Spasticity is a chronic, disabling motor symptom resulting from central nervous system lesions, characterized by a velocity-dependent increase in muscle tone and exaggerated stretch reflexes. Poststroke spasticity (PSS) is the most prevalent and widely studied etiology, affecting up to 43% of stroke survivors within the first year. ^, PSS significantly contributes to disability, particularly in those with severe motor impairment or delayed rehabilitation, and often coexists with weakness and poor postural control, which limits activity and participation. In multiple sclerosis (MS), spasticity affects 40% to 80% of patients, depending on disease stage, and contributes to impaired mobility, gait dysfunction, and fatigue, often requiring combined pharmacologic and rehabilitative treatment. ^, In cerebral palsy (CP), spasticity is the hallmark of the most common subtype, affecting 75% to 80% of individuals due to early, nonprogressive brain injury. It frequently coexists with dystonia and weakness, necessitating individualized, multidisciplinary management throughout life. ^, Spinal cord injury (SCI) is also associated with high spasticity prevalence, particularly in chronic stages. The quadriceps femoris muscle is commonly affected, regardless of lesion severity, and reflects spinal disinhibition and segmental hyperreflexia. Additionally, in SCI, spasms are often present, and their occurrence is commonly associated with walking disability. In particular, extensor spasm severity directly correlates with pain intensity below the lesional level and with poorer walking capability measured with the walking index for SCI. Interestingly, this relation does not seem to be established with flexor spasms.

Reframing spasticity as a chronic neurologic condition carries key clinical and systemic implications. It requires long-term care models that extend beyond acute rehabilitation, focusing on functional recovery, prevention of complications, and sustained quality of life. Within this paradigm, spasticity resembles other noncommunicable chronic diseases: persistent, progressive, and requiring individualized treatment to preserve independence and participation.

Furthermore, spasticity is a dynamic condition that evolves over time under the influence of neural, muscular, and systemic factors. In stroke populations, it may appear weeks to months post-event and progress, particularly in patients with incomplete recovery or limited rehabilitation access. Its course often shifts from a neural to a mixed pattern, with growing contributions from muscular changes such as stiffness, fibrosis, and fatty infiltration. Age-related dynapenia further accelerates mobility decline in those with pre-existing motor deficits. Morphofunctional changes, including reduced gait speed and increased muscle echogenicity, reflect chronic neuromuscular adaptation that worsens over time and correlates with diminished functional capacity. ^,

These progressive changes support the need for a proactive, continuous, and individualized treatment strategy. Chronic management can improve mobility and symptoms, particularly when combined with physical therapy, strength training, stretching, and orthotic support. ^, Long-term care planning is thus essential to mitigate complications, preserve motor function, and support autonomy. Like other chronic conditions, spasticity requires a rehabilitation approach centered on continuity and sustained outcome maintenance throughout life.

Chronic spasticity, particularly after upper motor neuron lesions such as stroke, triggers a cascade of morphostructural changes and functional limitations that progressively impair outcomes. Rather than static, spasticity evolves through neurogenic hyperactivity and secondary alterations in muscular and connective tissue, leading to stiffness, weakness, and restricted mobility.

Morphologically, spasticity causes muscle atrophy, particularly on the paretic side, alongside shifts in fiber type from type II to type I, which reduces contractile force and endurance. Alterations in fascicle length and pennation angle further compromise muscle function. These architectural changes are often irreversible and contribute significantly to disability.

Extracellular matrix (ECM) remodeling also plays a key role. Increased collagen and high-molecular-weight hyaluronan reduce fascial gliding and fiber extensibility, heightening stiffness and promoting fibrosis and joint contractures. This structural rigidity limits mobility even in the absence of active hypertonia.

Ultrasound and elastography studies confirm these findings, showing increased echogenicity indicative of fat infiltration and fibrosis. This imaging profile correlates with reduced responsiveness to interventions and aids in assessing muscle reversibility, as exemplified by the Stiffness-Echogenicity Matrix.

