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© 2000 American Academy of Neurology Articles Abnormal vergence with upper brainstem infarctsPseudoabducens palsyFrom the Department of Neurology, State University of New York at Buffalo. Address correspondence and reprint requests to Dr. P. Pullicino, Stroke Program, Department of Neurology/State University of New York at Buffalo, Buffalo NY 14203; e-mail: ppullici{at}acsu.buffalo.edu 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 pseudoabducens palsy. Pseudoabducens palsy and CRN are probably both manifestations of abnormal vergence activity. Inhibitory descending pathways for convergence may pass through the thalamus and decussate in the subthalamic region. This article has been cited by other articles:
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