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(Stroke. 1995;26:1467-1470.)
© 1995 American Heart Association, Inc.

Articles

Vertical Gaze Palsies From Medial Thalamic Infarctions Without Midbrain Involvement

Joni M. Clark, MD Gregory W. Albers, MD

From the Stanford Stroke Center, Palo Alto, Calif.

Correspondence to Joni Clark, MD, Stanford Stroke Center, 701 Welch Rd, Suite 325, Palo Alto, CA 94304.

Background Although the supranuclear pathways for vertical gaze control are not well defined, lesions of the mesencephalic reticular formation including the nucleus of Darkschewitsch, the rostral interstitial medial longitudinal fasciculus, the interstitial nucleus of Cajal, and the posterior commissure are known to produce vertical gaze palsies. MRI studies have not previously reported isolated thalamic lesions as the cause of vertical gaze palsies.

Case Descriptions Three patients with acute paralysis of vertical gaze were imaged with MRI. Sagittal T₁ and axial T₁, T₂, and proton-weighted images were obtained. All three patients had repeated scans performed from 3 days to 6 weeks after the original study. Two patients exhibited unilateral right thalamic infarcts (polar and paramedial territory), and one patient had a bilateral paramedian thalamic infarction. There was no evidence of midbrain involvement on any of the images.

Conclusions Vertical gaze palsies are known to be produced by lesions of the rostral interstitial medial longitudinal fasciculus. This MRI study reveals thalamic infarctions without associated midbrain infarctions in three patients with vertical gaze palsies. This may be explained by interruption of supranuclear inputs.

Key Words: eye abnormalities • magnetic resonance imaging • thalamus

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