Most people who live with a spinal cord injury (SCI) develop chronic pain. Pooled across studies, roughly two-thirds report pain that persists, and in some studies the figure reaches four-fifths [1]. The pain is often felt in parts of the body where sensation is reduced or absent, which is part of what makes it hard to explain and hard to treat [2][3]. It can begin within days of the injury or surface years later. In this article, we cover the main types of pain after SCI, why the injured nervous system produces them, how clinicians classify and assess them, and what the evidence says about the full range of treatments.
What Pain After Spinal Cord Injury Is
Pain after spinal cord injury is not one condition. It is a set of distinct pain types with different causes, different patterns over time, and different treatments. Sorting out which type a person has is where effective treatment begins, because a treatment aimed at nerve-generated pain will do little for a mechanical shoulder problem, and the reverse is equally true.
Clinicians group pain after SCI by its underlying cause. The widely used framework, the International Spinal Cord Injury Pain (ISCIP) Classification, sorts each pain a person reports into one of four broad types (nociceptive, neuropathic, other, and unknown) and then into subtypes within those [2]. Nociceptive pain comes from the activation of pain receptors in tissue such as muscle, joint, or an internal organ. Neuropathic pain comes from a lesion or disease of the nervous system itself. The sections below start with the nerve-generated pain that most defines the SCI experience, then move through the tissue-based pains that are just as common.
Nerve pain (neuropathic pain) after spinal cord injury
Nerve pain, which clinicians call neuropathic pain, is produced by damage to the nervous system itself, which then generates and processes pain abnormally. After spinal cord injury, nerve pain affects somewhere between half and roughly 60 percent of people, with pooled estimates of 53 percent, 57 percent, and 58 percent across three separate meta-analyses [1][4][5]. People describe it as burning, electrical, stabbing, or a pins-and-needles sensation, and it is frequently felt in regions where other sensation is dulled or gone [2].
The ISCIP framework splits SCI nerve pain by location relative to the injury. At-level pain appears in a band at the neurological level of injury or within three segments below it. Below-level pain appears farther down, in territory more distal to that band [2].
Where the pain is felt
At-level and Below-level Pain, by Location
Nerve pain after spinal cord injury is grouped by where it sits relative to the injury. The two bands behave differently, which is why naming them matters. The spine below shows an example injury at the sixth thoracic level (T6).
At-level pain
Felt at the injury level or within three segments below it, often as a band around the body. It is usually present within the first months after injury.
Below-level pain
Felt further down, in territory well below the injury. It tends to appear later and keep spreading over years, so it can be new even long after the injury.
The area above the injury is typically spared from SCI nerve pain.
Source: Bryce TN, Biering-Sorensen F, Finnerup NB, et al. International Spinal Cord Injury Pain Classification: part I. Background and description. Spinal Cord. 2012;50(6):413-417. PMID: 22182852. [2]
How nerve pain changes over time after spinal cord injury
The two types diverge over the years. In a five-year study of 100 people with traumatic SCI, Siddall and colleagues tracked how each type appeared and persisted [6]. Reported by 39 percent at two months and 42 percent at five years, at-level pain was already common within the first months and stayed fairly steady.
Below-level pain followed a different course, starting lower and climbing steadily, from 12 percent at two months to 34 percent at five years [6]. A person can be years past the injury and still develop new below-level pain, which is part of why this type is so often missed or dismissed.
At-level pain arrives early. Below-level pain keeps building.
Share of people with traumatic spinal cord injury reporting each type of nerve pain, measured at 2, 6, and 60 months after injury in a cohort of 100.
| Time since injury | At-level pain | Below-level pain |
|---|---|---|
| 2 months | 39% | 12% |
| 6 months | 46% | 18% |
| 60 months | 42% | 34% |
Musculoskeletal and shoulder pain after spinal cord injury
Musculoskeletal pain is nociceptive pain from muscles, joints, tendons, and bone. In the 2021 meta-analysis described earlier, Hunt and colleagues found this type of pain nearly as common as nerve pain, near 56 percent [1]. The most frequent site is the shoulder. Among people who use a manual wheelchair, shoulder pain is reported in a majority, with the wrist, hand, and elbow following [7].
The cause is mechanical load. The arms and shoulders take on the work of transfers, propulsion, and weight relief, and joints built for a smaller share of that load wear down under the strain. Prolonged daily manual wheelchair use and thoracic-level injury are among the factors tied to upper-limb overuse [7].
