Abstract Details

Title The Medulla and Horizontal Gaze: A Case of Contralateral Eye Deviation in Medial Medullary Infarction

Topic Neuro-ophthalmology/Neuro-otology

Presentation(s) P4 - Poster Session 4 (8:00 AM-9:00 AM)

Poster/Presentation
Number 17-017

Objective Conjugate eye deviation has been well described in lesions of frontal eye fields and the brainstem, particularly the pons. However, the role of medullary lesions in horizontal gaze control is rarely described in medical literature. We present a case of contralateral conjugate eye deviation presenting acutely in the setting of a left medial medullary infarct.

Background Several medullary structures are thought to play a role in the control of horizontal eye movement, including the nucleus prepositus hypoglossi, medial longitudinal fasciculus, climbing fibers, and inferior olivary nucleus. Conjugate eye deviation in medullary lesions is thought to result from an imbalance between excitatory and inhibitory inputs within these pathways.

Design/Methods Not Applicable

Results A 50-year-old male presented with forced right eye gaze deviation, left gaze palsy, dysarthria and right hemiparesis. Initial computed tomography (CT) scan of the head was negative for acute stroke, and CT angiography scan of head and neck showed no significant stenosis or occlusion of intracranial vasculature. A magnetic resonance imaging (MRI) of the brain showed an acute left medial medullary infarct. The patient was managed with Aspirin and Plavix. At discharge, 14 days after onset, his symptoms had improved, but he continued to have right conjugate eye deviation with left gaze palsy.

Conclusions Conjugate eye deviation is rarely described in medullary lesions. Our case highlights the role of key medullary structures including the nucleus prepositus hypoglossi, medial longitudinal fasciculus, and inferior olivary nucleus in the control of horizontal eye movements. Additional clinical data is needed to better define the incidence of gaze deviation and gaze palsies in medullary lesions and their association with other neurologic symptoms. These findings may help delineate a distinct medullary syndrome and assist clinicians in more accurate lesion localization.

Authors/Disclosures
Lubna Salih, MBBS PRESENTER	Dr. Salih has nothing to disclose.
Daniel Miller, MD	Dr. Miller has nothing to disclose.
Joudi Sharaf, MD (Henry Ford Hospital)	Dr. Sharaf has nothing to disclose.

��ɫ��

��ɫ��