TENS is a noninvasive modality. While traditionally known for its pain-relieving effects via mechanisms such as the gate-control theory, the application of TENS in spasticity leverages broader neuromodulatory effects on spinal excitability. Studies suggest that TENS applied to spastic muscles or nerve pathways can lead to immediate and sustained reductions in muscle tone and neurophysiological markers such as the H-reflex. ^, Emerging research suggests that TENS may enhance the efficacy of other spasticity management strategies, such as botulinum toxin injections, by promoting neuromuscular adaptation and prolonging treatment effectiveness. ^,

TENS could reduce spasticity through multiple neurophysiological mechanisms operating at different levels of the nervous system. The antispastic effects appear to be mediated through modulation of spinal inhibitory interneuronal circuits, potentially enhancing presynaptic inhibition and recurrent inhibitory pathways that regulate alpha-motoneuron excitability. At the supraspinal level, TENS can transiently modulate the excitability of sensorimotor cortical networks, inducing reciprocal inhibitory and facilitatory changes that may support cortical plasticity and functional reorganization. The therapeutic efficacy likely stems from synergistic interactions between these peripheral, spinal, and cortical mechanisms, culminating in normalized neuromuscular control parameters and reduced pathologic muscle tone. The relative contribution of each mechanism may vary depending on stimulation parameters, electrode placement, and the underlying pathophysiology of the specific upper motor neuron syndrome being addressed. ^,

TENS is usually applied at frequencies ranging from approximately 20 Hz up to 200 Hz, with 100 Hz being commonly reported in protocols. ^, Pulse durations are typically in the range of 100 to 300 μs. Stimulation intensity was set to a strong but comfortable sensory level, below the motor contraction threshold. TENS electrodes are placed over nerves or muscles corresponding to the spastic muscles. Sessions commonly last 20 to 60 minutes and may be performed daily or several times per week. A review by Mahmood and colleagues suggests that optimal TENS parameters for lower limb spasticity in stroke patients may include sessions over 30 minutes, extended for more than 2 weeks, with intensity levels described as “strong but comfortable” or “twice the sensory threshold,” and electrode placement along the nerve or on the muscle belly.

Neuromuscular electrical stimulation (NMES) has been shown to yield positive outcomes in spasticity management. NMES uses surface or garment-integrated electrodes to stimulate motor nerves, eliciting muscle contractions.

It reduces spasticity through specific neurophysiological pathways that regulate abnormal motor control mechanisms. ^, Stimulation of antagonistic muscles activates reciprocal Ia inhibitory circuits, decreasing excitatory signals to agonist α-motoneurons via segmental spinal pathways. At the same time, activation of motor units triggers Renshaw cell-mediated recurrent inhibition, helping to lower motoneuron hyperexcitability seen in upper motor neuron lesions. Additional modulation occurs through increased presynaptic inhibition of Ia afferents and the induction of post-activation depression—both mechanisms reduce synaptic strength at the Ia-motoneuron connection. NMES may also stimulate Ib afferents from Golgi tendon organs, enhancing autogenic inhibition and further stabilizing motoneuron firing ^,

The direct application of NMES to hypertonic muscles facilitates the activation of the propriospinal inhibitory network and modulates dorsal horn afferent processing, thereby inducing neuroplastic adaptations in motoneuronal excitability thresholds.

These complementary therapeutic mechanisms collectively modify aberrant sensorimotor integration at both spinal and supraspinal levels, resulting in immediate and potentially sustained reduction in pathologic muscle tone, as evidenced by quantitative measures of reflex threshold modulation and clinical spasticity scales.

Studies show that NMES can reduce spasticity levels by 45% to 60% while also improving range of motion, muscle function, and body composition in people with SCI. ^, Its effectiveness is often enhanced when combined with other therapeutic approaches, as demonstrated in randomized controlled trials. ^, A meta-analysis of 29 RCTs (940 subjects) found that NMES combined with conventional therapy significantly decreased spasticity and increased joint range of motion after stroke.