This pain tends to accrue with years of use, so its burden generally grows over the long term, the opposite of the pattern for at-level nerve pain. This type is also the most preventable. The strongest positive finding in the whole SCI pain literature concerns shoulder-preservation exercise, described in the treatment sections below. The Consortium for Spinal Cord Medicine addressed upper-limb preservation in a dedicated clinical practice guideline [7].
Visceral (abdominal) pain after spinal cord injury
Visceral pain arises from the internal organs, most often the bladder and bowel, and is the least common of the major SCI pain types, reported by about 20 percent of people [1]. It tends to be dull, cramping, or poorly localized, and it can be hard to separate from other abdominal sensations when sensation below the injury is altered.
Visceral pain deserves close attention for a reason beyond the discomfort. It often signals a treatable problem lower down, such as a distended bladder, constipation, or an infection. In a person with a high injury, an unaddressed noxious trigger of this kind can set off autonomic dysreflexia (AD), a medical emergency covered in the assessment section. Mechanism-level detail on bladder and bowel dysfunction lives in the NASCIC bladder resources.
Spasticity-related pain after spinal cord injury
Spasticity is the involuntary muscle tightness and spasm that follows many spinal cord injuries. When those contractions become painful, the discomfort is grouped with the nociceptive and musculoskeletal pains, since it comes from muscle rather than from damaged nerve tissue directly. People describe a cramping or pulling ache that tracks with the spasms, and it can interrupt sleep, seating, and transfers.
Spasticity-related pain sits at the boundary between a movement disorder and a pain problem, and its treatment reflects that, drawing on the medications and injections that target the spasticity itself, described in the treatment sections below. It is a strong candidate for its own article, since spasticity affects a large share of the SCI population and its painful component is often treated separately from the muscle tightness.
Why the injured spinal cord produces pain
The nerve pain that follows spinal cord injury is not simply a signal traveling up from a fresh wound. It comes from lasting changes in the spinal cord and brain that outlast the original trauma. After injury, the dorsal horn, the relay station in the cord where incoming sensory signals are first processed, becomes hyperexcitable. Gwak and Hulsebosch describe damaged nerve endings releasing more glutamate, neuropeptides, and inflammatory molecules while the local wiring reorganizes in ways that magnify incoming signals rather than dampen them [8].
Hulsebosch and colleagues mapped distinct mechanisms operating at different distances from the injury, which helps explain why at-level and below-level pain behave so differently [3]. The practical consequence is that established SCI nerve pain comes from a nervous system that has become too easy to set off and has lost some of its natural braking, not from ongoing damage to muscle or other tissue. The alarm keeps sounding even after the original injury has settled. That is why treatments that calm nerve signaling tend to matter more than treatments aimed at a single sore spot. The figure below traces how a small signal from below the injury is magnified into a large, ongoing one, and names the three changes behind it.
Why the pain does not stop
How the Injured Cord Magnifies Pain
Established nerve pain after spinal cord injury is not a signal traveling up from a fresh wound. It comes from lasting changes that leave the cord magnifying signals it should quiet. A small input from below the injury grows into a large, ongoing pain output.
-
Nerve cells fire too easily
After injury, voltage-gated sodium channels (Nav1.3) become abundant in pain-signaling neurons, and those neurons fire on light input. Blocking the channels lowers the over-firing in animal studies. [9]
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Immune cells keep it going
Microglia, the cord's own immune cells, switch into an activated state and sustain the pain. Quieting them restores more normal signaling in animal studies. [10]
-
The brakes weaken
The cord loses part of its inhibitory control. Signals that should calm a neuron instead fail, or even push it toward firing, which removes much of the built-in restraint on pain. [11]
Sources: Gwak YS, Hulsebosch CE. Curr Pain Headache Rep. 2011;15(3):215-222. [8] Hulsebosch CE, Hains BC, Crown ED, Carlton SM. Brain Res Rev. 2009;60(1):202-213. [3] Hains BC, et al. J Neurosci. 2003;23(26):8881-8892. [9] Hains BC, Waxman SG. J Neurosci. 2006;26(16):4308-4317. [10] Hasbargen T, et al. Ann N Y Acad Sci. 2010;1198:168-172. [11]
How common pain is after spinal cord injury
The best single estimate for overall chronic pain after spinal cord injury is 68 percent (95 percent confidence interval, 63 to 73), from Hunt and colleagues' 2021 meta-analysis [1]. Across the wider literature the figure ranges from roughly two-thirds to four-fifths, depending on how a study defines pain and when it measures [1]. The breakdown by type appears in the figure below, and because many people live with more than one type at once, those type figures add to more than the overall total.
