Jong S Kim1. 1. Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, Korea. jongskim@amc.seoul.kr
Abstract
OBJECTIVE: To describe the clinical features, MRI findings, and pathogenesis of strokes producing internuclear ophthalmoplegia (INO) as an isolated or predominant clinical manifestation. METHODS: Thirty patients presenting with INO without (n = 12) or with (n = 18) minimal other neurologic signs were studied. MRI and angiogram (conventional in 3, MR angiogram in 27) studies were performed in all of them. RESULTS: Twenty-four presented with INO, whereas six initially presented with one-and-a-half syndrome that changed into INO. Dorsal brainstem infarcts responsible for the INO were located in the caudal pons in 4, rostral pons in 8, rostral pons and isthmus in 2, isthmus area in 14, isthmus and midbrain in 1, and midbrain in 1 patient. Vascular lesions were found in the posterior circulation in 14 patients (47%): at the basilar artery (BA) in 4, superior cerebellar artery (SCA) in 4, posterior cerebral artery (PCA) in 4, and both the PCA and the SCA in 1. The INO eventually disappeared in all patients, tending to last longer (p = 0.05) when it was associated with other neurologic signs. CONCLUSIONS: Isolated or predominant INO is a unique clinical stroke syndrome caused by small dorsal brainstem infarction. The pathogenesis, however, is heterogeneous, including distal occlusion of small penetrating arteries, atheromatous branch occlusion from the BA, SCA, or PCA, or major BA occlusion. The functional prognosis of these patients is excellent, although the INO tends to last longer when there are other neurologic deficits.
OBJECTIVE: To describe the clinical features, MRI findings, and pathogenesis of strokes producing internuclear ophthalmoplegia (INO) as an isolated or predominant clinical manifestation. METHODS: Thirty patients presenting with INO without (n = 12) or with (n = 18) minimal other neurologic signs were studied. MRI and angiogram (conventional in 3, MR angiogram in 27) studies were performed in all of them. RESULTS: Twenty-four presented with INO, whereas six initially presented with one-and-a-half syndrome that changed into INO. Dorsal brainstem infarcts responsible for the INO were located in the caudal pons in 4, rostral pons in 8, rostral pons and isthmus in 2, isthmus area in 14, isthmus and midbrain in 1, and midbrain in 1 patient. Vascular lesions were found in the posterior circulation in 14 patients (47%): at the basilar artery (BA) in 4, superior cerebellar artery (SCA) in 4, posterior cerebral artery (PCA) in 4, and both the PCA and the SCA in 1. The INO eventually disappeared in all patients, tending to last longer (p = 0.05) when it was associated with other neurologic signs. CONCLUSIONS: Isolated or predominant INO is a unique clinical stroke syndrome caused by small dorsal brainstem infarction. The pathogenesis, however, is heterogeneous, including distal occlusion of small penetrating arteries, atheromatous branch occlusion from the BA, SCA, or PCA, or major BA occlusion. The functional prognosis of these patients is excellent, although the INO tends to last longer when there are other neurologic deficits.