Spasticity and Muscle Spasms: A Plain English Guide for People Living With Them

SpasticityFES CyclingFunctional Electrical Stimulation (FES)
Written By Derek Jones

When I demonstrate an FES cycling system, spasticity is usually in the room before I have finished setting up. A leg that will not settle onto the pedal. A knee that pushes out straight at the wrong moment. A foot that starts bouncing the instant it takes any weight. The person in the chair rarely calls it spasticity. They say their legs have a mind of their own, or that everything goes rigid when they transfer, or that the spasms wake them at three in the morning. The clinical word comes later, if it comes at all.

This article is for the person who has just been introduced to that word, or who has lived with the thing itself for years without anyone quite explaining it. I want to cover what spasticity and spasms actually are, why they happen after a spinal cord injury, a stroke or with multiple sclerosis, what they do to daily life, and what genuinely helps, from medication through to electrical stimulation. I will try to be clear about what the evidence shows and what it does not; if different people have told you contradictory things, that is partly because the field itself contains genuine uncertainty.

Spasm, spasticity, cramp, or clonus: which one is this?

One question appears in the patient forums over and over, in almost the same words: what is the difference between a spasm, spasticity and a cramp? Part of the answer is that even the specialists have not fully agreed; a 2025 handbook chapter from the International Federation of Clinical Neurophysiology states directly that there is no generally accepted definition of spasticity.

Here is the working version I use with clients.

Spasticity is the background state: muscles too ready to contract, so they feel stiff and resist being moved, especially quickly. It is a property your limb has rather than an event.

A spasm is an event: a sudden, involuntary contraction. Your legs jump, your knee shoots out straight (your therapist calls this an extensor spasm), your arm pulls in. Spasms often ride on top of spasticity as individual episodes rather than as the state itself.

Clonus is the rhythmic, bouncing version, most often seen at the ankle. You might put the foot on a footplate of the bike at the wrong angle and it starts tapping away on its own.

A cramp is different again: a painful, sustained knot of contraction that healthy muscles also produce, which is why cramps alone do not indicate a neurological problem.

The labels overlap, and I would not lose sleep over perfectly classifying your own symptoms. What genuinely helps your clinical team is a description of what happens and when it happens. It's your personal experience of what the limb does, what sets it off, and what it stops you from doing.

KEY POINT: Spasticity is the ongoing state of muscles being too ready to contract. Spasms are sudden episodes; clonus is the rhythmic bouncing effect, and cramps are something healthy muscles can also do. The names matter less than a clear description of what happens, when, and what it interferes with.

Why it happens: the brake that stopped working

I am not a neurophysiologist, but the core mechanism can be explained without a single Latin word.

In an uninjured nervous system, the brain sends a constant, quiet stream of signals down the spinal cord. Much of that traffic is not commanding movement at all; it is restraining the spinal cord's own reflexes, the way a brake restrains the movement of a car on a hill.

A spinal cord injury, a stroke or MS disrupts that stream of signal traffic. The reflexes below the level of the damage lose their braking effect and become overactive. A small, quick stretch that a calm nervous system would ignore now triggers a large contraction. That is why the stiffness is often worse with fast movements, why a simple thing like a catheter tube dragging across the skin can set a whole leg off, and why the resistance you feel is genuinely involuntary. Nobody is failing to relax.

Two features of the timeline confuse people. After a spinal cord injury there is often an early period, sometimes weeks, when the muscles are floppy and reflexes are absent; spasticity then emerges over the following weeks and months as the spinal circuits reorganise. And after a stroke, spasticity commonly appears weeks or months after the event itself, so a tight, pulling arm three months on is a known pattern rather than evidence of a second stroke, although new symptoms always deserve a conversation with your clinical team.

How common is this, and what does it disrupt?