How to read spinal cord injury pain estimates
Two things temper these numbers. The estimates vary partly because studies use different definitions and assessment methods, which is exactly the problem the ISCIP Classification was built to reduce [5].
The demographic pattern is also weaker than intuition suggests. Large pooled analyses find that whether a person develops nerve pain is not strongly predicted by age, sex, injury level, or completeness [5].
Individual cohorts do show signals. In a register study of 402 people, Werhagen and colleagues found nerve pain rising with older age at injury and below-level pain more common after complete injury, with no effect of sex or injury level [12]. The honest summary is that pain after SCI is common across the whole population, and no simple profile reliably marks out who will be spared.
How common each kind of pain is after spinal cord injury
Pooled share of people with SCI who report each pain type. Because many people have more than one type at once, the by-type figures add to more than the overall figure.
Any chronic pain
By type
| Pain type | Pooled prevalence | 95% confidence interval |
|---|---|---|
| Overall chronic pain | 68% | 63% to 73% |
| Nerve pain | 58% | 49% to 68% |
| Musculoskeletal pain | 56% | 41% to 70% |
| Visceral pain | 20% | 11% to 29% |
How Pain After Spinal Cord Injury Is Identified
Because the treatments differ so much from one pain type to the next, getting the classification right carries real weight. Two people can report pain of the same intensity and need opposite treatments, one a strengthening program for a worn shoulder, the other a medication that quiets nerve signaling.
Identifying SCI pain well means naming the type, measuring how much it interferes with daily life, and checking for a treatable cause underneath it before turning to long-term pain control.
The International Spinal Cord Injury Pain (ISCIP) Classification
For years, SCI pain was sorted by competing schemes, some with as few as two categories and one with as many as fifteen. The differences made it hard to compare studies or agree on treatment.
In 2012, Bryce and colleagues published a single consensus system, the International Spinal Cord Injury Pain Classification, in the journal Spinal Cord [2]. It merges the older schemes into one standard and was reviewed and endorsed through the major professional bodies before release.
How the spinal cord injury pain classification works
ISCIP works in three tiers, shown in the figure below. The first names the broad type of pain, the second names the subtype, and the third names the specific source when it can be identified. A clinician reaches the classification through interview, physical examination, and imaging.
The value of a shared standard is practical. When studies use the same definitions their results can be compared. Much of the reason prevalence figures vary is that older studies used different definitions, the very problem ISCIP was built to reduce [5].
How clinicians classify pain after spinal cord injury
The International Spinal Cord Injury Pain (ISCIP) Classification sorts each pain a person reports across three tiers, from broad type down to the specific source.
Nociceptive
Pain from tissue such as muscle, joint, or an internal organ.
- MusculoskeletalMuscle, joint, and bone, such as shoulder overuse
- VisceralInternal organs, such as bladder or bowel
- Other nociceptive
Neuropathic
Pain from a lesion or disease of the nervous system itself.
- At-level SCI painAt the injury level or within three segments below it
- Below-level SCI painFurther down, in more distal territory
- Other neuropathic
Other pain
A recognized condition not caused by the SCI, such as fibromyalgia or complex regional pain syndrome.
Unknown pain
Used when the pain cannot reasonably be placed in the categories above.
Tier 3. For any pain above, the clinician adds the specific source when it is known, down to the joint, organ, or lesion responsible. The classification is reached through interview, examination, and imaging.
How pain after spinal cord injury is assessed
Alongside the classification, clinicians use a standard recording tool, the International Spinal Cord Injury Pain Basic Data Set, now in its third version [13]. It captures the worst pain a person has, how often it occurs, where it sits, how long it has lasted, how much it interferes with daily activity, mood, and sleep, and which ISCIP category it falls into.
Both the classification and the data set are maintained jointly by the International Spinal Cord Society (ISCoS) and the American Spinal Injury Association (ASIA), and are free to download [13]. Self-report is central. Because sensation below the injury is often altered, a person's own account of what the pain feels like and where it sits carries information that an examination alone cannot supply.
Autonomic dysreflexia, when pain is an emergency signal
In people with an injury at the sixth thoracic level (T6) or above, a painful or otherwise noxious event below the injury can set off autonomic dysreflexia, a sudden and dangerous rise in blood pressure. The body cannot mount its normal correction below the lesion, so pressure climbs until the trigger is found and removed.
