Comparative analysis of gait and speech in Parkinson's disease: hypokinetic or dysrhythmic disorders?

International audienceGait and speech are automatic motor activities which are frequently impaired in Parkinson's disease (PD). Obvious clinical similarities exist between these disorders but were never investigated. We propose to determine whether there exist any common features in PD between spatiotemporal gait disorders and temporal speech disorders. Gait and speech were analyzed on eleven PP undergoing deep-brain-stimulation of the sub-thalamic-nucleus (STN-DBS) and eleven control subjects (CS) under 3 conditions of velocity (natural, slow and speed). The patients were tested with and without L-Dopa and stimulator ON or OFF. Locomotor parameters were recorded using an optoelectronic system. Speech parameters were recorded with a headphone while subjects were reading a short paragraph. The results confirmed that PP walk and read more slowly than controls. Patient's difficulties in modulating walking and speech velocities seem to be due mainly to an inability to internally control the step length and the interpause-speech duration ISD. STN-DBS and levodopa increased patients' walking velocity by increasing the step length. STN-DBS and levodopa had no effect on speech velocity but restored the patients' ability to modulate the ISD. The walking cadence and speech index of rythmicity (SPIR) tended to be lower in patients and were not significantly improved by STN-DBS or levodopa. Speech and walking velocity as well as ISD and step length were correlated in both groups. Negative correlations between SPIR and walking cadence were observed in both groups Similar fundamental hypokinetic impairment and probably a similar rhythmic factor affected similarly the patients' speech and gait. These results suggest a similar physiopathological process in both walking and speaking dysfunction

Analyse comparative des troubles rythmiques de la marche et de la parole chez le patient parkinsonien stimulé

Si l expression motrice des symptômes de la maladie de Parkinson se traduit principalement au niveau des membres, le clinicien constate souvent l émergence, au fur et à mesure de l évolution de la maladie, de signes axiaux caractéristiques. Ainsi, marche et parole sont souvent touchées par le syndrome akinéto-rigide de la maladie mais aussi par une dysrégulation du rythme de ces activités motrices automatisées se manifestant sur le plan clinique pour l une par des phénomènes de festination et de freezing de la marche et pour l autre par des phénomènes de répétitions et de blocage de la parole. C est à la relation qu il peut exister entre akinésie et rythme au cours de la marche et de la parole que nous nous sommes intéressés au cours de ce travail. Pour cela, nous avons comparé les performances de marche et de parole en lecture et en répétition de syllabes de 11 sujets témoins et de 11 patients parkinsoniens porteurs d une stimulation cérébrale profonde bilatérale du noyau sous-thalamique, dans les quatre conditions de traitement et dans cinq situations expérimentales. Nos résultats montrent une augmentation de la cadence de marche compensatoire à l akinésie de la marche chez le patient parkinsonien. Par l existence de corrélations positives entre cadence de marche et vitesse de parole d une part et longueur du pas et durée des suites sonores d autre part nos résultats suggèrent que l accélération du rythme de parole observée dans la maladie de Parkinson pourrait, de la même façon, être compensatoire à l akinésie de la parole. Cette première approche des corrélations entre marche et parole dans la maladie de Parkinson n a pu prouver avec certitude l hypothèse de déficits similaires sur l axe temporel entre ces deux activités motrices mais nos résultats prometteurs soulèvent l existence de processus physiopathologiques proches. Ainsi, si le dysfonctionnement des noyaux gris centraux explique l akinésie de la marche et de la parole et que le trouble du rythme de la marche trouve son origine dans un dysfonctionnement du noyau pédonculopontin, notre étude ouvre de nouvelle perspectives expérimentales qui peut être permettront de déterminer avec certitude la structure impliquée dans la dysrégulation du rythme de la parole chez le patient parkinsonien.AIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Agricultural Support in Eastern Europe: Discussion

Neuronal activity within and across the cortex and basal ganglia is pathologically synchronized, particularly at 20 Hz in patients with Parkinson's disease. Defining how activities in spatially distributed brain regions overtly synchronize in narrow frequency bands is critical for understanding disease processes like Parkinson's disease. To address this, we studied cortical responses to electrical stimulation of the subthalamic nucleus (STN) at various frequencies between 5 and 30 Hz in two cohorts of eight patients with Parkinson's disease from two different surgical centres. We found that evoked activity consisted of a series of diminishing waves with a peak latency of 21 ms for the first wave in the series. The cortical evoked potentials (cEPs) averaged in each group were well fitted by a damped oscillator function (r 0.9, P < 0.00001). Fits suggested that the natural frequency of the subthalamo-cortical circuit was around 20 Hz. When the system was forced at this frequency by stimulation of the STN at 20 Hz, the undamped amplitude of the modelled cortical response increased relative to that with 5 Hz stimulation in both groups (P 0.005), consistent with resonance. Restoration of dopaminergic input by treatment with levodopa increased the damping of oscillatory activity (as measured by the modelled damping factor) in both patient groups (P 0.001). The increased damping would tend to limit resonance, as confirmed in simulations. Our results show that the basal ganglia–cortical network involving the STN has a tendency to resonate at 20 Hz in Parkinsonian patients. This resonance phenomenon may underlie the propagation and amplification of activities synchronized around this frequency. Crucially, dopamine acts to increase damping and thereby limit resonance in this basal ganglia–cortical networ