Spasticity is a positive feature of the upper motor neuron syndrome, commonly observed in patients with stroke, multiple sclerosis, brain injury, spinal cord injury, or cerebral palsy. It “ results from hyperexcitable descending excitatory brainstem pathways and ” the consequent “ exaggerated stretch reflex responses ” manifesting “ as velocity- and muscle length–dependent increase in resistance to externally imposed muscle stretch. ” Alongside spasticity, “ other related motor impairments, including abnormal synergies, inappropriate muscle activation, and anomalous muscle coactivation may coexist and share similar pathophysiological origin. ”

Although spasticity may occasionally confer functional benefits (such as aiding limb stability or facilitating transfers), it more often leads to disability, pain, contractures, deformities, and reduced participation in daily activities, imposing a substantial socioeconomic and caregiving burden. Management strategies for spasticity have traditionally relied on pharmacologic, interventional, and rehabilitation approaches. Among these, botulinum toxin type A injection has emerged as the first-line treatment for focal or segmental muscle overactivity, owing to its proven efficacy and favorable safety profile. ^, Other antispastic agents, including baclofen, tizanidine, and benzodiazepines, exert systemic effects but are often limited by adverse events such as sedation and weakness. Nevertheless, the benefits of pharmacologic treatments are transient, prompting the implementation of interventional, long-term strategies such as therapeutic nerve blocks, cryoneurolysis, and selective neurotomy in patients with spasticity. Rehabilitation for spasticity relies on comprehensive, interdisciplinary approaches that integrate medical, physical, and functional interventions. Core components include prolonged positioning techniques, targeted muscle stretching, strengthening of both agonist and antagonist muscle groups, therapeutic exercise, and repetitive task-specific practice designed to promote motor relearning. ^, These interventions, combined with occupational therapy, gait training, and adaptive strategies, aim to normalize movement patterns, prevent secondary complications such as contractures and joint deformities, and enhance overall functional independence. Together, they support greater participation in daily activities and improve quality of life by fostering patient engagement and optimizing neuromuscular recovery within a coordinated, multidisciplinary rehabilitation framework.

Physical modalities, defined as interventions that apply physical energy to modulate physiologic processes, have long been integral to rehabilitation medicine and are gaining renewed attention as complementary tools in spasticity management. In recent years, an expanding body of research has investigated the efficacy of these modalities both as adjuncts to pharmacologic interventions (particularly botulinum toxin type A) and as standalone treatments for (mild-to-moderate) spasticity. ^, However, despite encouraging findings, the evidence remains heterogeneous, with considerable variability in treatment parameters, session frequency, and outcome measures. Against this backdrop, clarifying the clinical utility and limitations of physical modalities is essential for advancing individualized, patient-centered rehabilitation strategies. This literature overview aims to synthesize current evidence on the physiologic mechanisms, clinical effectiveness, and integration of physical modalities in spasticity management, examining their role within a multimodal framework to determine whether and how these interventions can enhance functional recovery, mitigate complications, and improve quality of life for individuals living with spasticity.

Spasticity is increasingly recognized as a condition with dual pathophysiological underpinnings: neural and nonneural. ^, The neural component originates from disinhibition of spinal reflex circuits following loss of supraspinal inhibitory control. In parallel, prolonged muscle overactivity, immobility, and maladaptive limb posturing lead to secondary biomechanical adaptations within the musculotendinous unit. These include increased collagen deposition, reduced sarcomeres arranged in series, altered fiber type composition, and remodeling of the extracellular matrix, all of which reduce tissue compliance and promote contracture formation. Such structural changes support a self-perpetuating cycle of stiffness and resistance to passive movement that persists even after pharmacologic reduction of neural excitability. Consequently, effective long-term management of spasticity must address both neural hyperexcitability and biomechanical soft-tissue alterations.

Within this conceptual framework, the application of physical modalities may serve as a therapeutic bridge between the neural and mechanical aspects of spasticity. By delivering controlled physical energy (eg, mechanical, thermal, or electromagnetic), these interventions act on multiple physiologic targets. ^,, They can modulate reflex activity through enhanced reciprocal inhibition and improved sensorimotor integration, while simultaneously inducing biological responses that remodel connective tissue architecture, increase local blood flow, and restore viscoelastic balance. ^, Collectively, these mechanisms contribute to reducing both neural-driven tone and nonneural stiffness, ultimately improving muscle compliance and functional mobility. Furthermore, physical modalities can enhance the efficacy of pharmacologic interventions such as botulinum toxin, providing additive or synergistic benefits through complementary or boosting (by facilitating toxin uptake and prolonging its therapeutic action) mechanisms.

