Description
A 77-year-old man was referred with a sudden-onset horizontal diplopia post-transcatheter aortic valve replacement. Oscillopsia (a visual disturbance in which objects appear to oscillate) was only noted by the patient on looking up.
Examination showed a right-sided internuclear ophthalmoplegia and bilateral gaze evoked upbeat nystagmus (video 1). Pupils were isocoric and reactive to light. Corrected visual acuity was 6/6 in the right eye and 6/9 in the left eye, and funduscopic examination was normal. MRI of the brain showed an acute infarct in the right dorsal pons (figure 1). The patient reported complete resolution of his symptoms within 4 months from onset, and detailed ocular examination was completely normal at 6 months.
video 1.
Figure 1.
(A) Diffusion-weighted image sequence MRI of the brain shows an acute right dorsal pontine infarct. (B) Illustration shows the pathway of the ventral tegmental tract (blue lines) originating from superior vestibular nuclei (yellow circles) in the pons. The tract decussates at the level of mid-pons to supply the eye elevator third nerve sub-nuclei (red circles). Each superior rectus receives innervation (yellow lines) from the contralateral oculomotor nucleus.
Pontine lesions disrupting the ventral tegmental tract (VTT) may cause upbeat nystagmus.1 This tract originates in the superior vestibular nucleus, passes through the ventral pons and sends excitatory upward vestibular signals to the superior rectus and inferior oblique subnuclei of the contralateral oculomotor nucleus. A VTT lesion, therefore, may lead to hypoactivity of the neuronal drive to the elevator muscles resulting in a downward drift with subsequent upbeat nystagmus. This case highlights the importance of careful clinical examination and good knowledge of neuroanatomy in the process of localising the lesion.
Learning points.
Vertical eye movement abnormalities may also occur in patients with internuclear ophthalmoplegia (INO).
The side of the lesion in patients with INO is ipsilateral to the side of ocular adduction limitation.
Although nystagmus is often called by the direction of its fast phase (upbeat nystagmus in the case described), it is the slow phase that points to the underlying defect.
bcr-2019-233130supp001.mp4 (1.8MB, mp4)
Footnotes
Contributors: ME and AB contributed equally to this work (co-first authors). They drafted the article and reviewed the literature. MGH interpreted the images and helped with the literature review. TMA acted as a senior author and reviewed the article for important intellectual content.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Patient consent for publication: Obtained.
Provenance and peer review: Not commissioned; externally peer reviewed.
Reference
- 1. Pierrot-Deseilligny C, Milea D. Vertical nystagmus: clinical facts and hypotheses. Brain 2005;128:1237–46. 10.1093/brain/awh532 [DOI] [PubMed] [Google Scholar]
Associated Data
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Supplementary Materials
bcr-2019-233130supp001.mp4 (1.8MB, mp4)