An episode is defined by a rise in systolic blood pressure of at least 20 points above a person's baseline [14]. Warning signs often appear above the injury, such as a pounding headache, flushing, or sweating, and the person may not consciously feel the stimulus that started it. Clinicians document these autonomic effects using the international standards for autonomic function after SCI [15]. The figure below traces how the trigger, the blocked signal, and the surge fit together, along with the emergency response.
Autonomic dysreflexia: the body divided at the injury
In an injury at the sixth thoracic level (T6) or above, the body cannot regulate itself across the lesion. A trigger below the injury sets off a surge above it that the brain cannot calm.
Above the injury
Blood pressure surges, defined by a systolic rise of at least 20 points above baseline. A pounding headache, flushing, and sweating appear here.
At the injury (T6 or above)
The brain's signal to calm the surge cannot pass the lesion, so nothing opposes the rising pressure.
Below the injury
A noxious trigger starts it, most often a full or blocked bladder, and next most often the bowel or the skin. The person may not feel it.
Respond right away
- Sit upright, so pressure in the head can settle
- Loosen anything tight, such as clothing, straps, or an abdominal binder
- Find and remove the trigger, which most often means draining the bladder
- If it does not settle, get emergency medical care
Ruling out treatable causes of pain
New or worsening pain after spinal cord injury is a reason to look for a fixable cause before escalating pain medication. A distended bladder, constipation, or a urinary infection can drive visceral pain and can trigger autonomic dysreflexia [15].
Two other sources are worth ruling out. Pressure injuries, which affect most people with SCI at some point, are a frequent nociceptive source, and their prevention and care are covered in the NASCIC wound resources. Heterotopic ossification, the formation of bone in soft tissue, can produce localized pain and is addressed in the NASCIC bone health resources.
Pain that is new or clearly changing years after the injury warrants prompt medical evaluation. In a minority of people it can signal post-traumatic syringomyelia, a fluid-filled cavity in the cord that is detectable on imaging.
How pain affects sleep, mood, and daily life
Chronic pain after spinal cord injury reaches well beyond the pain itself. It interferes with sleep, lowers mood, and reduces participation in work and social life, and it is consistently tied to higher rates of depression and anxiety [17]. Pain interference, meaning how much the pain gets in the way of daily activity, is the thread that connects pain severity to these wider effects. A mixed-methods study by Widerstrom-Noga and colleagues documents both the measured interference and the lived experience behind it [17].
How Pain After Spinal Cord Injury Is Treated
The evidence for treating SCI pain is uneven, and it helps to say so at the outset. The strongest positive finding in the whole field concerns exercise for shoulder pain. For nerve pain, several medications reduce pain more than placebo, but the effect is usually modest, and most people do not reach complete relief from any single drug [18].
Treatment works best when it is matched to the pain type and when more than one approach is combined. The figure below shows where treatment usually starts for each type.
Where treatment begins
Matching Treatment to the Type of Pain
Sorting out which type of pain a person has is where effective treatment begins. Each type has a different starting point, and a treatment aimed at one does little for another.
Nerve pain
From nerve damage, felt at or below the injury
Where treatment starts
Medication, usually pregabalin first, sometimes with stimulation or psychological support.
- Pregabalin
- Gabapentin
- Neuromodulation
Musculoskeletal pain
From muscles and joints, most often the shoulder
Where treatment starts
Strengthening and stretching exercise, plus changes to movement technique and equipment.
- Shoulder exercise
- Technique and equipment
Spasticity-related pain
From involuntary muscle tightness and spasm
Where treatment starts
Treat the spasticity itself. The pain benefit follows from reducing the spasm.
- Antispasticity medication
- Focal injections
Visceral pain
From internal organs, often the bladder or bowel
Where treatment starts
Find and fix the trigger, such as a full bladder, constipation, or an infection.
- Relieve bladder or bowel
- Treat infection
Most people have more than one type at once, so treatment is often combined. Talking through the mix with a care team is part of getting it right.
Sources: shoulder-preservation exercise [19][20] and the PVA upper-limb guideline [7]; the CanPain SCI medication ladder [21] and pregabalin's SCI approval [22]; treatable-trigger management for visceral pain and autonomic dysreflexia [16].
