Can Electrical Stimulation Reduce Spasticity After Stroke?

NeuroRehab Team
Thursday, January 15th, 2026

Stroke impacts 6.8 million Americans over age 20, which represents 2.8% of the population. Electrical stimulation for spasticity has become a key treatment option for these patients. The American Heart Association reports that spasticity affects 20% to 30% of stroke survivors. Research shows that 50% of patients develop contractures within 6 months after their stroke. These numbers make stroke one of the leading causes of serious long-term disability across the United States.

The good news is that electrical stimulation helps stroke patients in ways that go beyond traditional therapies. Research proves that patients who receive both electrical stimulation and physical therapy show better results than those who exercise alone. The evidence supporting electrical stimulation’s effectiveness against spasticity has grown rapidly, with clinical trials increasing fourfold in the last decade. Healthcare providers and patients need to understand these treatments as functional electrical stimulation for spasticity continues to advance. This knowledge helps them better manage this common post-stroke complication.

Understanding Spasticity After Stroke

Spasticity ranks among the most common complications after a stroke. The condition affects 19% to 43% of survivors in their first year ^[1]. Patients experience stiff or rigid muscles that create roadblocks in their rehabilitation and recovery. This complex motor disorder shows up through involuntary muscle contractions, changed movement patterns, and tight muscles.

What causes spasticity in stroke survivors

Damage to specific nerve pathways in the brain or spinal cord causes spasticity. These pathways normally control movement and stretch reflexes ^[2]. A stroke can harm brain areas that handle voluntary muscle control, particularly the upper motor neurons. This nerve damage throws off the normal balance between excitatory and inhibitory signals sent to muscles.

The brain loses control over muscle contractions, which guides the stretch reflex into overdrive. Research points to reticulospinal hyperexcitability as the likely mechanism behind post-stroke spasticity ^[3]. This happens because stroke disrupts the balanced signals that usually flow through descending reticulospinal projections.

Spasticity doesn’t pop up right after a stroke. Symptoms typically surface between 1 and 6 weeks after the original injury. The timing varies among patients ^[3]. This delayed onset suggests that spasticity develops from changes in the central nervous system rather than just direct injury. By the later stages, spasticity can affect up to 97% of stroke survivors who have moderate-to-severe motor problems ^[1].

Spasticity often teams up with other motor problems like weakness and poor control ^[1]. These combined issues create bigger functional challenges than spasticity would cause alone.

How spasticity affects daily function

Spasticity disrupts daily life in many ways. Severe cases interfere with simple activities and cause pain ^[2]. Life changes become clear in several areas:

Mobility and movement limitations – Leg muscle spasticity hurts balance and walking. Studies show that higher spasticity levels link to worse balance, poor position sense, and more falls ^[4].
Personal care challenges – Basic tasks like dressing, cleaning under arms, and personal hygiene become tough with stiff muscles ^[5]. Almost 98% of patients struggle with daily tasks because of spasticity ^[6].
Hand function impairment – Stiff wrist and finger muscles make it hard to grab and release objects. The “clenched fist” problem can lead to skin damage and nail infections ^[5]. About 98% of affected people have trouble carrying things ^[6].

Untreated spasticity creates more problems over time. These include frozen joints, bone fractures, joint dislocations, urinary infections, and chronic constipation ^[2]. Joints can freeze up when muscles stay shortened too long, which makes stretching harder ^[3].

Life quality takes a big hit, with 72% of patients saying spasticity hurts their overall wellbeing ^[6]. Many people (44%) lose independence and battle depression ^[7]. Family members feel the weight too – about 64% of people with spasticity need family care. Half of these caregivers cut back or quit their jobs ^[7].

Work life suffers as 38% of affected people can’t work or become disabled ^[7]. The condition most affects their careers, intimate relationships, and self-worth ^[6].

A clear picture of these effects helps develop better treatments, including electrical stimulation. This approach can tackle both main symptoms and stop additional problems from developing.