Functionally, these adaptations impair voluntary movement and postural control. Abnormal stretch resistance disrupts agonist recruitment, synergy timing, and inter-joint coordination. In chronic stroke, spasticity contributes to lower-limb gait deviations—equinovarus foot, stiff-knee gait, knee hyperextension, and circumduction—which are inefficient, painful, and destabilizing.

To overcome these deficits, patients adopt compensatory strategies such as hip hiking, vaulting, and pelvic tilting. While initially helpful, they increase energy expenditure and increase the risk of overuse injuries, potentially leading to maladaptive patterns and further functional decline.

Upper limb function is similarly affected. Spastic co-contractions, especially in flexor synergy patterns, often prevent effective hand use, particularly when combined with soft tissue shortening of wrist and finger flexors. Minimal voluntary movement becomes ineffective due to mechanical resistance and pain.

Chronic spasticity significantly reduces health-related quality of life, with patients reporting worse outcomes across SF-36, EQ-5D, and Stroke Impact Scale domains. Pain, fatigue, dependence, and reduced mobility are key drivers. Psychosocial consequences include emotional distress, frustration, and social isolation, often exacerbating depressive symptoms and reducing rehabilitation adherence.

Additionally, caregivers often experience excessive burden. Deformities and contractures can significantly impact daily care tasks, leading to increased caregiver burden, emotional fatigue, and a higher risk of burnout.

Effective long-term spasticity management relies on clear, patient-centered goals. In chronic neurologic conditions, where functional limitations evolve gradually and are shaped by personal and contextual factors, defining realistic and individualized goals is essential. A structured goal-oriented approach aligns treatment with patient priorities, supporting both clinical outcomes and satisfaction.

A feasible tool is the goal attainment scaling (GAS), adapted from mental health outcomes research, which is widely used in many parts of the world to quantify personalized outcomes in spasticity care. It involves predefined goals scored on a 5-point scale, enabling meaningful outcome measurement beyond standard clinical tools and focusing care on what matters most to the patient.

Observational studies confirmed the feasibility and responsiveness of GAS in real-world settings. Among over 1000 patients treated with botulinum toxin type A (BoNT-A) and multidisciplinary care, GAS captured improvements in domains such as ease of care, pain, function, and mobility, which are often underrepresented in conventional assessments. Furthermore, GAS allows for the assessment of clinicians’ accuracy in determining the correct leeway for therapeutic potential.

To support implementation of GAS, the GO-FAST tool guides clinicians in defining SMART goals, selecting target muscles, and integrating interventions such as BoNT-A, stretching, orthoses, and strengthening. This facilitates structured decision-making and team communication.

Together, GAS and GO-FAST promote a shift from impairment-based care to a function-oriented model aligned with the ICF framework. Goals—such as ambulation with an orthosis, independent transfers, or reduction of caregiver burden—are often more meaningful than changes in tone or range of motion.

Effective goal setting also requires ongoing dialogue and adjustments based on disease progression, comorbidities, and psychosocial context. Balancing realism and optimism ensures that goals remain motivating and achievable, reinforcing rehabilitation as a dynamic process focused on optimizing function, participation, and quality of life over time.

BoNT-A has emerged as a first-line pharmacologic intervention in the long-term management of focal and multifocal spasticity. Its role extends far beyond temporary symptom relief, encompassing chronic modulation of muscle overactivity, prevention of secondary complications, and enhancement of functional performance when integrated within a multidisciplinary rehabilitation program. In chronic spasticity, particularly in poststroke, CP, MS, and SCI, BoNT-A offers the flexibility to adapt treatment plans to changing functional demands over time. This aspect is due to its pharmacologic characteristics.

BoNT-A acts by inhibiting acetylcholine release at the neuromuscular junction, inducing transient and reversible chemodenervation, which leads to temporary muscle relaxation. The action onset typically occurs within 3 to 7 days postinjection, with peak effects around 4 weeks, and is followed by a gradual decline over 3 to 6 months, depending on the formulation and dose. This predictable pharmacokinetic profile enables cyclical, individualized administration, aligning with evolving patient goals and therapeutic windows.