The parameters of NMES application play a crucial role in spasticity reduction. Generally, a frequency range of 20 to 50 Hz is used to elicit tetanic muscle contractions, which are sustained muscle contractions without individual twitches. One systematic review focusing on SCI identified a frequency of 20 to 30 Hz, a pulse duration of 300 to 350 μs, and an amplitude of current greater than 100 mA as parameters associated with positive reductions in spasticity. The intensity of the stimulation should be above the motor threshold, meaning it should be sufficient to produce a visible or palpable muscle contraction. Treatment sessions usually last between 20 and 30 minutes and are typically conducted 3 times a week. A pulse width range of 100 to 500 μs is commonly used. ^, However, some researchers have suggested that a higher pulse width, such as 1000 μs, may have a greater effect on central activation. While these parameters provide a general guideline, it is important to recognize that the optimal settings for NMES likely vary depending on the specific neurologic condition, the targeted muscles, and the individual patient’s response to the stimulation.

FES is a rehabilitation technique that utilizes low-level electrical currents to stimulate nerves and muscles, aiming to elicit controlled muscle contractions that produce or augment functional movements. Unlike traditional electrical stimulation, which is primarily used for pain relief or muscle strengthening in isolation, FES focuses on creating movements that mimic natural, purposeful actions such as walking, grasping objects, or maintaining posture. This is achieved by applying electrical stimulation to specific muscles or muscle groups through electrodes placed on the skin over the targeted nerves or muscles. Combined with the patient’s effort to perform a functional task, FES aims to retrain the neuromuscular system, enhance motor control, and build strength in a functional context.

FES may reduce spasticity through several spinal inhibitory mechanisms ^, previously described as NMES. Furthermore, FES can help the CNS relearn the execution of impaired functions, thereby reorganizing the central motor network. Although FES can reduce spasticity as a secondary effect, it is not specifically designed to target spasticity. Indeed, FES has been successfully integrated into rehabilitation programs to improve gait, reach, and grasp functions in individuals with poststroke hemiparesis and SCI. ^,

In SCI, FES cycling (pedaling an ergometer with electrical stimulation of leg muscles) has been studied as an activity-based therapy that can help reduce spasticity. A 2021 meta-analysis of FES cycling in SCI showed that after a training program (typically 2–3 sessions per week for several weeks), lower extremity spasticity (Modified Ashworth scores) significantly decreased compared to baseline ( P =.013). Interestingly, the analysis suggested that approximately 20 FES cycling sessions were needed to achieve a meaningful reduction in spasticity.

FES uses core parameters similar to NMES, such as pulse amplitude, pulse width, and frequency, to activate motor and sensory pathways. However, in practical applications, FES also requires additional controls like duty cycle (on/off times), ramp-up and ramp-down durations, and electrode configuration to meet task-specific goals, such as coordinated limb movement and fatigue management. These parameters are essential for safety and effective function, especially during repetitive, patterned contractions used in gait and upper limb training.

Repetitive neuromuscular magnetic stimulation (rPMS) is a noninvasive method with negligible side effects that produces a magnetic field to stimulate the peripheral nervous system and muscles. In recent years, peripheral magnetic stimulation therapy has gained attention as an alternative to electrical stimulation for peripheral applications to reduce spasticity, promote motor abilities, and perceptual-function skills.

rPMS can effectively stimulate deep muscle structures that are less accessible to NMES. The electric coil in the applicator generates a magnetic field that propagates into the human body, inducing electric currents according to Michael Faraday’s law of magnetic induction. These induced currents travel along neurons, triggering muscle contractions. Unlike electrical stimulation, which is typically limited to stimulating structures at a depth of about 12 mm, magnetic stimulation penetrates deeper into the body without requiring direct contact between the applicator and the skin. Consequently, rPMS can be performed through clothing and bandages. Additionally, this technique minimizes the activation of pain receptors (Aδ, C fibers) in the skin, resulting in less discomfort during stimulation.