Extracorporeal shock wave therapy (ESWT) delivers short, high-pressure acoustic impulses that propagate through soft tissues and exert both neural and nonneural effects relevant to spasticity reduction. ^, Mechanistically, ESWT influences peripheral and central pathways of motor control by modulating nitric oxide (NO) signaling, a key mediator of neuromuscular junction maintenance, microcirculation, and synaptic plasticity. This NO-mediated response contributes to improved local perfusion, metabolic recovery, and remodeling of chronically hyperactive motor units. ^, At the same time, ESWT can transiently alter neuromuscular transmission by reducing acetylcholine receptor density or neurotransmitter release at the neuromuscular junction, thereby attenuating excessive excitatory drive to the muscle. At the spinal level, the therapy produces a mild inhibitory effect on alpha-motor neuron excitability, possibly through modulation of Ia afferent activity and interneuronal circuits, leading to decreased reflex hyperactivity and muscle spasm. ^,,, These neurophysiological adaptations, in conjunction with peripheral effects such as neovascularization and enhanced oxygen delivery, support a multimodal neuromodulatory influence that collectively helps to decrease muscle tone and may improve voluntary motor control. In parallel, ESWT induces beneficial changes in the mechanical and structural properties of spastic muscles. ^,, The repeated acoustic pulses trigger fibroblast activation, promote collagen realignment, and regulate extracellular matrix turnover, thereby improving viscoelasticity and reducing passive stiffness. By modifying the rheological environment of the muscle, ESWT counteracts the nonneural contributors to spasticity (stiffness, fibrosis, and loss of elasticity), thereby increasing muscle compliance and facilitating more efficient joint motion. ^, Clinical and experimental assessments using elastosonography, myotonometry, and thermal imaging confirm these rheological improvements, demonstrating reductions in tissue viscosity and stiffness together with enhanced trophic status.

Two main delivery formats are employed in clinical practice for wave therapy. Focused ESWT concentrates acoustic energy within a small focal zone and penetrates deeply (up to approximately 12 cm) using electromagnetic, electrohydraulic, or piezoelectric generators. In contrast, radial pressure wave therapy relies on pneumatic or ballistic mechanisms that disperse lower-intensity energy more superficially, reaching depths of about 3 to 4 cm. ^,, Current evidence indicates comparable clinical efficacy between the 2 modalities. Therefore, selection should be guided by the treating professional, considering the target muscle depth and specific therapeutic goals, as well as the professional qualifications required for each treatment modality. According to the guidelines of the International Society for Medical Shockwave Treatment, focused ESWT must be performed exclusively by trained physicians who have completed specific education in shockwave treatment, whereas pressure wave therapy may be administered by well-trained and certified physiotherapists or nurses, provided that a physician has carried out the appropriate diagnostic assessment and issued the treatment prescription. Together, these neural and mechanical effects make wave therapy a versatile, noninvasive option capable of reducing tone and stiffness while improving mobility in patients with spasticity.

From a clinical standpoint, limited comparative evidence suggests that targeting either the muscle belly or the myotendinous junction produces similar reductions in spasticity. The choice can be individualized: application over the muscle belly is consistent with hypothesized rheological and neuromuscular junction-mediated mechanisms, whereas stimulation at the myotendinous junction is thought to engage tendon organ pathways that influence motor neuron excitability. ^,, Both single-session and multi-session protocols have been described in the literature, with the latter often consisting of 2 to 3 treatments delivered over a few (eg, 1 to 2) weeks. Meta-analytic evidence indicates that a single application may provide only transient benefits, whereas repeated sessions within 4 weeks are more effective in sustaining tone reduction and functional gains. The duration of clinical benefit generally ranges from 4 to 6 weeks, although several studies have reported improvements persisting for up to 12 weeks, particularly when multi-session regimens are employed or when ESWT is combined with other therapeutic interventions such as antispastic medications or rehabilitation procedures.

When used as an adjunct, ESWT is typically introduced after botulinum toxin type A administration (most commonly within 1 to 2 weeks postinjection) once early chemodenervation has begun to take effect. This timing aims to maximize the potential synergistic interaction between the 2 approaches. The rationale for combination therapies lies in their distinct yet complementary mechanisms of action: botulinum toxin primarily acts on the neural component of spasticity by blocking acetylcholine release at overactive motor endplates, thereby reducing neural hyperexcitability, whereas ESWT exerts both rheological and microvascular effects that improve muscle compliance, modulate neuromuscular junction function, and enhance tissue perfusion. Together, these mechanisms can potentiate tone reduction, alleviate stiffness related to nonneural factors, and prolong the duration of clinical benefit. Evidence from randomized controlled trials supports this synergistic approach of combined ESWT with botulinum toxin type A as a biologically plausible and clinically effective strategy that addresses both neural and mechanical components of spasticity. ^,,,,

