Strength deficits in primary focal hand dystonia
Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperk...
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Published in | Movement disorders Vol. 21; no. 1; pp. 18 - 27 |
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Language | English |
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Abstract | Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co‐contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output. © 2005 Movement Disorder Society |
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AbstractList | Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output.Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output. Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output. Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co‐contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output. © 2005 Movement Disorder Society |
Author | Prodoehl, Janey MacKinnon, Colum D. Corcos, Daniel M. Comella, Cynthia L. |
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Cites_doi | 10.1097/01.PHM.0000087458.32122.14 10.1002/mds.870100516 10.1002/ana.410390112 10.1007/BF00253633 10.1136/jnnp.70.4.471 10.1136/jnnp.58.3.312 10.1016/0166-2236(90)90007-W 10.1093/brain/120.12.2179 10.1212/WNL.35.1.73 10.1016/S1388-2457(00)00460-0 10.1093/brain/113.3.691 10.1212/WNL.52.2.291 10.1093/brain/121.7.1195 10.1097/00004691-200206000-00006 10.1152/jn.1997.77.5.2842 10.1046/j.1468-1331.2000.t01-1-00102.x 10.1002/1531-8249(199907)46:1<22::AID-ANA6>3.0.CO;2-Z 10.1002/mds.10142 10.1212/WNL.53.8.1794 10.1002/mds.20017 10.1212/WNL.53.1.96 10.1016/j.neuroimage.2003.10.019 10.1093/brain/108.2.463 10.1093/brain/105.3.461 10.1093/brain/120.4.571 10.1006/nimg.2000.0615 10.1002/mds.870100607 10.1093/brain/115.5.1481 10.1093/brain/awh057 10.1016/S1388-2457(98)00045-5 10.1002/ana.10474 10.1136/jnnp.52.9.1043 10.1002/ana.410370313 |
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Keywords | Nervous system diseases Electrophysiology Hand Cerebral disorder Involuntary movement Writer cramp focal dystonia; writer's cramp; EMG Striated muscle disease Central nervous system disease Electromyography Dystonia Neurological disorder Strength Extrapyramidal syndrome weakness; muscle activation |
Language | English |
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Snippet | Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the... |
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SubjectTerms | Adult Biological and medical sciences Cerebral Cortex - physiopathology Diseases of striated muscles. Neuromuscular diseases Dystonic Disorders - diagnosis Dystonic Disorders - physiopathology Electromyography EMG EMG, weakness Female focal dystonia Hand - innervation Humans Isometric Contraction - physiology Male Medical sciences Middle Aged muscle activation Muscle Weakness - diagnosis Muscle Weakness - physiopathology Muscle, Skeletal - innervation Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Reference Values Torque weakness Wrist - innervation writer's cramp |
Title | Strength deficits in primary focal hand dystonia |
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