Many people assume they are alone with this; the numbers say otherwise. After a traumatic spinal cord injury, around two thirds of people report spasticity by the time they leave hospital; it is troublesome enough to need treatment in roughly one in three, and around one in five still report it interfering with function five years on. In multiple sclerosis, large surveys find between half and two thirds of people reporting spasticity, with about 40% of those rating it moderate or severe. After stroke, about one in four people develop spasticity overall, rising to about 40% among those with arm or leg weakness.

What does it disrupt? The research points at pain, contractures and tiredness as its closest companions, and the forums point, above everything else, at night: spasms that arrive when you lie down are the single most common complaint I encounter. For perspective, a Danish survey of over 2,000 people with MS found the symptoms most strongly linked to quality of life were fatigue, pain and disturbed sleep, with spasticity sitting alongside them rather than above them. Spasticity is one member of a gang, and treating it is often worthwhile precisely because of what it does to sleep and pain.

Are spasms a sign that movement is coming back?

You will find websites suggesting that spasms after a spinal cord injury are a sign of recovery. There is a grain of truth buried in the idea, but the claim as usually stated is wrong, and you deserve the accurate version.

The grain of truth: after the early floppy phase of spinal shock, the return of reflexes does mean the nervous system has moved into a new phase, and the timing can coincide with whatever recovery is going to happen. But the spasm itself is a reflex running without its brake as we described above. It's not a measure of the return of voluntary control. Someone can have powerful, frequent spasms and no useful movement; someone else can recover meaningful movement with very little tone. A second misunderstanding is related: a rigid limb can feel strong, but tone is not strength. A spastic limb is very often weak, stiff and poorly controlled all at once, which is why "just relax" and "build it up" both miss the point.

KEY POINT: Spasms mean the spinal reflexes are active without their normal restraint. They are not a signal that voluntary movement is returning, and their strength says nothing about the strength you can use. Real recovery is measured by what you can do on purpose.

When spasms suddenly get worse, check for a trigger first

If I could put one message from this article on a card in every wheelchair user's home, it would be this one. Spasticity fluctuates, and a sudden, marked worsening is very often not your fundamental condition deteriorating. It is frequently your body reporting a problem it cannot report any other way.

In a study of urinary tract infections in men with spinal cord injury, increased spasticity was one of the presenting signs in about 30% of confirmed infection episodes. The nervous system below an injury cannot always send you pain, so it sends you tone. Before concluding that your spasticity has permanently escalated, or reaching for a higher drug dose, check the list:

  • A urinary tract infection, or a catheter problem

  • A full bladder or bowel, or constipation

  • Skin damage: a pressure sore developing, an ingrown toenail, a tight seam or strap rubbing somewhere

  • Pain or injury anywhere below the level of damage, including fractures you may not feel

  • Any other infection or illness

  • For many people with MS, heat, hot weather, and hot baths are commonly reported to make stiffness worse. With climate changes this is obviously not a happy situation.

UK stroke guidance explicitly tells clinicians to teach this. If the "trigger hunt" yields no results and the change persists, involve your GP or clinical team.

KEY POINT: A sudden flare of spasms is often a messenger representing a source of triggering irritation. Check bladder, bowel, skin, and for signs of infection first. Treating a urinary tract infection will do more for that week's spasticity than any stimulator or tablet.

Is some spasticity worth keeping?

Here is something the leaflets rarely say: spasticity is not always the enemy. Some people use the stiffness in their legs to help them transfer or stand, and I have clients who would not thank anyone for abolishing their tone entirely, because they would lose the extensor thrust they rely on to get from chair to bed. The goal of treatment is never simply "less spasticity"; it is the level you can live and function with, decided with a clinician who has asked what your tone does for you as well as to you.

Contractures: when stiffness becomes fixed

There is a harder deadline hiding behind everything above. Spasticity is muscle overactivity: it fluctuates, responds to triggers, and can be turned down. A contracture is different. It is a structural shortening of the muscle and its connective tissue, and once established it does not relax away, because there is no longer anything to relax: the tissue is genuinely shorter, and careful measurement after stroke shows the shortening sits in the muscle itself rather than the tendon.

