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Spasticity in Multiple Sclerosis: Causes, Symptoms, and Modern Treatment Approaches

Spasticity — defined as increased muscle tone accompanied by “stiffness,” resistance to movement, and painful spasms — is one of the most common and functionally significant symptoms of multiple sclerosis (MS). According to large observational studies, various degrees of spasticity develop in most people with MS over the course of the disease, directly affecting gait, independence, and overall quality of life.

This article reviews what spasticity in MS is, why it occurs, how neurologists assess it, and which pharmacological and non-pharmacological treatments are currently recommended. We also discuss when intrathecal baclofen therapy (baclofen pump) and botulinum toxin injections are indicated, and outline emerging and experimental treatment directions. A Q&A section for patients is included at the end.

What Is Spasticity in Multiple Sclerosis?

The classical definition of spasticity is “a velocity-dependent increase in muscle tone with exaggerated tendon reflexes due to upper motor neuron damage.” In daily life, patients describe it as a feeling of “tight,” “rigid,” or “stone-like” muscles, painful spasms, or involuntary jerks triggered spontaneously or by movement.

In MS, inflammatory and degenerative damage to motor pathways in the brain and spinal cord disrupts the balance between excitatory and inhibitory influences on spinal reflex circuits. As a result, muscles receive excessive signals to contract, producing a characteristic pattern: increased tone, delayed relaxation, exaggerated reflexes, clonus, and pathological reflexes.

Epidemiological studies show that more than half of people with MS experience spasticity, and in progressive forms the prevalence approaches the vast majority. Patients may not identify spasticity as their primary complaint, but it often underlies difficulties with walking, dressing, and self-care, and increases the risk of falls.

How Spasticity Affects Gait and Daily Activities

Lower-limb spasticity is a major contributor to gait impairment in MS. Increased extensor tone in the hips and knees results in a “stiff,” straight-legged gait, reduced knee and ankle flexion, and spasms or clonus that cause unexpected “giving way” or leg “throwing” during a step.

In relatively mildly impaired patients, the earliest and most noticeable symptom may be foot dragging and foot drop — the inability to sufficiently lift the front of the foot during swing phase. Patients may still walk long distances but trip on uneven surfaces, fatigue quickly, and begin avoiding previously manageable activities.

With more pronounced spasticity, additional problems arise:

  • persistent tightness and cramping spasms,
  • pain worsened by attempts to stretch or flex a limb,
  • difficulties rising from a chair, turning in bed, or shifting weight,
  • problems with hygiene and dressing,
  • higher risk of contractures and joint deformities if untreated.

It is important to note that spasticity is not always purely harmful — in some individuals, mild tone helps compensate for significant weakness and allows standing or walking. Therefore, the goal of treatment is not to “eliminate spasticity,” but to find the optimal balance between reducing excessive tone and preserving functional stability.

How Neurologists Assess Spasticity: Scales and Tools

Assessment is always multifaceted and typically includes:

  • Neurological examination — evaluation of tone during passive movements, tendon reflexes, clonus, pathological reflexes, weakness, coordination, and sensation.
  • Standardized scales, most commonly:
    • Modified Ashworth Scale (MAS) — resistance to passive movement.
    • Tardieu Scale — considers velocity of stretch and presence of a catch.
    • Numeric Rating Scale for patient-reported spasticity and spasms.
  • Patient-reported questionnaires such as the PRISM scale, which assess pain, sleep, activity, and participation.
  • Gait analysis and functional walking tests (6-Minute Walk Test, Timed 25-Foot Walk), especially in patients with predominant lower-limb spasticity.

Regular standardized assessment allows clinicians to monitor progression, measure treatment response (medications, botulinum toxin, intrathecal therapy, physiotherapy), and promptly identify adverse effects.

Pharmacological Treatment of MS-Related Spasticity

The main goals of pharmacotherapy are:

  • reducing painful spasms and nocturnal jerks,
  • decreasing excessive tone interfering with movement and self-care,
  • improving or preserving function,
  • minimizing side effects (sedation, weakness, dizziness).

First-line medications

The most commonly recommended agents include:

  • Baclofen (baclofen) — a GABAB-receptor agonist that decreases spinal reflex activity. Side effects include sedation, weakness, and dizziness. Requires gradual titration and careful tapering.
  • Tizanidine (tizanidine) — an α2-adrenergic agonist effective for daytime and nocturnal spasms, with possible side effects such as drowsiness, dry mouth, hypotension, and liver enzyme elevation.
  • Gabapentin (gabapentin) — useful when spasticity coexists with neuropathic pain.
  • Diazepam (diazepam) — used sparingly due to sedation, coordination impairment, and dependence risk.
  • Dantrolene (dantrolene) — acts peripherally at the muscle level; requires liver function monitoring.

