Background: Spontaneous nystagmus caused by dorsolateral medullary infarction may be of vestibular origin. Objectives: To test if imbalance of the central pat hways of the semicircular canals contributes to spontaneou...Background: Spontaneous nystagmus caused by dorsolateral medullary infarction may be of vestibular origin. Objectives: To test if imbalance of the central pat hways of the semicircular canals contributes to spontaneous nystagmus in dorsola teral medullary syndrome. Methods: We examined four patients with dorsolateral m edullary syndrome and recorded spontaneous nystagmus binocularly at gaze straigh t ahead with the threedimensional search coil technique. The median slow phase velocity of the nystagmus was analysed in the light and in the dark, and the no rmalised velocity axes were compared with the rotation axes as predicted from an atomical data of the semicircular canal. Results: The slow phase rotation axes o f all patients aligned best with the rotation axes resulting from stimulation of the contralesional posterior and horizontal semicircular canals. This alignment cannot be explained by pure otolith imbalance. Conclusion: We propose that vest ibular imbalance caused by an ipsilesional lesion of the central semicircular ca nal pathways of the horizontal and anterior semicircular canals largely accounts for spontaneous nystagmus in dorsolateralmedullary syndrome.展开更多
文摘Background: Spontaneous nystagmus caused by dorsolateral medullary infarction may be of vestibular origin. Objectives: To test if imbalance of the central pat hways of the semicircular canals contributes to spontaneous nystagmus in dorsola teral medullary syndrome. Methods: We examined four patients with dorsolateral m edullary syndrome and recorded spontaneous nystagmus binocularly at gaze straigh t ahead with the threedimensional search coil technique. The median slow phase velocity of the nystagmus was analysed in the light and in the dark, and the no rmalised velocity axes were compared with the rotation axes as predicted from an atomical data of the semicircular canal. Results: The slow phase rotation axes o f all patients aligned best with the rotation axes resulting from stimulation of the contralesional posterior and horizontal semicircular canals. This alignment cannot be explained by pure otolith imbalance. Conclusion: We propose that vest ibular imbalance caused by an ipsilesional lesion of the central semicircular ca nal pathways of the horizontal and anterior semicircular canals largely accounts for spontaneous nystagmus in dorsolateralmedullary syndrome.
