What is spasticity in cerebral palsy?

Spasticity is a velocity-dependent increase in muscle tone — meaning the faster a limb is moved, the greater the resistance encountered. In cerebral palsy (CP), it occurs because the brain damage that causes CP removes the motor cortex’s ability to properly regulate muscle signals, leaving specific muscle groups in a state of persistent over-activation.

In daily life, a child with spastic CP may:

• Walk on tiptoe rather than with a flat foot, because the calf muscles are too tight to allow normal ankle flexion
• Cross their legs in a “scissor” walking pattern, due to tight hip adductor muscles pulling the thighs inward
• Hold one or both hands in a clenched fist that is difficult to open voluntarily
• Show jerky or exaggerated startle responses when moved quickly
• Demonstrate a “crouched gait” — walking with persistently bent knees due to tight hamstrings and hip flexors

It is important to distinguish spasticity from other motor abnormalities in CP. Dystonia involves uncontrolled, twisting involuntary movements. Ataxia refers to problems with coordination and balance. Spasticity specifically refers to velocity-dependent muscle hypertonicity caused by upper motor neuron damage — and it responds to specific treatments that are distinct from those used for dystonia or ataxia.

What causes spasticity in cerebral palsy?

The brain injury or abnormal brain development that causes cerebral palsy typically affects the corticospinal tract — the primary pathway that carries voluntary motor control signals from the brain’s motor cortex down to the spinal cord and then to the muscles. When this pathway is damaged, two interlocking changes occur:

1. Loss of descending inhibition. In a healthy nervous system, the brain continuously sends inhibitory signals down to the spinal cord’s reflex circuits, dampening their sensitivity and preventing muscles from overreacting to sensory stimuli. When the corticospinal tract is disrupted, these inhibitory signals are reduced or absent.
2. Hyperactive stretch reflexes. Without the brain’s restraining influence, the spinal cord’s muscle stretch reflex becomes hypersensitive. Any quick stretching of a muscle — even during normal movement — triggers an exaggerated reflex contraction. This is the observable, measurable phenomenon of spasticity.

The location of the brain lesion determines which muscles are affected:

• Spastic diplegia — both legs primarily affected; most commonly linked to periventricular leukomalacia (PVL), damage to white matter near the brain’s ventricles, frequently associated with premature birth.
• Spastic hemiplegia — one side of the body affected; often caused by a unilateral brain injury, hemorrhage, or stroke in the perinatal period.
• Spastic quadriplegia (tetraplegia) — all four limbs and typically the trunk affected; usually results from more extensive bilateral brain damage and is associated with the greatest functional impact.

An important distinction: the brain injury that causes CP is non-progressive — it does not worsen over time. However, the secondary consequences of spasticity — joint contractures, bone deformities, hip dislocation — can and do progress as the child grows, which is precisely why early treatment is so critical.

How spasticity affects daily life

Spasticity is not merely a clinical measurement. For children and adults with cerebral palsy, it translates into real, daily challenges that touch nearly every aspect of life — movement, independence, pain, social participation, and long-term physical health.

Gait and mobility

Tight muscles in the hips, knees, and ankles fundamentally alter walking patterns, producing the characteristic gait abnormalities of spastic CP. These abnormal movement patterns are less mechanically efficient than typical gait, dramatically more fatiguing, and create abnormal forces on joints that were not designed to bear load in these positions.

