O041 Dyskinesia-induced postural instability in Parkinson\'s disease

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Abstracts of the 17th Annual Meeting of ESMAC, Oral Presentations / Gait & Posture 28S (2008) S1–S48

to provide quantitative data on balance control during daily life facing environmental balance challenges. Its use is of interest for researchers evaluating daily life effects of disorders hampering the STS movement. References [1] Janssen WG, Bussmann JB, Horemans HL, Stam HJ. Validity of Accelerometry In Assessing the Duration of the Sit-to-Stand Movement. Med Biol Eng Comput 2008, submitted. [2] Janssen WG, Bussmann JB, Horemans HL, Stam HJ. Analysis and decomposition of accelerometric signals of trunk and thigh obtained during the sit-to-stand movement. Med Biol Eng Comput 2005; 43: 265−72. [3] Janssen WG, Geler K¨ulc¨u D, Horemans HL, Stam HJ, Bussmann JB. Sensitivity of Accelerometry to Assess Balance Control During Sit-to-Stand Movement. IEEE Trans Neural Syst Rehabil Eng 2008, accepted. [4] Janssen WGM, Geler D, Bussmann JBJ, Horemans HLD, Stam HJ. Sensitivity of accelerometry to assess trunk lateral sway during the sit-to-stand movement in patients with stroke. Gait & Posture 2006; 24: S211-S3.

O040 Ambulatory monitoring of motor fluctuations in Parkinson’s disease S. Moore1 , H. MacDougall2 , W. Ondo3 . 1 Neurology, Mount Sinai School of Medicine; 2 Psychology, University of Sydney; 3 Neurology, Baylor College of Medicine, USA Summary: We have developed a device which can be worn on the patient’s lower leg for extended periods (up to 24 h) that provides data on the locomotor response to levodopa (LD) and identifies freezing of gait (FOG) in Parkinson’s disease (PD). Conclusions: Ambulatory monitoring of gait in PD is sensitive to changes in stride length in response to levodopa, and can be used to characterize motor fluctuations. Frequency analysis of vertical leg acceleration can identify FOG episodes. Introduction: PD results from a progressive loss of dopaminergic and other sub-cortical neurons. One of the typical features of PD is locomotor dysfunction; shortened stride length, increased variability of stride, reduced walking speed and FOG. LD, the metabolic precursor to dopamine, is commonly used to manage the motor symptoms of PD by replacing endogenous dopamine at the striatum. Although initially effective, almost 60% of patients develop motor fluctuations after 3 years of treatment, including the “off/on’ phenomenon (abrupt and unpredictable responses to individual doses of LD) and ‘wearing off’ (declining dose duration). FOG is generally resistant to LD therapy. LD-related fluctuations in locomotor function can significantly limit mobility and complicate management of PD. Assessment of efficacy of various treatment regimes in PD is essentially subjective, utilizing rating scales (such as the UPDRS) and clinical observation. Patients/Materials and Methods: We have developed an ambulatory device for long-term (up to 24 h) measurement of stride length (SL) and for detection of FOG, utilizing a lightweight ankle-mounted sensor array [1]. SL was calculated from the vertical linear acceleration and pitch angular velocity of the leg with an accuracy of 5 cm. Power analysis showed high-frequency components of vertical leg movement during FOG in the 3– 8 Hz band that were not apparent during volitional standing, and this information was used to implement an automated FOG detection algorithm. Here we summarize results from preliminary

studies [1−3] of ambulatory monitoring of gait and FOG in patients (N = 26) diagnosed with idiopathic PD (UK PD Society Brain Bank diagnostic criteria). Results: Motor fluctuations [2]: SL following LD administration was fit with a Hill function, from which latency (time until SL increased 15% of the difference between baseline and maximum response) and Hill coefficient (H; shape of off-on transition) were determined (N = 13). Latency (range 4.7−53.3 min) inversely correlated with age at onset of PD (R = −0.83; p = 0.0004). H (range 0.9−16.9) correlated with disease duration (R = 0.67; p = 0.01). Freezing of gait [3]: FOG was characterized by highfrequency (3−8 Hz) components in vertical leg movement, and this information was used to autonomously detect FOG with an accuracy of 89% during unrestricted ambulation (N = 11). Latency to onset of orally disintegrating (OD) LD vs oral (PO) LD: Preliminary results (N = 12) in a single dose, placebo controlled, cross-over trial comparing latency to onset (time until SL increased 50% of the difference between baseline and maximum response) found that OD LD (29[15] min) had a faster onset than PO LD (40[21]). Discussion: The small, variable stride length characteristic of Parkinsonian gait, and fluctuations of efficacy associated with LD therapy, such as delayed onset, wearing off, and the ‘off/on’ effect, could reliably be detected from long-term changes in SL during ambulatory monitoring in the clinic [2] and the community [1]. Increasing abruptness (H) of the ‘off−on’ transition with disease duration is consistent with results from finger-tapping studies, and may reflect reduced buffering capacity of pre-synaptic nigrostriatal dopaminergic neurons. Ambulatory monitoring of gait objectively measures the dynamic locomotor response to levodopa, and this information could be used to improve daily management of motor fluctuations. There is currently no objective measure of FOG, and our FOG detection technique may significantly improve clinical management of this often intractable phenomenon. References [1] Moore ST, MacDougall HG, Gracies J-M, Cohen HS, Ondo WG. Long term monitoring of gait in Parkinson’s disease. Gait Posture 2007; 26: 200−7. [2] Moore ST, MacDougall HG, Gracies J-M, Ondo WG. Locomotor response to levodopa in fluctuating Parkinson’s disease. Exp Brain Res 2008; 84: 469–478. [3] Moore ST, MacDougall HG, Ondo WG. Ambulatory monitoring of freezing of gait in Parkinson’s disease. J NeuroSci Meth 2008; 167: 340–348.

