Spasticity Medication Guide: Which Treatment Works Best?
NeuroRehab Team
Thursday, December 11th, 2025
Multiple sclerosis patients report spasticity as a debilitating symptom, with 90% of cases showing this condition. The condition can progress beyond muscle tightness if left untreated. Patients may develop painful deformities, kyphoscoliosis, and contractures that can substantially affect their quality of life.
Spasticity’s severity ranges from mild muscle tightness to severe, uncontrollable stiffness. Painful spasms can interfere with daily activities. The good news is that patients have multiple treatment options. Oral medications remain common, but multimodal therapies with GRADE A evidence might deliver better outcomes than traditional oral medications. These traditional medications can sometimes slow down functional recovery. Recent network meta-analyzes of 1,930 patients show promising results. Botulinum toxin injections and shock wave therapies have demonstrated substantial improvements in reducing spasticity compared to control treatments.
This detailed guide explores the most effective spasticity treatments available in 2025. It compares everything from traditional medications to advanced interventions and emerging therapies. Healthcare providers and patients can make better decisions about managing this challenging condition by understanding each option’s benefits, limitations, and proper applications.
Understanding Spasticity and Its Impact
Spasticity stands as one of the toughest neurological symptoms patients face worldwide, affecting over 12 million people globally [1]. This complex condition makes muscles involuntarily tight and stiff, which can drastically affect mobility, independence, and quality of life.
What is spasticity?
Muscles stay contracted because of brain or spinal cord damage, which results in abnormal muscle tightness and involuntary contractions. Doctors define it as a velocity-dependent increase in muscle tone – the faster you move a muscle, the more it resists [2].
The condition develops from an imbalance between excitatory and inhibitory signals to alpha motor neurons [2]. Damage to the central nervous system disrupts normal communication that lets some muscles contract while others relax [3]. Many muscles contract at once, which makes controlled movement hard.
We see spasticity mostly in people with these neurological conditions:
- Multiple sclerosis (affecting up to 90% of patients) [4]
- Cerebral palsy (affecting approximately 80% of patients) [1]
- Stroke (affecting up to 45% of patients) [5]
- Spinal cord injury (affecting around 36% of patients) [5]
- Traumatic brain injury (affecting up to 50% of patients) [5]
How it affects daily life
Spasticity’s effects on daily functioning range from mild to severely debilitating. People with moderate to severe symptoms face substantial barriers to independence and comfort.
Common signs include:
- Muscle stiffness and tightness that limit movement
- Painful muscle spasms and contractions
- Abnormal posture and joint positioning
- Involuntary crossing of the legs
- Clonus (rapid, rhythmic muscle contractions)
- Exaggerated reflexes and the clasp-knife phenomenon [3]
These symptoms get in the way of simple activities. Research shows that spasticity most often disrupts stair climbing, walking, and sleep [5]. On top of that, it creates significant challenges with hygiene, dressing, eating, and other self-care tasks [4].
The psychological impact runs deep. Many adults with this condition pull away from others because of reduced mobility, increased fatigue, and pain [5]. A survey of multiple sclerosis patients showed that more than 35% struggled significantly with stiffness, spasms, or pain, mainly in their lower extremities [5].
Why treatment is essential
Untreated spasticity often progresses from muscle tightness to permanent structural changes. Joints develop contractures over time as muscles become permanently shortened and fixed [3]. This leads to further decreased mobility as joints freeze or become immobilized [3].
Serious complications of unmanaged spasticity include:
- Bone fractures and joint dislocations [1]
- Pressure sores that can lead to infection and sepsis [1]
- Chronic constipation and urinary tract infections [3]
- Inhibition of longitudinal muscle growth [6]
- Muscle and joint deformities including kyphoscoliosis [4]
- Sleep disruption and chronic pain [7]
Children with spasticity face especially severe risks that affect normal growth and might cause permanent deformities [1]. As the condition worsens, caregivers find it harder to provide needed care, which creates additional health risks [3].
Proper treatment becomes crucial not just to manage symptoms but to prevent irreversible damage. You can’t cure spasticity, but proper management through appropriate medications and therapies can improve comfort, function, and quality of life by a lot [5]. Early intervention helps prevent the cascade of complications that untreated spasticity can trigger.
Oral Medications for Spasticity
Oral medications are the life-blood of spasticity management. Doctors prescribe them as first-line treatments before trying more invasive options. These medications work through different mechanisms and give unique benefits and limitations to patients with various neurological conditions.