Secondary musculoskeletal complications

If spasticity goes inadequately treated during childhood, the continuously overactive muscles exert abnormal pulling forces on bones and joints through the growth years. The consequences include:

• Joint contractures — muscles and tendons permanently shorten, fixing joints in abnormal positions that restrict movement even after spasticity is later treated
• Hip displacement and dislocation — tight hip adductors and flexors progressively pull the femoral head out of the acetabulum; a painful complication common in spastic quadriplegia that can require major reconstructive surgery
• Scoliosis — asymmetric muscle tone around the spine creates lateral curves that worsen during adolescence and can become severe enough to impair breathing and seated posture
• Rotational bone deformities — long-term abnormal forces during bone growth lead to torsional deformities of the femur and tibia that further impair gait alignment

Pain and fatigue

Spastic muscles are muscles in a state of constant, low-grade overwork. This produces chronic muscular fatigue, cramps, and — particularly in older patients — persistent pain in affected limbs and joints. Pain can become a primary barrier to participation in rehabilitation, creating a cycle in which inadequate spasticity treatment leads to less effective therapy, which leads to less functional progress.

Upper limb and communication impact

In children with spastic hemiplegia or quadriplegia, spasticity in the hand, wrist, and arm limits self-care, writing, feeding, and use of assistive technology. When spasticity involves the muscles of the mouth, jaw, larynx, and tongue — called bulbar spasticity — it affects speech clarity and the development of effective communication.

How spasticity is diagnosed

Quantifying spasticity requires a structured clinical examination, sometimes supplemented by instrumental assessment to guide treatment planning.

Modified Ashworth Scale (MAS)

The most widely used bedside tool, the MAS grades resistance to passive movement on a scale from 0 (no increase in muscle tone) to 4 (affected part is rigid in flexion or extension). It is quick, requires no equipment, and reproducible across clinical settings.

Observational gait analysis

A trained clinician systematically observes the patient’s walking pattern, identifying specific gait deviations and the muscle groups functionally responsible. This does not always correlate directly with MAS scores — some patients have objectively high scores but retain reasonable walking ability, while others with lower scores face more significant functional barriers.

Instrumented (3D) gait analysis

For complex surgical planning, a full three-dimensional computerized gait analysis uses motion capture cameras, ground reaction force plates, and electromyography (EMG) to provide precise data on joint angles, forces, and muscle activation timing throughout the gait cycle. This enables surgeons to identify exactly which muscles require intervention and to predict the functional impact of each possible procedure.

Neuroimaging

Brain MRI characterizes the type, location, and extent of the underlying cerebral injury — information that informs prognosis, predicts which muscle groups are at risk, and helps guide families’ expectations about the likely functional ceiling after treatment.

Treatment options: the full spectrum

Effective spasticity management in cerebral palsy is rarely a single intervention. The strongest outcomes come from a carefully tailored combination of treatments, delivered by a coordinated multidisciplinary team and adjusted as the patient grows and their needs evolve. Below is the full range of available options, organized from least to most invasive.

1. Physical therapy and rehabilitation

Physiotherapy is the cornerstone of spasticity management at every stage and should begin as early as possible — even in infancy, before spasticity has fully established itself. Core goals include maintaining and improving joint range of motion, strengthening the opposing (antagonist) muscles, preventing contracture formation, and optimizing functional movement patterns.

Effective physiotherapy approaches include:

• Passive and active stretching — regular, sustained elongation of spastic muscles to counteract their tendency to permanently shorten
• Strengthening exercises — building antagonist muscles to create better movement balance around spastic joints
• Constraint-induced movement therapy (CIMT) — for hemiplegia, restraining the unaffected limb to intensively promote use and cortical reorganization in favor of the affected side
• Hydrotherapy — warm water temporarily reduces muscle tone and facilitates movement, used therapeutically for range-of-motion work and motor skill practice
• Ankle-foot orthoses (AFOs) — maintain proper joint positioning and prevent contractures between therapy sessions
• Massage therapy — particularly valuable under 2 years of age, before surgery is appropriate, to minimize the progression of muscle shortening

2. Oral medications

Several oral drugs can reduce global muscle tone by acting centrally on the nervous system. Their systemic nature — affecting all muscles, not only spastic ones — limits their use in patients who need to preserve selective muscle function for daily activities.