What Is Electrical Stimulation and How Does It Work?

Electrical stimulation helps stroke patients recover by sending controlled electrical impulses to muscles and nerves. This therapy reduces spasticity and improves function. The technology has come a long way in 2026, giving stroke survivors new hope by mimicking and boosting natural neural processes.

Simple principles of neuromuscular electrical stimulation (NMES)

NMES works by sending short electrical pulses through skin-placed electrodes that excite peripheral nerves. These pulses copy the natural electrical signals your brain sends to muscles. This creates contractions even when you can’t move voluntarily ^[3]. NMES works best when lower motor neurons remain intact, making it ideal for stroke patients whose paralysis comes from upper motor neuron damage ^[8].

Therapists can adjust several important settings to make NMES work:

Frequency – Set between 12-50 Hz, which determines pulses per second ^[8]
Pulse amplitude – Ranges from 0-100 mA to control stimulation strength ^[8]
Pulse width/duration – Ranges from 0-300 microseconds to affect stimulation depth ^[8]
Duty cycle – Balances “on time” and “off time” to prevent muscle fatigue ^[2]

Modern NMES devices let therapists fine-tune these settings in 2026. This creates customized rehabilitation plans that help patients recover better.

How electrical impulses activate muscles

Simple nerve physiology explains how electrical stimulation works. Your brain normally starts an action potential that travels down motor neurons to reach muscle fibers. Electrical stimulation skips this process. It directly depolarizes axons to their threshold potential (about -55 mV), which triggers action potentials moving in both directions ^[3].

Natural and electrically stimulated contractions differ in how they recruit motor units. Your nervous system naturally activates smaller, slow-twitch Type I muscle fibers first, followed by larger, fast-twitch Type II fibers ^[9]. Electrical stimulation does the opposite – it activates larger fibers first ^[9]. This explains why NMES first recruits fast-twitch muscle fibers, which create stronger but faster-tiring contractions ^[9].

The stimulation mainly targets large-diameter afferent fibers that handle proprioception ^[3]. These fibers spread throughout the spinal cord and create multiple therapeutic pathways. They connect directly with alpha-motoneurons in the ventral gray matter and affect opposing muscles through interneuron connections ^[3]. A single stimulation can activate muscles while inhibiting their opposites, creating coordinated movements.

Role of neuroplasticity in recovery

Your brain’s ability to rewire itself by forming new neural connections – neuroplasticity – makes electrical stimulation work for stroke recovery. Research shows electrical stimulation aids neuroplastic remodeling in several ways ^[3]. Changes start in neural pathways by activating spinal motor pools and boosting synaptic connections. Muscle fiber changes happen later ^[9].

The therapy works through multiple channels. Electrical stimulation synchronizes presynaptic and postsynaptic activity, which promotes Hebbian plasticity – when cells fire together, they wire together ^[8]. This strengthens existing neural pathways and helps create new ones around damaged brain areas.

Research shows that combining electrical stimulation with voluntary effort boosts cortical excitability more than stimulation alone ^[8]. This happens because activating remaining upper motor neurons while stimulating muscles creates perfect conditions for neural reorganization ^[8]. Sensory feedback during stimulation also triggers long-term changes in the sensorimotor cortex, which helps motor learning ^[9].

These benefits go beyond just the treated areas. Balogun’s research showed a 24% strength increase in stimulated limbs and 10% in untreated opposite limbs. This proves electrical stimulation creates both local and central neural changes ^[9]. Through these mechanisms, electrical stimulation helps the brain rebuild itself, potentially restoring movement even years after a stroke.

Types of Electrical Stimulation Used in Stroke Rehabilitation

Different types of electrical stimulation help treat post-stroke spasticity. Each type works differently and serves unique purposes. Rehabilitation professionals need to know these differences to choose the right treatment for each patient.

