ParkinsonFranceV1, PascalFrancis, Corpus, bibRecord, 000E55

A computer model of rigidity and related motor dysfunction in Parkinson's disease

Identifieur interne : 000E55 ( PascalFrancis/Corpus ); précédent : 000E54; suivant : 000E56

A computer model of rigidity and related motor dysfunction in Parkinson's disease

Auteurs : Philippe Le Cavorzin ; Guy Carrault ; Francis Chagneau ; Pierre Rochcongar ; Hervé Allain

Source :

Movement disorders [ 0885-3185 ] ; 2003.

RBID : Pascal:04-0130059

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Hypertonie spastique, Trouble moteur, Modèle, Traitement informatique, Physiopathologie, Homme.

English descriptors

KwdEn :
- Computerized processing, Human, Models, Motor system disorder, Parkinson disease, Pathophysiology, Spasticity.

Abstract

This work explores the involvement of spinal circuits in the generation of parkinsonian rigidity and related motor dysfunction. A computer model of spinal proprioceptive input processing, derived from previous work on spasticity modeling, was adapted to the simulation of parkinsonian rigidity. Model parameters were varied to generate simulations reproducing experimental data obtained using the pendulum test of the leg in 10 parkinsonian patients and 3 healthy subjects. Convenient reproductions of experimental traces in rigidity were obtained by the combination of a low reflex gain and a decrease in reflex threshold. These findings are consistent with studies reporting an increase of spinal interneuron excitability and proprioception deficits in Parkinson's disease (PD). Moreover, as the threshold parameter was much lowered, our model generated typical features of parkinsonian resting tremor, endorsing the hypothesis of a participation of a spinal oscillator in this disorder. Finally, tuning the reflex gain during simulations of rigidity resulted in the generation of active movement, opening some hypotheses on pathophysiology of motor dysfunction in PD, and notably, of akinesia. More generally, this work accredits the hypothesis of the involvement of an aperiodic, altered supra-spinal motor drive in PD, resulting in spinal dysfunction, through specific descending motor pathways. This may lead to a search for new (spinal) pharmacological targets in PD. It emphasizes further the value of computer modeling in understanding motor control in health and disease.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 04-0130059 INIST
ET :	A computer model of rigidity and related motor dysfunction in Parkinson's disease
AU :	LE CAVORZIN (Philippe); CARRAULT (Guy); CHAGNEAU (Francis); ROCHCONGAR (Pierre); ALLAIN (Hervé)
AF :	Laboratoire de Pharmacologie Expérimentale et Clinique, Faculté de Médecine de Rennes/Rennes/France (1 aut., 5 aut.); Centre de Réeducation Fonctionnelle de Rennes-Beaulieu/Rennes/France (1 aut.); Laboratoire de Traitement du Signal et de l'Image, Université de Rennes I/Rennes/France (2 aut.); Laboratoire de Mécanique Appliquée, Institut Universitaire de Technologie de Rennes/Rennes/France (3 aut.); Laboratoire de Physiologie, Faculté de Médecine, Université de Rennes I/Rennes/France (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2003; Vol. 18; No. 11; Pp. 1257-1265; Bibl. 31 ref.
LA :	Anglais
EA :	This work explores the involvement of spinal circuits in the generation of parkinsonian rigidity and related motor dysfunction. A computer model of spinal proprioceptive input processing, derived from previous work on spasticity modeling, was adapted to the simulation of parkinsonian rigidity. Model parameters were varied to generate simulations reproducing experimental data obtained using the pendulum test of the leg in 10 parkinsonian patients and 3 healthy subjects. Convenient reproductions of experimental traces in rigidity were obtained by the combination of a low reflex gain and a decrease in reflex threshold. These findings are consistent with studies reporting an increase of spinal interneuron excitability and proprioception deficits in Parkinson's disease (PD). Moreover, as the threshold parameter was much lowered, our model generated typical features of parkinsonian resting tremor, endorsing the hypothesis of a participation of a spinal oscillator in this disorder. Finally, tuning the reflex gain during simulations of rigidity resulted in the generation of active movement, opening some hypotheses on pathophysiology of motor dysfunction in PD, and notably, of akinesia. More generally, this work accredits the hypothesis of the involvement of an aperiodic, altered supra-spinal motor drive in PD, resulting in spinal dysfunction, through specific descending motor pathways. This may lead to a search for new (spinal) pharmacological targets in PD. It emphasizes further the value of computer modeling in understanding motor control in health and disease.
CC :	002B17G
FD :	Parkinson maladie; Hypertonie spastique; Trouble moteur; Modèle; Traitement informatique; Physiopathologie; Homme
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Muscle strié pathologie; Trouble tonus; Trouble neurologique
ED :	Parkinson disease; Spasticity; Motor system disorder; Models; Computerized processing; Pathophysiology; Human
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Striated muscle disease; Muscle tonus alteration; Neurological disorder
SD :	Parkinson enfermedad; Hipertonia espástica; Trastorno motor; Modelo; Tratamiento informático; Fisiopatología; Hombre
LO :	INIST-20953.354000118857050060
ID :	04-0130059