Numerous studies have demonstrated that repeated BoNT-A injections yield cumulative functional benefits, particularly when combined with rehabilitation. In poststroke patients, longitudinal improvements in walking speed, passive range of motion, and Modified Ashworth Scale scores have been reported following serial treatments. A recent study demonstrated significant gains across multiple injection cycles in individuals with chronic poststroke conditions, even in late recovery phases.

In chronic spasticity, morphostructural changes in muscle tissue are both a consequence of the disease and a target of intervention. On the other hand, it has been hypothesized that chronic exposure to BoNT-A can modulate and potentially exacerbate some of these changes. Histologic studies in both animal and human models report muscle fiber atrophy, alterations in fiber-type composition, and increased ECM following BoNT-A injection. ^,

However, interpreting these structural effects requires caution. Some changes may indicate underlying pathology rather than toxin-induced damage. For example, Fridén and Lieber demonstrated that spastic muscles in CP are inherently stiffer and shorter, even in BoNT-A-naïve patients, highlighting that disease-related maladaptation must be considered.

Additionally, muscle tissue changes such as a reduction in fiber cross-sectional area and a shift from type IIx to type I and IIa fibers have been observed 3 months after BoNT-A injection in the medial gastrocnemius of naïve children with CP. These changes seem to decrease 6 months after treatment and were less severe than those reported in animal models.

Even in adult stroke survivors who undergo multiple cycles of BoNT-A treatment over many years, muscle fibroadipose degeneration and overall structural decline seem to rely on residual walking ability and the severity of spasticity. This finding may suggest that maintaining a higher functional level, also due to stable spasticity control with BoNT-A, can help preserve muscle structure.

The relationship between BoNT-A and muscle strength is a nuanced and frequently debated topic. On one hand, chemodenervation inherently leads to reduced voluntary contraction in injected muscles. On the other, reduced spastic co-contraction can facilitate more efficient movement, improve motor selectivity, and reduce fatigue. Clinical studies show that BoNT-A does not consistently impair global strength or function—particularly when injections target antagonistic muscles or when rehabilitative strategies are integrated post-injection. ^, Therefore, careful muscle selection, timing, and dosing remain critical to minimize unwanted weakening, especially in weight-bearing or stability-related muscles.

The safety and tolerability of long-term BoNT-A use have been thoroughly studied and are generally excellent. Adverse effects are rare and usually mild, including local pain, temporary fatigue, or minor systemic symptoms. Serious complications—such as widespread weakness or difficulty swallowing—are more commonly linked to overdosing, improper targeting, or off-label use, and remain rare with current standard practices. There is concern that repeated use might lead to neutralizing antibodies, which could decrease effectiveness, but the occurrence is very low when using purified preparations at regular intervals and doses. Switching formulations or considering different serotypes may help restore response if clinical nonresponse occurs. ^,

To fully unlock the therapeutic potential of BoNT-A in managing chronic spasticity, its application must be integrated into a comprehensive rehabilitation framework that addresses the multifactorial aspects of the condition and promotes long-term functional improvement. Numerous studies and international guidelines stress that BoNT-A alone is not sufficient to achieve the best outcomes in chronic spasticity. Instead, the toxin should be seen as a window of opportunity during which targeted rehabilitation can use temporary muscle relaxation to encourage neural plasticity, restore joint mobility, and develop effective motor patterns. Rehabilitation strategies should therefore be planned proactively around the timing and objectives of BoNT-A treatment. Stretching is one of the most frequently employed adjunct therapies following BoNT-A injection. Both manual and device-assisted stretching protocols have shown efficacy in maintaining muscle length, reducing passive stiffness, and slowing the progression of soft tissue contractures in spastic muscles. The effects are magnified when performed during the period of chemodenervation and sustained through consistent repetition. Evidence supports the use of serial casting or dynamic splinting in conjunction with BoNT-A to achieve sustained elongation of shortened musculotendinous units. ^,

