A computer model of rigidity and related motor dysfunction in Parkinson's disease.
Identifieur interne : 001070 ( PubMed/Corpus ); précédent : 001069; suivant : 001071A computer model of rigidity and related motor dysfunction in Parkinson's disease.
Auteurs : Philippe Le Cavorzin ; Guy Carrault ; Francis Chagneau ; Pierre Rochcongar ; Hervé AllainSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- Computer Simulation, Electromyography (instrumentation), Humans, Models, Biological, Muscle Rigidity (diagnosis), Muscle Rigidity (etiology), Neural Networks (Computer), Parkinson Disease (complications), Parkinson Disease (diagnosis), Parkinson Disease (physiopathology), Proprioception (physiology), Reflex, Stretch (physiology), Spinal Cord (physiopathology), Time Factors.
- MESH :
- complications : Parkinson Disease.
- diagnosis : Muscle Rigidity, Parkinson Disease.
- etiology : Muscle Rigidity.
- instrumentation : Electromyography.
- physiology : Proprioception, Reflex, Stretch.
- physiopathology : Parkinson Disease, Spinal Cord.
- Computer Simulation, Humans, Models, Biological, Neural Networks (Computer), Time Factors.
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.
DOI: 10.1002/mds.10532
PubMed: 14639665
Links to Exploration step
pubmed:14639665Le document en format XML
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<author><name sortKey="Carrault, Guy" sort="Carrault, Guy" uniqKey="Carrault G" first="Guy" last="Carrault">Guy Carrault</name>
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<author><name sortKey="Chagneau, Francis" sort="Chagneau, Francis" uniqKey="Chagneau F" first="Francis" last="Chagneau">Francis Chagneau</name>
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<author><name sortKey="Rochcongar, Pierre" sort="Rochcongar, Pierre" uniqKey="Rochcongar P" first="Pierre" last="Rochcongar">Pierre Rochcongar</name>
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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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<Abstract><AbstractText>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.</AbstractText>
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