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A possible role in strength regulation to maintain an upright position and adjustment of coherent postural reactions during body displacement has been suggested for the basal ganglia. 1 Controlling upright posture also requires the constant use of sensory information analyzed by different neural networks, most often unconsciously.2 These signals proceed from proprioceptors (vestibular, muscular, and tendinous), and exteroceptors (visual and cutaneous) used for stability.3 Patients with advanced Parkinson's disease (PD) show difficulties in keeping a body position, 4 particularly the body center of mass, within specific spatial and stability limits in order to maintain equilibrium between stabilizing and destabilizing forces, resulting in falls and injuries that become more and more frequent as the disease progresses.2 Their balance difficulties are characterized by a loss of postural balance reactions as well as a decrease in anticipatory postural adjustments. 5 In one study, 6 lateral oscillations differentiated PD patients from control subjects while anteriorposterior mean values were comparable in both groups, but greater anterior-posterior than lateral oscillations have also been reported. 7 The participants in the latter two studies had different mean disease duration (7 and 16 years, respectively).Postural stability control is a crucial aspect of motor function at all PD stages but has not been fully characterized early in the ABSTRACT: Objective: To characterize postural stability control and levodopa responsiveness in early Parkinson's disease (PD). Methods: Postural sway was studied during quiet stance in ten patients within six years of PD onset, both before (OFF) and after (ON) regular oral levodopa dosing. Postural sway was recorded using a force platform during 30 sec with eyes open, and six dependent variables were examined. Results: Mild baseline subclinical changes in postural sway were recorded in our patients. Clear benefit was observed in five out of six characteristics (mean sway, transversal sway, sagittal sway, sway intensity, and sway area) in the ON condition. Conclusion: Postural control mechanisms are affected early in PD and modulated by dopamine.

The mechanism by which chronic, high frequency, electrical deep brain stimulation (HF-DBS) suppresses tremor in Parkinson's disease is unknown. Rest tremor in subjects with Parkinson's disease receiving HF-DBS was recorded continuously throughout switching the deep brain stimulator on (at an effective frequency) and off. These data suggest that the stimulation induces a qualitative change in the dynamics, called a Hopf bifurcation, so that the stable oscillations are destabilized. We hypothesize that the periodic stimulation modifies a parameter affecting the oscillation in a time dependent way and thereby induces a Hopf bifurcation. We explore this hypothesis using a schematic network model of an oscillator interacting with periodic stimulation. The mechanism of time-dependent change of a control parameter in the model captures two aspects of the dynamics observed in the data: (1) a gradual increase in tremor amplitude when the stimulation is switched off and a gradual decrease in tremor amplitude when the stimulation is switched on and (2) a time delay in the onset and offset of the oscillations. This mechanism is consistent with these rest tremor transition data and with the idea that HF-DBS acts via the gradual change of a network property. (c) 2001 American Institute of Physics.

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The effect of chronic high frequency deep brain stimulation (DBS) on rest tremor was investigated in subjects with Parkinson's disease (PD). Eight PD subjects with high amplitude tremor (Group 1) and eight PD subjects with low amplitude tremor (Group 2, used as a reference group) were examined by a clinical neurologist and tested with a velocity laser to quantify time and frequency domain characteristics of tremor. Possible rebound effects in rest tremor when DBS was stopped for 60 min were also explored. Participants received DBS of the internal globus pallidus (GPi) (n = 7), the subthalamic nucleus (STN) (n = 6) or the ventrointermediate nucleus of the thalamus (Vim) (n = 3). Tremor was recorded with a velocity laser under two conditions of DBS (on-off) and two conditions of medication (L-Dopa on-off). Correlations between clinical and experimental results for tremor amplitude was 0.70 with no medication and no stimulation. In Group 1, DBS decreased tremor amplitude but also increased spectral concentration and median frequency significantly. Under medication, the changes in tremor with and without stimulation were not statistically significant (Group 1). When stimulation was stopped for 60 min, a rebound in tremor amplitude was observed and median frequency remained stable in Group 1. None of the comparisons examined produced significant effects in Group 2. Taken together, these results suggest that beyond its effect on tremor amplitude DBS acted also on tremor frequency and did not modify tremor characteristics in subjects with low amplitude tremor.