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A 63-year-old man with transient vertical diplopia
Teaching NeuroImages Neurology Resident and Fellow Section © 2015 American Academy of Neurology
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Vignette He consistently developed a transient right hypertropia (with left supraduction deficit) after looking down for ~10 seconds and then back to primary. Aside from presumed transient tonic contraction of the left inferior rectus, there was no evidence that other IIIrd-innervated muscles were involved. Gold © 2015 American Academy of Neurology
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Imaging Gold © 2015 American Academy of Neurology
Figure 1) Tonic left inferior rectus contraction causing diplopia in ONM: Right hypertropia in primary and eccentric gaze (aside from downgaze), maximal in right and upgaze with a left supraduction deficit. Gold © 2015 American Academy of Neurology
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Imaging Gold © 2015 American Academy of Neurology
Supplementary Figure) Neurovascular contact in ONM: (A) Axial CISS imaging shows compression of left IIIrd nerve by PCA. (B) Magnified view showing PCA (arrow heads), and IIIrd nerve (arrow). Gold © 2015 American Academy of Neurology
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Ocular Neuromyotonia: An under-recognized cause of transient diplopia
When vascular compression of an ocular motor nerve causes ocular neuromyotonia (ONM), it is thought that ephaptic transmission is responsible. Axonal “cross-talk” causes irritability and abnormal firing independent of the synapse. Without thin, heavily T2-weighted CISS or FIESTA sequences, neurovascular contact can be missed. ONM has also been associated with radiation therapy, thyroid eye disease, mass lesions, or superior oblique myokymia. If diplopia manifests or worsens after prolonged eccentric gaze, ONM should be considered. 1. Roper-Hall G, Chung SM, Cruz OA. Ocular neuromyotonia: differential diagnosis and treatment. Strabismus 2013;21: 2. Cruz FM, Blitz AM, Subramanian PS. Partial third nerve palsy and ocular neuromyotonia from displacement of posterior communicating artery detected by high-resolution MRI. J Neuro-ophthalmol 2013;33: Gold © 2015 American Academy of Neurology
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