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Two patients exhibiting "primary" oculomotor misdirection caused by intracavernous mass lesions, and a third boy with transient oculomotor synkinesis after migrainous ophthalmoplegia provide background for a reassessment of the currently accepted explanation of anomalous synkineses subsequent to oculomotor nerve palsies. The hypothesis of peripheral misdirection of regenerating motor axons is inconsistent with these clinical observations, and an alternate mechanism is suggested, based on concepts of ephaptic neuronal transmission of impulses or on chromatolysis-induced reorganization of nuclear synapses.
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Frederick E. Lepore (1980) studied this question.
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