Functional electrical stimulation (FES)

FES has become a promising rehabilitation tool to restore motor skills in stroke survivors ^[10]. This method sends electrical impulses through the skin to stimulate specific nerves and triggers movements in affected muscles. The electrical stimulations create useful functional movements instead of random ones ^[10].

FES systems come in two main types. Open-loop FES uses therapist-applied, preprogrammed patterns that patients can’t control ^[10]. Closed-loop FES systems use patient feedback through brain-computer interfaces (BCI) or electromyogram (EMG) control ^[10]. EMG-controlled systems work particularly well for stroke rehabilitation because they measure electrical currents during muscle contraction ^[10]. This feedback lets the system analyze muscle activity and adjust stimulation based on what the muscle needs ^[10].

Stroke patients with foot drop can benefit from commercial devices like the WalkAide system and NESS L300. These devices stimulate during walking’s swing phase to lift the ankle properly ^[11]. The NESS H200 stands as the only commercial FES device for upper limb rehabilitation. It uses five electrodes to stimulate forearm and hand muscles for gripping and grasping ^[11].

Transcutaneous electrical nerve stimulation (TENS)

TENS has helped treat chronic hemiplegia in the last decade. Research shows it can boost motor function when used on the common peroneal nerve ^[1]. Unlike FES, TENS doesn’t try to create functional movements but works through other mechanisms.

Research proves that 60 minutes of TENS, applied five times weekly for three weeks, substantially reduced ankle plantarflexor spasticity and hyperactive stretch reflexes ^[1]. Patients showed better voluntary control of ankle dorsiflexors. This happens mainly by exciting large-diameter Aα and β afferents, including sensory and motor fibers ^[1].

TENS does more than just reduce spasticity. It regulates spasticity by increasing presynaptic inhibition and reducing stretch reflex excitability ^[5]. Meta-analysis shows that applying TENS over nerve or muscle belly for more than 30 minutes creates strong therapeutic effects on spasticity in stroke patients ^[5].

Interferential current (IFC)

IFC offers another way to manage post-stroke spasticity. This technique uses crossing medium-frequency currents to create a therapeutic low-frequency effect where they meet. These currents penetrate tissues deeper than other stimulation types.

Clinical trials show impressive results. A single 60-minute IFC stimulation of the gastrocnemius, combined with air-pump massage, reduced gastrocnemius spasticity more than placebo treatment ^[12]. Patients using IFC showed better balance and walking abilities. Their scores improved on functional reach tests, Berg Balance Scale, timed up-and-go tests, and 10-meter walk tests ^[12].

IFC reduces muscle tone using interfering middle frequencies between 4,000 Hz and 4,100 Hz ^[12]. The electrical stimulation decreases muscle tone by boosting presynaptic inhibition ^[12]. Middle frequency current faces less skin resistance, so it reaches deep tissues better than TENS, making it potentially more effective at reducing spasticity ^[12].

NMES vs FES: Key differences

Neuromuscular electrical stimulation (NMES) and FES both help with voluntary contractions, but they serve different purposes:

Goal orientation: Traditional NMES focuses on strength building in training programs, while FES promotes functional activity ^[13].
Patient involvement: NMES runs passively with preset patterns, but FES works with voluntary contractions during functional tasks ^[6].
Parameter settings: FES uses shorter pulse frequency (20-60 Hz) and lower amplitude than traditional NMES ^[7].
Application context: NMES builds muscle strength when active movement is limited, while FES helps recover functional movement for specific tasks like grasping or walking ^[6].

Clinical practice doesn’t always show clear lines between NMES and FES. However, knowing their unique features helps clinicians pick the best treatment based on each patient’s rehabilitation goals and current abilities.

How Electrical Stimulation Reduces Spasticity

The complex mechanisms behind spasticity reduction through electrical stimulation affect neural pathways in both spinal and cortical levels. Scientists now better understand how these treatments help stroke survivors regain normal muscle tone and function.