Strengthening programs represent another critical component of integrated spasticity care. Contrary to historical concerns, resistance training does not exacerbate spasticity and may, in fact, reduce reflex hyperexcitability and improve voluntary control. ^, Strengthening is particularly important in chronic stages, where deconditioning, disuse atrophy, and BoNT-A-related weakness may coexist. Recent studies support the safety and benefit of eccentric training protocols in individuals with chronic hemiparesis, showing improvements in motor output, balance, and walking speed without increasing muscle tone. Eccentric loading, which involves lengthening contractions, is particularly relevant in spastic muscles with shortened resting lengths, as it provides both neural and mechanical stimuli for adaptation.

Functional task training should be prioritized as a key pillar of post-injection rehabilitation. Engaging patients in repetitive, goal-oriented activities such as walking, sit-to-stand transfers, or reaching tasks helps reinforce motor learning during periods of reduced spastic interference. This principle is supported by international clinical practice guidelines (NICE, ISWP, ESO), which strongly recommend task-specific training for both upper and lower limbs after stroke.

Another peculiar treatment strategy is guided self-rehabilitation contracts (GSCs). In this context, a personalized program of home-based stretching exercises demonstrated to improve the composite active range of motion, if combined with abobotulinumtoxinA injections, both in the upper and in the lower limb. Additionally, the diary-based monitoring and the contractual nature of this technique provided an elevate patients and clinicians’ satisfaction, increasing treatment adherence and patients’ active involvement and motivation in the care process. Thanks to this feature, a systematic deployment of GSCs could deliver a broader dissemination of rehabilitation effects. Particularly, in the chronic phase after stroke, in which in-clinic treatment is often difficult to maintain due to higher costs, lack of resources, and possible imbalance between costs and benefits, promoting patients’ empowerment could provide a steadier maintenance of functional outcomes.

Orthotic devices play an important role in the post-BoNT-A phase. Their use should be guided by specific functional goals and tailored to the patient’s neurologic and orthopedic profile. Recent advances in 3D-printed and dynamic orthoses have further enhanced comfort and compliance, enabling continuous wear during daily activities.

Neuromuscular electrical stimulation (NMES) and robot-assisted therapy represent other modalities that can complement BoNT-A and facilitate recovery of voluntary movement. NMES can be applied to antagonistic muscles to rebalance tone and improve coordination, while robotic gait or arm training can enhance intensity and repetition in task execution—both key drivers of neural reorganization. ^,

The choice of multimodal non-pharmacological therapy should also be provided in a goal- and target-oriented scenario. Notably, the various mentioned tools act on different aspects of spasticity physiopathology and clinical manifestation, and the combination of techniques may better address antagonist strength, rheological properties of spastic muscles, articular range of motion, motor control, pain reduction, hypertonia reduction, or spinal motor neuron excitability. Generally speaking, the neural pathways could benefit from electrical stimulation, transcranial magnetic stimulation, drugs (such as BoNT-A or baclofen), transcutaneous electrical nerve stimulation, and extracorporeal shock wave therapy. On the other hand, nonneural aspects can be targeted with casting, splinting, stretching, transcutaneous electrical nerve stimulation, extracorporeal shock wave therapy, and robotic training.

It should be noted that said strategies need to be considered in the context of a multimodal treatment approach and not only as adjunctive treatment. Indeed, multimodal spasticity management, involving both pharmacologic and non-pharmacologic strategies (simultaneously or in succession) and targeting both neural and nonneural components, is determined in advance through goal-setting and clinical assessment. In contrast, adjunctive therapies refer to interventions chosen to enhance the effectiveness of a primary treatment, typically administered after the main intervention has been delivered. In some cases, adjunctive therapies may be considered part of a multimodal approach.

