How to Decrease Tone in Stroke Patients

Post-stroke muscle tone responds to a layered combination of physical, pharmacological, and sometimes surgical interventions, and the right mix depends on how severe the spasticity is, which limbs are involved, and how long ago the stroke occurred. The stiffness many stroke survivors feel is not a single problem with a single fix. It involves changes in the brain’s motor pathways, shifts in how muscles and connective tissue respond to stretch, and sometimes actual shortening of muscle fibers into contracture. Addressing tone effectively means understanding which piece of the puzzle is dominant and choosing treatments accordingly.

Why Tone Increases After Stroke

When a stroke damages the brain’s motor areas, the normal balance between signals that excite muscles and signals that inhibit them gets disrupted. In the early weeks, the brain attempts to reorganize itself, and motor recovery during this window is driven largely by beneficial changes in the cortex. But when damage is extensive, a less desirable adaptation takes hold: pathways running through the brainstem, particularly the reticulospinal tract, become overactive. This hyperexcitability is now considered the most plausible explanation for the involuntary muscle tightness that develops weeks to months after a stroke.¹

There is an important wrinkle here. A classic study of 24 stroke patients found that while half developed measurable resistance to passive movement, most of that resistance came from muscle contracture rather than overactive reflexes. Contracture appeared as early as two months post-stroke, and the increased stiffness correlated with tissue changes in the muscle, not with reflex hyperexcitability.² This means a limb that feels “spastic” to the touch may be stiff because the muscle itself has shortened and become less compliant, because the nervous system is firing too much, or both. Effective treatment starts with figuring out which component dominates.

Measuring Tone Before Choosing a Treatment

Clinicians most often grade spasticity using the Modified Ashworth Scale, which rates resistance to passive movement on a simple ordinal scale. Its reliability is solid: studies have found inter-rater agreement values around 0.84, which means two different therapists examining the same patient will usually arrive at the same score.³ More elaborate scales exist, such as the Tone Assessment Scale, but the portions that measure posture and associated reactions are less consistent between raters. Where the Tone Assessment Scale does perform well is in scoring passive movement, which is essentially what the Modified Ashworth Scale already captures. In practice, the Modified Ashworth Scale remains the workhorse for deciding whether an intervention is actually reducing tone, and nearly every trial referenced in this article uses it as a primary outcome.

Brain imaging adds another layer of prediction. Stroke lesions that involve the internal capsule and striatum carry a particularly high risk of later spasticity, even when the total volume of damaged brain tissue is small. In a study of 103 patients imaged within the first week, supratentorial lesions smaller than half a cubic centimeter did not usually lead to spasticity unless those specific structures were hit.⁴ Identifying high-risk patients early opens the door to preventive strategies such as positioning, stretching, and early splinting before tone becomes entrenched.

Stretching, Casting, and Splinting

Prolonged low-load stretch is one of the oldest approaches to managing tone, and it still forms the backbone of most rehabilitation programs. Serial casting takes this idea to its logical extreme: a limb is placed in a stretched position inside a plaster or fiberglass cast, and the cast is changed periodically to push the joint further into range. Research confirms that casting is effective for fixed contractures caused by increased tone of cerebral origin.⁵ One recent study examined whether adding serial casting before botulinum toxin injections could make the toxin’s effects last longer. Patients who received both casting and toxin held their gains more steadily over follow-up, though the advantage over toxin alone was not statistically confirmed.⁶ While the evidence base for casting is promising, a review of upper-limb casting after stroke found that most studies so far lack controlled designs and large sample sizes, making it hard to draw strong conclusions about long-term benefit.⁷

Splints offer a less intensive alternative for home use. A randomized controlled trial of a 3D-printed dynamic hand-wrist splint found that chronic stroke survivors who wore the device showed meaningful reductions in wrist and finger flexor spasticity, along with improvements in functional hand movements. Users rated the splint highly for comfort and ease of use.⁸ Another case series using a dynamic progressive orthosis for the wrist found increased passive range of motion and reduced resistance to passive movement over several weeks of wear.⁹ Dynamic splints, which apply a gentle spring-loaded stretch rather than locking the joint in a fixed position, seem particularly suited to patients who need both tone management and the ability to attempt functional movements during the day.

Exercise and Functional Electrical Stimulation

One of the most persistent myths in stroke rehabilitation is that strengthening exercises will worsen spasticity. A systematic review specifically targeting this question found the opposite: resistance training programs benefit stroke survivors without increasing spasticity, and they also improve motor function.¹⁰ A progressive resistance training trial confirmed this: muscle strength went up significantly, muscle tone stayed the same, and the improvements persisted at follow-up.¹¹ If your therapist has been cautious about adding resistance work, the evidence firmly supports safe incorporation of strengthening.