Choice of medication and dose is individualized. Not only tone reduction but also strength, balance, gait, cognition, and fatigue must be considered. Often the best result comes from a minimal effective combination that the patient tolerates well.

Cannabinoids (nabiximols and others)

For patients whose spasticity persists despite first-line agents, cannabinoid-based medications such as the THC/CBD oromucosal spray (nabiximols) may be considered where legally available.

Systematic reviews show a moderate but statistically significant improvement in subjective spasticity scores in some patients, although not all respond. Side effects include dizziness, coordination problems, and mood changes. Dose titration must be cautious.

Intrathecal Baclofen Therapy (Baclofen Pump)

In severe generalized spasticity that does not respond to oral medications or causes intolerable side effects at higher doses, intrathecal baclofen therapy may be recommended.

How the method works:

  • a pump with a drug reservoir is implanted under the skin (usually in the abdomen),
  • a catheter delivers baclofen directly into the cerebrospinal fluid,
  • this allows the use of doses many times lower than oral equivalents,
  • with more stable and pronounced tone reduction.

Before implantation, a test dose of intrathecal baclofen is administered to evaluate effectiveness and tolerability. If spasticity reduction improves comfort, positioning, or rehabilitation without excessive weakness, the pump may become a long-term component of treatment.

Risks include infection, catheter issues, overdose, or under-delivery. Therefore, indications must be discussed in a specialized center with a neurologist, rehabilitation specialist, and neurosurgeon.

Botulinum Toxin Therapy for Spasticity in MS

Botulinum neurotoxin type A (onabotulinumtoxinA, abobotulinumtoxinA and others) is one of the most effective and safest local treatments for focal and multifocal spasticity. The toxin blocks acetylcholine release at the neuromuscular junction, temporarily reducing muscle overactivity.

In MS, botulinum toxin injections are used for:

  • focal or multifocal lower-limb spasticity (equinus, inversion, flexor spasms),
  • upper-limb spasticity interfering with hygiene, dressing, or assistive device use,
  • painful tonic spasms and spastic deformities affecting quality of life.

Effect develops gradually over 7–14 days, peaks at 4–6 weeks, and lasts about 3–4 months. Repeated injections allow dose and muscle selection adjustments. Best outcomes occur when combined with physiotherapy, stretching, orthotics, and functional gait or upper-limb training.

Botulinum toxin can:

  • reduce tone without excessive weakness,
  • improve gait and weight transfer, including in foot drop,
  • improve hygiene and reduce skin complications and pain,
  • create a “window of opportunity” for rehabilitation.

Physiotherapy, Rehabilitation, and Specialized Programs

Non-pharmacological treatment is essential in MS-related spasticity. Systematic reviews show that physical activity and rehabilitation significantly reduce spasticity and improve function, especially when combined with medication.

Physiotherapy and exercise therapy

  • Individualized exercise programs focusing on stretching spastic muscles, strengthening antagonists, and training balance and coordination.
  • Robotic or assisted gait training to normalize gait patterns, reduce spasticity, and improve weight-bearing.
  • Functional electrical stimulation (including systems for correcting foot drop) to activate muscles at the appropriate phase of gait.
  • Vibration and shockwave modalities, which may provide temporary relief in selected patients.

Hydrotherapy (aquatic therapy)

Warm-water exercise is often well tolerated because water:

  • reduces joint loading and allows safe balance and gait training,
  • facilitates gentle stretching of spastic muscles,
  • improves endurance and confidence in movement.

Programs should be designed by a rehabilitation specialist familiar with MS-specific considerations (heat sensitivity, fatigue, balance impairment).

Hippotherapy and other specialized methods

Hippotherapy — therapeutic horseback-based movement — may help coordinate balance, core stability, and lower-limb tone patterns. Evidence is still limited, but it can be included as part of comprehensive MS rehabilitation.

Advanced and Experimental Methods

Several new approaches for MS-related spasticity are under active investigation:

  • Optimized botulinum toxin protocols — dose refinement, expanded indications, combination with electrical stimulation and robotic training.
  • Neuromodulation — non-invasive brain stimulation (rTMS, iTBS), spinal and peripheral nerve stimulation. Early studies show potential benefits, but methods remain experimental.
  • Advances in intrathecal baclofen delivery — improved pumps, individualized programming, and investigation of broader biological effects.
  • Spasticity-Plus concept — viewing spasticity as part of a broader cluster of symptoms (pain, spasms, sleep problems, bladder dysfunction) and addressing them together through integrated management.

Frequently Asked Questions

Can spasticity in MS be completely eliminated?

Complete elimination is rare, especially in long-standing MS with structural spinal cord changes. However, most patients achieve meaningful improvement in spasms, tone, gait, and sleep through a combination of medications, botulinum toxin, rehabilitation, and intrathecal baclofen when appropriate. The true goal is maximal comfort and functional independence.

Is long-term use of baclofen and other muscle relaxants safe?

