[External ophthalmoplegia caused by amitriptyline poisoning]
Related Experiment Video
Updated: Oct 1, 2026

Visual Evoked Potential Recording in a Rat Model of Experimental Optic Nerve Demyelination
Published on: July 29, 2015
S von Stuckrad-Barre1, G Wekerle, T Pfefferkorn
1Neurologische Klinik, Universität München, Klinikum Grosshadern, Marchioninistrasse 15, 81377 München.
Abstract:
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.
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