Kinematic and Electromyographic Tools for Characterizing Movement Disorders in Mice
Identifieur interne : 000C35 ( PascalFrancis/Corpus ); précédent : 000C34; suivant : 000C36Kinematic and Electromyographic Tools for Characterizing Movement Disorders in Mice
Auteurs : Hans C. Scholle ; H. A. Jinnah ; Dirk Arnold ; Frank H. W. Biedermann ; Bernd Faenger ; Roland Grassme ; Ellen J. Hess ; Nikolaus P. SchumannSource :
- Movement disorders [ 0885-3185 ] ; 2010.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Increasing interest in rodent models for movement disorders has led to an increasing need for more accurate and precise methods for both delineating the nature of abnormal movements and measuring their severity. These studies describe application of simultaneous high-speed video kinematics with multichannel electromyography (EMG) to characterize the movement disorder exhibited by tottering mutant mice. These mice provide a uniquely valuable model, because they exhibit paroxysmal dystonia superimposed on mild baseline ataxia, permitting the examination of these two different problems within the same animals. At baseline with mild ataxia, the mutants exhibited poorly coordinated movements with increased variation of stance and swing times, and slower spontaneous walking velocities. The corresponding EMG showed reduced mean amplitudes of biceps femoris and vastus lateralis, and poorly modulated EMG activities during the step cycle. Attacks of paroxysmal dystonia were preceded by trains of EMG bursts with doublets and triplets simultaneously in the biceps femoris and vastus lateralis followed by more sustained coactivation. These EMG characteristics are consistent with the clinical phenomenology of the motor phenotype of tottering mice as a baseline of mild ataxia with intermittent attacks of paroxysmal dystonia. The EMG characteristics of ataxia and dystonia in the tottering mice also are consistent with EMG studies of other ataxic or dystonic animals and humans. These studies provide insights into how these methods can be used for delineating movement disorders in mice and for how they may be compared with similar disorders of humans.
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Format Inist (serveur)
NO : | PASCAL 10-0161566 INIST |
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ET : | Kinematic and Electromyographic Tools for Characterizing Movement Disorders in Mice |
AU : | SCHOLLE (Hans C.); JINNAH (H. A.); ARNOLD (Dirk); BIEDERMANN (Frank H. W.); FAENGER (Bernd); GRASSME (Roland); HESS (Ellen J.); SCHUMANN (Nikolaus P.) |
AF : | Division Motor Research, Pathophysiology and Biomechanics, Department of Trauma, Hand and Reconstructive Surgery, University Hospital, Friedrich Schiller University/Jena/Allemagne (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 8 aut.); Departments of Neurology and Human Genetics, Emory University/Atlanta, Georgia/Etats-Unis (2 aut.); Departments of Pharmacology and Neurology, Emory University/Atlanta, Georgia/Etats-Unis (7 aut.); Prevention Department, Berufsgenossenschaft Nahrungsmittel und Gaststätten/Erfurt/Allemagne (6 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 3; Pp. 265-274; Bibl. 42 ref. |
LA : | Anglais |
EA : | Increasing interest in rodent models for movement disorders has led to an increasing need for more accurate and precise methods for both delineating the nature of abnormal movements and measuring their severity. These studies describe application of simultaneous high-speed video kinematics with multichannel electromyography (EMG) to characterize the movement disorder exhibited by tottering mutant mice. These mice provide a uniquely valuable model, because they exhibit paroxysmal dystonia superimposed on mild baseline ataxia, permitting the examination of these two different problems within the same animals. At baseline with mild ataxia, the mutants exhibited poorly coordinated movements with increased variation of stance and swing times, and slower spontaneous walking velocities. The corresponding EMG showed reduced mean amplitudes of biceps femoris and vastus lateralis, and poorly modulated EMG activities during the step cycle. Attacks of paroxysmal dystonia were preceded by trains of EMG bursts with doublets and triplets simultaneously in the biceps femoris and vastus lateralis followed by more sustained coactivation. These EMG characteristics are consistent with the clinical phenomenology of the motor phenotype of tottering mice as a baseline of mild ataxia with intermittent attacks of paroxysmal dystonia. The EMG characteristics of ataxia and dystonia in the tottering mice also are consistent with EMG studies of other ataxic or dystonic animals and humans. These studies provide insights into how these methods can be used for delineating movement disorders in mice and for how they may be compared with similar disorders of humans. |
CC : | 002B17; 002B17A01 |
FD : | Ataxie; Dystonie; Pathologie du système nerveux; Cinématique; Animal; Souris; Modèle animal; Electromyographie |
FG : | Rodentia; Mammalia; Vertebrata; Pathologie de l'encéphale; Pathologie du système nerveux central; Trouble neurologique; Syndrome extrapyramidal; Mouvement involontaire; Pathologie du muscle strié; Electrophysiologie |
ED : | Ataxia; Dystonia; Nervous system diseases; Kinematics; Animal; Mouse; Animal model; Electromyography |
EG : | Rodentia; Mammalia; Vertebrata; Cerebral disorder; Central nervous system disease; Neurological disorder; Extrapyramidal syndrome; Involuntary movement; Striated muscle disease; Electrophysiology |
SD : | Ataxia; Distonía; Sistema nervioso patología; Cinemática; Animal; Ratón; Modelo animal; Electromiografía |
LO : | INIST-20953.354000181820230030 |
ID : | 10-0161566 |
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<series><title level="j" type="main">Movement disorders</title>
