or neoplastic lesions can interrupt this pathway. The cocaine test is used to confirm the diagnosis.2 Cocaine, 10%, is applied topically to both eyes. Normally, cocaine produces dilation of the pupil by preventing the reuptake of norepinephrine that has been released into the synaptic junctions of the iris dilator muscle. If the sympathetic innervation to the eye is interrupted, cocaine should have no mydriatic effect. This patient's left pupil did not dilate in response to topical cocaine, which confirmed the suspected diagnosis of Horner syndrome. Hydroxyamphetamine is used to help distinguish a preganglionic or central lesion from a postganglionic lesion.2This drug is an indirectly acting α-adrenergic agonist that dilates the pupil only in the presence of endogenous norepinephrine. In patients who have central or preganglionic lesions, the postganglionic sympathetic pathway is undisturbed; thus, the norepinephrine contained within the presynaptic vesicles is released, and normal mydriasis occurs. In patients with postganglionic lesions (which are considered to be secondary to "benign" causes, such as endarterectomy or other neck surgery, trauma, or migraine variants), the involved pupil does not dilate when topical hydroxyamphetamine is applied. Instilled hydroxyamphetamine caused this patient's pupil to dilate, signaling the presence of either a central or a preganglionic lesion. Because of her history of longterm smoking, a chest film was obtained. An apical lung neoplasm known as a Pancoast tumor was found; it was later identified as an oat cell carcinoma. The patient was referred to a pulmonologist, and the neoplasm was successfully treated.

 
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