Contractures develop when a joint is held in a shortened position for long periods, and paralysis and spasticity are exactly the forces that hold joints there. They are dismayingly common. I see them just about every week.

In a study following 200 people admitted to hospital with stroke, 52% had developed at least one contracture within six months; in a similar study of 92 people with new spinal cord injuries, 66% had done so within a year.

In high-level spinal cord injuries, the arms are especially vulnerable, something I see regularly in people with cervical injuries who come to us years on, with elbows, wrists, and hands that no longer open fully. In one multicentre review of 74 arms in people with complete C5 or C6 injuries, half could no longer be fully straightened at the elbow, and the arms at greatest risk were those whose triceps no longer responded to anything, including electrical stimulation.

What does the evidence say about prevention?
Less than most people assume. A large Cochrane review of 49 trials found high-quality evidence that stretching, as delivered in those trials, does not produce clinically important changes in joint mobility. The average effect in neurological conditions was about 2 degrees. A randomised trial of overnight wrist splinting after stroke found no benefit, and NICE stroke guidance now says not to offer wrist and hand splints routinely, but to consider them for people at risk, with a clear purpose, proper fitting and a review plan. Whether regular passive movements help is, on the published evidence, simply unclear, and adding electrical stimulation to a standing programme made no measurable difference to ankle contractures in one careful trial in brain injury.

I read that evidence with two eyes, though. Every trial in the Cochrane review applied stretch for less than seven months, so what sustained positioning over years achieves has never been tested, rather than answered negatively.

What the evidence discourages is relying on a few minutes of stretching to do a job it has not been shown to do; sustained time in good alignment, active movement wherever possible, and early escalation when a limb starts drifting remain the sensible course. For established or fast-developing contractures there are stronger tools: in one small but well-designed trial, botulinum toxin followed by serial casting improved ankle range by around 26 degrees, and early botulinum toxin after stroke slowed contracture formation in a placebo-controlled trial of 93 people, though it did not improve arm function. Surgical release is sometimes considered as a last resort.

I have to say that I do encourage persons, especially with high-level spinal cord injuries, to use reverse arm cranking as part of their FES Cycling exercise regime, either with passive movement only or with the addition of electrical stimulation. Why reverse arm cranking? Well that's the subject of a future article.

There is one more practical reason to care about contractures. Studies of FES cycling routinely exclude people with severely limited hip and knee range. No formal guideline names contracture as a contraindication, and there is no magic number of degrees; the reason is mechanical. A pedal crank turns through a fixed arc, and joints that cannot travel through that arc cannot be cycled safely, whatever the muscles could do. I have met people for whom this door had closed by the time they found us.

KEY POINT: Spasticity is negotiable; a contracture much less so. Half of stroke patients develop one within six months and two thirds of people with new spinal cord injuries within a year. Short bouts of stretching have not been shown to prevent them, so take a drifting joint seriously early, ask about escalation, and remember that severely restricted hips and knees can rule out options such as FES cycling and even standing in a standing frame later.

What medication can and cannot do

Baclofen is where most people start, usually because their doctor prescribes it, and UK guidance supports that. Most of our FES Cycling clients seem to use it. NICE recommends oral baclofen first for MS spasticity and considers it for generalised spasticity after stroke, with gabapentin as a second option in MS and referral to a specialist spasticity service when initial treatment fails.

Two things about baclofen are interesting but not that well known.
First, the trial evidence behind the tablets is thinner than its almost universal use suggests. A 2023 systematic review gathered 98 studies of baclofen in spinal cord injury and found only four that were highest quality, randomised, double-blind and placebo-controlled, with most of the efficacy data concerning the surgically implanted pump rather than the tablets. That does not mean baclofen does nothing. It means the confident tone in which it is sometimes prescribed outruns the trials. Second, the side effects that fill the patient forums are real and common: drowsiness, weakness and a foggy head are frequently reported, and for many people that trade is the reason they go looking for alternatives. Over the years we have had many clients who embrace FES cycling in the hope that they can reduce their medication. If that is you, one safety rule is not negotiable: never stop baclofen abruptly. Sudden withdrawal is dangerous, and any reduction belongs in a plan agreed with your prescriber.

