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+44 (0)141 628 8222Before you invest in FES cycling, one question decides whether it can work at all: is the nerve between your spinal cord and your muscles still intact? A nerve conduction study answers it. Here is how to read one, in plain English.
There is a question that decides, before anything else, whether FES cycling can do anything for you at all. It is not about your fitness, your commitment, or how much of your leg you can feel. It is a question about your "wiring". Is the nerve between your spinal cord and your leg muscles still intact and working?
If it is, FES cycling has something to work with. If it is not, no amount of stimulation delivered the conventional way will turn the pedals, and you would be better served by a different approach entirely.
The good news is that this is not a guessing game. There is a test that answers the question directly, and most people who have had a spinal or nerve injury have either already had one or can ask for one. It is called a nerve conduction study, usually paired with a needle examination called EMG. The report it produces is written for one specialist to read to another, and almost nobody translates it for the person it describes. This article is a translation.
Conventional functional electrical stimulation, the kind that drives an FES bike, works by activating a motor nerve from outside the skin. Sticky electrodes on the thigh deliver a brief electrical pulse, typically less than a millisecond, repeated 20 to 50 times per second. That pulse triggers the nerve. The nerve triggers the muscle to contract, and the leg pushes the pedal.
The whole arrangement rests on one assumption: that there is a working nerve running from your spinal cord to the muscle that the pulse activates. FES does not directly command the muscle. It borrows the muscle's own nerve to do the work, which is exactly why it is so efficient. The nerve amplifies the tiny electrical pulse into a full contraction.
Take that nerve away, and the whole thing falls apart. The muscle is still there, still alive, but the means of switching it on from outside is gone. Setting the stimulator to maximum and hoping does nothing. This is the situation that a nerve conduction study is designed to detect, and it is the reason the test matters so much before you spend money on a system.
Every movement you ever made ran through a physiological two-stage relay. The first stage, the so-called upper motor neuron, runs from your brain down through the spinal cord. The second stage, the lower motor neuron, leaves the cord and travels out along a peripheral nerve to the muscle.
Most of the spinal cord injuries you read about damage the first stage. The relay is broken at the level of the cord, but the second stage, the nerve from the cord to the muscle, is untouched. For these injuries, FES cycling works fine. The stimulator can reach the intact lower motor neuron from outside the skin and make the muscle contract, even though your brain can no longer and there is paralysis.
Some injuries damage the second stage instead. If the injury is to the cauda equina or the conus, at the lower end of the spine, or to a peripheral nerve further out in a limb, it is the lower motor neuron itself that is harmed. Now the muscle is not just cut off from the brain; it is cut off from everything else in the nervous system. This is called denervation, and it changes the entire picture. In these cases, conventional FES has nothing left to activate.
KEY POINT: In an upper motor neuron injury, the muscle has lost its commander but keeps its nerve, and FES cycling can work. In a lower motor neuron injury, the muscle has lost its nerve altogether, and conventional FES cannot help. These look similar from the outside. A nerve conduction study distinguishes them.
This distinction is not a fine technicality. It is the single most important thing to establish before pursuing FES cycling, and it is precisely what the test is best at.
A full examination is really two tests that answer two questions.
The nerve conduction study looks at the nerve's structural wiring. A nerve is stimulated at one point on the skin, and the response is recorded from the muscle it supplies. The size of that response, its amplitude, is the key figure. It is roughly proportional to how many nerve fibres are still working. A big response means plenty of working fibres. A tiny response means most have stopped. No response means the motor supply is, to a first approximation, gone.
Because of that, the examiner compares your affected side against your unaffected side. If one leg produces a healthy signal and the other produces almost nothing, you are looking at a serious loss of working nerve fibres on the weak side. If both produce healthy signals but one limb is still weak, the problem is more likely central, upstream, in the cord or brain, with the peripheral nerve intact. That second picture is the FES-friendly one.
The needle examination looks at the muscle. A fine needle records electrical activity from inside the muscle. A healthy resting muscle is electrically silent. A muscle that has lost its nerve is not: its fibres begin to fire spontaneously, and the needle picks this up as fibrillation potentials and positive sharp waves. These are the clearest signs that a muscle has been denervated. The needle also watches how the muscle recruits when you try to contract it. Few or no motor units firing is a sign of lost nerve supply. Larger, messier units appearing later are a sign that repair has begun.
