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Precision grip deficits in cerebellar disorders in man.
Authors:S J Fellows  J Ernst  M Schwarz  R T?pper  J Noth
Institution:1. Department of Neurology, Daisan Hospital, The Jikei University School of Medicine, Tokyo, Japan;2. Department of Neurology, The Jikei University School of Medicine, Tokyo, Japan;1. Department of Neurology, Brain Research Institute, Niigata University, Japan;2. Department of Neurology and Geriatrics, Gifu University School of Medicine, Japan;1. PET/CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3-3-20 Shinsuna, Koto-ku, Tokyo 136-0075, Japan;2. Yokohama Hoyu Hospital, Psychiatry, Yokohama 241-0812, Japan;3. Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan;4. Department of Psychiatry, Juntendo University School of Medicine, Tokyo 113-8421, Japan;5. Department of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan;6. Daigo Hospital, Psychogeriatric Center, Miyazaki 889-1911, Japan;1. Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea;2. Department of Neurosurgery, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
Abstract:OBJECTIVE: To investigate the effect of a variety of cerebellar pathologies on a functional motor task (lifting an object in a precision grip). METHODS: The study involved 8 patients with unilateral damage in the region of the posterior inferior cerebellar artery (PICA), 6 with damage in the region of the superior cerebellar artery (SUPCA), 12 patients with familiar or idiopathic cortical cerebellar degeneration, and 45 age-matched normal subjects. Subjects lifted an object of unpredictable load (internally guided task) or responded to a sudden load increase while holding the object steadily (externally guided task). RESULTS: Damage to the dentate nucleus (SUPCA) or its afferent input (cerebellar atrophy) resulted in disruption of the close coordination normally seen between proximal muscles (lifting the object) and the fingers (gripping the object) during a self-paced lift. Both the SUPCA group and, more markedly, the atrophy group, showed exaggerated levels of grip force. All patients showed a normal rate of grip force development. Damage in the PICA region had no significant effect on any of the measured lifting parameters. All patient groups retained the ability to scale grip force to different object loads. The automatic grip force response to unexpected load increase of a hand held object showed normal latency and time course in all patient groups. The response was modulated by the rate of the load change. Response magnitude was exaggerated in the atrophy patients at all 3 rates tested. CONCLUSIONS: Disturbances associated with cerebellar disorders differed from those seen following damage to the basal ganglia, with no evidence of slowed rates of grip force development. Disruption of temporal coordination between the proximal muscles (lifting) and the fingers (gripping) in a lift was apparent, supporting the role of the cerebellum in coordinating the timing of multi-joint movement sequences. Exaggeration of grip force levels was found in association with damage to the dentate nucleus or, in particular, to its afferent input. This could support a role or the cerebellum in sensorimotor processing, but might also represent a failure to time correctly the duration of grip force generation.
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