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Abstract
Earlier works on rabbits have demonstrated that destruction of both labyrinths leads to a defective OKN in acute stage. The aim of this study was to examine whether this defect is to be ascribed to changes in brain stem mechanisms of OKN or due to possible disturbances of alertness. In 10 intact rabbits and in 6 hemilabyrinthectomized rabbits (HL-rabbits) OKN and EEG were studied. Alertness was controlled with vibration. In intact rabbits OKN reached a maximum velocity slowly, during several minutes. Simultaneously, theta waves were observed in EEG indicating increase in brain activity. Exposure to vibration caused a sooner increase and higher a maximum velocity of OKN and a momentary increase in EEG activity, than without vibration stimuli. In HL-rabbits OKN remained reduced in both directions still two months after operation. Vibration only slightly improved OKN responses while EEG was normally activated. OKN was decreased to about the same extent as was vestibular nystagmus. Attention seems to influence OKN in intact rabbits but not in HL-rabbits. The study confirms the dependence of optokinetic mechanism on vestibular mechanisms. The enhancing effect of alertness on OKN in intact rabbits and lack of this enhancement in HL-rabbits support the idea that the disturbance in the brain stem pathways may be reason for defective OKN.