Kinematic and electromyographic tools for characterizing movement disorders in mice.
Identifieur interne : 001A22 ( PubMed/Corpus ); précédent : 001A21; suivant : 001A23Kinematic 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 : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Age Factors, Animals, Biomechanical Phenomena, Calcium Channels, N-Type, Calcium Channels, P-Type (genetics), Calcium Channels, Q-Type (genetics), Disease Models, Animal, Electromyography (methods), Exercise Test (methods), Female, Locomotion (genetics), Mice, Mice, Transgenic, Movement Disorders (genetics), Movement Disorders (pathology), Movement Disorders (physiopathology), Muscle, Skeletal (abnormalities), Muscle, Skeletal (physiopathology), Mutation (genetics), Time Factors, Videotape Recording.
- MESH :
- chemical , genetics : Calcium Channels, P-Type, Calcium Channels, Q-Type.
- chemical : Calcium Channels, N-Type.
- abnormalities : Muscle, Skeletal.
- genetics : Locomotion, Movement Disorders, Mutation.
- methods : Electromyography, Exercise Test.
- pathology : Movement Disorders.
- physiopathology : Movement Disorders, Muscle, Skeletal.
- Age Factors, Animals, Biomechanical Phenomena, Disease Models, Animal, Female, Mice, Mice, Transgenic, Time Factors, Videotape Recording.
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.
DOI: 10.1002/mds.22933
PubMed: 20077474
Links to Exploration step
pubmed:20077474Le document en format XML
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Biedermann</name></author><author><name sortKey="Faenger, Bernd" sort="Faenger, Bernd" uniqKey="Faenger B" first="Bernd" last="Faenger">Bernd Faenger</name></author><author><name sortKey="Grassme, Roland" sort="Grassme, Roland" uniqKey="Grassme R" first="Roland" last="Grassme">Roland Grassme</name></author><author><name sortKey="Hess, Ellen J" sort="Hess, Ellen J" uniqKey="Hess E" first="Ellen J" last="Hess">Ellen J. Hess</name></author><author><name sortKey="Schumann, Nikolaus P" sort="Schumann, Nikolaus P" uniqKey="Schumann N" first="Nikolaus P" last="Schumann">Nikolaus P. Schumann</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.22933</idno><idno type="RBID">pubmed:20077474</idno><idno type="pmid">20077474</idno><idno type="wicri:Area/PubMed/Corpus">001A22</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Kinematic and electromyographic tools for characterizing movement disorders in mice.</title><author><name sortKey="Scholle, Hans C" sort="Scholle, Hans C" uniqKey="Scholle H" first="Hans C" last="Scholle">Hans C. Scholle</name><affiliation><nlm:affiliation>Division Motor Research, Pathophysiology and Biomechanics, Department of Trauma, Hand and Reconstructive Surgery, University Hospital, Friedrich Schiller University, Jena, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Jinnah, H A" sort="Jinnah, H A" uniqKey="Jinnah H" first="H A" last="Jinnah">H A Jinnah</name></author><author><name sortKey="Arnold, Dirk" sort="Arnold, Dirk" uniqKey="Arnold D" first="Dirk" last="Arnold">Dirk Arnold</name></author><author><name sortKey="Biedermann, Frank H W" sort="Biedermann, Frank H W" uniqKey="Biedermann F" first="Frank H W" last="Biedermann">Frank H W. Biedermann</name></author><author><name sortKey="Faenger, Bernd" sort="Faenger, Bernd" uniqKey="Faenger B" first="Bernd" last="Faenger">Bernd Faenger</name></author><author><name sortKey="Grassme, Roland" sort="Grassme, Roland" uniqKey="Grassme R" first="Roland" last="Grassme">Roland Grassme</name></author><author><name sortKey="Hess, Ellen J" sort="Hess, Ellen J" uniqKey="Hess E" first="Ellen J" last="Hess">Ellen J. Hess</name></author><author><name sortKey="Schumann, Nikolaus P" sort="Schumann, Nikolaus P" uniqKey="Schumann N" first="Nikolaus P" last="Schumann">Nikolaus P. Schumann</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Biomechanical Phenomena</term><term>Calcium Channels, N-Type</term><term>Calcium Channels, P-Type (genetics)</term><term>Calcium Channels, Q-Type (genetics)</term><term>Disease Models, Animal</term><term>Electromyography (methods)</term><term>Exercise Test (methods)</term><term>Female</term><term>Locomotion (genetics)</term><term>Mice</term><term>Mice, Transgenic</term><term>Movement Disorders (genetics)</term><term>Movement Disorders (pathology)</term><term>Movement Disorders (physiopathology)</term><term>Muscle, Skeletal (abnormalities)</term><term>Muscle, Skeletal (physiopathology)</term><term>Mutation (genetics)</term><term>Time Factors</term><term>Videotape Recording</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Calcium Channels, P-Type</term><term>Calcium Channels, Q-Type</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Calcium Channels, N-Type</term></keywords><keywords scheme="MESH" qualifier="abnormalities" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Locomotion</term><term>Movement Disorders</term><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electromyography</term><term>Exercise Test</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Movement Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Movement Disorders</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Biomechanical Phenomena</term><term>Disease Models, Animal</term><term>Female</term><term>Mice</term><term>Mice, Transgenic</term><term>Time Factors</term><term>Videotape Recording</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20077474</PMID><DateCreated><Year>2010</Year><Month>03</Month><Day>03</Day></DateCreated><DateCompleted><Year>2010</Year><Month>06</Month><Day>02</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>3</Issue><PubDate><Year>2010</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Kinematic and electromyographic tools for characterizing movement disorders in mice.</ArticleTitle><Pagination><MedlinePgn>265-74</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22933</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>(c) 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Scholle</LastName><ForeName>Hans C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Division Motor Research, Pathophysiology and Biomechanics, Department of Trauma, Hand and Reconstructive Surgery, University Hospital, Friedrich Schiller University, Jena, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jinnah</LastName><ForeName>H A</ForeName><Initials>HA</Initials></Author><Author ValidYN="Y"><LastName>Arnold</LastName><ForeName>Dirk</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Biedermann</LastName><ForeName>Frank H W</ForeName><Initials>FH</Initials></Author><Author ValidYN="Y"><LastName>Faenger</LastName><ForeName>Bernd</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Grassme</LastName><ForeName>Roland</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Hess</LastName><ForeName>Ellen J</ForeName><Initials>EJ</Initials></Author><Author ValidYN="Y"><LastName>Schumann</LastName><ForeName>Nikolaus P</ForeName><Initials>NP</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS33592</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS40470</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS033592</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS040470</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS040470-09</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020864">Calcium Channels, N-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020865">Calcium Channels, P-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020907">Calcium Channels, Q-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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Test</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008124">Locomotion</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051379">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008822">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009069">Movement Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018482">Muscle, Skeletal</DescriptorName><QualifierName 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