Muscle and reflex changes with varying joint angle in hemiparetic stroke.
BACKGROUND
Despite intensive investigation, the origins of the neuromuscular abnormalities associated with spasticity are not well understood. In particular, the mechanical properties induced by stretch reflex activity have been especially difficult to study because of a lack of accurate tools separating reflex torque from torque generated by musculo-tendinous structures. The present study addresses this deficit by characterizing the contribution of neural and muscular components to the abnormally high stiffness of the spastic joint.


METHODS
Using system identification techniques, we characterized the neuromuscular abnormalities associated with spasticity of ankle muscles in chronic hemiparetic stroke survivors. In particular, we systematically tracked changes in muscle mechanical properties and in stretch reflex activity during changes in ankle joint angle. Modulation of mechanical properties was assessed by applying perturbations at different initial angles, over the entire range of motion (ROM). Experiments were performed on both paretic and non-paretic sides of stroke survivors, and in healthy controls.


RESULTS
Both reflex and intrinsic muscle stiffnesses were significantly greater in the spastic/paretic ankle than on the non-paretic side, and these changes were strongly position dependent. The major reflex contributions were observed over the central portion of the angular range, while the intrinsic contributions were most pronounced with the ankle in the dorsiflexed position.


CONCLUSIONS
In spastic ankle muscles, the abnormalities in intrinsic and reflex components of joint torque varied systematically with changing position over the full angular range of motion, indicating that clinical perceptions of increased tone may have quite different origins depending upon the angle where the tests are initiated.Furthermore, reflex stiffness was considerably larger in the non-paretic limb of stroke patients than in healthy control subjects, suggesting that the non-paretic limb may not be a suitable control for studying neuromuscular properties of the ankle joint. Our findings will help elucidate the origins of the neuromuscular abnormalities associated with stroke-induced spasticity.
Mirbagheri
Mehdi M
MM
Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Chicago, USA. mehdi@northwestern.edu
Alibiglou
Laila
L
Thajchayapong
Montakan
M
Rymer
William Z
WZ
D000368:Aged; D000842:Ankle / Q000294:innervation / Q000503:physiopathology; D000843:Ankle Joint / Q000294:innervation / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D007866:Leg / Q000294:innervation / Q000503:physiopathology; D008875:Middle Aged; D009069:Movement Disorders / Q000209:etiology / Q000503:physiopathology; D009122:Muscle Hypertonia / Q000209:etiology / Q000503:physiopathology; D009128:Muscle Spasticity / Q000209:etiology / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology*; D009460:Neurologic Examination / Q000379:methods; D010291:Paresis / Q000209:etiology / Q000503:physiopathology*; D011237:Predictive Value of Tests; D016059:Range of Motion, Articular / Q000502:physiology; D012021:Reflex, Abnormal / Q000502:physiology*; D012026:Reflex, Stretch / Q000502:physiology; D020521:Stroke / Q000150:complications / Q000503:physiopathology*; D013710:Tendons / Q000503:physiopathology; D019415:Torque