Pain and Spasticity: 70 Per Cent Have It, and It Gets Dismissed

Pain and spasticity after spinal cord injury: 70 per cent have it, and it gets dismissed as impossible

“But you can’t feel your legs.”

People with spinal cord injury hear versions of that sentence from clinicians, family members and strangers, and it is the reason a great deal of treatable pain goes untreated for years.

The logic seems sound and it is wrong. The pain after a spinal cord injury is frequently generated by the damaged cord and the nervous system above it, not by the body part that appears to be the source. A person with a complete injury who cannot feel a pin in their foot can simultaneously experience burning, crushing or electric pain that they locate in that same foot. The sensation is real, the suffering is real, and the mechanism is well described.

The numbers are not marginal. The AlphaBeta report prepared for SpinalCure Australia in 2020 found that chronic pain lasting more than six months affects 70 per cent of people with spinal cord injury, with about a third reporting severe pain.

Seventy per cent. It is more common than the mobility impairment that defines the condition in the public mind, and when people with spinal cord injury are asked what they would most want resolved, pain is consistently near the top of the list — often above walking.

This comes from a New South Wales disability provider working with spinal cord injury every day. We are not a pain service and nothing in this guide is medical advice. What follows is an account of how pain and spasticity after spinal cord injury are understood and managed, written so that people can have a better-informed conversation with the clinicians who do make these decisions.

The four kinds of pain, and why the distinction decides the treatment

Getting the type right matters enormously, because treatments that work for one type do essentially nothing for another. A great deal of failed pain management after spinal cord injury is the right drug for the wrong pain.

Musculoskeletal nociceptive pain. Ordinary pain from joints, muscles and tendons, in the parts of the body that still have sensation. After spinal cord injury this is dominated by the shoulders, because arms become the means of transferring, propelling and weight-shifting — doing load-bearing work they were never designed for, thousands of times a day, for decades. Neck and upper back pain from posture and from looking up at standing people is close behind.

This responds to the things musculoskeletal pain normally responds to: load management, physiotherapy, technique change, equipment change, anti-inflammatories, injection. Importantly, it also responds to reducing the load, which usually means equipment — a power chair for longer distances, a tilt function so shoulders are not doing pressure relief, a hoist instead of a manual transfer. There is more on this in the guide to equipment and shoulders in this library.

Visceral nociceptive pain. Pain from internal organs — bladder, bowel, abdomen. Often felt as poorly localised abdominal discomfort, bloating or cramping.

This category carries a specific warning. Visceral pain may be the only signal the body can send about something serious: an impaction, a bladder stone, appendicitis, a gallbladder problem, an obstruction. In somebody with an injury at or above T6, autonomic dysreflexia may be the only other signal. New or unexplained abdominal pain after spinal cord injury should be investigated, not managed with analgesia.

At-level neuropathic pain. Pain in a band at or just below the level of injury, generated by damage to the cord and nerve roots at that level. Typically described as burning, tight, banding, or like sunburn. Often worse with touch or clothing. Frequently present where sensation is otherwise altered.

Below-level neuropathic pain — also called central pain. Pain felt below the level of injury, in regions with reduced or absent sensation, generated centrally rather than in the tissues where it is felt. Descriptions are distinctive and consistent: burning, electric, shooting, crushing, like ice, like being in boiling water, like the legs are being twisted. It can be constant or paroxysmal. It is often worse at night, worse with fatigue, worse with stress, and worse when something else is going on in the body — an infection, a pressure injury, a loaded bowel.

That last point is clinically useful. A sudden worsening of neuropathic pain is frequently the body reporting a problem elsewhere. The pain is not necessarily getting worse on its own; something has triggered it. The response is to look for the trigger — urinary infection, pressure injury, impaction, ingrown toenail, fracture — before escalating medication.

Neuropathic pain does not respond meaningfully to paracetamol, anti-inflammatories or, in most cases, opioids. It requires different drug classes entirely, which is why misclassification matters so much.

What the evidence supports

This is the honest version, and the honesty includes an uncomfortable headline: complete relief of neuropathic pain after spinal cord injury is uncommon. The realistic goal in most cases is meaningful reduction — enough to sleep, enough to work, enough to think about something else. Anybody promising elimination is overselling.

For neuropathic pain, the gabapentinoids have the strongest evidence. Pregabalin and gabapentin are the best-supported medications for central neuropathic pain after spinal cord injury and are generally first-line. They take weeks to titrate to an effective dose, which means a two-week trial at a low dose is not an adequate trial — a very common reason people conclude they “don’t work”. Side effects include drowsiness, dizziness, weight gain and ankle swelling, and dose needs adjusting in impaired renal function.

