Abstract

IntroductionVertical gaze palsy is a recognized manifestation of midbrain lesions. It rarely is a consequence of unilateral thalamic infarction.Case presentationWe report the case of a 48-year-old African-American woman who presented to our facility with vertical gaze palsy and evidence of left medial thalamic infarct on diffusion-weighted imaging without coexisting midbrain ischemia. The etiology of infarct was determined to be small vessel disease after extensive investigation.ConclusionsThis report suggests a possible role of the thalamus as a vertical gaze control center. Clinicoradiological studies are needed to further define the role of the thalamus in vertical gaze control.

Highlights

  • Vertical gaze palsy is a recognized manifestation of midbrain lesions

  • This report suggests a possible role of the thalamus as a vertical gaze control center

  • Stenosis of the right vertebral artery at the C4 transverse foramen secondary to extrinsic osteophyte compression was seen on magnetic resonance angiography and confirmed by catheter angiography

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Summary

Introduction

Vertical gaze palsy is usually associated with lesions of the mesencephalic rostral interstitial nucleus of the medial longitudinal fasiculus, the interstitial nucleus of Cajal, the posterior commissure and the peri-aqueductal gray matter. Vertical gaze palsies can be a manifestation of paramedian thalamic infarction [1,2,3]. We describe the case of a patient presenting with upward gaze palsy secondary to isolated medial thalamic infarct. Case presentation A 48-year-old African-American woman with diabetes, hypertension and hyperlipidemia presented to our facility with acute onset of dizziness and vertical diplopia. A physical examination revealed upward gaze paresis, which could be overcome by the doll’s eye maneuver and skew deviation of the right eye. A magnetic resonance imaging (MRI) scan, which was performed 12 hours after the onset of symptoms, showed an acute left paramedian thalamic infarct (Figure 1, Figure 2 and 3) without associated midbrain lesions (Figure 4), and a chronic right cerebellar infarct.

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