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<front><div type="abstract" xml:lang="en">Increasing interest in rodent models for movement disorders has led to an increasing need for more accurate and precise methods for both delineating the nature of abnormal movements and measuring their severity. These studies describe application of simultaneous high-speed video kinematics with multichannel electromyography (EMG) to characterize the movement disorder exhibited by tottering mutant mice. These mice provide a uniquely valuable model, because they exhibit paroxysmal dystonia superimposed on mild baseline ataxia, permitting the examination of these two different problems within the same animals. At baseline with mild ataxia, the mutants exhibited poorly coordinated movements with increased variation of stance and swing times, and slower spontaneous walking velocities. The corresponding EMG showed reduced mean amplitudes of biceps femoris and vastus lateralis, and poorly modulated EMG activities during the step cycle. Attacks of paroxysmal dystonia were preceded by trains of EMG bursts with doublets and triplets simultaneously in the biceps femoris and vastus lateralis followed by more sustained coactivation. These EMG characteristics are consistent with the clinical phenomenology of the motor phenotype of tottering mice as a baseline of mild ataxia with intermittent attacks of paroxysmal dystonia. The EMG characteristics of ataxia and dystonia in the tottering mice also are consistent with EMG studies of other ataxic or dystonic animals and humans. These studies provide insights into how these methods can be used for delineating movement disorders in mice and for how they may be compared with similar disorders of humans.</div>
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<s5>09</s5>
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<fC03 i1="04" i2="X" l="SPA"><s0>Cinemática</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Animal</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Souris</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Mouse</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Ratón</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Modèle animal</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Animal model</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Electromyographie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Electromyography</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Electromiografía</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>42</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>42</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Pathologie du muscle strié</s0>
<s5>43</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Striated muscle disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Músculo estriado patología</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Electrophysiologie</s0>
<s5>44</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Electrophysiology</s0>
<s5>44</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Electrofisiología</s0>
<s5>44</s5>
</fC07>
<fN21><s1>102</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 10-0161566 INIST</NO>
<ET>Kinematic and Electromyographic Tools for Characterizing Movement Disorders in Mice</ET>
<AU>SCHOLLE (Hans C.); JINNAH (H. A.); ARNOLD (Dirk); BIEDERMANN (Frank H. W.); FAENGER (Bernd); GRASSME (Roland); HESS (Ellen J.); SCHUMANN (Nikolaus P.)</AU>
<AF>Division Motor Research, Pathophysiology and Biomechanics, Department of Trauma, Hand and Reconstructive Surgery, University Hospital, Friedrich Schiller University/Jena/Allemagne (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 8 aut.); Departments of Neurology and Human Genetics, Emory University/Atlanta, Georgia/Etats-Unis (2 aut.); Departments of Pharmacology and Neurology, Emory University/Atlanta, Georgia/Etats-Unis (7 aut.); Prevention Department, Berufsgenossenschaft Nahrungsmittel und Gaststätten/Erfurt/Allemagne (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 3; Pp. 265-274; Bibl. 42 ref.</SO>
<LA>Anglais</LA>
<EA>Increasing interest in rodent models for movement disorders has led to an increasing need for more accurate and precise methods for both delineating the nature of abnormal movements and measuring their severity. These studies describe application of simultaneous high-speed video kinematics with multichannel electromyography (EMG) to characterize the movement disorder exhibited by tottering mutant mice. These mice provide a uniquely valuable model, because they exhibit paroxysmal dystonia superimposed on mild baseline ataxia, permitting the examination of these two different problems within the same animals. At baseline with mild ataxia, the mutants exhibited poorly coordinated movements with increased variation of stance and swing times, and slower spontaneous walking velocities. The corresponding EMG showed reduced mean amplitudes of biceps femoris and vastus lateralis, and poorly modulated EMG activities during the step cycle. Attacks of paroxysmal dystonia were preceded by trains of EMG bursts with doublets and triplets simultaneously in the biceps femoris and vastus lateralis followed by more sustained coactivation. These EMG characteristics are consistent with the clinical phenomenology of the motor phenotype of tottering mice as a baseline of mild ataxia with intermittent attacks of paroxysmal dystonia. The EMG characteristics of ataxia and dystonia in the tottering mice also are consistent with EMG studies of other ataxic or dystonic animals and humans. These studies provide insights into how these methods can be used for delineating movement disorders in mice and for how they may be compared with similar disorders of humans.</EA>
<CC>002B17; 002B17A01</CC>
<FD>Ataxie; Dystonie; Pathologie du système nerveux; Cinématique; Animal; Souris; Modèle animal; Electromyographie</FD>
<FG>Rodentia; Mammalia; Vertebrata; Pathologie de l'encéphale; Pathologie du système nerveux central; Trouble neurologique; Syndrome extrapyramidal; Mouvement involontaire; Pathologie du muscle strié; Electrophysiologie</FG>
<ED>Ataxia; Dystonia; Nervous system diseases; Kinematics; Animal; Mouse; Animal model; Electromyography</ED>
<EG>Rodentia; Mammalia; Vertebrata; Cerebral disorder; Central nervous system disease; Neurological disorder; Extrapyramidal syndrome; Involuntary movement; Striated muscle disease; Electrophysiology</EG>
<SD>Ataxia; Distonía; Sistema nervioso patología; Cinemática; Animal; Ratón; Modelo animal; Electromiografía</SD>
<LO>INIST-20953.354000181820230030</LO>
<ID>10-0161566</ID>
</server>
</inist>
</record>
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