Peripheral and Central Changes Combined Induce Movement Disorders on the Basis of Disuse or Overuse
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2011/04/01
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Description:To gain new insights into the underpinning mechanisms of movement disorders observed with both cerebral palsy and repetitive motion disorders, we have investigated the long-term effects of movement disuse or overuse on musculoskeletal tissues and topographical organization of the primary somatosensory and primary motor cortices, using two different rat models. We provide strong evidence that experience-dependent movements play a crucial role in shaping normal as well as aberrant movement abilities. Cerebral palsy is a developmental neurological disorder characterized by spasticity of some muscles, but also disuse in other muscles, and motor abnormalities. Our data from a rat model of cerebral palsy shows that aberrant sensorimotor inputs during development resulting from prolonged disuse (i.e. hind limb immobilization during the first month of life) induces peripheral tissue changes, such as muscle atrophy and extracellular matrix changes, joint degeneration, and drastic topographical disorganization of primary somatosensory and motor cortical hind limb representations. These peripheral and central tissue changes were associated with increased muscular tone at rest and with active flexion and extension around movement-restricted joints that resulted in abnormal walking patterns. Observed tissue changes and movement disorders were worsened when developmental disuse was combined with neonatal asphyxia. In contrast, repetitive motion disorders, such as carpal tunnel syndrome and focal hand dystonia, are a type of overuse associated with tasks that require prolonged, repetitive behaviors. Our data from a rat model of repetitive reaching and grasping shows that peripheral tissue changes are induced with cumulative task exposure, including myofiber fray, fibrotic nerve compression, and increased macrophages and inflammatory cytokines. These tissue changes were associated with declines in reach performance, grip strength and agility. The motor declines also correlated with disorganization of the forepaw representation in the primary somatosensory cortex, including the emergence of large receptive fields, and a drastic enlargement of the overall forepaw map area of the primary motor cortex, in which emerged the representation of joint movements specifically involved in the repetitive task. Peripheral inflammation correlated with signs of central sensitization (mechanical allodynia, myalgia, and increased neurochemicals and cytokines in the spinal cord), and with the reduced amount of current needed in the motor cortex to evoke forelimb movements. Our data from a rat model of repetitive motion injuries show that peripheral inflammation, spinal cord neuroplasticity and cortical neuroplasticity jointly contribute to the development of chronic repetitive motion disorders. In conclusion, both prolonged disuse and overuse lead to both peripheral and central changes that are interdependent to drive cerebral plasticity and altered motor output function. [Description provided by NIOSH]
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ISBN:9781612092003
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Pages in Document:1-41
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NIOSHTIC Number:nn:20056308
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Citation:Movement disorders: causes, diagnoses and treatments. Larsen BJ ed. New York: Nova Science Publishers, 2011 Apr; :1-41
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Contact Point Address:Mary F Barbe, Department of Anatomy and Cell Biology, Temple University, 3500 North Broad Street, Philadelphia, PA 19140, USA
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Email:mary.barbe@temple.edu
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Federal Fiscal Year:2011
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Performing Organization:Temple University
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Peer Reviewed:False
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Start Date:20000601
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Source Full Name:Movement disorders: causes, diagnoses and treatments
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End Date:20120731
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Main Document Checksum:urn:sha-512:7039a10f15d2bea99f2e79c04ec19efd648a6ce3140a416ef33f5f92d1351bd3c64ef7b770446c560fb6a61e26a458d9cb3f7e0503b781c3b7416c2318a1a8b6
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