Agnes M F Wong1, Douglas Tweed, James A Sharpe. 1. Division of Neurology, University Health Network-Toronto Western Hospital, University of Toronto, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8.
Abstract
OBJECTIVE: To detect and determine the magnitude of vertical deviation in patients with unilateral sixth nerve palsy. DESIGN: Prospective consecutive comparative case series. PARTICIPANTS: Twenty patients with unilateral peripheral sixth nerve palsy, 7 patients with central palsy caused by brainstem lesions, and 10 normal subjects. METHODS: Subjects were tested by the prism and cover test, Maddox rod and prism test, and magnetic search coil recordings in nine diagnostic eye positions. They were also tested during static lateral head tilt by the prism and cover, and Maddox rod and prism tests. MAIN OUTCOME MEASURES: The magnitudes of horizontal and vertical deviations. RESULTS: All patients had an abduction deficit and incomitant esodeviation that increased in the field of action of the paretic muscle, indicating sixth nerve palsy. Mean vertical deviations, for all positions of gaze in peripheral palsy were 0.3 +/- 0.8 prism diopters (PD) by prism and cover test, 1.3 +/- 1.6 PD by Maddox rod and prism test, and 2.0 +/- 1.4 PD by coil recordings. Mean vertical deviations in normal subjects were 0.0 +/- 0.0 PD by prism and cover test, 1.0 +/- 0.9 PD by Maddox rod and prism test, and 1.9 +/- 2.1 PD by coil recordings. Therefore, peripheral palsy did not cause abnormal vertical deviation. In central palsy, for all positions together mean vertical deviations were 0.9 +/- 1.3 PD by prism and cover test, 1.4 +/- 1.6 PD by Maddox rod and prism test, and 2.5 +/- 1.6 PD by coil recordings; they were not different from normal values. During static head roll, patients with peripheral palsy had a right hyperdeviation on right head tilt and a left hyperdeviation on left head tilt, regardless of the side of the palsy. In contrast, in central palsy, head tilt caused vertical strabismus that remained on the same side on head tilt to either side. CONCLUSIONS: Small vertical deviations in sixth nerve palsy are consistent with normal hyperphorias that become manifest in the presence of esotropia. In peripheral sixth nerve palsy, static head roll to either side induces hyperdeviation in the eye on the side of the head tilt. Hyperdeviation of the same eye induced by head tilt to either direction implicates a brainstem lesion as the cause of paretic abduction. Quantitative study of sixth nerve palsy demonstrates that if a vertical deviation falls within the normal range of hyperphoria, multiple cranial nerve palsy or skew deviation may not be responsible. Conversely, vertical deviation > 5 PD indicates skew deviation or peripheral nerve palsy in addition to abduction palsy.
OBJECTIVE: To detect and determine the magnitude of vertical deviation in patients with unilateral sixth nerve palsy. DESIGN: Prospective consecutive comparative case series. PARTICIPANTS: Twenty patients with unilateral peripheral sixth nerve palsy, 7 patients with central palsy caused by brainstem lesions, and 10 normal subjects. METHODS: Subjects were tested by the prism and cover test, Maddox rod and prism test, and magnetic search coil recordings in nine diagnostic eye positions. They were also tested during static lateral head tilt by the prism and cover, and Maddox rod and prism tests. MAIN OUTCOME MEASURES: The magnitudes of horizontal and vertical deviations. RESULTS: All patients had an abduction deficit and incomitant esodeviation that increased in the field of action of the paretic muscle, indicating sixth nerve palsy. Mean vertical deviations, for all positions of gaze in peripheral palsy were 0.3 +/- 0.8 prism diopters (PD) by prism and cover test, 1.3 +/- 1.6 PD by Maddox rod and prism test, and 2.0 +/- 1.4 PD by coil recordings. Mean vertical deviations in normal subjects were 0.0 +/- 0.0 PD by prism and cover test, 1.0 +/- 0.9 PD by Maddox rod and prism test, and 1.9 +/- 2.1 PD by coil recordings. Therefore, peripheral palsy did not cause abnormal vertical deviation. In central palsy, for all positions together mean vertical deviations were 0.9 +/- 1.3 PD by prism and cover test, 1.4 +/- 1.6 PD by Maddox rod and prism test, and 2.5 +/- 1.6 PD by coil recordings; they were not different from normal values. During static head roll, patients with peripheral palsy had a right hyperdeviation on right head tilt and a left hyperdeviation on left head tilt, regardless of the side of the palsy. In contrast, in central palsy, head tilt caused vertical strabismus that remained on the same side on head tilt to either side. CONCLUSIONS: Small vertical deviations in sixth nerve palsy are consistent with normal hyperphorias that become manifest in the presence of esotropia. In peripheral sixth nerve palsy, static head roll to either side induces hyperdeviation in the eye on the side of the head tilt. Hyperdeviation of the same eye induced by head tilt to either direction implicates a brainstem lesion as the cause of paretic abduction. Quantitative study of sixth nerve palsy demonstrates that if a vertical deviation falls within the normal range of hyperphoria, multiple cranial nerve palsy or skew deviation may not be responsible. Conversely, vertical deviation > 5 PD indicates skew deviation or peripheral nerve palsy in addition to abduction palsy.