Novel Evidences of Extracorporeal Shockwave Therapy for Spasticity

Spasticity is defined as ‘a disorder of sensorimotor control, resulting from an upper motor neuron (UMN) lesion, presenting as intermittent or sustained involuntary activation of muscles’. It is characterized by increased involuntary velocity-dependent tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex. In the recent years, a range of non-pharmacological interventions has been used to manage spasticity. Among the novel of all therapies, extracorporeal shock wave therapy (ESWT) is attractive for many researchers since the noninvasive, easy application after well training and safety property. Moreover, the evidences of regeneration of musculoskeletal tissues made ESWT more interesting than other novel therapies. This article will show the evidences, practical clinical use and precaution to guide treating for the clinicians in the novel therapy of ESWT for spasticity. The review of the scientific evidences including methodology components and main results of ESWT treatment on upper limb and lower limb muscles affected by post-stroke spasticity are demonstrated. However, reducing spasticity alone without addressing the negative components of the upper motor neuron syndrome will limit meaningful recovery. A combination of rehabilitation techniques is needed to facilitate functional improvements.

Keywords: Spasticity, Extracorporeal Shock Wave Therapy (ESWT), Rehabilitation

Spasticity is defined as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motor neuron syndrome [1]. It can be associated with a variety of signs and symptoms of the upper motor neuron syndrome. These symptoms include the neural components and the biomechanical components. The neural components consist of positive phenomena as clonus, dystonia (involuntary muscle contraction resulting in abnormal posturing of a joint or limb), extensor or flexor spasms, spastic co-contraction (contraction of both the agonist and antagonist muscles caused by an abnormal pattern of commands in the descending supraspinal pathway), abnormal reflex responses (exaggerated deep tendon reflexes and associated reaction), and negative phenomena as the loss of dexterity, muscle fatigue, weakness, and loss of limb control. The biomechanical components consist of stiffness, contracture, fibrosis, and atrophy [2-7]. Many disease conditions of the central nervous system, including stroke, cerebral palsy, traumatic brain injury, multiple sclerosis, and spinal cord injury, can provoke spasticity.

Pathophysiology, spasticity results from an abnormal intraspinal processing of primary afferent inputs due to the dissociation of the motor and sensory components of the diastaltic arch [8]. This dissociation is caused by lesions in the brainstem, the cerebral cortex (in the primary, secondary, and supplementary motor areas) or the spinal cord (pyramidal tract), which leads to an inhibitory/excitatory imbalance in the spinal network with a consequent segmental hyperexcitability, including increased muscle activity and exaggerated spinal reflex responses to a peripheral stimulation [9-16]. Furthermore, multiple sclerosis induced spasticity is believed to be due to the occurrence of either axonal degeneration or demyelination within the specific descending tracts in the central nervous system. The inhibitory/excitatory imbalance results from damage-induced dysfunction and maladaptive connectivity among several brain structures such as the supplementary motor, cingulate motor, premotor, posterior and inferior parietal areas, and the cerebellum [9].The spasticity treatments available can be categorized as pharmacological and nonpharmacological treatments. The pharmacological treatment includes oral (eg, baclofen, tizanidine, benzodiazepine, etc) and injectable (eg, botulinum toxins, alcohol and phenol). In recent years, a range of non-pharmacological interventions has been used to manage spasticity, include: physical interventions (stretching, passive movements); transcutaneous electric nerve stimulation (TENS); transcranial direct current stimulation (tDCS); extracorporeal shock wave therapy (ESWT); vibratory stimulation (whole body vibration); electromyography biofeedback; repetitive transcranial magnetic stimulation (TMS); therapeutic ultrasound; acupuncture; orthotics (splints, casts), thermotherapy, cryotherapy and others. In practice, these categories can be implemented in a neurorehabilitation program, either as a stand-alone therapy or in a combination of 2 or more treatment modalities. Among the novel of all therapies, extracorporeal shock wave therapy (ESWT) is attractive for many researchers since the noninvasive, easy application after well training and safety property. Moreover, the evidences of regeneration of musculoskeletal tissues made ESWT more interesting than other novel therapies. However, reducing spasticity alone without addressing the negative components of the upper motor neuron syndrome will limit meaningful recovery. A combination of rehabilitation techniques is needed to facilitate functional improvements.

ESWT uses biphasic acoustic energy that goes from positive high peak pressures (10-100 MPa (mega pascals) for fESWT; 0.1-1 MPa for rESWT) to negative phase (10 MPa); short rise times (10-100 μs for F-ESWT; 0.5-1 μs for rESWT), short duration (0.2-0.5 μs for fESWT; 0.2-0.5 μs for rESWT). Focused and radial shockwaves are generated in different ways. Focused shockwaves are generated electrically, either within the applicator (electrohydraulic technique), or externally to it in the focal zone (electromagnetic or piezoelectric techniques), and then propagate to a designated focal point in order to treat it. rESWT are ballistic pressure waves generated at lower pressures over a longer time and propagate divergently within the tissue [17-23]. The induced energy is propagating in the tissue and converges into a focal or radial area, depending on the equipment used and the settings selected for intensity, angle and other parameters [17]. The energy of fESWT decreased within the target tissue consists of bone, calcifications, water, etc., more than 50% in occasionally, whereas consistent energy flux density was found in Reswt [17-39].