Cycling combined with functional electrical stimulation (FES) takes a different route to the same goal. In a study comparing cycling alone with cycling plus FES, both groups showed reduced muscle tone after just 20 minutes. Adding FES made a bigger difference for patients who started with higher tone, as measured by both the Hoffmann reflex ratio and a pendulum test of the knee.¹² The timing of FES matters, too. Research examining different on-to-off ratios during electrical stimulation of the lower limb found that a longer off period (a 1:5 on-to-off ratio) produced a greater reduction in calf muscle tone than a shorter off period. Interestingly, the upper limb did not respond as clearly to the same stimulus parameters.¹³

Oral Medications

When spasticity is widespread and bothersome enough to interfere with sleep, comfort, or daily activities, oral medications enter the picture. A meta-analysis of oral antispasticity drugs in non-progressive neurological conditions, including stroke, found them moderately effective at reducing tone.¹⁴ The three most commonly prescribed agents are baclofen, tizanidine, and diazepam. Clinical trials have shown that tizanidine works about as well as baclofen or diazepam, but patients tend to tolerate it somewhat better overall.¹⁵

All three drugs share a common drawback: they act on the entire nervous system, not just the affected muscles. That means sedation, dizziness, and muscle weakness are routine side effects, and these effects can undermine the very rehabilitation activities that help stroke survivors recover. For this reason, clinicians often prefer focal treatments like botulinum toxin when spasticity is concentrated in a few muscle groups rather than widespread.

Botulinum Toxin Injections

Botulinum toxin type A works by blocking the nerve signal that tells a muscle to contract. Injected directly into a spastic muscle, it weakens that muscle for roughly three to four months, creating a window for more effective stretching and functional training. The BoTULS trial, the largest randomized study of upper-limb botulinum toxin after stroke, showed that the treatment group had significantly lower muscle tone at one month, improved arm strength at three months, and gains in basic functional tasks like hand hygiene and dressing that persisted out to 12 months. Pain also improved at the one-year mark.¹⁶

From an economic standpoint, early use of botulinum toxin appears cost-effective. A secondary analysis of a randomized trial found that patients treated early spent substantially less on contracture-related costs, and the cost per unit of functional improvement was negative, meaning the treatment both saved money and produced better outcomes.¹⁷ A separate cost-utility analysis of rehabilitation combined with botulinum toxin versus rehabilitation alone found that the combination produced more quality-adjusted life years gained over two years, at a cost that fell within accepted willingness-to-pay thresholds.¹⁸ These numbers matter because insurers and health systems sometimes view repeated injections as expensive without considering the downstream costs they prevent.

Intrathecal Baclofen for Severe Cases

When spasticity is severe, widespread across multiple limbs, and unresponsive to oral medications or focal injections, intrathecal baclofen (ITB) becomes an option. A surgically implanted pump delivers baclofen directly into the fluid surrounding the spinal cord, bypassing the blood-brain barrier and achieving high local concentrations with a fraction of the oral dose. A meta-analysis found that ITB significantly reduced spasticity scores and improved gait speed in stroke patients.¹⁹ Canadian Stroke Best Practice Recommendations now suggest ITB for severe, intractable, disabling, or painful spasticity.

The SISTERS trial, a randomized multicenter study, compared ITB therapy against conventional oral antispasticity medications in patients with spasticity affecting at least two extremities.²⁰ ITB requires surgical implantation and ongoing pump refills, so it is typically reserved for the subset of patients whose daily function and quality of life are most compromised. It is not a first-line treatment, but for the right patient, the reduction in tone can transform caregiving demands and comfort.

Non-Invasive Brain Stimulation

Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are emerging tools that target spasticity at its source: the brain. Two meta-analyses have addressed their effectiveness. One found that both rTMS and tDCS produced significant reductions in Modified Ashworth Scale scores compared to sham controls, with tDCS showing a slightly larger pooled effect size.²¹ The other reported that low-frequency rTMS applied to the unaffected hemisphere was particularly beneficial, and that anodal tDCS outperformed other stimulation setups.²²

The overall quality of evidence is moderate. Most trials are small, and the optimal stimulation parameters, including session number, intensity, and which hemisphere to target, are still being worked out. Brain stimulation is not widely available outside research centers, and it is rarely used as a standalone treatment. Its real promise may lie in priming the brain before a physical therapy session, making the motor cortex more receptive to exercises that follow. That combination approach is where current research is heading.

