We present a 50-year-old woman who sustained spastic left hemiplegia secondary to the right thalamic hemorrhage 6 years ago. She complained of persistent severe left calf pain after serial casting for the treatment of shortened plantar flexors of the left ankle. Two months later, magnetic resonance T1-weighted images showed diffuse high signal intensity involving the whole muscle bulk of the soleus and normal signal intensity of thin atrophied gastrocnemius. Needle electromyography of the soleus revealed myopathic patterns. Histologic findings of the soleus showed necrotic muscle fibers with phagocytosis, endomyseal collagen and fat deposition. We concluded that prolonged passive stretch of spastic plantar flexors of the ankle under serial casting induced soleus myopathy with segmental myonecrosis, and which developed left calf pain. Selective induction of soleus myopathy could be explained by the higher stretch tension produced by ankle dorsiflexion in the soleus compared to the gastrocnemius because of different proximal ends.

Objective: This study was designed to evaluate the effect of stretching on decreasing spasticity of ankle plantar flexor muscles by biomechanical assessments.

Method: Twenty two ankle joints of nineteen patients with upper motor neuron lesion were included. The spasticity was assessed both clinically and biomechanically before and after stretching of ankle plantar flexor muscles by tilt table. For clinical assessment modified Ashworth scale (MAS) was used. For biomechanical assessment, ankle plantar flexor muscles were stretched isokinetically while EMG signals were recorded simultaneously and peak eccentric torque, stiffness index and stretch reflex threthold speed (SRTS) were measured.

Results: Two cases showed improvement in MAS after stretching but the others did not. SRTS of ankle plantar flexor was increased significantly while peak eccentric torque and stiffness index were unchanged.

Conclusion: Passive stretching of ankle plantar flexor muscles decreased the stretch threshold, that is a neural component of spasticity but it did not decrease the mechanical component of spasticity.