Mechanisms of spasticity reduction

Electrical stimulation helps reduce spasticity by changing spinal reflexes and their excitability. Neuromuscular electrical stimulation (NMES) can trigger neuroplasticity in spinal cord pathways. These adaptive changes help reduce spasticity by reorganizing neural connections ^[4]. The changes happen at several levels throughout the nervous system.

Large-diameter afferent fibers responsible for proprioception respond to electrical stimulation ^[2]. These fibers spread extensively through the spinal cord and connect directly with alpha-motoneurons. They also influence opposing muscles through interneuron connections. This process changes how the stretch reflex behaves, which plays a key role in spasticity.

The therapeutic impulses boost presynaptic inhibition of overactive reflexes ^[9]. This happens because stimulation creates synchronized presynaptic and postsynaptic activity. Neuroscientists call this Hebbian plasticity—following the principle that “neurons that fire together, wire together.” This mechanism strengthens helpful neural connections while weakening harmful ones.

Evidence from clinical trials

Research strongly supports the use of electrical stimulation to reduce spasticity. A systematic review of 29 randomized clinical trials showed that NMES led to significant reduction in spasticity in 14 studies compared to control groups ^[4]. NMES combined with other treatments gave meaningful reductions in spasticity (−0.30 [95% CI, −0.58 to −0.03]) and improved range of motion (2.87 [95% CI, 1.18–4.56]) after stroke ^[14].

Different approaches yield different results. The active NMES group expressed significant improvements in plantarflexor muscles spasticity with a 35% improvement compared to the sham NMES group’s -10.74% change ^[4]. TENS combined with exercise programs also helped improve standing posture and lower extremity somatosensory function ^[9].

Treatment protocols make a difference. High-frequency TENS (99-100 Hz) with narrow pulse widths (≤125 µs) works better at relieving spasticity than lower frequencies ^[2]. Studies of TENS revealed significant spasticity relief measured by reduced Modified Ashworth Scale scores versus control groups (SMD = –0.71; 95% CI = –1.11 to –0.30; p = 0.0006) ^[9].

Targeting specific muscle groups

Results vary based on which muscle groups receive treatment. Leg muscle stimulation produces better results than upper extremity treatment. Five studies using NMES on leg muscles showed substantial spasticity reduction compared to control (−0.78 [95% CI, −1.02 to −0.54]) ^[14]. However, six studies on wrist NMES showed no significant improvement (0.12 [95% CI, −0.41 to 0.64]) ^[14].

Clinicians in 2026 use these parameters to reduce spasticity:

Frequency: 20-30 Hz for NMES/FES ^[8]
Pulse duration: 300-350 μs ^[8]
Amplitude: Greater than 100 mA ^[8]
Session duration: Minimum 30 minutes to work ^[9]

Electrode placement plays a crucial role in treatment success. Stimulation works better when applied over nerves that supply spastic muscles rather than other areas like dermatomes ^[2]. Placing electrodes on common peroneal and tibialis nerves gives better results for ankle spasticity ^[2].

Upper limb spasticity responds well to specific treatments. Lin et al.’s study showed a significant MAS score decrease (p<.005) with 30 Hz NMES applied to spastic carpal extensor muscles. These benefits lasted through the one-month follow-up ^[15]. NMES also helped reduce static and dynamic spasticity of plantarflexors and improved plantarflexion push-off in stroke-affected lower limbs ^[4].

Benefits Beyond Spasticity: Range of Motion and Strength

Electrical stimulation helps stroke survivors regain lost function and offers amazing benefits beyond reducing spasticity. Research shows these treatments improve physical recovery through several connected mechanisms.

Improving joint flexibility

Stroke patients often face range of motion limits even after treating spasticity. The good news is electrical stimulation works well to increase joint mobility. A meta-analysis of 13 randomized clinical trials shows that NMES with regular therapy increased range of motion by 2.87 degrees compared to control groups ^[14]. We saw these improvements when electrical stimulation worked together with other therapeutic techniques.