Baclofen: still the first-line?
Baclofen remains the preferred first-line treatment for spasticity, especially with spinal cord injuries [1]. This GABA-B receptor agonist reduces excitatory neurotransmitter release in presynaptic neurons while stimulating inhibitory signals in postsynaptic neurons [1]. Such dual action reduces muscle tone and relieves flexor spasms, clonus, and associated pain.
Baclofen’s effectiveness comes with several challenges. Poor blood-brain barrier penetration means patients need higher oral doses to get therapeutic effects [8]. The gastrointestinal tract absorbs 70-85% of oral baclofen, and peak plasma concentrations show up 2-3 hours after ingestion [1].
Network meta-analyzes have showed baclofen works well, with substantial spasticity reduction compared to placebo on the modified Ashworth scale [5]. Notwithstanding that, patients often experience transient sedation, confusion, muscle weakness, vertigo, and nausea [1]. Patients who feel too drowsy with oral doses might get better results with fewer side effects from an intrathecal baclofen pump [5].
Tizanidine and clonidine: pros and cons
Tizanidine and clonidine work as alpha-2 adrenergic agonists with notable differences in their application and side effects. Tizanidine increases presynaptic inhibition of motor neurons to reduce spasticity [5].
Patient satisfaction surveys gave tizanidine a 6.2 out of 10 rating from 394 users. The results showed 48% had positive effects while 29% reported negative outcomes [9]. Side effects include drowsiness (19.5%), dry mouth (9.9%), hallucinations (7.1%), and dizziness (6.1%) [9]. Tizanidine causes nowhere near the muscle weakness of baclofen and only slightly lowers blood pressure compared to clonidine [9].
Doctors originally prescribed clonidine more often for hypertension. Now it helps manage spasticity by inhibiting excessive afferent sensory transmission [5]. Patients rated it higher at 7.1 out of 10, with 61% reporting positive effects [9]. Side effects like hypotension, bradycardia, and drowsiness limit its use as a standalone spasticity treatment [5].
Gabapentin and benzodiazepines
Gabapentin started as an anticonvulsant and now shows promise in spasticity management. A randomized, double-blind, placebo-controlled study showed that gabapentin administration (2400 mg over 48 hours) reduced spasticity by 11% on the Ashworth Scale and 20% on the Likert Scale in spinal cord injury patients [10]. Scientists believe it acts on calcium channels to inhibit muscle contractions [5].
Benzodiazepines, especially diazepam, work as GABA-A agonists that depress central nervous system activity [5]. These medications help reduce nighttime spasticity and promote uninterrupted sleep through their sedative effects [5]. Recent studies confirm diazepam reduces spasticity significantly compared to placebo [5].
Benzodiazepines work best on flexor reflexes, making them more suitable for spinal rather than cerebral spasticity [5]. Tolerance and dependence issues limit their long-term use [5].
Dantrolene: peripheral action and risks
Dantrolene differs from other medications as the only FDA-approved oral peripherally-acting antispasmodic medication [4]. This drug works directly on skeletal muscles by stopping calcium release from the sarcoplasmic reticulum, which blocks muscle contractions [4].
This unique mechanism makes dantrolene work exceptionally well for cerebral-origin spasticity from stroke, cerebral palsy, and traumatic brain injury [10]. Patients often experience less pain, better residual motor function, and improved use of assistive devices after careful dose adjustment [11].
Adults start with 25 mg daily for seven days, then gradually increase to 400 mg per day maximum [4]. Children over five years old start at 0.5 mg/kg/day and may take up to 100 mg four times daily [4].
Dantrolene’s benefits come with a black box warning about potential hepatotoxicity, including overt hepatitis [4]. This serious risk means doctors must check liver function before treatment and monitor it regularly [4]. Patients must stop taking the medication immediately if their liver function becomes impaired [4].
Botulinum Toxin Injections: A Focal Solution
Botulinum toxin injections have become a precise, focused solution for spasticity management in 2025. These injections target specific overactive muscles without affecting the entire body, unlike systemic oral medications.
How botulinum toxin works
Bacteria from the Clostridium botulinum family produce botulinum neurotoxin (BoNT), a 150 kilodalton protein [12]. This potent neurotoxin blocks acetylcholine release at the neuromuscular junction [6]. BoNT cleaves specific proteins that are vital for vesicle docking and neurotransmitter release—especially the 25 kDa synaptosomal protein [6]. Muscle activity becomes temporarily paralyzed and muscle hypertonia decreases, making it perfect for targeted spasticity reduction.
