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Methods appropriate for use in research, particularly into the mechanism of spasticity did not satisfy the needs of the clinician and the need for an objective but clinically applicable tool was identified. A clinical assessment may need to generate more than one 'value' and should include evaluation of other components of the upper motor neurone syndrome. There is therefore a need for standardized protocols for 'best practice' in application of spasticity measurement tools and scales.

The clinical and experimental use of the three methods is restricted due to moderate reliability and sensitivity. It is recommended to perform combined neurophysiological-biomechanical assessment of spasticity during active, functional movement.

Objective: To investigate the effect of body weight support on the gait of hemiparetic subjects walking on a treadmill. Design: Survey. Patients: Eleven nonambulatory hemiparetic subjects. Methods: Subjects walked on the treadmill with full weight bearing and with 15%, 30%, 45%, and 60% body weight support at constant walking velocity. Cycle parameters, symmetry ratios, and the kinematic EMG of several lower limb muscles of the affected leg were recorded. Video-analysis served for assessment of posture and hip and knee angle displacement. Results: With body weight support the relative double support time decreased, the relative single stance period of the affected limb increased, and the functional activity of the vastus and soleus diminished. The activity of the gluteus tended to increase. Patients walked more upright and with less hip and knee flexion. The extensor spasticity did not change and the qualitative activation pattern of all recorded muscles remained unchanged. Conclusion: Body weight support did not facilitate a less physiological gait. By reducing double support duration, body weight support resulted in a greater stimulus for balance training. The facilitation of gluteus medius is favorable with respect to training pelvic alignment. The reduction of the activity of other antigravity muscles suggests a limit of 30% BWS not be exceeded.

This study further supports the beneficial effects of botulinum toxin in the treatment of lower limb extensor spasticity. A correlation was observed between the clinical reduction of muscle tone, functional gait parameters, and a more normal EMG pattern with a predominant reduction of the premature activity of the plantar flexors. The qualitative type of EMG pattern corresponding to an increased stretch-reflex excitability (type I) was a positive predictor for the outcome.

Twelve chronic hemiparetic outpatients with pronounced lower limb extensor spasticity were injected with 400 units of botulinum toxin A, EMG guided into the soleus, tibialis posterior, and both heads of the gastrocnemius muscles. Botulinum toxin A caused a definite reduction of plantar flexor spasticity, in 10 patients two weeks after the injection, as assessed by the Ashworth scale. Four of the patients were able to achieve active dorsiflexion of their affected ankle. Gait analysis including the measurement of vertical ground reaction forces showed a statistically significant (p < 0.01) improvement in velocity, stride length, stance symmetry, and the length of the force point of action under the affected foot. Qualitative improvements on the force diagrams indicated a better loading, advancement of the body, and push off of the affected limb in seven patients. Eight weeks after the injection the effects waned.

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