Different body parts respond differently to treatment. Research on NMES applied to the leg among other treatments showed a 3.13-degree increase in range of motion ^[14]. The elbow treatments showed a 4.57-degree improvement ^[14]. These results prove how important it is to target specific body regions with the right stimulation protocols.

Patients with foot drop saw better ankle dorsiflexion range of motion when electrical stimulation joined conventional rehabilitation therapy. This worked best during recovery phases (1-6 months post-stroke) ^[16]. The targeted approach helps fix walking patterns that don’t improve with traditional therapy alone.

Preventing muscle atrophy

Muscle wasting creates serious problems for stroke survivors. Electrical stimulation curbs this issue through several body processes. Research shows NMES reduces stroke-related sarcopenia by promoting satellite cell myogenic differentiation via the AMPK-ULK1-Autophagy axis ^[17]. This means it helps rebuild muscles at the cellular level.

The body responds by releasing myokines—especially insulin-like growth factor-1 (IGF-1)—which builds skeletal muscle ^[3]. NMES also lowers MuRF-1 and Atrogin-1, genes that cause muscle shrinkage ^[3]. This explains why regular stimulation can change muscle fiber makeup, turning Type II glycolytic fibers into more resilient Type I oxidative skeletal muscle fibers ^[18].

The numbers tell a clear story. Studies found more muscle mass and better myogenic differentiation in stroke-related sarcopenia models after NMES treatment ^[17]. Human tests showed dorsiflexor muscle strength increased by 56.6% with FES plus conventional rehabilitation, compared to just 27.7% with conventional rehabilitation alone ^[3].

Improving voluntary movement

Electrical stimulation’s biggest impact might be how it aids voluntary motor control. It does more than strengthen muscles. Stroke patients who exercise during electrical stimulation rebuild their brain-muscle connection faster ^[19].

Research proves that mixing electrical stimulation with physical therapy exercises leads to better movement and function than traditional therapy alone ^[20]. This happens because electrical stimulation sends rich sensory signals, including position feedback from joints, tendons, muscles, and mechanoreceptors ^[18].

FES really shines at improving functional movements. Studies confirm FES treatment of the dorsiflexors fixes foot drop and balances walking patterns ^[3]. Using it on both hip abductors and dorsiflexors improves walking speed and symmetry. This helps with uneven weight shifts that regular approaches don’t fix well ^[3].

Combining Electrical Stimulation with Other Therapies

Research shows that combining electrical stimulation with other rehabilitation methods creates better results than using either therapy alone. Stroke survivors who struggle with spasticity can benefit from these combined approaches that lead to better recovery.

Physical and occupational therapy integration

Combining electrical stimulation with conventional rehabilitation leads to better therapeutic outcomes. Muscles that receive electrical stimulation while doing physical exercises show a collaborative effect ^[21]. This combined approach targets different aspects of motor learning. Electrical stimulation strengthens neuromotor pathways through muscle activation. Physical therapy allows multiple repetitions of functional movements ^[21].

A notable advance combines synergy-based functional electrical stimulation (FES) with robotic-assisted therapy (RAT). This combination creates an effective intervention for upper limb rehabilitation because each method complements the other’s recovery aspects ^[21]. The Fourier intelligence upper-limb robotic system shows this approach well. It provides passive, assistive, and active planar movements around shoulder, elbow, and wrist joints while FES activates specific muscle groups ^[21].

Botulinum toxin and NMES

Botulinum toxin injections combined with electrical stimulation create a powerful combination to manage post-stroke spasticity. A randomized, placebo-controlled study revealed that patients who received both botulinum toxin A (BtxA) and electrical stimulation had better outcomes than those who got toxin alone ^[22].