Non-drug and rehabilitation approaches
Whichever type dominates, the treatment options fall into a few families, and the non-drug approaches come first because the single strongest result in the whole field sits among them. Shoulder-preservation exercise produced the largest treatment effect of any intervention in the major Cochrane review of non-drug SCI pain care, led by Boldt and colleagues [19]. In the flagship trial, STOMPS (Strengthening and Optimal Movements for Painful Shoulders), a twelve-week home program of shoulder exercise plus movement-technique advice cut shoulder pain to about a third of its starting level, while the comparison group did not change [20].
That result comes with one honest note about scope. The trials tested exercise for shoulder pain that was already present, so the evidence is strongest for treating existing pain rather than for preventing it from developing [23]. That reflects what has been formally studied, not a reason to hold off. Clinicians commonly encourage protecting the shoulders proactively, which is the focus of a dedicated upper-limb preservation guideline [7].
The mind-body approaches are a weaker but real second strand. Cognitive behavioral therapy for SCI pain, tested in the definitive Dutch CONECSI trial, missed its main pain outcomes even as it improved anxiety and activity [24], and a Cochrane review of psychological therapies for nerve pain reached the same cautious verdict [25]. The brightest recent signal is hypnotic cognitive therapy. In a 2026 trial by Bombardier and colleagues, 127 people saw a small but durable benefit that kept growing after the sessions ended [26].
Pain medications studied for spinal cord injury
When exercise and therapy are not enough, or when the pain is nerve pain rather than mechanical, medication is the next move, and one drug is the clear exception. Pregabalin holds a United States Food and Drug Administration (FDA) approval specifically for nerve pain after spinal cord injury, granted in 2012 on the strength of two placebo-controlled trials, and it carries the strongest evidence of any SCI pain treatment [22][27]. Gabapentin usually follows, prescribed for the same purpose though not formally approved for it, and the tricyclic antidepressant amitriptyline is a further option whose clearest benefit appeared in people who also had depressive symptoms [28].
Even the best of these offers a measured benefit, not a cure. The large review by the International Association for the Study of Pain (IASP) found that for any single drug, the most likely outcome is falling short of a fifty percent reduction in pain [18]. That is a case for realistic expectations, for combining approaches, and for weighing side effects honestly. This article gives no doses, which belong to a person and their prescriber. Where pain is driven by spasticity, the useful medicines are the ones that reduce the spasticity itself.
Neuromodulation and interventional options
For pain that resists both exercise and drugs, a set of procedures aims at the nervous system directly, though the evidence thins as the procedures grow more invasive. Transcranial direct current stimulation, a weak current applied over the scalp, gave a moderate reduction in a pooled analysis by Mehta and colleagues, but the benefit faded once treatment stopped [29]. Repetitive transcranial magnetic stimulation has a smaller, contested record and has not clearly beaten sham stimulation, an inactive placebo version of the procedure, in SCI [30].
The implanted options carry more weight and more caution. Spinal cord stimulation has only weak SCI evidence and works better in incomplete than complete injury, with a recent review calling its role poorly defined [31]. Deep brain stimulation and motor cortex stimulation are last-resort measures, and the numbers usually quoted for them come from central pain after stroke, not after SCI, so they should not be read as SCI outcomes [32].
At the far end, a surgical procedure on the cord itself, dorsal root entry zone lesioning, sits in the Canadian guideline as a last resort for exceptional cases [21]. These pain uses are worth separating from the neurotechnology aimed at restoring movement and communication after SCI, which is a different goal.
What the guidelines recommend
Pulling these choices together, three guidelines organize the drug decisions, and they line up at the top. The Canadian CanPain guideline is the one written specifically for nerve pain after spinal cord injury. The United Kingdom's National Institute for Health and Care Excellence (NICE) guideline covers nerve pain in general [33], and the IASP recommendations, updated in 2025, set the international standard [34]. The ladder below lays out the CanPain tiers, from first-line down to the drugs it advises against.
What the guidelines recommend
The SCI Nerve Pain Treatment Ladder
The Canadian CanPain guideline is written specifically for nerve pain after spinal cord injury. It ranks options by how strong the SCI evidence is, from a first-line tier down to two drugs it advises against. It does not give doses, which a prescriber sets for each person.
- First-line Strong recommendation, high-quality evidence
- PregabalinStrongest SCI evidence. The only drug FDA-approved for SCI pain.
- GabapentinThe usual next choice after pregabalin.
