Abstract
Ocular lateropulsion is known to be a sign which is frequently seen in patients with lateral medullary syndrome, and is characterized by following findings; (1) no limitation of eye movements, (2) tonic bias of the eyes toward the side of the lesion when fixation is interrupted and (3) asymmetry in the amplitude of horizontal saccades (hypermetric toward the side ipsilateral to the lesion and/or hypometric toward the side contralateral to the lesion).
In the present study, patients who presented with all items (1) to (3) were defined as definite ocular lateropulsion, and those who met only the items (1) and (3) were thought to have possible ocular lateropulsion. We present 2 definite and 7 possible cases having ocular lateropulsion among 11 patients with lateral medullary syndrome. An additional case with supratentorial cerebral infarction, involving the frontal eye field, who met all the criteria for ocular lateropusion is presented.
Two patients, one with lateral medullary syndrome and the other with supratentorial cerebral infarction, presented with conjugate deviation in the acute stage of stroke, and later showed findings compatible with ocular lateropulsion including tonic bias of the eyes. From the findings of these cases, tonic bias of the eyes is thought to be an aborted form of conjugate deviation. Concerning the tonic eye deviation toward the affected side in medullary lesion, its occurrence in patients with unilateral peripheral vestibular disease by removal of visual fixation had been reported. Thus, an involvement of vestibular nucleus in dorsolateral aspect of medulla oblongata appears to cause tonic bias of the eye balls to the affected side.
Among 9 cases with definite and possible ocular lateropulsion, hypometric saccade toward the side contralateral to the lesion was seen in 7, but hypermetric saccade toward the side ipsilateral to the lesion was detected in ony 2 cases.
The former is explained by persisting effect of conjugate deviation to the affected side caused by involvement of vestibular nucleus in the medulla, but in the latter, an effect of cerebellar dysfunction on the eye movement must have been present in producing hypermetric saccade. Therefore, these 2 cases with hypermetric saccade should be distinguished from remaining 7 cases who showed only hypometric saccade, when the mechanism and pathophysiology of ocular lateropulsion are discussed.
In six of seven patients with definite or possible ocular lateropulsion in whom MRI was performed, lesions responsible for the lateral medullary syndrome were clearly demonstrated in the dorsolateral aspect of the medulla oblongata. In one patient who did not present with ocular lateropulsion, the lesion located more ventrally. However, there were no differences in localization of the lesion between the cases presenting with hypometric saccade alone and those with both hypermetric and hypometric saccades.
