On the interest of computer modelling in the validation of ambulatory measurement of movement disorders in man.

Continuous ambulatory monitoring is a promising technique for objective evaluation of movement disorders in man. Although technological progress make such devices currently available, no validated measurements exist. We propose an original approach to validate instrumental measurements in central neurological diseases, based upon the use of computer modeling of movement disorders. In such an approach, computer simulations of altered movement were used to validate accelerometric-derived measurements in spasticity and Parkinson's disease. We found that some measurements, derived from the frequency power spectrum of distal acceleration at the upper limb, may be suitable for evaluation of some motor disorders, as spasticity, parkinsonian rigidity and related motor disability. Direct applications are expected in ambulatory monitoring of neurological diseases.

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

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.