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Bradykinesia is not a "systematic" feature of adult-onset Huntington's disease; implications for basal ganglia pathophysiology

Identifieur interne : 000663 ( PascalFrancis/Corpus ); précédent : 000662; suivant : 000664

Bradykinesia is not a "systematic" feature of adult-onset Huntington's disease; implications for basal ganglia pathophysiology

Auteurs : Alison Fenney ; Mandar S. Jog ; Christian Duval

Source :

RBID : Pascal:08-0158112

Descripteurs français

English descriptors

Abstract

Our goal was to determine whether bradykinesia is present in choreic adult-onset Huntington's disease (HD) patients, and determine the impact of chorea on their voluntary movements. We recorded whole-body involuntary movements (WBIM) and voluntary motor acts simultaneously, using a magnetic tracker system, in 15 choreic HD patients and 15 healthy age- and gender-matched control subjects. Participants were asked to perform two distinct tasks; a manual-tracking (MT) task yielding a measure of chorea intrusion during accurate movements, and a rapid alternating movement (RAM) task, yielding measures of bradykinesia. Results show that patients with HD presented with deviations from the target that hindered their ability to match the target velocity during the MT task. Furthermore, error in performance was correlated with the amplitude of whole-body chorea (Rho=0.67), illustrating the deleterious effect of chorea during accurate movements. However, patients with choreic HD presented with significantly higher RAM range and velocity than matched controls, therefore ruling out the idea that bradykinesia is a systematic feature of HD even when chorea is predominant. The present results imply that patients may have benefited from an intact direct pathway ("select ON" pathway in the focused attention model of basal ganglia function) that allowed them to supersede any dysfunctions associated with the progressive alteration of the "control function" (striatal-globus pallidus-subthalamic) pathway responsible for generating the chorea. Finally, the present results suggest that patients with adult-onset HD having chorea would greatly benefit from improved treatments aiming at reducing their involuntary movements while maintaining proper motor function.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11 02  1    @1 JOG (Mandar S.)
A11 03  1    @1 DUVAL (Christian)
A14 01      @1 Département de kinanthropologie, Université du Québec à Montréal @2 Montréal, Québec @3 CAN @Z 1 aut. @Z 3 aut.
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C01 01    ENG  @0 Our goal was to determine whether bradykinesia is present in choreic adult-onset Huntington's disease (HD) patients, and determine the impact of chorea on their voluntary movements. We recorded whole-body involuntary movements (WBIM) and voluntary motor acts simultaneously, using a magnetic tracker system, in 15 choreic HD patients and 15 healthy age- and gender-matched control subjects. Participants were asked to perform two distinct tasks; a manual-tracking (MT) task yielding a measure of chorea intrusion during accurate movements, and a rapid alternating movement (RAM) task, yielding measures of bradykinesia. Results show that patients with HD presented with deviations from the target that hindered their ability to match the target velocity during the MT task. Furthermore, error in performance was correlated with the amplitude of whole-body chorea (Rho=0.67), illustrating the deleterious effect of chorea during accurate movements. However, patients with choreic HD presented with significantly higher RAM range and velocity than matched controls, therefore ruling out the idea that bradykinesia is a systematic feature of HD even when chorea is predominant. The present results imply that patients may have benefited from an intact direct pathway ("select ON" pathway in the focused attention model of basal ganglia function) that allowed them to supersede any dysfunctions associated with the progressive alteration of the "control function" (striatal-globus pallidus-subthalamic) pathway responsible for generating the chorea. Finally, the present results suggest that patients with adult-onset HD having chorea would greatly benefit from improved treatments aiming at reducing their involuntary movements while maintaining proper motor function.
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Format Inist (serveur)

NO : PASCAL 08-0158112 INIST
ET : Bradykinesia is not a "systematic" feature of adult-onset Huntington's disease; implications for basal ganglia pathophysiology
AU : FENNEY (Alison); JOG (Mandar S.); DUVAL (Christian)
AF : Département de kinanthropologie, Université du Québec à Montréal/Montréal, Québec/Canada (1 aut., 3 aut.); Clinical Neurological Sciences, University of Western Ontario Health Centre-University Hospital/London, Ontario/Canada (2 aut.)
DT : Publication en série; Niveau analytique
SO : Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2008; Vol. 1193; Pp. 67-75; Bibl. 1 p.1/4
LA : Anglais
EA : Our goal was to determine whether bradykinesia is present in choreic adult-onset Huntington's disease (HD) patients, and determine the impact of chorea on their voluntary movements. We recorded whole-body involuntary movements (WBIM) and voluntary motor acts simultaneously, using a magnetic tracker system, in 15 choreic HD patients and 15 healthy age- and gender-matched control subjects. Participants were asked to perform two distinct tasks; a manual-tracking (MT) task yielding a measure of chorea intrusion during accurate movements, and a rapid alternating movement (RAM) task, yielding measures of bradykinesia. Results show that patients with HD presented with deviations from the target that hindered their ability to match the target velocity during the MT task. Furthermore, error in performance was correlated with the amplitude of whole-body chorea (Rho=0.67), illustrating the deleterious effect of chorea during accurate movements. However, patients with choreic HD presented with significantly higher RAM range and velocity than matched controls, therefore ruling out the idea that bradykinesia is a systematic feature of HD even when chorea is predominant. The present results imply that patients may have benefited from an intact direct pathway ("select ON" pathway in the focused attention model of basal ganglia function) that allowed them to supersede any dysfunctions associated with the progressive alteration of the "control function" (striatal-globus pallidus-subthalamic) pathway responsible for generating the chorea. Finally, the present results suggest that patients with adult-onset HD having chorea would greatly benefit from improved treatments aiming at reducing their involuntary movements while maintaining proper motor function.
CC : 002B17G; 002B18C13
FD : Noyau gris central; Physiopathologie; Mouvement corporel; Dyskinésie; Chorée de Huntington; Maladie de Parkinson; Adulte; Contrôle moteur
FG : Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Encéphale; Système nerveux central; Motricité; Mouvement involontaire; Trouble neurologique; Homme
ED : Basal ganglion; Pathophysiology; Body movement; Dyskinesia; Huntington disease; Parkinson disease; Adult; Motor control
EG : Degenerative disease; Genetic disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Central nervous system; Motricity; Involuntary movement; Neurological disorder; Human
SD : Núcleo basal; Fisiopatología; Movimiento corporal; Disquinesia; Corea Huntington; Parkinson enfermedad; Adulto; Control motor
LO : INIST-12895.354000183573360080
ID : 08-0158112