- AmitriptylineClearest benefit when depression is also present.
- B options Strong recommendation, moderate-to-high evidence
- Oxcarbazepine
- Tramadol
- LamotrigineOnly in incomplete injury.
- C options Weak recommendation
- Botulinum toxin AFor below-level pain, injected at the painful area.
- Transcranial direct current stimulation
- D options Weak recommendation, last among the options
- Cannabinoids
- TENS
- OxycodoneAn opioid, weighed against real harms in SCI.
- Advised against Trials found no benefit in SCI
- Levetiracetam
- Mexiletine
The general nerve pain guidelines from NICE and the IASP largely agree on the first-line drugs. They differ from CanPain on a few later options, mostly because CanPain limits itself to SCI-specific trials while the others draw on all nerve pain evidence.
Source: Loh E, Mirkowski M, Agudelo AR, et al. The CanPain SCI clinical practice guidelines for rehabilitation management of neuropathic pain after spinal cord injury: 2021 update. Spinal Cord. 2022;60(6):548-566. [21] Pregabalin FDA approval for SCI neuropathic pain, 2012. [22]
What the evidence does not support
Being clear about what does not work is as useful as naming what does.
Two anticonvulsant drugs, levetiracetam and mexiletine, are actively advised against for SCI pain, because controlled trials found no benefit over placebo [21].
If those two are simply ineffective, cannabinoids are the opposite problem, a case where the popular impression is well ahead of the evidence. A meta-analysis of the SCI-specific trials found no clear pain benefit and a higher rate of side effects such as dizziness and drowsiness, and guidelines are split on whether to allow even a cautious trial [35].
Opioids land in a different place again, late in every major guideline. The SCI-specific efficacy evidence is thin, and the harms are real and particular to this population, including worsening of neurogenic bowel through constipation, dependence, and a paradoxical increase in pain sensitivity with long-term use [21][34]. Tramadol, a weaker opioid, reduced pain in one small SCI trial, but most of the participants stopped taking it because of side effects [36].
What realistic pain relief looks like
No single treatment reliably eliminates nerve pain after spinal cord injury. The workable goal is meaningful reduction, reached by matching treatment to the pain type, combining a drug with a rehabilitation or psychological approach, and reviewing what helps and what does not over time. Anyone weighing these options should do so with their care team, who can account for the person's full medical picture.
A resource for understanding and talking about SCI pain: SeePain
Pain after spinal cord injury is hard to see and hard to describe, and many people have been told they should not be feeling it at all. SeePain is a free education resource built to close that gap. It was developed by a research team at The Miami Project to Cure Paralysis, led by Eva Widerstrom-Noga, with Kimberly Anderson-Erisman, PhD, a professor of physical medicine and rehabilitation at MetroHealth and Case Western Reserve University who directs the Northeast Ohio Regional Spinal Cord Injury System and lives with a spinal cord injury, as a co-leader. It draws on the published pain research and on interviews with people living with SCI and pain, the people closest to them, and clinicians who specialize in SCI, and the team has published how SeePain was developed [37].
SeePain comes in two free modules. Module 1 explains what pain after SCI is, how it is classified, and how it affects daily life. Module 2 covers ways to manage pain, from non-drug approaches to medication, and makes clear that no single option works for everyone. In a follow-up study, people with SCI who reviewed the resource reported that it helped them understand their pain and talk about it with their healthcare providers [38]. NASCIC also hosted a webinar with the SeePain team where the walkthrough of the resource begins about six minutes in.
Clinical disclaimer
This article is intended for educational purposes. Decisions about your own care or the care of someone you support should be made with your healthcare team, who can apply the information here to your specific situation. This content does not replace professional medical advice, diagnosis, or treatment. If your pain is new, worsening, or accompanied by warning signs of autonomic dysreflexia, contact your care team or call emergency services.
