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James J. Corbett, MD; Matthew Rizzo, MD
Department of Neurology University of Iowa Iowa City, IA 52242

Arch Neurol. 1984;41(7):703.

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

In Reply.

—It was our intention to suggest possible mechanisms for the reversal of internuclear ophthalmoplegia in a patient who used several psychopharmacologic agents in addition to opiate agonists. We did not intend to overemphasize the possible nonopioid action of naloxone.

We stand by our statement that "opiate receptors have not been anatomically demonstrated within the medial longitudinal fasciculus or associated structures."^1,2 Gillman and Sandyk correctly cite evidence from Herkenham and Pert as well as Cuello that opioid receptors exist in primary sensory nuclei. Fibers from primary sensory nuclei may travel in the medial lemniscus but they are not a component of the medial longitudinal fasciculus. In addition, they quote DeQuincy as further evidence for involvement of centers related to visual and auditory perception. We are not sure what this evidence has to do with internuclear ophthalmoplegia. Internuclear ophthalmoplegia is caused by dysfunction in specific oculomotor-vestibular connections in or around the . . . [Full Text PDF of this Article]

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