KEY POINT: A big drop in the nerve response on the weak side, together with spontaneous firing in the muscle at rest, is the signature of denervation. That combination means conventional FES will not work, and it points instead to a specialised approach.
A nerve conduction study gives a different answer depending on when it is done.
When a nerve is cut off, the part beyond the injury does not fail instantly. It degenerates over days to weeks, a process called Wallerian degeneration. The spontaneous firing that marks denervation takes roughly two to three weeks to appear and shows up in muscles close to the injury before those further away. So a test done in the first week or so can understate things. It is too early for the muscle's denervation signals to have developed, and far too early to show any signs of recovery, which takes longer still.
This is why clinicians often repeat the study, frequently at around three months. A first test taken soon after injury captures what has been lost. A second test, weeks or months later, reveals whether anything is coming back: more motor units firing, a growing nerve response, and enlarged, messy motor units that signal a nerve repairing itself. If you have only had one early study, it is worth knowing that a later one may tell a very different and more hopeful story.
If your study shows denervation, being told "stimulation will not work for you" is only half the truth. Conventional FES will not work. But denervated muscle can be stimulated. It just needs a completely different kind of stimulation, and this is where a great many people give up too soon.
The physics explains why. To make a muscle contract through its nerve takes very little energy, because the nerve does the amplifying. To make a denervated muscle contract, you have to directly activate the muscle membrane, which requires roughly 1,000 times more energy, delivered over a much longer pulse. Not a fraction of a millisecond, but tens to hundreds of milliseconds. This is far beyond what any FES bike or consumer stimulator can produce. It needs dedicated equipment, large electrodes, and high currents.
The evidence that this works is strong, and it comes mainly from the European RISE project led by Helmut Kern's group in Vienna, who spent two decades on it. In their home-based programme for people with complete lower motor neuron injuries, around ninety per cent of those who trained recovered or increased sustained muscle contractions, and about a quarter regained enough force to stand during stimulation with support. There is a time pressure, though: a denervated muscle wastes away and is gradually replaced by fat and scar tissue, with the window for rescue closing over roughly 12 to 18 months. Starting sooner protects more.
If this is your situation, we have written about it in more depth. Our companion article on cauda equina and lower motor neuron injury sets out what an at-home programme for denervated muscle actually looks like, and the evidence behind it.
Let me make this concrete with a recent case, fully de-identified.
A woman in her forties developed a drop foot immediately after routine lumbar spine surgery, unable to lift the front of her foot. Her nerve conduction study told a clear story. The nerve to her main foot-lifting muscle produced a response of 0.3 millivolts on the affected side, against 3.1 millivolts on the other: about a tenth of the normal signal. The needle examination found active denervation and only a single motor unit firing when she tried to lift the foot. But her sensory readings were normal and she had no numbness, which placed the injury very close to the spinal cord, on the motor side, a more recoverable pattern than it first looked.
When conventional stimulation settings were tried, a short pulse at a typical frequency, nothing happened, even at the highest current she could tolerate. With only a tenth of the nerve fibres conducting, there was too little for conventional stimulation to work with. But when long pulses were used, tens to hundreds of milliseconds each, the muscle produced a visible twitch. The muscle was alive. It simply needed to be addressed directly, not through its depleted nerve.
That is the whole value of the test in one example. Without it, you might buy a conventional system and conclude, wrongly, that stimulation had failed. With it, you know exactly which path has a chance of working, and which does not.
If you are considering FES cycling but worry that denervation might be an issue, a nerve conduction study is one of the most useful tests you can have before making the decision. Ask your clinicians four things about it: is the peripheral nerve to the target muscles intact, roughly how much of it is still working, is the muscle showing signs of denervation, and where does the injury sit. The answers sort you cleanly onto one of two paths.
If your nerves are intact and the problem is upstream in the cord, FES cycling has a real chance, and the rest of this site is written for you.
If your muscles are denervated, conventional FES cycling is not your route, but that is not the end of the conversation. A different kind of stimulation may still preserve your muscle and, in the right cases, restore useful force. The mistake to avoid is spending on the wrong equipment because nobody read the test to you.
We work with both types of stimulation and read these reports routinely. If you have a study and are not sure what it means for your options, we are glad to talk it through, alongside whatever your own clinical team advises. The aim is simple: to make sure the equipment you pursue is the equipment that can actually work for your particular wiring.
https://www.anatomicalconcepts.com
https://denervatedmuscle.com
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