References
- Hunt C, Moman R, Peterson A, Wilson R, Covington S, Mustafa R, Murad MH, Hooten WM. Prevalence of chronic pain after spinal cord injury: a systematic review and meta-analysis. Reg Anesth Pain Med. 2021;46(4):328-336. DOI: 10.1136/rapm-2020-101960
- Bryce TN, Biering-Sorensen F, Finnerup NB, Cardenas DD, Defrin R, Lundeberg T, Norrbrink C, Richards JS, Siddall P, Stripling T, Treede RD, Waxman SG, Widerstrom-Noga E, Yezierski RP, Dijkers M. International Spinal Cord Injury Pain Classification: part I. Background and description. Spinal Cord. 2012;50(6):413-417. PMID: 22182852. DOI: 10.1038/sc.2011.156
- Hulsebosch CE, Hains BC, Crown ED, Carlton SM. Mechanisms of chronic central neuropathic pain after spinal cord injury. Brain Res Rev. 2009;60(1):202-213. PMID: 19154757. DOI: 10.1016/j.brainresrev.2008.12.010
- Burke D, Fullen BM, Stokes D, Lennon O. Neuropathic pain prevalence following spinal cord injury: a systematic review and meta-analysis. Eur J Pain. 2017;21(1):29-44. PMID: 27341614. DOI: 10.1002/ejp.905
- Prevalence of neuropathic pain following spinal cord injury: an updated systematic review and meta-analysis. J Clin Neurosci. 2025.
- Siddall PJ, McClelland JM, Rutkowski SB, Cousins MJ. A longitudinal study of the prevalence and characteristics of pain in the first 5 years following spinal cord injury. Pain. 2003;103(3):249-257. PMID: 12791431. DOI: 10.1016/S0304-3959(02)00452-9
- Consortium for Spinal Cord Medicine. Preservation of upper limb function following spinal cord injury: a clinical practice guideline for health-care professionals. J Spinal Cord Med. 2005;28(5):434-470. PMID: 16869091
- Gwak YS, Hulsebosch CE. Neuronal hyperexcitability: a substrate for central neuropathic pain after spinal cord injury. Curr Pain Headache Rep. 2011;15(3):215-222. PMID: 21387163. DOI: 10.1007/s11916-011-0186-2
- Hains BC, Klein JP, Saab CY, Craner MJ, Black JA, Waxman SG. Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury. J Neurosci. 2003;23(26):8881-8892. PMID: 14523090. DOI: 10.1523/JNEUROSCI.23-26-08881.2003
- Hains BC, Waxman SG. Activated microglia contribute to the maintenance of chronic pain after spinal cord injury. J Neurosci. 2006;26(16):4308-4317. PMID: 16624951. DOI: 10.1523/JNEUROSCI.0003-06.2006
- Hasbargen T, Ahmed MM, Miranpuri G, et al. Role of NKCC1 and KCC2 in the development of chronic neuropathic pain following spinal cord injury. Ann N Y Acad Sci. 2010;1198:168-172. PMID: 20536931
- Werhagen L, Budh CN, Hultling C, Molander C. Neuropathic pain after traumatic spinal cord injury: relations to gender, spinal level, completeness, and age at the time of injury. Spinal Cord. 2004;42(12):665-673. DOI: 10.1038/sj.sc.3101641
- Widerstrom-Noga E, Biering-Sorensen F, Bryce TN, Cardenas DD, Finnerup NB, Jensen MP, Richards JS, Siddall PJ. The International Spinal Cord Injury Pain Basic Data Set (version 3.0). Spinal Cord. 2023;61(9):536-540. PMID: 37491608. DOI: 10.1038/s41393-023-00919-w
- Consortium for Spinal Cord Medicine. Evaluation and Management of Autonomic Dysreflexia and Other Autonomic Dysfunctions: Preventing the Highs and Lows. Washington, DC: Paralyzed Veterans of America; 2020.
