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Nancy M. Newman, MD
Department of Ophthalmology Neuro-ophthalmology Division

Peter S. Levin, MD
Department of Ophthalmology Pacific Presbyterian Medical Center PO Box 7999 San Francisco, CA 94120

Arch Neurol. 1987;44(5):471.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—In the February 1986 issue of the ARCHIVES, Stone et al¹ convincingly documented a case of hypothalamic infarction caused by a Horner's syndrome that disrupted the preganglionic sympathetic pathway of the first-order neuron. They pointed out the importance of detecting a preganglionic lesion as a cause of Horner's syndrome (in contrast to the more common postganglionic lesion).

To exclude postganglionic sympathetic pathway disruption, the authors used a direct-acting adrenergic agent (epinephrine hydrochloride diluted 1:1000) to test for denervation hypersensitivity of the iris sphincter muscle. This method of testing for postganglionic Horner's syndrome may result in inconclusive responses, as it is dependent on precise and equal doses reaching the iris sphincter.² Thus it is affected by disruption of the corneal epithelial barrier³ (as may occur after testing corneal sensation and/or intraocular pressure, or from corneal exposure in patients having seventh cranial nerve palsy or decreased . . . [Full Text PDF of this Article]

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