Ocular ipsipulsion elicited by closing eyes in lateral medullary infarction
Shi-Lin Yang1, Tao Yang2, Xiang Han1, Qiang Dong1 1 Department of Neurology, Huashan Hospital, Fudan University, Shanghai, PR China 2 Department of Emergency, Huashan Hospital, Fudan University, Shanghai, PR China
Date of Web Publication
Correspondence Address: Dr. Qiang Dong Department of Neurology, Huashan Hospital, No. 12, Wulumuqi Road (M), Jing'an District, Shanghai 200040 PR China
Source of Support: None, Conflict of Interest: None
How to cite this article: Yang SL, Yang T, Han X, Dong Q. Ocular ipsipulsion elicited by closing eyes in lateral medullary infarction. Neurol India 2019;67:331
An 86-year-old man presented to the emergency room complaining of sudden onset of vertigo. Neurological examination showed a primary position left-beating nystagmus, decreased sensation of pain and temperature in the left limbs, and right Horner's syndrome. Extraocular movement was full in all directions. When he was asked to close his eyes, the eyes deviated to the extreme right lateral position; when he opened his eyes, they turned towards mid-position [Video 1]. He could perform right gaze effortlessly, but left gaze required effort. Saccades towards the right side were hypermetric and saccades towards the left side were hypometric [Video 1]. Right gaze deviation was also unveiled by computed tomography (CT) scan [Figure 1]a. Magnetic resonance imaging (MRI) showed restricted diffusion in right lateral medulla, confirming the diagnosis of acute lateral medullary infarction, also known as Wallenberg's syndrome [Figure 1]b.
Figure 1: (a) Right gaze deviation appeared during a computed tomography scan in the absence of visual fixation. Note that the position of the junction of eyeballs and optic nerves (arrows) demonstrated an ocular right deviation. (b) Magnetic resonance imaging showed restricted diffusion in the right lateral medulla, suggestive of an acute infarction
Ocular ipsipulsion, a unique sign of a lateral medullary lesion, manifests as a tonic deviation of eyes toward the damaged side despite the presence of full extraocular movements. It should be distinguished from conjugate gaze palsy, the inability to move both eyes in the same direction, which is associated with lesions in the pons or frontal lobe. Ocular ipsipulsion is most prominent when visual fixation is interrupted, for example, when eyes are closed or during the performance of a CT scan, as seen in our case. Despite being a sign with localizing value, it is often overlooked in patients with lateral medullary infarction.
The mechanism of ocular ipsipulsion has not been well elucidated. It is believed that ocular ipsipulsion results from interruption of the contralateral olivocerebellar pathways passing through the ipsilateral inferior cerebellar peduncle. Due to loss of inhibitory signal from the ascending fibers, Purkinje cell projections increase activity to inhibit the ipsilateral vestibular nuclei. As a result, the predominant activity of the contralateral vestibular nuclei generates a slow-phase drift towards the side of lesion.
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