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Asymmetric Optokinetic Afterresponse in Patients with Small Acoustic Neurinomas1

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Directional asymmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 20 patients with small acoustic neurinomas (⩽20 mm), and results were compared to those for 24 normal controls. The optokinetic afterresponse was induced by 60 s of horizontal whole-field optokinetic stimulation in both directions. Among patients, the optokinetic afterresponse was asymmetric, OKAN I and OKAN II beating toward the lesioned ear being significantly weaker than the OKAN I and OKAN II beating toward the healthy ear. Hence, in these patients with gradual deterioration of vestibular function, the vestibular side-difference was reflected both in OKAN I and OKAN II. Although asymmetry in OKAN I was frequently observed among controls, it was significantly more pronounced among the patients. Moreover, patients could be distinguished by the occurrence of OKAN II, as it did not occur at all among controls exposed to the same stimulation.
Title: Asymmetric Optokinetic Afterresponse in Patients with Small Acoustic Neurinomas1
Description:
Directional asymmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 20 patients with small acoustic neurinomas (⩽20 mm), and results were compared to those for 24 normal controls.
The optokinetic afterresponse was induced by 60 s of horizontal whole-field optokinetic stimulation in both directions.
Among patients, the optokinetic afterresponse was asymmetric, OKAN I and OKAN II beating toward the lesioned ear being significantly weaker than the OKAN I and OKAN II beating toward the healthy ear.
Hence, in these patients with gradual deterioration of vestibular function, the vestibular side-difference was reflected both in OKAN I and OKAN II.
Although asymmetry in OKAN I was frequently observed among controls, it was significantly more pronounced among the patients.
Moreover, patients could be distinguished by the occurrence of OKAN II, as it did not occur at all among controls exposed to the same stimulation.

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