Transcutaneous electrical nerve stimulation (TENS) is a noninvasive neuromodulation technique that delivers brief electrical pulses through surface electrodes to activate large-diameter cutaneous afferents, primarily A-beta fibers. In individuals with upper motor neuron lesions, TENS mitigates spasticity through several converging mechanisms, including enhancement of presynaptic (D1) inhibition within spinal circuits, facilitation of reciprocal inhibition, modulation of stretch-reflex excitability, and improved sensorimotor integration. ^, High-frequency stimulation (≥50–100 Hz) at sensory intensity selectively recruits A-beta fibers and, to a lesser extent, A-delta afferents, thereby diminishing α-motor-neuron overactivity without inducing visible muscle contraction. Frequencies around 200 Hz appear to potentiate D1 inhibition further, reflecting a spinal mechanism that suppresses reflex hyperexcitability. Neurophysiological studies support these effects, reporting reductions in H-reflex amplitude, decreased Hmax/Mmax ratios, and prolonged reflex latency (all consistent with lower motor-pool excitability). ^,,

Clinically, TENS has demonstrated significant efficacy in reducing limb spasticity when used as an adjunct to physiotherapy compared with placebo. The most consistent improvements are observed when sessions exceed 30 minutes, and stimulation is applied over the nerve trunk or muscle belly (both electrode placements proving effective and well tolerated). Comparable results have been obtained across high-frequency (≈100 Hz) and low-frequency (5–20 Hz) protocols, suggesting that therapeutic benefit depends more on sufficient session duration and integration with rehabilitation than on stimulation frequency alone.

When combined with pharmacologic agents, particularly botulinum toxin type A, TENS may amplify and prolong therapeutic outcomes through complementary mechanisms. Botulinum toxin acts peripherally by blocking acetylcholine release at the neuromuscular junction, reducing excessive muscle activation and neural-driven tone. In contrast, TENS primarily modulates central and spinal excitability by reinforcing presynaptic inhibition, facilitating reciprocal inhibition, and promoting adaptive sensorimotor reorganization. The simultaneous engagement of these neural pathways provides a physiologic rationale for synergistic use. From a practical perspective, TENS is typically introduced one to 2 weeks after botulinum toxin injection, coinciding with the onset of chemodenervation. Applied over the nerve trunk or muscle belly of the injected region (generally for 30–60 minutes, 5 times per week, over 2 to 4 weeks), TENS may potentiate and extend the toxin’s effects by sustaining descending inhibitory control and preserving neural adaptations induced by pharmacologic treatment. ^, Clinical studies indicate that this combined approach yields greater reductions in muscle tone, enhanced motor performance, and longer-lasting functional gains than toxin alone, reinforcing its role as a safe, accessible, and cost-effective adjunct in spasticity management.

Neuromuscular electrical stimulation (NMES) involves applying surface electrodes over the motor points of target muscles to evoke visible, controlled contractions. Within the spectrum of upper motor neuron syndromes, NMES influences both neural and nonneural mechanisms underlying spasticity. Repeated electrically induced contractions increase Ia afferent input in a patterned way that enhances presynaptic inhibition, facilitates reciprocal inhibition between agonist–antagonist pairs, and reduces stretch-reflex excitability at the spinal level. ^,, At the cortical level, sustained sensory–motor feedback promotes neuroplastic reorganization and improved sensorimotor integration, which may lessen co-contraction and support more refined voluntary control. Meanwhile, the repetitive, low-load contractions produce peripheral benefits by improving muscle elasticity, blood flow, and extracellular matrix remodeling, thereby counteracting stiffness and preventing early contracture. ^,, Through this dual action, NMES serves as a bridge between neural modulation and mechanical conditioning.

When applied as a standalone rehabilitation modality, NMES can directly reduce spasticity and maintain soft tissue flexibility. Typical protocols involve sessions lasting 30 to 60 minutes, delivered 3 to 5 times per week for 2 to 6 weeks. Optimal outcomes are achieved when NMES is incorporated into broader rehabilitation programs that include stretching, strengthening, and task-specific training, facilitating both tone reduction and functional recovery.

When combined with botulinum toxin injection, NMES provides a synergistic enhancement of therapeutic effects through complementary physiologic mechanisms. Botulinum toxin type A acts peripherally by blocking acetylcholine release at the neuromuscular junction via receptor-mediated internalization and SNAP-25 cleavage. This activity-dependent uptake occurs within minutes after injection, offering a rationale for immediate postinjection NMES. Delivering stimulation during this short uptake window accelerates toxin binding and internalization at cholinergic terminals, amplifying and prolonging chemodenervation. Evidence from clinical and experimental studies indicates that a single 30 to 60 min NMES session applied immediately after injection produces the most effective biological response. ^,, Early stimulation optimizes botulinum toxin absorption, whereas delayed application (initiated hours or days later) yields only the general antispastic effects of NMES rather than a true booster effect. ^,