Moreover, timing is critical. Several studies suggest that the most robust functional gains occur when rehabilitation is initiated within the first 7 to 10 days post-injection, corresponding to the early phase of BoNT-A action. Delayed rehabilitation may fail to capitalize on the transient reduction in tone, leading to suboptimal outcomes. As such, coordination among physiatrists, therapists, and orthotists is essential to ensure the timely implementation of the rehabilitation plan.

Despite the substantial progress achieved in the pharmacologic and rehabilitative management of chronic spasticity, a significant unmet need remains in terms of individualized care, durable functional outcomes, and the biological modulation of maladaptive plasticity. Advances in neurorehabilitation research and technology are progressively redefining what is possible in long-term care for individuals with spasticity. Several emerging strategies, including neuromodulation, robotics, and biomarker-guided interventions, offer promising avenues for enhancing treatment efficacy, extending therapeutic windows, and achieving more durable changes in motor function and quality of life. Even simpler strategies may provide interesting results. For example, high-velocity training, consisting of plyometric exercise and procedures stimulating high movement speed similar to playing activities, has been shown to improve muscle strength, gait speed, and overall functional mobility in children with CP. ^,

Technological advances are transforming the way spasticity care is delivered. Robotics and sensor-based devices now enable precise measurement of joint stiffness, muscle resistance, and voluntary control. These technologies provide objective outcome metrics that surpass traditional clinical scales, allowing for more detailed monitoring of progression and responses to interventions. Digital health technologies are also becoming increasingly relevant. Wearable sensors, remote monitoring platforms, and mobile applications offer novel ways to track patient progress, support self-management, and guide home-based rehabilitation. These tools are especially valuable in the context of long-term care, where continuity, adherence, and patient engagement are crucial for sustaining therapeutic gains.

On the biological front, increased attention is being given to the muscle tendon unit as a dynamic and modifiable structure. Research using ultrasound elastography and MRI is refining our understanding of muscle stiffness, fibrosis, and architectural remodeling in spasticity. Moreover, investigations into molecular biomarkers of spasticity and denervation, such as changes in inflammatory markers, gene expression profiles, and muscle histology, may 1 day enable clinicians to predict treatment responses and customize interventions based on biological factors.

In the context of a chronic and long-term follow-up, the role of intrathecal baclofen (ITB) is noteworthy. In children with CP, ITB has been shown to improve body functions, such as pain, ease of care, social participation, mental health, and a significant therapeutic goal reaching even during adulthood. The effect onset typically occurs 6 months after implantation, when reaching a plateau phase, and the highest level of benefit seems to be delivered in nonambulatory patients. Even in adult stroke survivors, ITB plays a considerable role in reducing pain and improving perceived quality of life from 6 months after implant. When conservative treatment reaches its limits and structural modification is necessary, a valid treatment option is functional surgery. In this context, guidelines are scarce, and therapeutic approaches may vary significantly. The most important aspect before addressing surgery is an accurate clinical evaluation, differentiating between muscle and tendon contractures and muscle overactivity. In this scenario, motor nerve blocks, dynamic electromyography, and 3 dimensional gait analysis are necessary for a correct differential diagnosis. In particular, in stroke survivors, surgical correction of spastic equinovarus foot could improve walking, spatial and temporal parameters, foot clearance, and better stance support. Even though ankle power may decrease both in the absorption and push-off phases, the gained stability could compensate for the deficit.

Finally, a broader cultural and clinical shift is occurring in the conceptualization of spasticity itself. No longer viewed solely as a symptom to suppress, chronic spasticity is now recognized as a complex, dynamic condition requiring a longitudinal, personalized, and multidimensional approach. This shift echoes recent calls for integrating spasticity care into chronic disease management models, with a focus on prevention, functional maintenance, and quality of life over time.

In this framework, the true impact of an efficient and effective treatment program became evident when, due to the COVID-19 pandemic, access to spasticity care was limited. The postponement of reassessment visits and therapeutic interventions resulted in increased self-reported stiffness, decreased independence, and a reduced quality of life, affecting all ICF domains. This is especially true in relation to BoNT-A discontinuation. This point should be recognized as crucial, shifting the focus from just the symptom to the person.