Beyond tablets sit the focal and the severe-case options. Botulinum toxin injections target specific overactive muscles, wear off over roughly three months, and are supported by UK guidance for focal spasticity; a 2024 review of 54 studies found no change in the injected muscle's strength in most results, though it judged the question not fully settled. For severe spasticity that has not responded to oral medication, an intrathecal baclofen pump delivers tiny doses directly into the spinal fluid, and a 2024 review in MS found it effective in that refractory group, with most complications related to the surgery rather than the drug. And because MS readers ask constantly, cannabis-based nabiximols (Sativex) have genuine trial evidence, with an interesting wrinkle, in that patients consistently report a larger improvement than clinicians can measure on their tone scales. Whether it is an option for you is a conversation for your MS team, since prescribing criteria are specific.

KEY POINT: Medication is a legitimate tool with real costs. Baclofen remains the guideline first choice even though the trial base for the tablets is surprisingly thin, and its sedation and weakness are the most common reasons people look further. Botulinum toxin suits focal problems, the pump suits severe refractory cases, and no reduction in baclofen should ever be abrupt.

Can electrical stimulation help?

This is the question I am asked most, and I will answer it carefully, because this is territory where sellers sometimes overclaim and charities say nothing at all.

Starting with the strongest anchor available, NICE's 2023 stroke rehabilitation guideline explicitly says clinicians should consider a trial of NMES, FES or TENS for focal spasticity after stroke. Electrical stimulation for spasticity is not a fringe idea and it is in mainstream UK guidance, framed as something worth trying properly. As usual, there tends to be confusion over terminology and a lack of understanding of what stimulation parameters are associated with these terms.

What does the research show? For TENS, the gentle, sensory-level stimulation most people have met through pain machines, two independent meta-analyses in stroke both found a moderate reduction in spasticity when TENS was added to physiotherapy, with sessions longer than 30 minutes appearing to matter. One analysis favoured 100 Hz over lower frequencies, though the direct comparison between frequencies was not itself conclusive, and a less flattering network analysis ranked TENS behind other approaches, so the effect size quoted depends on who is quoting. In spinal cord injury, a small crossover trial found a single 30-minute session of either TENS or FES reduced spasticity for up to four hours. In MS specifically, a 2024 review rated the certainty of evidence for TENS as very low, which is worth knowing before spending money.

For FES cycling, the evidence is genuinely mixed, and I say so as someone who sells the equipment. One meta-analysis found a significant reduction in spasticity, but only in programmes that ran for more than 20 sessions, which aligns with my practical experience that this is a cumulative training effect, not a quick fix. A 2025 systematic review of sixteen studies still describes the overall evidence as inconclusive, with the best long-term results coming from programmes of an hour, three times a week, for sixteen weeks. My own reading is that the positive studies, the mechanism, and what I see in clients all line up, but I hold that view as experience alongside evidence, not as proof.

One research finding deserves special mention. A 2022 meta-analysis found that stimulation reduced spasticity whether or not it caused the muscle to visibly contract. In FES Cycling we tend to aim for visible contractions as this allows for active cycling exercise. However, it's nice to know that sensory-level stimulation, with parameters set to deliver lower intensity, worked too. As with many applications of electrical stimulation, we can't say there is one "best" set of stimulation parameters to use; however, we do know settings that tend to work for most people, and some experimentation generally bears fruit.

The active ingredient appears to be the stream of sensory signals flowing into the spinal cord, gently retraining the reflex circuits, rather than the muscle work itself. Which explains something I hear often: "I bought a cheap TENS unit and it did nothing." A consumer device used briefly, at the wrong settings, for the wrong purpose, tells you almost nothing about what a properly set up programme can do.

KEY POINT: UK stroke guidance recommends considering a trial of NMES, FES or TENS for focal spasticity. The research shows moderate, real, but not universal effects, with longer sessions and programmes past twenty sessions performing best, and the benefit appears to come through the sensory nerves rather than the muscle contraction itself.