Certain antidepressants have supporting evidence, notably tricyclics such as amitriptyline and the serotonin-noradrenaline reuptake inhibitors such as duloxetine. These are prescribed for pain in their own right, not because the pain is psychological — a distinction worth insisting on if it is presented badly. Amitriptyline’s anticholinergic effects include constipation, which interacts badly with neurogenic bowel.

Opioids have poor evidence for central neuropathic pain and substantial harms in this population. They slow the bowel considerably, in people for whom constipation is already a serious problem and a trigger for autonomic dysreflexia. They depress respiratory drive, in people who may have limited respiratory reserve and undiagnosed sleep-disordered breathing. Tolerance and dependence develop. None of that means opioids are never appropriate, but it means they are not the obvious answer they appear to be, and a long-term opioid regimen for neuropathic pain deserves a proper review.

Non-drug approaches have better evidence than people expect. Exercise and physical activity have a reasonable evidence base for pain after spinal cord injury. Transcutaneous electrical nerve stimulation helps some people. Psychological therapies — cognitive behavioural approaches, acceptance and commitment therapy, mindfulness-based programmes, and hypnosis, which has a surprisingly respectable evidence base in this specific population — address the suffering and functional impact even where pain intensity changes little.

This needs stating clearly because people take offence at the suggestion and the offence is understandable: being referred to a psychologist for pain is routinely heard as being told the pain is imaginary. It is not that. Chronic pain of any origin involves nervous system processes that psychological therapy demonstrably influences, and the treatment works in people whose pain has an unambiguous physical cause. A good pain service will explain this properly. A bad referral that does not explain it damages trust.

Multidisciplinary pain services are the best setting for complex cases, and a referral is reasonable to request if pain has not been properly addressed.

Intrathecal drug delivery is used in selected refractory cases.

What to be careful about. This field attracts expensive interventions with thin evidence. Before paying for something, the questions worth asking are what the evidence is specifically in spinal cord injury, what the realistic expected benefit is, and what happens if it does not work.

Spasticity, and why treating it harder is not always better

Spasticity is increased muscle tone with exaggerated reflexes, caused by loss of the descending inhibitory signals that normally damp spinal reflexes. After spinal cord injury those signals cannot cross the damaged segment, so reflexes below the injury become unopposed and overactive.

It shows up as stiffness, involuntary jerks, clonus, spasms triggered by movement or touch, and muscles that resist being stretched.

It needs distinguishing from contracture, which is permanent shortening of muscle and connective tissue. Spasticity is active resistance that varies; contracture is fixed. Untreated spasticity leads to contracture, and contracture does not respond to antispasticity treatment — it requires stretching, splinting or surgery. Which is why early management matters.

Here is the nuance that gets missed: spasticity is not uniformly bad, and eliminating it can remove function.

Many people use their spasticity. Extensor tone in the legs can assist standing transfers and support weight. Tone maintains muscle bulk, which provides padding over bony prominences and reduces pressure injury risk. It supports circulation and may reduce deep vein thrombosis risk. It maintains bone density to some degree.

Reduce that tone too aggressively and a person who was transferring independently may no longer be able to, their legs may become genuinely flaccid, muscle bulk may decline, and pressure risk may rise.

So the clinical question is not “how do we remove the spasticity” but “is this spasticity causing a problem that outweighs its usefulness?” The problems that justify treatment are: pain, interference with transfers or positioning, disturbed sleep, difficulty with seating and posture, skin damage from shear during spasms, difficulty providing care, and contracture risk.

If none of those apply, the answer may be to leave it alone — and a person who says “I need that tone to transfer” should be listened to carefully.

New or worsening spasticity means look for a cause

This is the same logic as autonomic dysreflexia and it is just as important.

A sudden increase in spasticity, in somebody whose spasticity was stable, is usually the body reporting a problem below the injury that it cannot report any other way. The usual suspects:

• Urinary tract infection — a very common cause
• Pressure injury
• Faecal impaction or constipation
• Ingrown toenail, or anything painful in the feet
• Fracture the person cannot feel
• Deep vein thrombosis
• Heterotopic ossification — abnormal bone forming in soft tissue, usually around hips or knees, which presents with swelling, warmth, reduced range of movement and increased spasticity
• Syringomyelia — see below
• New medication, or a missed dose of an existing one

The first response to increased spasticity is investigation, not more medication. Giving baclofen for spasticity caused by an untreated pressure injury treats the alarm and leaves the fire.