Muscle relaxation starts 1-3 days after injection, rather than immediately [13]. The toxin reaches its peak effectiveness at 5 weeks post-injection [14]. The injected muscles weaken during this process, and this controlled paralysis helps break the cycle of spastic muscle contractions.
Best practices for injection sites
Proper injection technique and muscle targeting lead to successful outcomes. Doctors use several methods to ensure precision:
- Electrical stimulation: An injection needle delivers electrical pulses that make specific muscles contract, confirming correct muscle injection [3]
- Electromyography (EMG): This helps identify muscles in obese patients whose neck muscles can’t be properly felt [2]
- Ultrasound guidance: Doctors can see where the needle goes
- Anatomical landmarks: These work alone or with other techniques [7]
Most patients need multiple injection sites—about 22.71% get one injection site, 27.05% get two sites, 16.91% get three sites, and 19.81% get four sites [6]. Doctors choose techniques based on anatomical region and muscle activity, sometimes using multiple detection methods on one patient [6].
Comparing BoNT-A types: Botox, Dysport, Xeomin
Clinical practice in 2025 features three main BoNT-A preparations:
- OnabotulinumtoxinA (Botox): Contains the neurotoxin with accessory proteins in a 900 kD complex [15]
- AbobotulinumtoxinA (Dysport): Has the neurotoxin with different amounts of accessory proteins [16]
- IncobotulinumtoxinA (Xeomin): Contains just the purified 150 kD neurotoxin without complexing proteins [6]
Potency units between these products are not interchangeable [16]. The conversion ratios vary by a lot—OnaA and IncoA have a ratio of about 1:1 [6]. OnaA to AboA conversion usually ranges from 1:3 to 1:4, though clinical practice shows ratios from 1:1 to as high as 1:11 [6].
OnaA:AboA dose ratios change based on specific muscles—from 1:2.2 in biceps muscles to 1:4.1 in pronator teres muscles [16]. Doctors need to adjust doses based on individual patient responses rather than strict conversion formulas.
Duration of effect and repeat dosing
BoNT typically works for 78.5 ± 28.4 days (about 3 months) [1]. The specific toxin used, doses given, and patient characteristics affect this timeline [1]. Research shows that onaBoNT-A lasts longer than incoBoNT-A, regardless of clinical condition and doses [1].
Patients usually get treatments every 100 days (99-102 days depending on formulation) [16]. Repeated BoNT-A treatments continue to improve function and tone [17]. Multiple treatments can increase functional improvements over time—one study revealed that five sessions reduced spasticity more than a single session [8].
Side effects become less common with more treatments—dropping from 40.2% in cycle 1 to 13.6% by cycle 4—and most are mild to moderate [3]. Patients most often experience pain, soreness, stiffness, and mild swelling where they get injections [13].
Advanced Interventions: ITB and Phenol Injections
Advanced interventions offer powerful alternatives to patients with severe spasticity who don’t respond to conservative treatments in the 2025 treatment landscape. These options deliver medication straight to target sites and often yield better results for people with debilitating symptoms.
Intrathecal baclofen pumps: who benefits?
Intrathecal baclofen (ITB) therapy delivers liquid baclofen directly into the intrathecal space around the spinal cord. This method works better because it bypasses the blood-brain barrier and uses about 100 times less medication than oral administration while providing better relief [18].
ITB might be right in these cases:
- Patients with severe spasticity who don’t respond to oral medications [9]
- People who can’t tolerate side effects from oral baclofen [10]
- Patients who meet threshold criteria of level 3 on the Ashworth Scale and level 2 on the Spasm Frequency Scale for at least 12 months [10]
Doctors need to give patients a test dose through lumbar puncture during screening. This test helps predict how well the treatment will work, with peak effects usually happening within 4 hours [10]. The programmable titanium pump measures about 3 inches in diameter and 1 inch thick. It delivers exact baclofen doses through a catheter placed between the first and second lumbar vertebrae [10].
Studies of long-term ITB therapy reveal lasting improvements in spasticity control and reduced spasms. Most patients say they can transfer more easily, sit better, handle daily activities better, and feel much less pain [10].
Phenol and alcohol neurolysis: when it’s right
Phenol (usually 5%) or ethyl alcohol (45-100%) neurolysis provides another way to manage focal spasticity [18]. These substances denature proteins in neural tissue and block nerve transmission effectively [18].