The current status of knowledge about ESWT from can be shortly summarized as follows: (i) ESWT is effective. (ii) ESWT is safe. (iii) For certain conditions such as plantar fasciopathy or calcifying tendonitis of the shoulder, randomized controlled trials (RCTs) on ESWT have become the predominant type of RCT listed in the highly prestigious Physiotherapy Evidence Database (PEDro*; www.pedro.org.au), and/or obtained the highest PEDro quality scores among all investigated treatment modalities. (iv) among those RCTs listed in the PEDro database, there is no difference in the “quality” of RCTs with positive or negative outcome. (v) Application of local anesthesia adversely affects outcome of ESWT. (vi) Application of insufficient energy adversely affects outcome of ESWT. (vii) There is no scientific evidence in favor of either rESWT or fESWT with respect to treatment outcome. (viii) The frequently used distinction between rESWT as “low-energy ESWT” and fESWT as “high-energy ESWT” is not correct and should be abandoned. (ix) ESWT has become an attractive alternative for treating newly diagnosed tendinopathies and myofascial pain syndrome. (x) An optimum treatment protocol for ESWT appears to be three treatment sessions at one-week intervals, with 2000 impulses per session and the highest energy flux density that can be applied [17-39].

The advantage for treatment with ESWT are as the follows;17,27,28,37,38 (1) effectively relieves pain in more than 80 percent of patients even after just three treatments, (2) can replace surgery in many cases of diseases of the musculoskeletal system, (3) requires compliance by the patient that can easily be achieved (three times five to ten minutes treatment, usually once a week), (4) can be fully performed on an outpatient basis, (5) can be combined with other PRM treatments ,(6) No medication ,and (7) Gentle and effective.

The mechanism of shock wave therapy on spastic muscles is still are still unclear and require further investigation. There are studies investigated the mechanisms of the shock waves as the following hypotheses follows; (1) can induce non-enzymatic and enzymatic nitric oxide (NO) synthesis [40-43]. NO is involved in neuromuscular junction formation in the peripheral nervous system [44] and in important physiological functions of the CNS, including neurotransmission, memory and synaptic plasticity [45]. NO synthesis has been suggested as an important mechanism to explain the effectiveness of shock waves in the anti-inflammatory treatment of different tendon diseases [40-43]. However, the reduction in hypertonia in patients after stroke after shock wave therapy is not produced by denervation or lesion of the peripheral nerve, as shown by neurophysiological findings in a previous study [46].; (2) A direct effect of shock waves on fibrosis and on the rheological properties of the chronic hypertonic muscles should be considered together with the documented therapeutic effect on bone and tendon diseases [47-53].; (3) possible tixotrophy effects of shock waves on tissues and vessels of the treated muscles [41, 42].; (4) The effect of mechanical stimuli of shock waves on the muscle fibers next to the tendon cannot be excluded; (5) pain itself may be contributing to increased muscle tone. Therefore, treating the pain may reduce muscle tone [54, 55]. (6) the effect of rESWT on muscle fibrosis and non-reflex hypertonia. The reduced extensibility, due to soft tissue changes, causes pulling forces to be transmitted more readily to the muscle spindles. In this condition, an exaggerated spindle discharge in response to muscle stretch might lead to an increased stretch reflex. Thus, the reduction of non-reflex hypertonia could modify muscle spindles’ excitability, leading to a secondary reduction of spasticity [46,56].; (7) a neuroregenerative properties of the ESWT characterized by strong growth in the rate of axonal regeneration, connected with the removal of degenerated axons initially and obtaining a greater capacity for the creation of new axons as a result of partial destructive impact of ESWT [57].; (8) low-energy ESWT enhances the neuroprotective effect in reducing secondary injury and leads to better locomotor recovery following spinal cord injuries [58].; (9) early application of ESWT facilitated the activity of macrophages and Schwann cells, which affect the survival and regeneration of neurons [59,60]. 10) ESWT treatment is effective in improving the function of peripheral nerves and also show a positive effect on the prevention of atrophy associated with denervation [61].

Review of the scientific evidences including methodology components and main results of ESWT treatment on upper limb and lower limb muscles affected by post-stroke spasticity are as in the Table 1 and Table 2, respectively.

Guo P, et al conducted a meta-analysis to combine the results of previous studies to arrive at a summary conclusion. The pooled data immediately after ESWT and 4 weeks after ESWT compared with baseline date all suggested that ESWT had a significant effect on relieving spasticity caused by stroke measured by MAS grades. Moreover, no serious adverse effects were observed in any patients after shock wave therapy. But the differences in the subtype of shock wave, therapeutic energy, treatment sessions, and tested muscles might lead to the varied effects reported in selected studies, leading to a significant level of heterogeneity among the studies [72].

ESWT is effective in treating spasticity and improving some parameters, although the improvement more significant immediately after apply ESWT and diminished with time. The non-invasive nature of ESWT and its much fewer adverse effects, it can be a useful alternative for treating spasticity especially in stroke patients or combined with other therapies as botulinum toxin injection, oral antispasticity drugs and stretching exercises. The various mechanisms are evidenced for ESWT in decreasing spasticity and enhance functions. However, the neurorehabilitation treatment as strengthening exercises for the antagonist muscles, endurance exercises, balance and coordination training are also need for enhancement the movement ability and the functional outcome of the patients.