With proper monitoring, baclofen, tizanidine, gabapentin, and related medications can be used safely long term. Important aspects include monitoring for sedation, weakness, blood pressure changes, and liver function (for some drugs). Abrupt withdrawal should be avoided. If side effects limit tolerability, botulinum toxin or intrathecal baclofen are alternatives.

When should a baclofen pump be considered?

A pump is considered in severe generalized spasticity that significantly limits sitting, transfers, hygiene, or turning in bed, and is not controlled by oral medications or requires intolerably high doses. A test dose is performed first. The final decision is made jointly in a specialized center with the patient and family.

Do exercise and hydrotherapy help, or are medications enough?

Medications are only part of the strategy. Without regular stretching, strengthening, balance training, gait practice, and assistive devices, pharmacological effects tend to be weaker. Aquatic therapy, physiotherapy, and functional electrical stimulation systems (including for foot drop) substantially enhance overall outcomes.

How is botulinum toxin different from oral medications?

Oral medications act systemically and are limited by side effects such as sedation. Botulinum toxin is a localized treatment targeting the specific muscles that impair walking, hygiene, or function, without affecting the rest of the body. The best strategy often combines low-dose oral therapy, botulinum toxin, and structured rehabilitation.

Is there a “magic pill” for spasticity?

There is no universal, side-effect-free medication that completely eliminates spasticity in MS. The most effective approach is individualized multimodal therapy: oral drugs, botulinum toxin, rehabilitation, intrathecal baclofen when needed, and active patient participation.

Key References

  1. Pandyan AD, Gregoric M, Barnes MP, et al. Spasticity: clinical perceptions, neurological realities and meaningful measurement. Disabil Rehabil. 2005;27(1–2):2–6. DOI: 10.1080/09638280400014576
  2. Patejdl R, Zettl UK. Spasticity in multiple sclerosis: contribution of inflammation, autoimmune mediated neuronal damage and therapeutic interventions. Autoimmun Rev. 2017;16(9):925–936. DOI: 10.1016/j.autrev.2017.07.004
  3. Rizzo MA, Hadjimichael OC, Preiningerova J, Vollmer TL. Prevalence and treatment of spasticity in MS patients. Mult Scler. 2004;10(5):589–595. DOI: 10.1191/1352458504ms1085oa
  4. Stevenson VL, Gras A, Bárdos JI, Broughton J. The high cost of spasticity in MS to individuals and society. Mult Scler. 2015;21(12):1583–1592. DOI: 10.1177/1352458514566416
  5. Otero-Romero S, Sastre-Garriga J, Comi G, et al. Pharmacological management of spasticity in MS: systematic review and consensus. Mult Scler. 2016;22(11):1386–1396. DOI: 10.1177/1352458516643600
  6. Etoom M, Khraiwesh Y, Lena F, et al. Effectiveness of physiotherapy on spasticity in MS: systematic review and meta-analysis. Am J Phys Med Rehabil. 2018;97(11):793–807. DOI: 10.1097/PHM.0000000000000970
  7. Amatya B, Khan F, Song K, Galea M. Effectiveness of non-pharmacological interventions for spasticity in MS. Ann Rehabil Med. 2024;48(5):305–343. DOI: 10.5535/arm.240064
  8. Azadvari M, Pourshams M, Guitynavard F, et al. Cannabinoids for spasticity in MS: systematic review and meta-analysis. Mult Scler J Exp Transl Clin. 2024;10(4):20552173241282379. DOI: 10.1177/20552173241282379
  9. Emami Razavi SZ, Azadvari M, Mirmosayyeb O, et al. Botulinum toxin injection for spasticity in MS: systematic review and meta-analysis. Middle East J Rehabil Health Stud. 2025;12(2):e156825. DOI: 10.5812/mejrh-156825
  10. Fernandez O, Costa-Frossard L, Martínez-Ginés ML, et al. Integrated management of MS spasticity and related symptoms using the Spasticity-Plus concept. Front Neurol. 2021;12:722801. DOI: 10.3389/fneur.2021.722801

Spasticity in multiple sclerosis is closely linked with gait impairment, balance problems, and fall risk. Modern treatment approaches include not only oral medications but also botulinum toxin injections, intrathecal baclofen therapy, physiotherapy, orthotic support, and individualized rehabilitation programs aimed at maintaining independence and quality of life.

Dr. Lidiia Prakhova
Author
Dr. Lidiia Prakhova
Neurologist, expert in demyelinating diseases, migraine and botulinum toxin therapy

Dr. Prakhova is a neurologist practicing in Israel. She consults patients with MS, NMOSD, MOGAD, chronic migraine, dystonia and spasticity.

  • Over 35 years of clinical experience in neurology.
  • Main specialization — demyelinating CNS diseases and migraine.
  • Experience with modern MS/NMOSD/MOGAD therapies.
  • Advanced botulinum toxin therapy training.
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