This treatment works best for:
- Focal spasticity that other treatments can’t help [19]
- Patients who have no functional movement in affected limbs [9]
- People who have lost bladder and bowel function [9]
- Patients with impaired sensation in the treatment area [9]
The procedure needs high technical expertise and often uses electrical stimulation with a Teflon-coated needle to find motor points [20]. Sometimes doctors use ultrasound guidance to locate peripheral nerves during injection [20]. Spasticity reduction typically lasts more than six months [18], which beats botulinum toxin injections for duration.
Recent clinical data shows that phenol neurolysis stays effective with repeated treatments and works well alongside botulinum toxin therapy [21]. Phenol starts working within minutes of injection, while botulinum toxin takes 3-5 days to help [21].
Risks and complications of invasive options
These advanced treatments work well but come with serious risks that require careful patient selection and monitoring.
ITB therapy risks include:
- Catheter problems or disconnections [18]
- Pump battery running out or mechanical failure [4]
- Life-threatening baclofen withdrawal symptoms like spasms, tremors, high temperature, seizures, and rarely, death [9]
- Overdose signs such as drowsiness, extreme muscle weakness, breathing problems, and loss of consciousness [11]
Neurolysis can cause these problems:
- Dysesthesias affecting 2-32% of adults, especially near mixed motor and sensory nerves [20]
- Skin damage and muscle death from wrong injection placement [19]
- Body-wide effects including low blood pressure, tremor, or seizures from absorbed medication [18]
- Anesthesia dolorosa—uncomfortable numbness from disrupted nerve signals [9]
Both treatments need specialized medical expertise and thorough patient screening. ITB patients must be able to make regular pump refill appointments to avoid dangerous withdrawal [18]. Doctors should only use phenol neurolysis on patients who have no functional movement in the targeted area [9].
Emerging and Adjunctive Therapies
Non-invasive therapies are now recognized as valuable options for managing spasticity, beyond traditional medications and invasive procedures. Patients looking for extra relief can choose from these emerging approaches along with their standard treatments.
Extracorporeal shock wave therapy (ESWT)
ESWT uses high-energy acoustic waves that create therapeutic effects through mechanical stimulation in target tissues. Two types of ESWT exist: focused ESWT concentrates energy in specific areas with penetration depths up to 12 cm, while radial ESWT spreads energy in a diffuse pattern reaching about 3.5 cm deep [22].
ESWT works through several mechanisms:
- It produces nitric oxide that reduces acetylcholine at neuromuscular junctions [22]
- The vibratory stimulation decreases motor neuron excitability [22]
- Better muscle microcirculation helps relieve muscle spasm [22]
The largest longitudinal study with 1,930 patients showed that ESWT works as well as botulinum toxin injections. Radial shock wave (RSW) therapy proved most effective with a 72.3% probability of reducing mid-term spasticity [23].
Repetitive peripheral magnetic stimulation (rPMS)
rPMS creates painless muscle contractions using magnetic fields, unlike the discomfort that comes with electrical stimulation. Treatment plans usually need 1-20 sessions over periods from a single day to two weeks [24].
Meta-analyzes reveal that rPMS substantially reduces spasticity with a moderate clinically meaningful improvement (standardized mean difference of -0.55) [24]. Patients who received rPMS showed 36% better Modified Ashworth Scale scores compared to conventional therapy [25].
Localized muscle vibration (LMV)
LMV targets spastic muscles or their antagonists with mechanical vibration. Most research uses vibration frequencies between 75-120 Hz to activate proprioceptive muscle afferents specifically [5].
The benefits go beyond simple muscle relaxation. Patients show quick improvements in motor coordination and reduced spasticity [5]. These positive changes often last for weeks or months after completing treatment [5].
Combining physical therapy with medication
Treatments work better together than alone. Research strongly supports using anti-spasticity medications with physical therapies to get the best results [26].
Adding other therapies after botulinum toxin injections improves outcomes:
- Modified Ashworth Scale scores improve by at least one grade with electrical stimulation, modified constraint-induced movement therapy, and physiotherapy [27]
- Casting works better than taping, and taping shows better results than electrical stimulation by itself [27]
New clinical trials are exploring oral medications that target endocannabinoid systems. These medications help muscles relax naturally without making patients drowsy like traditional drugs [28].
These new therapies are great additions to existing treatments. They work effectively without being invasive and cause fewer side effects than conventional medications.
Comparing Effectiveness: What Works Best?
The best spasticity medication depends on many factors beyond how well it works.
