TY - JOUR
T1 - Differentiation between non-neural and neural contributors to ankle joint stiffness in cerebral palsy
AU - De Gooijer-Van De Groep, Karin L.
AU - De Vlugt, Erwin
AU - De Groot, Jurriaan H.
AU - Van Der Heijden-Maessen, Hélène Cm
AU - Wielheesen, Dennis Hm
AU - Van Wijlen-Hempel, Rietje S.
AU - Arendzen, J. Hans
AU - Meskers, Carel Gm
PY - 2013/1/1
Y1 - 2013/1/1
N2 - Background: Spastic paresis in cerebral palsy (CP) is characterized by increased joint stiffness that may be of neural origin, i.e. improper muscle activation caused by e.g. hyperreflexia or non-neural origin, i.e. altered tissue viscoelastic properties (clinically: "spasticity" vs. "contracture"). Differentiation between these components is hard to achieve by common manual tests. We applied an assessment instrument to obtain quantitative measures of neural and non-neural contributions to ankle joint stiffness in CP. Methods. Twenty-three adolescents with CP and eleven healthy subjects were seated with their foot fixated to an electrically powered single axis footplate. Passive ramp-and-hold rotations were applied over full ankle range of motion (RoM) at low and high velocities. Subject specific tissue stiffness, viscosity and reflexive torque were estimated from ankle angle, torque and triceps surae EMG activity using a neuromuscular model. Results: In CP, triceps surae reflexive torque was on average 5.7 times larger (p =.002) and tissue stiffness 2.1 times larger (p =.018) compared to controls. High tissue stiffness was associated with reduced RoM (p <.001). Ratio between neural and non-neural contributors varied substantially within adolescents with CP. Significant associations of SPAT (spasticity test) score with both tissue stiffness and reflexive torque show agreement with clinical phenotype. Conclusions: Using an instrumented and model based approach, increased joint stiffness in CP could be mainly attributed to higher reflexive torque compared to control subjects. Ratios between contributors varied substantially within adolescents with CP. Quantitative differentiation of neural and non-neural stiffness contributors in CP allows for assessment of individual patient characteristics and tailoring of therapy.
AB - Background: Spastic paresis in cerebral palsy (CP) is characterized by increased joint stiffness that may be of neural origin, i.e. improper muscle activation caused by e.g. hyperreflexia or non-neural origin, i.e. altered tissue viscoelastic properties (clinically: "spasticity" vs. "contracture"). Differentiation between these components is hard to achieve by common manual tests. We applied an assessment instrument to obtain quantitative measures of neural and non-neural contributions to ankle joint stiffness in CP. Methods. Twenty-three adolescents with CP and eleven healthy subjects were seated with their foot fixated to an electrically powered single axis footplate. Passive ramp-and-hold rotations were applied over full ankle range of motion (RoM) at low and high velocities. Subject specific tissue stiffness, viscosity and reflexive torque were estimated from ankle angle, torque and triceps surae EMG activity using a neuromuscular model. Results: In CP, triceps surae reflexive torque was on average 5.7 times larger (p =.002) and tissue stiffness 2.1 times larger (p =.018) compared to controls. High tissue stiffness was associated with reduced RoM (p <.001). Ratio between neural and non-neural contributors varied substantially within adolescents with CP. Significant associations of SPAT (spasticity test) score with both tissue stiffness and reflexive torque show agreement with clinical phenotype. Conclusions: Using an instrumented and model based approach, increased joint stiffness in CP could be mainly attributed to higher reflexive torque compared to control subjects. Ratios between contributors varied substantially within adolescents with CP. Quantitative differentiation of neural and non-neural stiffness contributors in CP allows for assessment of individual patient characteristics and tailoring of therapy.
KW - Ankle joint
KW - Cerebral palsy
KW - Contracture
KW - Movement disorder
KW - Neuromechanics
KW - Neuromuscular modeling
KW - Spasticity
KW - Stiffness
KW - System identification
UR - http://www.scopus.com/inward/record.url?scp=84880335605&partnerID=8YFLogxK
U2 - https://doi.org/10.1186/1743-0003-10-81
DO - https://doi.org/10.1186/1743-0003-10-81
M3 - Article
C2 - 23880287
SN - 1743-0003
VL - 10
JO - Journal of NeuroEngineering and Rehabilitation
JF - Journal of NeuroEngineering and Rehabilitation
IS - 1
M1 - 81
ER -