In addition to electrically stimulating the targeted nerves, rPMS generates enhanced somatosensory input compared to NMES. When applied to the muscle, rPMS induces proprioceptive signals in the CNS through both direct activation of sensorimotor nerve fibers and indirect activation of mechanoreceptors during rhythmic contraction, relaxation, and muscle vibration. This increased proprioceptive inflow influences and modulates neural network activity involved in motor control. Previous studies have demonstrated that rPMS, applied in single or multiple sessions, can significantly reduce spasticity and improve upper limb motor function in patients with CNS lesions. Furthermore, improvements in the kinematics of finger movements have been observed after rPMS, accompanied by activation of the parietal premotor network, suggesting a central modulatory effect on the brain through enhanced sensorimotor input. Upregulation of corticomotor excitability can result in heightened inhibitory control of the stretch reflex, thereby reducing spasticity. The effect on the nonneural component is also not negligible: rPMS may decrease muscle hardness and increase cephalic venous blood flow of the extensor digitorum muscle, after 600 magnetic pulses were delivered at 20 Hz to the radial in healthy subjects. ^, Electrical stimulation of peripheral nerves could activate group Ia afferent nerve fibers from stimulated muscle, group Ib afferent nerve fibers from the Golgi-tendon organ, and group II afferent nerve fibers from the skin, potentially reducing muscle hardness. There is no current consensus on the optimal intensity, stimulation frequency, and application methods due to the variability in study protocols and patient populations. Frequencies ranging from 1 Hz to 150 Hz have been previously used, with 25 Hz being the most commonly used frequency in most reviewed trials. The effectiveness of rPMS for spasticity depends not only on frequency but also on intensity, pulse duration, train duration, the total number of stimuli, and the location of stimulation (e.g., nerve roots, muscle belly).

Vibration therapy, including both focal vibration (FV) and whole-body vibration (WBV), uses mechanical vibration waves to reduce reflex hyperexcitability and spasticity, especially in individuals after a stroke and children with cerebral palsy. ^,

WBV is transmitted upward to the rest of the body through the contact site, which can produce vibration stimulation to multiple muscle groups simultaneously. It has been suggested that WBV inhibits muscle spindle Ia afferent activity by presynaptic inhibition and, thus, permits control of the increased muscle spindle and gamma motor neuron activity. Studies with transcranial magnetic stimulation suggest that WBV can influence the CNS by increasing the excitability of the corticomotor pathway, contributing to a reduction in the overactivity of motor neurons. This finding was confirmed by the modification of F-wave parameters observed after 5 minutes of WBV at 30 Hz in poststroke patients. This reduction persisted for at least 20 minutes post-interventions.

A recent meta-analysis highlighted that WBV combined with conventional rehabilitation at a lower vibration frequency (<20 Hz) for approximately 10 minutes was effective in reducing both upper and lower limb spasticity in acute and subacute stroke patients. A study comparing different WBV protocols (7–18 Hz vs static 11 Hz) suggested that while 7 to 18 Hz might offer superior immediate results in spasticity reduction, an 11 Hz static protocol showed better results after 8 weeks. FV works by delivering mechanical oscillations to specific muscles or tendons, thereby activating neuromuscular receptors, including muscle spindles and Golgi tendon organs. These receptors transmit signals to the CNS, influencing sensory and motor pathways. Research indicates that FV can alter spinal cord and cortex excitability, improve motor output, and reduce muscle stiffness.

