Differentiation between non-neural and neural contributors to ankle joint stiffness in cerebral palsy

Abstract

BackgroundSpastic 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.MethodsTwenty-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.ResultsIn 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.ConclusionsUsing 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.

Impaired gait function in adults with cerebral palsy is associated with reduced rapid force generation and increased passive stiffness

“…It should also be pointed out that the short stretch we used may have prevented us from determining a contribution from stretch reflex activity that might have been elicited with a longer stretch resembling the clinical evaluation to a larger extent. Indeed, this could potentially explain why we, in contrast to other studies in which longer stretches were used (de Gooijer-van de Groep et al, 2013), did not observe reflex hyperexcitability in this patient group.…”

“…It was therefore not surprising that neither of the two scales showed any correlation with reflex-mediated stiffness at rest in this patient population. This is somewhat in contrast to a recent study that reported a significantly larger reflex-mediated stiffness in 23 adolescents (range 12-19 years) with CP compared to an age-matched, healthy control group (de Gooijer-van de Groep et al, 2013). However, in that study a stretch of 30° lasting 250 ms was used.…”

European consensus on the concepts and measurement of the pathophysiological neuromuscular responses to passive muscle stretch

“…However, it is yet not defined what velocity and movement profile should be applied. In physical examination the movement profile is determined by constraints of human performance of the examiner, as opposed to motorized tests in which a particular movement profile can be imposed [40][41][42][43]. However, a motorized test is less feasible in clinical practice and constant velocities do not represent natural movement profiles [44].…”

Effects of Selective Dorsal Rhizotomy on Ankle Joint Function in Patients With Cerebral Palsy

“…Patients with CP develop muscle contractures that are thought to be multifactorial, including chronic muscle shortening (13) and decreased joint ROM (14) resulting in increased joint stiffness (15). The determinants of joint stiffness are (i) the passive component defined by the changes of the material properties of muscles and connective tissues, and (ii) the active component, which is the stiffness during dynamic conditions due to neural impairments (i.e., chronic muscle overactivity or spasticity) (16). Spasticity is believed to contribute to abnormal joint stiffness via changes of not only active but also passive muscle components due to adaptation (17).…”