Transcutaneous spinal cord stimulation: where the evidence stands

The newest entrant works one level further up (on the spine rather than stimulating a limb). Transcutaneous spinal cord stimulation, tSCS, delivers stimulation through electrodes on the skin over the spine, usually around the T11 to T12 level, to affect the legs, with return electrodes on the abdomen, aiming to calm the spinal circuits at their source. The "established" research protocol runs at 50 Hz with millisecond-long paired pulses for 30 minutes, at an intensity just below the level that would produce muscle twitches.

The case for it is genuinely interesting. Work from the Vienna group found that a single 30-minute session reduced stiffness, clonus and spasms in people with spinal cord injury, with large effect sizes two hours later, and their own title contains the operative word: temporary. In 2024, the same group published elegant work showing why it works. Spasticity involves specific inhibitory circuits in the cord running below normal strength, and tSCS measurably restores them towards normal for a time. A study in MS without a control group found similar effects lasting for hours, and repeated sessions may lead to longer carryover.

In 2025, the first randomised, sham-controlled trial of this protocol for spasticity, in sixteen people with progressive MS, found the difference between real and sham stimulation did not reach statistical significance. More people improved with the real stimulation than with the sham, 10 versus 7, but not by a large enough margin to rule out chance. The research group has links to SensorStim, the Berlin company that designed the Stim2Go device we supply, one author having co-founded it.

A company-adjacent trial reporting an unflattering result is, if anything, a mark of research done properly! Other studies add texture to the picture and a randomised study in subacute spinal cord injury found no significant spasticity change; another found benefit only in people who started with high spasticity, with one stimulation pattern making mild calf spasticity slightly worse, a concrete argument for individual assessment over standard settings. The systematic reviews grade the evidence as limited for effectiveness and reassuring for safety, with adverse events confined to skin irritation and tingling.

Certainly, the Stim2Go product, now the core product of our FES Cycling offer and our general-purpose NMES stimulator, supports several tSCS applications. Some programmes are for spasticity, some targeting pain, and some being incorporated with FES Cycling for these effects. Our clients include spinal cord injured and those with MS. Our experience with this is very positive, even if not backed by extensive research at present.

So where does that leave you? The fairest summary I can give is this: the mechanism is well established, the safety record is good, the short-term effects in spinal cord injury appear real in several studies, and our practical experience supports this. The technology has not yet beaten a sham in a controlled trial, but that can change in either direction, and we follow the literature closely.

On the practical side, the Stim2Go we supply includes tSCS spasm-reduction programmes at 33 Hz and 50 Hz among its licensed indications for severe spasms, with the working intensity set individually by a calibration programme that finds your individual reflex threshold and works just below it. That is a description of what the device offers, not a claim about what it will do for you; an assessed trial with before-and-after measurements is how you find out whether you respond.

KEY POINT: tSCS has a well-demonstrated mechanism, a clean safety record, and encouraging short-term effects on spasticity in spinal cord injury, but the first sham-controlled randomised trial, in MS, did not reach statistical significance. Anyone offering it to you as proven is ahead of the evidence but it's also the case that anyone dismissing it outright is behind it.

What you can do yourself, starting this week

Some of the most useful moves cost nothing. Keep a trigger diary for a fortnight and when the spasms flare, note bladder, bowel, skin, sleep, temperature and stress level. Patterns emerge quickly and give your clinician something concrete. Protect your positioning. I visited a client this week who had his legs fixed in an extended knee position due to a wheelchair mechanical fault and this was leading to pressure ulcer risk and knee stiffness. Time spent with joints in good alignment, day and night, is basic care for tone and the best insurance against contracture, even though short stretching bouts alone have not earned the faith often placed in them. Keep moving whatever moves: rhythmic, repeated activity over a good range of motion is consistently associated with calmer tone in practice. And treat infections and skin problems as urgent rather than minor, because below a spinal cord injury, they so often announce themselves through your spasticity first.