O041 Dyskinesia-induced postural instability in Parkinson’s disease S. Armand1 , T. Landis2 , R. Sztajzel2 , P. Burkhard2 . 1 Willy Taillard Laboratory of Kinesiology, Geneva University Hospitals and Faculty of Medicine; 2 Department of Neurology, Geneva University Hospitals and Faculty of Medicine, Switzerland Summary: Levodopa-induced dyskinesia (LID) is a frequent cause of functional disability in Parkinson’s disease (PD). The aim of this study was to quantify postural stability using static and dynamic posturography in 11 patients with advanced PD and 12 controls. The center of pressure (COP) parameters showed increased postural instability when patients were ON with LID compared to the OFF state.

Abstracts of the 17th Annual Meeting of ESMAC, Oral Presentations / Gait & Posture 28S (2008) S1–S48 Conclusions: Our results suggest that LID may compromise balance and independently contribute to postural instability in advanced PD. In those instances, reducing LD or using other antidyskinetic strategies may be beneficial to patients. Introduction: In the presence of LID, PD patients may complain of unsteadiness and impaired balance, yet the influence of LID upon postural stability has not been specifically examined. In this study, we addressed this issue using static and dynamic posturography in patients with advanced PD and typical LID. Patients/Materials and Methods: Eleven patients were OFF and ON, and 12 age-matched healthy controls were included in this study. Relevant postural stability parameters were measured on two force platforms (Kistler, CH), either in quiet standing or when performing leaning tasks designed to stress postural stability. Simultaneously, LID was assessed clinically using a dyskinesia rating scale of severity. Displacement of the center of pressure (COP), range of COP in the medio-lateral (ML) and antero-posterior (AP) directions, and 95% confidence ellipse area were measured as indicators of postural stability and used for comparison analyses (Wilcoxon signed-rank test). Results: There was a good correlation between the clinical scores of dyskinesia severity and the COP displacement (R = 0.74). We found a significant increase of COP displacement in all tasks up to 556% (mean: 125±165%) when patients were ON with LID (888.4±704.2 mm, p = 0.004), compared to the OFF state (371.4±106.7 mm). In about half of the patients, this increase was marked (>100%). In the presence of LID, the range of COP displacement was significantly higher both in the ML direction (20.5±9.4 vs 56.6±50.6 mm, p = 0.003) and in the AP direction (25.1±6.5 vs 40.6±25.3 mm, p = 0.041), but with more marked difference in the ML direction. As shown in Figure 1, the 95% confidence ellipse area was also considerably increased in the presence of LID (385±239 vs 2035±2742 mm2 , p = 0.004).

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the presence of LID predominates in the ML direction which may be linked with an increased risk of falling [1]. Third, patients tend to transfer body weight on the side less affected by dyskinesia, probably in an unconsicous attempt to attenuate the deleterious consequence of lower limb dyskinesia upon postural stability. References [1] Mitchell SL et al., 1995, Neurosci Lett, 197, 133–136.

O042 Influence of upper-extremity pathologies on daily life activities L. Fradet. Department of Orthopaedic Surgery, University of Heidelberg, Germany Summary and Conclusions: The activity related range of motion (ARRoM) can be a good tool to characterize the consequence of diverse UX pathologies on daily life movements. Introduction: Daily life movements have been analysed to assess the effect of various upper-extremity (UX) pathologies on patients’ life. However, the standardized protocol to use and the parameters characterizing these effects are still under debate [1]. The present study defines a new parameter, the activity related range of motion (ARRoM) [2] applied here on 10 daily life movements, to explore the consequence of an UX pathology on movements. Patients/Materials and Methods: 11 healthy UX and 11 UX diagnosed with synosthose were analysed. The subjects performed 10 daily life movements: to eat with a spoon; to comb; to wash with a face cloth; to phone; to tape on a computer; to drink; to turn a key; to turn a page, to pour water; and to draw. Following the movement analysis (vicon system, 10 cameras, 120 Hz), the upperarm abduction/adduction, ante/retroversion, internal/external rotation, the forearm flexion/extension, and pronation/supination were computed using an UX model developed in the laboratory [3]. For each UX group and movements, the average of the minimun and maximum reached by these angles was computed. Each angle ARRoM was then defined using the extreme values found for the 10 movements.

ARRoM for each angle

Figure 1. Discussion: Our study allowed the delineation of three mechanisms by which dykinesia may induce postural instability in PD. First, dyskinesia increases body sway during ON periods by increasing COP displacement irrespective of postural position. Second, we have shown that increased COP displacement occurring in

ARRoM (min; max)

Healthy

Synosthose

add; abd retro; ante ext; int flex; ext supi; pro

−17; 107 −37; 105 −127; 102 21; 148 −87; 49

−23; 116 −36; 128 −96; 106 17; 145 −1; 47

Results: The extreme angle values obtained for each movement and the ARRoMs are represented for the two groups on the figure