The combined approach showed remarkable improvements:

Better cleaning of the palm of the hand (p = 0.004)
Reduced elbow spasticity (p = 0.011)
Improved ability to put the arm through a sleeve (p = 0.020) ^[22]

Electrical stimulation makes botulinum toxin more effective in treating chronic upper limb flexor spasticity after stroke ^[22]. This collaborative effect might happen because electrical stimulation increases blood flow to target muscles, which helps spread the toxin better.

Mirror therapy and FES

Mirror therapy (MT) with functional electrical stimulation creates another powerful rehabilitation tool. MT activates mirror neurons through visual feedback. FES directly stimulates affected muscles to cause contraction ^[23]. Each method fills gaps in the other’s approach. MT doesn’t produce spontaneous muscle contractions well, and FES alone doesn’t help with motor relearning ^[23].

A systematic review of the combined approach found significant improvements. Patients showed better walking speed, Berg Balance Scale scores, cadence, step length, and stride length compared to control groups ^[23]. Studies showed that MT combined with FES led to significant upper extremity motor improvements based on the Fugl-Meyer Assessment ^[24]. Patients also showed notable improvements in wrist and hand function subscores ^[24].

This combined therapy works especially well for severe stroke patients. One study found that patients receiving both therapies showed significant improvements in Fugl-Meyer scores. These improvements included better hand, wrist, arm coordination and wrist flexion power compared to patients who received just one therapy ^[25].

Risks, Contraindications, and Safety Guidelines

Electrical stimulation provides great benefits for managing spasticity, but safety must come first. Patients and caregivers need a clear understanding of risks and contraindications to make this therapy work safely.

Who should avoid electrical stimulation

Patients with cardiac pacemakers or implanted electrical devices must never use electrical stimulation. This restriction exists because the treatment could cause device malfunction or life-threatening heart rhythm problems ^[26]. The therapy presents absolute risks for patients with active deep vein thrombosis. Blood clots might break loose and cause pulmonary embolism or stroke ^[26].

You should not use electrical stimulation on these areas:

Malignant tumors (risk of accelerated tumor growth from increased metabolism) ^[26]
Pregnant uterus or lumbo-pelvic area (especially during first trimester) ^[26]
Open wounds, broken bones, or infected areas ^[27]
Front of neck, eyes, or reproductive organs ^[27]
Areas with exposed metal like pins or staples ^[27]

Common side effects and how to manage them

Most side effects of electrical stimulation stay mild. Skin irritation tops the list of problems, usually from using adhesive electrodes too much ^[28]. Some patients might experience muscle tears, burns, or discomfort ^[27].

Clean skin properly before applying electrodes to minimize side effects. Persistent redness might mean your stimulation settings need adjustment ^[1]. Keep track of any bad reactions to help make future sessions better.

Safe electrode placement and usage tips

The right electrode placement makes all the difference in treatment success. Place electrodes on motor points where nerves enter muscles. This approach creates efficient muscle contractions with minimal current ^[5]. Wrong placement often results in weak contractions, quick fatigue, or odd movement patterns ^[5].

Clean the skin surface well before putting on electrodes. Alcohol prep pads do the job nicely, but skip the lotion – it blocks electrical flow ^[1]. Remember to switch off the device completely before taking off the electrodes ^[29].

Choosing the Right Device and Parameters in 2026

Electrical stimulation devices have evolved faster than ever, and 2026 gives stroke survivors more choices to manage spasticity both at home and in clinical settings.

Home-use vs clinical devices

Rehabilitation equipment used to be designed for hospitals, and patients needed medical staff for assistance. Now, home-based rehabilitation devices let stroke patients do upper limb training on their own ^[30]. These new systems help healthcare professionals monitor remotely and adjust programs based on individual needs ^[30].