Getting help in the UK

Two referral routes are written into national guidance, and it is worth knowing them by name. For stroke, NICE recommends referring to a specialist spasticity service when spasticity is not responding, treatments are not tolerated, or needs are complex. For MS, the equivalent recommendation is referral to a multidisciplinary team experienced in spasticity management when function is significantly affected. Spasticity clinics do exist across the UK, and you are entitled to ask your GP, consultant or physiotherapist directly whether a referral is appropriate.

Equipment is where expectations need managing. Electrical stimulation devices for home use, including FES cycling systems and stimulators such as the Stim2Go, are not routinely funded by most NHS integrated care boards. What funding does exist is generally case-by-case, and many of the people we work with self-fund or use case-managed or medico-legal funding. It is also why an assessment matters before any purchase because the right question is not "is this technology good" but "does this technology do something measurable for me".

What realistic improvement looks like

Nothing here is a cure. Successful spasticity management looks like fewer bad nights, easier transfers, a calmer session on the bike, perhaps a reduced medication dose agreed with your prescriber, sustained by things you do regularly rather than once. Single sessions of stimulation buy hours of relief in the studies and repeat programmes appear to build longer carry-over. Stopping stimulation lets things drift back. That is not a failing of the tools. It is the nature of a long-term condition, and the people who do best are the ones whose expectations were set accurately at the start. We go to the gym regularly if we want the benefits. We don't expect to go just once and be healthy for ever.

Quick answers to the questions I hear most

Why do my legs jump at night? Lying down changes the input stimulus provided to overactive spinal reflexes, and the day's accumulated triggers, a filling bladder among them, often surface at night. Frequent night spasms are worth reporting rather than enduring.

What is the difference between a spasm and spasticity? Spasticity is the ongoing state of muscles being too ready to contract; a spasm is the individual sudden episode. One is the weather pattern, the other is "the lightning".

Do spasms mean my injury is healing? No. They mean the reflexes below the injury are active without their normal restraint. Recovery is measured by regaining voluntary control, not by tone.

Does baclofen stop spasms? It reduces them for many people, at the common cost of drowsiness and weakness. Sometimes your body adapts to the dose, and effectiveness may rely on higher doses over time. Never stop it abruptly; reduce only with your prescriber.

Can I get FES on the NHS? Rarely as a routine provision. Most integrated care boards fund it case by case at best, so many people self-fund or use case-managed funding, which makes a proper assessment before purchase essential. Remember, too, that FES is not one thing. Even many clinicians have a poor practical understanding of electrical stimulation and how to apply it.

What I would suggest

If spasticity or spasms are shaping your days, start with your own clinical team. Ask whether a trigger could explain any recent worsening; ask whether a referral to a spasticity service or multidisciplinary team is appropriate, since both are named in national guidance; and if stiffness is focal, ask about the options NICE lists, including a trial of electrical stimulation. If a joint is losing range, raise it now, not at the next review. Once contractures become established, it is very difficult to reverse these effects.

Where we come in is assessment. At Anatomical Concepts, we have spent decades working with electrical stimulation in neurological rehabilitation, and the useful starting point is always the same: establishing what your spasticity pattern is, what your goals are, whether any of your tone is working for you, and whether stimulation produces a measurable response in your case, before any equipment is discussed. Decisions about your treatment belong with you and your clinicians, and nothing we do replaces that relationship.

If you would like to talk any of this through, whether you are weighing an alternative to a difficult medication or simply trying to understand what your legs are doing at three in the morning, do get in touch. A conversation costs nothing, and we would rather help you ask the right questions than see you spend money answering the wrong ones.

Further reading

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  • Cozzi FM, Zuckerman D, Sacknovitz A, et al. Outcomes, complications, and dosing of intrathecal baclofen in the treatment of multiple sclerosis: a systematic review. Neurosurgical Focus 2024; 56(6): E14. https://doi.org/10.3171/2024.3.FOCUS2464

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