• Baclofen — acts on GABA-B receptors to reduce spinal cord excitability; effective but associated with sedation, generalized weakness, and cognitive dulling at therapeutic doses
• Tizanidine — an alpha-2 adrenergic agonist; effective for moderate spasticity, associated with sedation and requires liver function monitoring
• Diazepam — enhances GABA-A activity; effective for acute episodes but problematic for long-term use due to tolerance and dependence
• Dantrolene — acts directly at the muscle level rather than the central nervous system, reducing muscle contraction strength; requires regular liver monitoring

3. Botulinum toxin A (Botox) injections

Injecting BTX-A into targeted spastic muscles temporarily reduces their activity by blocking acetylcholine release at the neuromuscular junction. Effects typically last 3–6 months and must be repeated. Botox is most useful for:

• Focal spasticity affecting a limited number of specific muscles
• Facilitating more effective physiotherapy by temporarily reducing tone
• Delaying the need for surgery in younger children not yet appropriate surgical candidates
• Managing residual spasticity in specific muscle groups after surgery

Repeated injections lose efficacy over time due to the development of neutralizing antibodies, and they cannot reverse contractures that have already developed.

4. Intrathecal baclofen pump (ITB)

For patients with severe whole-body spasticity — particularly those with spastic quadriplegia — a surgically implanted pump delivers baclofen directly into the cerebrospinal fluid around the spinal cord. This achieves far higher local drug concentrations with much lower systemic exposure than oral baclofen, providing better spasticity control with fewer side effects. The pump requires refilling every 2–3 months and carries risks of catheter complications, infection, and — critically — life-threatening baclofen withdrawal syndrome if the system fails.

5. Selective Dorsal Rhizotomy (SDR)

SDR is a major neurosurgical procedure in which specific lumbar sensory nerve rootlets in the spinal cord are selectively cut, permanently reducing the abnormal sensory drive that sustains lower limb spasticity. It can produce lasting spasticity reduction in carefully selected patients with spastic diplegia who are ambulatory and cognitively able to participate in intensive post-operative therapy.

SDR requires general anesthesia, spinal laminectomy, intraoperative electrophysiological monitoring, and a very intensive multi-year rehabilitation program. The ideal surgical window is typically between 3–8 years of age in children with pure spasticity and good baseline walking function.

6. Orthopedic procedures — tendon lengthening, SPML, and SFDM

Surgical interventions at the level of the muscles and tendons address both the spasticity itself and its secondary contractures and deformities:

• Traditional tendon lengthening — open surgery to elongate shortened tendons (Achilles, hamstrings, hip flexors, hip adductors); effective but involves visible scars, cast immobilization, and longer recovery
• Selective Percutaneous Myofascial Lengthening (SPML) — a minimally invasive evolution developed by Dr. Roy Nuzzo, using small percutaneous incisions with specialized instruments to lengthen muscle-fascial units without the invasiveness of open tendon surgery
• Selective Fibrotomy of Damaged Muscles (SFDM) — a further-developed minimally invasive approach created by Professor Vigein Tovmasian at the CP Clinic; described in detail in the next section

SFDM: minimally invasive surgical treatment for CP spasticity

Selective Fibrotomy of Damaged Muscles (SFDM) is a proprietary minimally invasive surgical technique developed by Professor Vigein Tovmasian, head surgeon at the CP Clinic in Vinnytsia, Ukraine — part of Tovmed Medical Center. It represents one of the most comprehensive and least traumatic surgical approaches currently available for treating the muscular manifestations of spasticity in cerebral palsy.

How the SFDM procedure works

SFDM is performed under general anesthesia and typically completed within one hour. The surgeon makes up to 40 microincisions — each just 2–3 mm in diameter — targeting all affected muscle groups simultaneously across multiple body segments in a single session. Each microincision is itself a microsurgery, precisely addressing the fibrotic (scarred and damaged) tissue within spastic muscles that restricts their extensibility and normal function.

Because the incisions are so small, no sutures (stitches) are required. The procedure leaves no significant visible scars. Patients can typically be discharged the same day, within 12 hours of the surgery concluding.

