ESWT is known to be effective in musculoskeletal diseases for treating pain, inflammation, or injury of a ligament. ESWT produces mechanical effects such as regeneration of degenerated tissue, neovascularization, and resorption of calcium deposit,24
and also physiological responses such as changes of epithelial cell permeability, free radical formation, change of cell membrane permeability, NO formation, and variable growth factor formation.14
The mechanisms of ESWT on spasticity due to central nervous system injury are still unknown. Mariotto et al.14
stated that ESWT can induce NO synthesis and NO is involved in improvement of variable tendon disease. NO is involved in neuromuscular junction formation in the peripheral nervous system27
and in physiological functions of the central nervous system, including neurotransmission, and synaptic plasticity.28
Likewise, variable mechanisms have been proposed, including acting on fibrosis of chronic hypertonic muscles,20
decreasing spinal excitability,29
and mechanical vibratory stimulation.29
Considering the therapeutic effects of ESWT on bones and tendons Manganotti and Amelio20
proposed that reduction of spasticity could be caused by improving the stiffness of connective tissue by directly acting on fibrosis of chronic hypertonic muscles.
In this study, we attempted to evaluate the antispastic mechanism of ESWT by using F waves and H-reflexes that reflect spinal excitability. Results showed no significant changes in F wave minimal latency, H-reflex latency, or H-M ratio after treatment. Therefore, those factors can be eliminated as the mechanism by which ESWT reduces spasticity by decreasing spinal excitability. Manganotti and Amelio20
also reported that the effect of ESWT on spinal excitability can be excluded as the main mechanism, because no change of F wave latency or amplitude after treatment was demonstrated.
Another possible mechanism was mechanical vibratory stimulation, which reduces excitability of motor neurons and induces the change of F wave.29
In this study, we can rule out this theory because no significant change of F wave or H-reflex were detected. Considering the clinical anti-spastic effect observed up to 4 weeks after treatment,20
mechanical vibratory stimulation, which is transitory and short lasting, could also be excluded as a major effect.
Because the latency and amplitude of compound muscle action potential and conduction velocity of tibial nerve were not changed in this study, we can rule out a significant effect of ESWT on peripheral nerves and the effect of botulinum toxin A on neuromuscular blockage.
Results of this study could not reveal the exact mechanism of ESWT for reducing spasticity. However, we can rule out several proposed mechanisms such as decreased spinal excitability, peripheral nerve injury, and mechanical vibratory stimulation by using electrophysiologic studies. It was previously reported that range of motion of the joint increased after ESWT;20
however, we did not evaluate range of motion of the joint in the study, and therefore the mechanisms proposed by Maganotti and Amelio20
for reducing spasticity mediated by improving stiffness of connective tissue affecting fibrosis of chronic hypertonic muscles were not confirmed in this study.
Similar to previous studies performed in stroke patients with upper limb spasticity, an immediate therapeutic effect of ESWT in reducing spasticity was found for stroke patients with ankle spasticity. ESWT can reduce spasticity in stroke patients with lower limb spasticity and prevent complications of spasticity, such as equinovarus deformity. This study only measured the immediate effect of ESWT, but Manganotti and Amelio20
and Yoo et al.21
reported that the therapeutic effect of ESWT on upper limb spasticity could last at least 4 weeks, maximally 12 weeks, and that ESWT had a therapeutic effect on reducing spasticity for a considerable time. There were several cases where the patient complained of pain during treatment, but the degree of pain was not severe (< VAS 3), and not all subjects reported pain after treatment; other side effects were not found in this study. ESWT appears to be safe and noninvasive and can reduce financial burden compared to treatment using botulinum toxin A. ESWT can be helpful in treatment of chronic stroke patients with spasticity.
There are several limitations in this study. First, the mechanism of ESWT for reducing spasticity was not fully evaluated in this study. Further studies are needed to elucidate the mechanism of ESWT for reducing spasticity by comparing the anti-spastic effects; for example, stiffness of connective tissue for acute stroke patients compared with chronic stroke patients. Second, this study used F wave minimal latency to assess the spinal excitability instead of F wave amplitude or F-M ratio, which are well known and widely used. Further studies concerning the correlation between F wave minimal latency and spinal excitability are needed. Third, similar to results from previous studies conducted for upper limb spasticity,20
range of motion of the joint should be measured. Reduced effect of spasticity on functional abilities such as ambulation or activities of daily living should be assessed. Finally, further studies concerning the most effective level of intensity, number of ESWT treatments, and duration of therapeutic effect, need to be conducted in a larger number of patients.