Abstract

Blinking and opening/closing of the eyelid are considered to be different movements with independent control mechanisms. Apraxia of lid opening (ALO) is a clinical syndrome in which patients experience difficulty in opening their eyes voluntarily. Our previous study with fluorodeoxyglucose and positron emission tomography (PET) has suggested that functional impairments in the supplementary motor area (SMA) and the anterior cingulate gyrus may be involved in the pathophysiology of ALO. The aim of this study was to explore the physiological mechanisms for voluntary eyelid opening/closing and the difference between self-initiated and triggered movements, using [(15)O]H(2)O and PET. We measured the regional cerebral blood flow in 8 healthy subjects under 3 conditions: [A] at rest with eyes closed, [B] with self-paced lid opening/closing, and [C] with triggered lid opening/closing. All tasks were done with a blindfold to exclude the influence of visual input. The SMA proper and the angular gyrus were activated during self-paced and triggered lid opening/closing movements; however, the pre-SMA and the primary motor area (M1) were activated only during self-paced movements. The anterior cingulate gyrus and the cerebellum were activated during self-paced condition over triggered condition. The roles of SMA, M1 and cerebellum were assumed in eyelid opening/closing movements: the preparation and processing of movements in SMA, execution of movements in M1, and rhythmic generation in pre-SMA, M1 and cerebellum. We suggest that the activation in pre-SMA, anterior cingulate gyrus, and cerebellum may be responsible for the self-initiated eyelid opening/closing movements.

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