[
home]
[
Personal Program]
[
Help]
tag
11:00
15 mins
A WAY TO ASSESS THE ROLE OF IMPROPER JOINT STIFFNESS AND ITS CONTRIBUTORS IN PATIENTS WITH CENTRAL NEUROLOGICAL DISEASE DURING FUNCTIONAL MOVEMENT
Karin de Gooijer-van de Groep, Stijn Van Eesbeek, Lizeth Sloot, Hans Arendzen, Jurriaan de Groot, Jaap Harlaar, Carel Meskers, Erwin de Vlugt
Session: Motor Control I
Session starts: Friday 25 January, 10:30
Presentation starts: 11:00
Room: Lecture room 558
Karin de Gooijer-van de Groep (Dept. Rehabilitation Medicine, Leiden University Medical Center, The Netherlands)
Stijn Van Eesbeek (Biomechanical Engineering, Delft University of Technology, The Netherlands)
Lizeth Sloot (Dept. Rehabilitation Medicine , VU University Medical Center, MOVE Research Institute, Amsterdam, The Netherlands)
Hans Arendzen (Dept. Rehabilitation Medicine, Leiden University Medical Center, The Netherlands)
Jurriaan de Groot (Dept. Rehabilitation Medicine, Leiden University Medical Center, The Netherlands)
Jaap Harlaar (Dept. Rehabilitation Medicine , VU University Medical Center, MOVE Research Institute, Amsterdam, The Netherlands)
Carel Meskers (Dept. Rehabilitation Medicine, Leiden University Medical Center, The Netherlands)
Erwin de Vlugt (Biomechanical Engineering, Delft University of Technology, The Netherlands)
Abstract:
Movement disorders of central neurological origin are characterized by increased joint stiffness, i.e. resistance to movement by improper muscle activation (neural) and/or changes in viscoelastic properties of connective tissues (non-neural). Differentiation between neural and non-neural components is hard to achieve by common manual tests. Most importantly, current passive clinical tests are not able to assess functional effects of therapy. This leaves the clinician with uncertainties in treatment selection and doses assignment. The ROBIN project (ROBot aided system Identification: novel tools for diagnosis and assessment in Neurological rehabilitation) aims to understand the role of improper joint stiffness in movement (walking) and the effects of intervention.
The assessment of causal relations between neuromechanical contributors to joint stiffness, requires combined biomechanical and control engineering approach using open and closed loop system identification and parameter estimation (SIPE) techniques under different experimental (task, environment) conditions. The ROBIN assessment goes from identification of single ankle joint stiffness during passive conditions all the way up to identification of ankle joint stiffness during walking. We designed a hierarchical assessment protocol, consisting of the following elements:
1) Neural and non-neural parameter estimation over the whole range of motion (RoM) under passive conditions using the Achilles, a 1-DOF ankle perturbator (MOOG, The Netherlands). This part most closely resembles current clinical tests like the Ashworth test.
2) Instantaneous neural and non-neural parameter estimation during tasks requiring active changes of muscle force and joint angle, resembling walking activity using the Achilles and time variant identification.
3) Identification of ankle joint stiffness during actual walking using small amplitude belt perturbations delivered by a high end dual belt treadmill (Forcelink, the Netherlands).
The first part of the ROBIN protocol was successfully applied on patients with stroke and cerebral palsy (CP). In CP, calf muscle reflexive torque was on average 5.7 times larger (p = 0.002) and tissue stiffness 2.1 times larger (p = 0.018) compared to controls. High tissue stiffness was associated with reduced RoM (p < 0.001).
The next step is to integrate ROBIN into current clinical care to assess sensitivity, specificity and repeatability of the ROBIN assessment compared to current clinical assessment with respect to specific current therapy for either non-neural and neural contributors to enhanced joint stiffness. ROBIN is a step forward in determining patient and component specific therapy to tune improper joint stiffness and to optimize mobility in patient with movement disorders after central neurological diseases.