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John S. Elston
London

Arch Ophthalmol. 1987;105(1):24.

	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.

—Although Shults and colleagues¹ refer to the possible role of central synaptic reorganization following peripheral nerve injury in the pathogenesis of ocular neuromyotonia, they favor the alternative hypothesis of injured motor axons generating spontaneous impulses. The clinical data provided, however, may be interpreted as supporting a central cause.

In three of the four cases described involving the oculomotor nerve, the neuromyotonic phase involved the extraocular muscles innervated by the third nerve, but not the pupil and ciliary muscle, as would be expected with ephaptic transmission. All of these patients showed lid retraction on downgaze in the neuromyotonic phase, ie, an increased innervation of one third nerve-innervated muscle on attempted use of another in a stereotyped pattern, suggesting that the function of the subnuclei of these two muscles was abnormally coordinated. Moreover, slight lid retraction on downgaze was a feature outside the neuromyotonic phase in all four cases, . . . [Full Text PDF of this Article]

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