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Abstract

carbamazepine monotherapy in newly diagnosed patients with epilepsy. Arch Neurol 1995;52:989 -996. 16. Marmor MF, Zrenner E. Standard for clinical electroretinography. Doc Ophthalmol 1995;89:199 -210. 17. Arden GB, Barrada A. Analysis of the electrooculograms of a series of normal subjects. Role of the lens in the development of the standing potential. Br J Ophthalmol 1962;46:468 -482. 18. Hanley JA, McNeill BJ. The meaning and use of the area under a receiver operator characteristic (ROC) curve. Radiology 1082;143:29 -36. 19. Bayer A, Zrenner E, Reid S, Schmidt D. Effects of anticonvulsant drugs in retinal function. Psychophysical and electrophysiological findings in patients with epilepsy. Invest Ophthalmol Vis Sci 1990;31:427. Abstract. 20. Harding GFA, Jones LA, Tipper VJ, Betts TA, Mumford JP. Electroretinogram, pattern electroretinogram and visual evoked potential assessment in patients receiving vigabatrin. Epilepsia 1995;36(suppl):108. Abstract. 21. Harding GFA, Robertson KA, Edson AS, Barnes P, Wild JM. Visual electrophysiological effect of a GABA transaminase blocker. Doc Ophthalmol 1999;97:179 -188. 22. Butler WH, Ford GP, Newberne JW. A study of the effects of vigabatrin on the central nervous system and retina of Sprague Dawley and Lister-Hooded rats. Toxicol Pathol 1987; 15:143-148. 23. Coupland SG, Rudd T, Zackon D. Visual electrophysiological correlates of vigabatrin therapy. Invest Ophthalmol Vis Sci 1999;40(suppl):767. Abstract. 24. Bareil FB, Delplaco MP, De Toffol B, Majzoub F, Rossazza C. Electrophysiological evaluation of visual disturbances associated with vigabatrin. Invest Ophthalmol Vis Sci 1999; 40(suppl):18. Abstract.Article abstract-Background: Infarcts of the rostral brainstem often cause vertical gaze palsies but may also produce inappropriate convergence that manifests as pseudoabducens palsy and convergence-retraction nystagmus (CRN). Although the substrate for vergence has been defined in the monkey as lying dorsal and lateral to the oculomotor nucleus, the human homologue is unknown. Method: The authors reviewed the clinical features, ocular findings, and CT or MR lesions in seven patients with pseudoabducens palsy and "top-of-the-basilar" infarction. They reviewed the literature for infarcts causing pseudoabducens palsy or CRN with precise autopsy localization. The authors then mapped the location of the infarcts on anatomic templates. Results: The smallest MR infarct produced an ipsilateral pseudoabducens palsy and CRN, and was located just rostral to the oculomotor nucleus, near the midbrain-diencephalic junction. Two patients with only contralateral pseudoabducens palsy had both subthalamic and thalamic infarction. Four patients with bilateral pseudoabducens palsy had larger infarcts involving the midbrain. All patients with pseudoabducens palsy had upgaze palsy. Two patients with CRN from the literature had small infarcts near the midbrain-diencephalic junction at autopsy. Conclusions: Lesions near the midbrain-diencephalic junction are important for the development of ps...