Robotic Rehabilitation

Robots can deliver highly repetitive, precisely controlled movements that would be exhausting for a human therapist to provide manually. An upper-extremity robot stretching and strengthening program was compared head-to-head with conventional occupational therapy for spastic stroke patients: both groups showed significant drops in spasticity scores, with the robot group achieving similar benefits.²³ A separate study of robot-assisted hand passive mobilization found that a single session significantly reduced wrist and finger spasticity scores and improved patients’ self-reported heaviness, stiffness, and pain.²⁴

Robots are not magic. They do roughly what a skilled therapist does, just with the capacity for more repetitions and consistent range of motion. Their value is practical: they can supplement limited therapy hours, maintain range when a therapist is not present, and standardize the dose of stretching a patient receives. For patients with severe hand spasticity who struggle to participate in conventional exercises, a robotic device that moves the fingers through a full arc can keep tissues mobile.

Dry Needling

Dry needling involves inserting thin filament needles into taut bands within spastic muscles, aiming to disrupt the feedback loop that keeps those muscles overactive. A meta-analysis found large effect sizes for spasticity reduction at short-term follow-up, with the lower extremity responding more consistently than the upper.²⁵ When dry needling was combined with Bobath therapy (a widely used neurological rehabilitation approach), significantly more patients experienced a decrease in spasticity compared with Bobath alone.²⁶

A review of the broader dry needling literature confirmed that the technique decreases spasticity when applied to muscles of the shoulder, arm, wrist flexors, and calf, with improvements in both range of motion and gait. The quality of evidence is rated moderate.²⁷ Dry needling is inexpensive, carries minimal side effects beyond temporary soreness, and can be performed in outpatient settings. It is best thought of as a useful adjunct rather than a primary treatment.

Cryotherapy and Heat

Applying cold to a spastic muscle can temporarily dampen tone, and the mechanism appears to act on the muscle tissue itself rather than the reflex arc. One crossover study found that cryotherapy reduced plantarflexor tone without changing muscle strength or gait kinematics.²⁸ Another confirmed that ice-pack application reduced plantar flexor spasticity without affecting joint position sense, an important safety consideration since you do not want to trade tone reduction for loss of awareness of where the ankle is in space.²⁹

There is a catch, though. A lab study that directly compared cold and heat stimulation found that while heat decreased total resistance by about 6%, cold actually increased total torque by about 11%. The reflex component did not change significantly under either condition.³⁰ The likely explanation is that cold stiffens the non-neural tissue of the muscle even as it quiets the nervous system’s contribution. So the clinical takeaway is nuanced: brief cold applications before a stretching session can reduce the reflex-driven portion of resistance, making the limb easier to move through range, but prolonged cooling may increase passive tissue stiffness. Heat may do the reverse, softening the tissue itself. Some clinicians use heat before passive stretching and cold after active exercise, though this combination strategy has not been tested in controlled trials.

Surgery for the Spastic Hand

When spasticity in the hand has become fixed and no longer responds adequately to injections, therapy, or medication, surgical options exist. A systematic review of surgical treatment for post-stroke spastic hands identified several commonly reported procedures: transfer of the superficialis to profundus flexor tendons, muscle-tendon releases, wrist fusion, and selective nerve cuts.³¹ These operations aim to rebalance forces across joints, improve hygiene in a clenched fist, reduce pain, and in some cases restore limited grasp. Surgery is rarely about returning normal hand function; it is more often about comfort, appearance, and making the hand easier to care for.

The Caregiver Side of Spasticity Management

Spasticity does not just affect the person who had the stroke. Caregivers of stroke survivors with spasticity report poorer physical and emotional health compared with the general population.³² The difficulty of daily tasks like dressing, bathing, and transferring a person with stiff limbs drives anxiety and depression in caregivers, and reducing the difficulty of caregiving tasks appears to matter more than reducing the time spent on them.³³ The economic toll is steep: employed caregivers in one study experienced an average of 32% overall work restriction and lost-productivity costs exceeding $10,000 per year, most of it from reduced effectiveness on the job rather than missed days.³⁴

These numbers reinforce why aggressive, early management of tone is worth pursuing. Treatments that reduce how difficult it is to handle an affected limb, even modestly, cascade outward to improve the whole household’s functioning.

Practical Barriers to Staying on Track

The best treatment plan only works if the patient can actually follow it. A mixed-methods study of home-based exercise programs for stroke survivors identified the most common barriers: difficulty managing time around other daily demands, lack of a caregiver available to assist with exercises, and problems with the design or interface of home exercise systems.³⁵ These barriers are worth discussing openly with a rehabilitation team. If a splint is uncomfortable, it will sit in a drawer. If an exercise program assumes two free hours a day, it will be abandoned within a week. Matching the intervention to the patient’s actual life, not just their clinical needs, is the difference between tone that gradually comes under control and tone that worsens unchecked.