Home FES devices have several advantages compared to clinical-only options:

Patients with mobility limitations can access them easily
Therapy continues beyond scheduled appointments
Daily activities become part of the treatment
Long-term treatment costs less

The MyoCycle stands out as a popular choice that stimulates up to 10 different muscles during at-home therapy ^[31]. The FDA-cleared TrainFES Advanced device delivers smart electrical stimulation therapy designed specifically for stroke and spinal cord injury patients ^[32].

Recommended frequency and duration

Therapy sessions in 2026 usually last 30-45 minutes for the best results ^[12]. Research shows patients need at least 10 FES sessions, though better outcomes happen after about 16 sessions ^[12].

The right pulse amplitude makes a vital difference—it should be strong enough to bring out muscle response while staying comfortable ^[1]. Patients can reduce pulse amplitude gradually as their muscles get stronger, which helps them continue therapy comfortably ^[1].

Emerging technologies and smart devices

New devices come with impressive advances. NeuroSkin®, a textile-based FES system, combines embedded dry electrodes with immediate gait analysis and AI-driven stimulation timing ^[12]. The system learns to adapt to individual patients after recording about 20 steps ^[12].

NeuStim takes less than 90 seconds to set up and lets clinicians control stimulation through a tablet interface ^[33]. It uses over 150 small electrodes to deliver precise electrical impulses without repositioning ^[33]. Some patients respond to this targeted approach within seconds ^[33].

Conclusion

Electrical stimulation stands out as a powerful tool to fight post-stroke spasticity. This piece explains how different stimulation techniques help change neural pathways, reduce muscle tone problems and aid recovery through neuroplastic mechanisms. Research shows that the right application of electrical stimulation will give a better range of motion. It prevents muscle atrophy and improves voluntary movement while reducing spasticity.

The benefits of electrical stimulation go beyond standard therapies. A collaborative effort emerges when you combine it with physical therapy, botulinum toxin injections, or mirror therapy. This approach tackles multiple aspects of motor recovery at once. Patients who receive combined treatments show better functional improvements than those who use just one method.

Patient safety comes first with electrical stimulation. All but one of these groups should stay away from this therapy – people with cardiac pacemakers, active thrombosis, or malignancies in the treatment area. The right stimulation settings, electrode placement, and treatment duration will keep patients safe and ensure the therapy works well.

The digital world of available devices has changed substantially. By 2026, stroke survivors will have better access to home-based systems than ever before. New technology lets patients continue their therapy outside clinical settings. Smart devices with AI-driven stimulation timing and textile-based electrodes customize treatment based on individual needs.

Healthcare providers and stroke survivors should tap into the potential of electrical stimulation as part of a complete rehabilitation plan. While spasticity creates major hurdles in recovery, electrical stimulation offers a proven path to better function and quality of life. Patients with post-stroke spasticity should ask their rehabilitation team about these options to find the best approach for their condition.

Key Takeaways

Electrical stimulation has emerged as a scientifically-backed treatment for post-stroke spasticity, offering stroke survivors multiple pathways to recovery beyond traditional therapies alone.

• Electrical stimulation effectively reduces spasticity by modulating spinal reflexes and promoting neuroplasticity, with clinical trials showing significant improvements in muscle tone and function.

• Combined therapies produce superior results – pairing electrical stimulation with physical therapy, botulinum toxin, or mirror therapy creates synergistic effects that exceed single-treatment approaches.

• Benefits extend beyond spasticity reduction including improved range of motion (2.87° increase), prevention of muscle atrophy, and enhanced voluntary movement control.

• Home-based devices now available in 2026 allow continuous therapy with AI-driven systems like NeuroSkin® and TrainFES, enabling personalized treatment beyond clinical settings.

• Safety requires careful patient selection – avoid use with pacemakers, active blood clots, or malignancies, and ensure proper electrode placement for optimal results.

The key to success lies in working with healthcare providers to develop personalized protocols that combine electrical stimulation with other rehabilitation approaches, maximizing recovery potential while maintaining safety standards.

References