Links to Exploration step

Pascal:04-0130059

Le document en format XML

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<front><div type="abstract" xml:lang="en">This work explores the involvement of spinal circuits in the generation of parkinsonian rigidity and related motor dysfunction. A computer model of spinal proprioceptive input processing, derived from previous work on spasticity modeling, was adapted to the simulation of parkinsonian rigidity. Model parameters were varied to generate simulations reproducing experimental data obtained using the pendulum test of the leg in 10 parkinsonian patients and 3 healthy subjects. Convenient reproductions of experimental traces in rigidity were obtained by the combination of a low reflex gain and a decrease in reflex threshold. These findings are consistent with studies reporting an increase of spinal interneuron excitability and proprioception deficits in Parkinson's disease (PD). Moreover, as the threshold parameter was much lowered, our model generated typical features of parkinsonian resting tremor, endorsing the hypothesis of a participation of a spinal oscillator in this disorder. Finally, tuning the reflex gain during simulations of rigidity resulted in the generation of active movement, opening some hypotheses on pathophysiology of motor dysfunction in PD, and notably, of akinesia. More generally, this work accredits the hypothesis of the involvement of an aperiodic, altered supra-spinal motor drive in PD, resulting in spinal dysfunction, through specific descending motor pathways. This may lead to a search for new (spinal) pharmacological targets in PD. It emphasizes further the value of computer modeling in understanding motor control in health and disease.</div>
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<s5>19</s5>
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<s5>19</s5>
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<s5>37</s5>
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<s5>37</s5>
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<s5>38</s5>
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<s5>38</s5>
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<s5>39</s5>
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<s5>39</s5>
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<s5>40</s5>
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<s5>40</s5>
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<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
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<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
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<s5>41</s5>
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<s5>41</s5>
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<s5>45</s5>
</fC07>
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<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Músculo estriado patología</s0>
<s5>45</s5>
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<fC07 i1="07" i2="X" l="FRE"><s0>Trouble tonus</s0>
<s5>46</s5>
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<fC07 i1="07" i2="X" l="ENG"><s0>Muscle tonus alteration</s0>
<s5>46</s5>
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<fC07 i1="07" i2="X" l="SPA"><s0>Trastorno tono muscular</s0>
<s5>46</s5>
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<s5>48</s5>
</fC07>
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<s5>48</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>48</s5>
</fC07>
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<fN82><s1>PSI</s1>
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<server><NO>PASCAL 04-0130059 INIST</NO>
<ET>A computer model of rigidity and related motor dysfunction in Parkinson's disease</ET>
<AU>LE CAVORZIN (Philippe); CARRAULT (Guy); CHAGNEAU (Francis); ROCHCONGAR (Pierre); ALLAIN (Hervé)</AU>
<AF>Laboratoire de Pharmacologie Expérimentale et Clinique, Faculté de Médecine de Rennes/Rennes/France (1 aut., 5 aut.); Centre de Réeducation Fonctionnelle de Rennes-Beaulieu/Rennes/France (1 aut.); Laboratoire de Traitement du Signal et de l'Image, Université de Rennes I/Rennes/France (2 aut.); Laboratoire de Mécanique Appliquée, Institut Universitaire de Technologie de Rennes/Rennes/France (3 aut.); Laboratoire de Physiologie, Faculté de Médecine, Université de Rennes I/Rennes/France (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2003; Vol. 18; No. 11; Pp. 1257-1265; Bibl. 31 ref.</SO>
<LA>Anglais</LA>
<EA>This work explores the involvement of spinal circuits in the generation of parkinsonian rigidity and related motor dysfunction. A computer model of spinal proprioceptive input processing, derived from previous work on spasticity modeling, was adapted to the simulation of parkinsonian rigidity. Model parameters were varied to generate simulations reproducing experimental data obtained using the pendulum test of the leg in 10 parkinsonian patients and 3 healthy subjects. Convenient reproductions of experimental traces in rigidity were obtained by the combination of a low reflex gain and a decrease in reflex threshold. These findings are consistent with studies reporting an increase of spinal interneuron excitability and proprioception deficits in Parkinson's disease (PD). Moreover, as the threshold parameter was much lowered, our model generated typical features of parkinsonian resting tremor, endorsing the hypothesis of a participation of a spinal oscillator in this disorder. Finally, tuning the reflex gain during simulations of rigidity resulted in the generation of active movement, opening some hypotheses on pathophysiology of motor dysfunction in PD, and notably, of akinesia. More generally, this work accredits the hypothesis of the involvement of an aperiodic, altered supra-spinal motor drive in PD, resulting in spinal dysfunction, through specific descending motor pathways. This may lead to a search for new (spinal) pharmacological targets in PD. It emphasizes further the value of computer modeling in understanding motor control in health and disease.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Hypertonie spastique; Trouble moteur; Modèle; Traitement informatique; Physiopathologie; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Muscle strié pathologie; Trouble tonus; Trouble neurologique</FG>
<ED>Parkinson disease; Spasticity; Motor system disorder; Models; Computerized processing; Pathophysiology; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Striated muscle disease; Muscle tonus alteration; Neurological disorder</EG>
<SD>Parkinson enfermedad; Hipertonia espástica; Trastorno motor; Modelo; Tratamiento informático; Fisiopatología; Hombre</SD>
<LO>INIST-20953.354000118857050060</LO>
<ID>04-0130059</ID>
</server>
</inist>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

A computer model of rigidity and related motor dysfunction in Parkinson's disease

A computer model of rigidity and related motor dysfunction in Parkinson's disease

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