Physiotherapists inherit the consequences of the first weeks after a stroke, a brain injury or a spinal cord injury twice over.

The first consequence is at the ankle itself. A foot that has spent weeks driven into plantarflexion by tone and gravity arrives in the rehabilitation gym short of the range it needs. A foot that cannot reach plantigrade cannot take weight properly, and everything that needs attention (standing practice, transfers, gait work) gets harder.

The second inherited problem relates to the skin. A heel pressure ulcer acquired during the acute phase can halt weight-bearing for weeks or months, right at the point in recovery when time matters most. Every day that the patient remains in bed results in loss of muscle mass. We also know that such an ulcer, even when healed, is much more likely to recur due to changes in the tissue's mechanical properties.

Most writing about heel pressure relief devices treats these as separate problems, one belonging to tissue viability and one to physiotherapy. In my experience, if we want continuity of care, they are best considered as part of the same problem seen from two directions, and the device on the end of the bed is where they meet. This article is about that meeting point, including some evidence that does not say what many people assume it says.

In 1994, I was visiting the Cleveland Clinic and saw a product design I came to know as the PRAFO (pressure relief ankle-foot orthosis). I recognised this as a practical orthosis being used to reduce the risk of heel pressure ulcers developing in at-risk patients following orthopaedic procedures. It's true that I liked the concept so much that we created a company, Anatomical Concepts (UK), to bring the products to the UK. Thirty years have now gone by, and we still deal with the PRAFO range. We still see the challenge that heel pressure ulcers present to affected individuals and our healthcare systems. For decades, we've emphasised prevention, yet acquired ulcers remain a widespread problem. We have some understanding of the mechanical and medical factors that heighten risk and lead to pressure ulcers, but something is missing.

If you've lost sensation in a hand or foot due to nerve injury, you'll notice that most of the information available focuses on muscle. Muscle wasting, muscle strengthening, preventing atrophy, stimulating a weak limb. Page after page of content. Then you look for something about the numbness, the part that actually bothers you most, and there is very little content available.

I want to address that gap, because there is real evidence that electrical stimulation improves sensory recovery. There is also, as far as I am aware, no evidence that any device you can buy and use at home will bring feeling back to a numb hand. Those two statements sit together and seem to be opposing; the difference between them is worth understanding before anyone sells you anything.

We see many people with foot drop, but the cause can vary a great deal and the treatment approach consequently will need to be personalised to the situation. One person has broken a leg; another has dislocated a knee or is recovering from a hip replacement or lumbar spine surgery, and now the foot on that side will not lift. They are catching their toe on every kerb. They have discovered foot drop stimulators online, watched the videos of people walking along a corridor without a brace, and they want to know how to get one.

The videos are genuine. The devices do what they appear to do. But almost every person in those videos has had a stroke, and that difference is not a minor detail. It decides whether that type of device can work for you at all.

I want to explain what a foot drop stimulator is actually doing, why it may do nothing whatsoever for a peroneal nerve injury, and what does matter in the first few months after that kind of injury.

Someone has damaged a nerve. Perhaps because of a fracture, perhaps a fall, perhaps a complication of surgery they were told would be routine. They have read that electrical stimulation can help prevent muscle wasting. They have bought a device, often an inexpensive TENS unit, sometimes a consumer muscle stimulator. They have put the pads on, turned the intensity up as far as it will go, and nothing has happened. No contraction. No twitch. Nothing at all.

Then, usually near the end of the call, comes the question, and it is nearly always some version of this:

Could I have made it worse?

If you have a nerve injury, whether at the spine or further out in a limb, at some point, someone may send you for a nerve conduction study. You will lie on a couch while a neurophysiologist delivers small electrical pulses to your skin and, a little later, puts a fine needle into one or two muscles. A few weeks after that, a report lands with your consultant. It is dense, full of numbers and abbreviations, and it is written for one clinician to read to another. Almost nobody explains it to the person whose nerve it describes. Just this morning, I read a note from a client who said, "I had a nerve conduction test, which indicated severe injury to the nerves." You might wonder, like me, what severe means, and what do I do about it?