Short-term vs long-term outcomes
Botulinum toxin and other temporary treatments work best around 5 weeks after injection but only last about 3 months [29]. Surgical treatments give longer-lasting benefits. Studies that compared selective dorsal rhizotomy (SDR) with standard treatment showed that SDR patients kept their walking speed while other patients slowed down by 25% [30]. The combination of repetitive transcranial magnetic stimulation (rTMS) with intermittent theta burst stimulation showed better motor function even after 3 months [31].
Modified Ashworth Scale (MAS) improvements
MAS serves as the gold standard to assess spasticity and guides treatment choices worldwide [32]. Its reliability can vary though. A study where four physiotherapists checked the same patient came up with MAS scores from 0 to 2 [33]. Surgical methods brought the biggest drops in MAS scores (2.7 points compared to 1.1 for botulinum toxin) [29]. The MAS gives us just a partial view of spasticity’s complex nature since it only measures resistance during fast stretching.
Patient-specific factors in treatment choice
Doctors need to look at several things when picking a treatment:
- Whether spasticity comes from the brain or spine
- Other health issues that affect how drugs work
- What the patient wants to achieve beyond reducing muscle tone
- How well they handle sedation or weakness
Dantrolene works great for brain-related spasticity but causes too much weakness in patients with spinal cord injuries [34].
Cost and accessibility considerations
Spasticity hits wallets hard – patients with post-stroke spasticity spend 39.6% more on healthcare ($62,875 versus $44,472) [35]. Among available options, abobotulinumtoxinA costs less per injection than other treatments [36]. The good news is that onabotulinumtoxinA therapy cut total healthcare costs by 66% and spasticity-related expenses by 51% by reducing hospital stays [37].
Conclusion
Each patient needs a tailored approach to manage spasticity based on their unique needs and goals. Oral medications are still the basic first-line treatments, but healthcare practitioners now see the value of using multiple strategies together. Of course, research shows better outcomes when doctors combine drugs with physical therapies instead of using medication alone.
Doctors need to think over several factors beyond just how well a treatment works. The medical team must first assess if the spasticity comes from cerebral or spinal sources. On top of that, they must balance possible side effects against benefits, especially when drowsiness or muscle weakness could hurt functional improvements. Then, what works well for one patient might not suit another.
Botulinum toxin injections are a great option with minimal body-wide effects. All the same, these injections last only three months and need regular doses. Patients who have severe, widespread spasticity might do better with intrathecal baclofen pumps, even though these are invasive and can have complications.
New non-drug options like extracorporeal shock wave therapy and repetitive peripheral magnetic stimulation show promise with fewer side effects. These approaches can work alongside traditional treatments and might help reduce medication doses.
Spasticity’s cost goes beyond just treatment expenses. Poor management leads to hospital stays, special care needs, and lower productivity. Good management strategies can cut these costs by a lot while making life better for patients.
Treatment for spasticity keeps moving toward more tailored, complete approaches. The best results come through teamwork between patients and healthcare teams to find the right treatment plan. This cooperative approach helps patients reach their goals while having fewer side effects and more independence. Looking at each patient’s needs, goals, and progress remains vital to manage spasticity well in 2025 and beyond.
Key Takeaways
Understanding the diverse spasticity treatment landscape in 2025 helps patients and healthcare providers make informed decisions about managing this challenging neurological condition that affects over 12 million people globally.
• Multimodal therapy outperforms single treatments – Combining medications with physical therapy shows Grade A evidence for superior outcomes compared to oral medications alone.
• Botulinum toxin injections offer precise focal relief – These targeted injections provide 3-month effectiveness with minimal systemic side effects, making them ideal for specific muscle groups.
• Baclofen remains the gold standard first-line treatment – Despite side effects like sedation and weakness, baclofen continues as the preferred initial oral medication for spasticity management.
• Advanced interventions serve severe cases effectively – Intrathecal baclofen pumps and phenol injections provide powerful relief for patients unresponsive to conservative treatments.
• Emerging non-invasive therapies show promise – Extracorporeal shock wave therapy and repetitive magnetic stimulation offer effective alternatives with fewer side effects than traditional medications.
• Treatment selection requires individualized assessment – Success depends on considering spasticity origin (cerebral vs spinal), patient goals, comorbidities, and tolerance for side effects rather than one-size-fits-all approaches.
The key to successful spasticity management lies in collaborative care between patients and multidisciplinary teams, emphasizing personalized treatment strategies that balance effectiveness with quality of life improvements.
References
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