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Pascal:08-0158112

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<s5>54</s5>
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<s5>54</s5>
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<s5>69</s5>
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<fC03 i1="08" i2="X" l="ENG">
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<s5>69</s5>
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<s5>69</s5>
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<s5>20</s5>
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<s5>20</s5>
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<s5>21</s5>
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<s5>21</s5>
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<s5>21</s5>
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<s5>22</s5>
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<s5>22</s5>
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<s5>22</s5>
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<s5>23</s5>
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<s0>Cerebral disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>23</s5>
</fC07>
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<s0>Syndrome extrapyramidal</s0>
<s5>24</s5>
</fC07>
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<s0>Extrapyramidal syndrome</s0>
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<s5>24</s5>
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<s5>25</s5>
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<s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>26</s5>
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<fC07 i1="07" i2="X" l="ENG">
<s0>Encephalon</s0>
<s5>26</s5>
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<s0>Encéfalo</s0>
<s5>26</s5>
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<s0>Système nerveux central</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>27</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>27</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Motricité</s0>
<s5>28</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Motricity</s0>
<s5>28</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Motricidad</s0>
<s5>28</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Mouvement involontaire</s0>
<s5>29</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Involuntary movement</s0>
<s5>29</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Movimiento involuntario</s0>
<s5>29</s5>
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<fC07 i1="11" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>30</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>30</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>30</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE">
<s0>Homme</s0>
</fC07>
<fC07 i1="12" i2="X" l="ENG">
<s0>Human</s0>
</fC07>
<fC07 i1="12" i2="X" l="SPA">
<s0>Hombre</s0>
</fC07>
<fN21>
<s1>098</s1>
</fN21>
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<server>
<NO>PASCAL 08-0158112 INIST</NO>
<ET>Bradykinesia is not a "systematic" feature of adult-onset Huntington's disease; implications for basal ganglia pathophysiology</ET>
<AU>FENNEY (Alison); JOG (Mandar S.); DUVAL (Christian)</AU>
<AF>Département de kinanthropologie, Université du Québec à Montréal/Montréal, Québec/Canada (1 aut., 3 aut.); Clinical Neurological Sciences, University of Western Ontario Health Centre-University Hospital/London, Ontario/Canada (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2008; Vol. 1193; Pp. 67-75; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Our goal was to determine whether bradykinesia is present in choreic adult-onset Huntington's disease (HD) patients, and determine the impact of chorea on their voluntary movements. We recorded whole-body involuntary movements (WBIM) and voluntary motor acts simultaneously, using a magnetic tracker system, in 15 choreic HD patients and 15 healthy age- and gender-matched control subjects. Participants were asked to perform two distinct tasks; a manual-tracking (MT) task yielding a measure of chorea intrusion during accurate movements, and a rapid alternating movement (RAM) task, yielding measures of bradykinesia. Results show that patients with HD presented with deviations from the target that hindered their ability to match the target velocity during the MT task. Furthermore, error in performance was correlated with the amplitude of whole-body chorea (Rho=0.67), illustrating the deleterious effect of chorea during accurate movements. However, patients with choreic HD presented with significantly higher RAM range and velocity than matched controls, therefore ruling out the idea that bradykinesia is a systematic feature of HD even when chorea is predominant. The present results imply that patients may have benefited from an intact direct pathway ("select ON" pathway in the focused attention model of basal ganglia function) that allowed them to supersede any dysfunctions associated with the progressive alteration of the "control function" (striatal-globus pallidus-subthalamic) pathway responsible for generating the chorea. Finally, the present results suggest that patients with adult-onset HD having chorea would greatly benefit from improved treatments aiming at reducing their involuntary movements while maintaining proper motor function.</EA>
<CC>002B17G; 002B18C13</CC>
<FD>Noyau gris central; Physiopathologie; Mouvement corporel; Dyskinésie; Chorée de Huntington; Maladie de Parkinson; Adulte; Contrôle moteur</FD>
<FG>Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Encéphale; Système nerveux central; Motricité; Mouvement involontaire; Trouble neurologique; Homme</FG>
<ED>Basal ganglion; Pathophysiology; Body movement; Dyskinesia; Huntington disease; Parkinson disease; Adult; Motor control</ED>
<EG>Degenerative disease; Genetic disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Central nervous system; Motricity; Involuntary movement; Neurological disorder; Human</EG>
<SD>Núcleo basal; Fisiopatología; Movimiento corporal; Disquinesia; Corea Huntington; Parkinson enfermedad; Adulto; Control motor</SD>
<LO>INIST-12895.354000183573360080</LO>
<ID>08-0158112</ID>
</server>
</inist>
</record>

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