The suggested mechanism of action of FV on spasticity involves the depression of the H reflex within spinal motoneurons and reciprocal inhibition between agonist and antagonist muscles, as assessed by the H reflex and M wave. The duration of the treatment appears to influence the effect of vibration on motoneuron excitability. Furthermore, mechanical vibrations applied to the muscle belly and/or its tendon activate muscle spindles, which have been demonstrated to evoke an involuntary reflex contraction called the tonic vibration reflex and inhibit the antagonist muscle, a phenomenon known as “reciprocal inhibition”. Vibrations applied near the tendon might also have a more direct influence on Golgi tendon organs, which are sensitive to muscle tension. In a recent observational pilot study, tendon vibration showed greater improvement in finger flexor tone compared to both stretching and muscle belly vibration. Most studies employed vibration frequencies between 85 and 120 Hz, with amplitudes ranging from 0.01 to 2 mm and a duration of approximately 30 minutes per session. Whether it is more effective to apply FV over the spastic muscle or on its antagonistic muscles remains controversial, despite the fact that vibration of the antagonist muscles has been the most prevalent approach in multiple studies. Conversely, FV also produces mechanical waveforms perpendicular to the soft tissue. The transmission of energy leads to muscle deformation, which in turn causes structural modifications. This is considered a potential rationale for treating agonist muscles, particularly as adjuvant therapy alongside botulinum toxin.

Extracorporeal shockwave therapy (ESWT) applies high-energy acoustic waves that induce mechanical stress in tissues, leading to biochemical and neurophysiological responses that contribute to spasticity reduction. ESWT is delivered either as focused (fESWT) or radial (rESWT) acoustic pulses. ESWT may work by reducing motor neuron excitability, inducing neuromuscular transmission dysfunction, and affecting the rheological properties of muscles. Mechanistically, ESWT is thought to decrease spasticity through multiple pathways: (1) modulation of spinal excitability via decreased alpha motor neuron activity ; (2) disruption of abnormal neuromuscular transmission ; (3) stimulation of nitric oxide (NO) production, which enhances local vasodilation and muscle relaxation ; and (4) reduction of fibrosis and improvement of muscle compliance through extracellular matrix remodeling. Shockwave-induced cavitation and microtrauma can trigger NO release and temporarily reduce acetylcholine availability at the neuromuscular junction, dampening hyperactive stretch reflexes. Concurrently, ESWT disrupts the fibrous cross-links in spastic muscles, improving their viscoelastic properties and thereby reducing passive stiffness. Studies suggest that ESWT could influence sensory afferent input, reducing exaggerated stretch reflex responses and facilitating long-term plasticity in neuromuscular function.

Recent systematic reviews and meta-analyses confirm that ESWT produces significant reductions in poststroke spasticity as measured by the Modified Ashworth Scale (MAS). Improvements were greatest immediately after treatment and remained significant (though diminished) at 4 to 12 weeks post-intervention. Both focused and radial ESWT yield spasticity relief ; some evidence suggests that radial ESWT may confer slightly greater improvements in joint range of motion, likely due to its broader dispersion of shockwave energy in superficial tissues. ^,

ESWT has been compared with botulinum toxin injections and has shown similar benefits in reducing spasticity. However, further research is needed to establish optimal protocols and long-term efficacy. ESWT is generally safe, with few reported side effects such as transient skin irritation or muscle soreness.

Optimal treatment parameters remain under debate. Typical antispastic protocols use 500 to 4000 impulses per session, an energy flux density of 0.03 to 0.30 mJ mm ², and a strike frequency of 4 to 12 Hz. Most trials consisted of 1 to 3 sessions (range 1–6 for fESWT; 1–8 for rESWT), administered at weekly (fESWT) or 2 to 3 day (rESWT) intervals, delivering 1500–3000 shocks per session. Higher-pressure stimuli and increased session frequency tend to enhance MAS score reductions, but additional sessions beyond 1 to 3 treatments do not consistently augment efficacy (potentially due to developing tolerance). The ideal application site remains unresolved; one trial noted greater immediate spasticity reduction when targeting the musculotendinous junction rather than the muscle belly, although the lasting effects in that study were minimal.