The thing that needs flagging: post-traumatic syringomyelia

A syrinx is a fluid-filled cavity that can develop within the spinal cord years or decades after injury. It can expand and cause progressive neurological deterioration, and it is treatable surgically if caught — which makes recognising it important.

What should prompt investigation:

• New or changing pain, particularly ascending pain
• New weakness, especially in arms or hands in somebody with a thoracic injury
• Sensation changing level — loss ascending above the previous injury level
• New or markedly increased spasticity
• New sweating changes or new autonomic dysreflexia pattern
• Loss of function the person previously had

The principle: anybody whose stable spinal cord injury starts changing needs imaging and a specialist opinion. Spinal cord injury is supposed to be stable. Progressive deterioration is not expected, and it should never be accepted as the condition simply getting worse.

Recurrent autonomic dysreflexia is also noted in clinical guidance as a possible sign of a developing syrinx.

The intrathecal baclofen warning

For people with severe spasticity, an implanted pump delivering baclofen directly into the spinal fluid can be transformative, achieving with very small doses what oral medication cannot achieve at any tolerable dose.

There is a safety point that everybody around such a person must know.

Abrupt withdrawal of intrathecal baclofen is a medical emergency and can be fatal. If a pump fails, a battery depletes, a catheter kinks or disconnects, or a refill is missed, the person can develop severe rebound spasticity, high fever, altered consciousness, muscle breakdown and cardiovascular instability. It can progress quickly and it has killed people.

Practically:

• Know whether the person has an intrathecal pump
• Know when the refill is due, and treat that appointment as unmissable
• Know the alarm the pump makes and what it means
• Have the pump clinic’s contact details, including after hours, on the fridge and in the file
• Treat sudden severe spasticity, fever or deterioration in somebody with a pump as a possible withdrawal emergency and say exactly that when calling 000 or presenting to hospital, because emergency staff may not consider it

The other treatment options, for context: stretching and positioning programmes, which remain foundational; oral baclofen, tizanidine, dantrolene and benzodiazepines; botulinum toxin injection for focal spasticity in specific muscles; serial casting or splinting; and in selected cases surgical options including tendon lengthening or neurotomy.

Mental health, which belongs in this guide

Pain and mood are not separable, and the figures in this population are substantial.

The AlphaBeta report found that up to 40 per cent of people experience post-traumatic stress disorder after traumatic spinal cord injury, and up to 30 per cent are at risk of depression.

The 70-year British mortality study also found suicide rates around 2.7 times the general population in this group.

Those numbers are not a reason for alarm about any individual, and they are not an inevitability — but they are a reason that psychological support should be a standard part of long-term care rather than something offered when a crisis appears. Several things make it harder than it should be: pain that disturbs sleep, a mechanism of injury that was often traumatic in itself, loss of role and work, relationship change, and the ordinary difficulty of accessing mental health care while also managing a complex physical condition.

What helps is unglamorous and real: psychological therapy with somebody who understands disability rather than treating adjustment as pathology, treating the pain and the sleep properly because both drive mood, peer connection with other people who have a spinal cord injury — which people consistently describe as more useful than almost anything professional — meaningful activity and work, and treating a request for help as the ordinary thing it is.

If you or somebody you support is struggling, Lifeline is on 13 11 14, available 24 hours. Beyond Blue is on 1300 22 4636. Spinal Cord Injuries Australia can connect people with peer support, which for this specific thing is often what makes the difference.

What good long-term pain and spasticity care looks like

• The pain is classified properly, into musculoskeletal, visceral, at-level neuropathic and below-level neuropathic, because the treatment differs completely.
• Nobody tells the person their pain is impossible.
• Adequate medication trials at adequate doses over adequate periods, rather than a fortnight at a starting dose followed by abandonment.
• New or worsening pain or spasticity triggers investigation for a cause below the injury, before medication is escalated.
• Progressive change triggers imaging and a specialist opinion, because stable injuries are not supposed to change.
• Load on the shoulders is managed with equipment, not endured.
• Spasticity is treated only where it causes problems that outweigh its usefulness, and the person’s own view of what they use it for is taken seriously.
• Intrathecal pump safety is understood by everybody around the person.
• Psychological support is standard, offered early and framed properly.
• Sleep is assessed, because sleep-disordered breathing is common, under-diagnosed and drives both pain and mood.
• A multidisciplinary pain service is involved where pain is complex or refractory.