Who is suitable for SFDM?

SFDM is appropriate for patients who:

• Have a diagnosis of cerebral palsy with mobility limitations attributable to muscle spasticity
• Are at least 24 months (2 years) of age — the minimum at which spasticity is sufficiently established to make surgical intervention effective
• Are medically fit for general anesthesia

There is no maximum age limit. The clinic has successfully treated patients up to 60 years old with meaningful improvements in function and quality of life. International patients are assessed remotely via telemedicine — submitting videos of their movement limitations and a medical questionnaire — before traveling for treatment.

Expected outcomes

Outcomes are closely related to the severity of the patient’s CP and their age at treatment. In mild to moderate spastic CP with well-preserved cognitive development, SFDM surgery followed by the individualized rehabilitation program can result in mobility that is practically indistinguishable from that of neurotypical peers. In more severe forms of CP, treatment goals are calibrated to achieve the greatest possible gains in independence, comfort, and quality of life.

The procedure carries a reported success rate of 98%, making it the primary procedure at the CP Clinic. Post-operative rehabilitation is conducted at the patient’s home, based on a personalized program designed by Professor Tovmasian during the final day of the clinic stay.

Read the full guide to the SFDM procedure →

Why early intervention changes outcomes

The single most influential factor in the outcome of spasticity treatment in cerebral palsy is timing. This is grounded in the neuroscience of brain and musculoskeletal development, not merely in clinical convention.

During early childhood, several biological processes make early intervention distinctly more effective:

• Contracture prevention — spastic muscles treated early, before significant shortening occurs, never develop the fixed contractures that would otherwise require far more invasive and complex surgery to address
• Motor learning during the critical window — when abnormal muscle tone is reduced during the prime years of motor development, children can learn typical movement patterns during a neurological period when the brain is most receptive to establishing new motor pathways
• Protecting bone development — bones grow in response to the forces placed on them during childhood; normalizing muscle forces early means bones are more likely to develop with proper alignment, significantly reducing the risk of hip dislocation, torsional deformities, and scoliosis
• Rehabilitation responsiveness — young children respond more rapidly to physiotherapy when spasticity has been effectively reduced; the combination of surgical spasticity reduction and intensive early therapy consistently produces better outcomes than either alone

This is the clinical basis for the approach at the CP Clinic: parents of children diagnosed with CP are strongly encouraged to pursue physiotherapy — particularly massage — as early as possible, and to seek specialist evaluation promptly once the child reaches 24 months of age. Every month of unnecessary delay during the critical early years represents a real opportunity cost in potential functional outcome.

Frequently asked questions about cerebral palsy spasticity

References and clinical sources

1. Rosenbaum P, et al. (2007). “A report: the definition and classification of cerebral palsy April 2006.” Developmental Medicine & Child Neurology, 49(s109), 8–14. PubMed ↗
2. Sanger TD, et al. (2003). “Classification and definition of disorders causing hypertonia in childhood.” Pediatrics, 111(1), e89–e97. PubMed ↗
3. Novak I, et al. (2020). “State of the Evidence Traffic Lights 2019: Systematic Review of Interventions for Preventing and Treating Children with Cerebral Palsy.” Current Neurology and Neuroscience Reports. PubMed ↗
4. Tedroff K, et al. (2018). “Long-term effects of selective dorsal rhizotomy in children with cerebral palsy: a systematic review.” Developmental Medicine & Child Neurology. PubMed ↗
5. Nuzzo R. (2020). “Selective Percutaneous Myofascial Lengthening.” PMC, National Library of Medicine. PMC ↗
6. Koman LA, et al. (2004). “Botulinum toxin type A in the management of cerebral palsy.” Pediatric Drugs, 6(4), 219–232. PubMed ↗
7. Pin T, et al. (2006). “The effectiveness of passive stretching in children with cerebral palsy.” Developmental Medicine & Child Neurology. PubMed ↗