Drug-induced ocular motor disorders occurring during coma may be difficult to distinguish from structural cerebral lesions. We recently encountered a case of reversible amitriptyline-induced external ophthalmoplegia, which was first described by Mladinich and Carlow in 1977. We suggest that the mechanism for gaze paresis and loss of vestibulo-ocular reflex due to amitriptyline overdose involves the modulation of neurons of the pontine paramedian reticular formation, the rostral fasciculus longitudinalis medialis, and the vestibulo-ocular reflex. Clinical features that might be useful when distinguishing amitriptyline-induced ophthalmoplegia from structural brain lesions--such as basilar thrombosis--include the preservation of corneal response, purposeful withdrawal from noxious stimuli, rapid recovery within 24 hours, and the reversal of symptoms by physostigmine.