- Wecht JM, Krassioukov AV, Alexander M, et al. International Standards to document Autonomic Function following SCI (ISAFSCI), Second Edition. Top Spinal Cord Inj Rehabil. 2021;27(2):23-49. PMID: 34108833. DOI: 10.46292/sci2702-23
- Krassioukov A, Warburton DE, Teasell R, Eng JJ; SCIRE Research Team. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. 2009;90(4):682-695. PMID: 19345787. DOI: 10.1016/j.apmr.2008.10.017
- Widerstrom-Noga E, Anderson KD, Perez S, Hunter JP, Martinez-Arizala A, Adcock JP, et al. Living with chronic pain after spinal cord injury: a mixed-methods study. Arch Phys Med Rehabil. 2017;98(5):856-865. PMID: 27894730. DOI: 10.1016/j.apmr.2016.10.018
- Finnerup NB, Attal N, Haroutounian S, McNicol E, Baron R, Dworkin RH, et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14(2):162-173. DOI: 10.1016/S1474-4422(14)70251-0
- Boldt I, Eriks-Hoogland I, Brinkhof MWG, de Bie R, Joggi D, von Elm E. Non-pharmacological interventions for chronic pain in people with spinal cord injury. Cochrane Database Syst Rev. 2014;(11):CD009177. PMID: 25432061. DOI: 10.1002/14651858.CD009177.pub2
- Mulroy SJ, Thompson L, Kemp B, et al. Strengthening and optimal movements for painful shoulders (STOMPS) in chronic spinal cord injury: a randomized controlled trial. Phys Ther. 2011;91(3):305-324. PMID: 21292803. DOI: 10.2522/ptj.20100182
- Loh E, Mirkowski M, Agudelo AR, et al. The CanPain SCI clinical practice guidelines for rehabilitation management of neuropathic pain after spinal cord injury: 2021 update. Spinal Cord. 2022;60(6):548-566. PMID: 35124700. DOI: 10.1038/s41393-021-00744-z
- Siddall PJ, Cousins MJ, Otte A, Griesing T, Chambers R, Murphy TK. Pregabalin in central neuropathic pain associated with spinal cord injury: a placebo-controlled trial. Neurology. 2006;67(10):1792-1800. PMID: 17130411. DOI: 10.1212/01.wnl.0000244422.45278.ff
- Wellisch M, Lovett K, Harrold M, et al. The effectiveness of active physiotherapy interventions on shoulder pain in people with spinal cord injury who use a manual wheelchair: a systematic review and meta-analysis. Spinal Cord. 2022;60(2):107-114. PMID: 34373591. DOI: 10.1038/s41393-021-00673-x
- Heutink M, Post MWM, Bongers-Janssen HMH, Dijkstra CA, Snoek GJ, Spijkerman DCM, Lindeman E. The CONECSI trial: a randomized controlled trial of a multidisciplinary cognitive behavioral program for coping with chronic neuropathic pain after spinal cord injury. Pain. 2012;153(1):120-128. PMID: 22100355. DOI: 10.1016/j.pain.2011.09.029
- Eccleston C, Hearn L, Williams AC de C. Psychological therapies for the management of chronic neuropathic pain in adults. Cochrane Database Syst Rev. 2015;(10):CD011259. DOI: 10.1002/14651858.CD011259.pub2
- Bombardier CH, Mendoza D, Thomas W, Barber J, Jensen MP. Hypnotic cognitive therapy for chronic pain in people with spinal cord injury: a randomized controlled trial. Neurology. 2026;106(8):e214836.
- Cardenas DD, Nieshoff EC, Suda K, Goto S, Sanin L, Kaneko T, et al. A randomized trial of pregabalin in patients with neuropathic pain due to spinal cord injury. Neurology. 2013;80(6):533-539. DOI: 10.1212/WNL.0b013e318281546b
- Rintala DH, Holmes SA, Courtade D, Fiess RN, Tastard LV, Loubser PG. Comparison of the effectiveness of amitriptyline and gabapentin on chronic neuropathic pain in persons with spinal cord injury. Arch Phys Med Rehabil. 2007;88(12):1547-1560. PMID: 18047869. DOI: 10.1016/j.apmr.2007.07.038
- Mehta S, McIntyre A, Guy S, Teasell RW, Loh E. Effectiveness of transcranial direct current stimulation for the management of neuropathic pain after spinal cord injury: a meta-analysis. Spinal Cord. 2015;53(11):780-785. PMID: 26193817. DOI: 10.1038/sc.2015.118
- Repetitive transcranial magnetic stimulation for pain after spinal cord injury: a systematic review and meta-analysis. 2016. PMID: 27603408
- Spinal cord stimulation for pain management following spinal cord injury: a systematic review. J Pain Res. 2026. DOI: 10.2147/JPR.S573333
- Deep brain stimulation and motor cortex stimulation for central post-stroke pain: a systematic review and meta-analysis. Pain Med. 2025;26(5). PMID: 39798142
- National Institute for Health and Care Excellence. Neuropathic pain in adults: pharmacological management in non-specialist settings. NICE clinical guideline CG173. Published 2013, updated 2020. https://www.nice.org.uk/guidance/cg173
- Soliman N, Moisset X, Ferraro MC, et al. Pharmacotherapy and non-invasive neuromodulation for neuropathic pain: a systematic review and meta-analysis. Lancet Neurol. 2025;24(5):413-428. DOI: 10.1016/S1474-4422(25)00068-7
- Cannabinoid use for pain reduction in spinal cord injuries: a meta-analysis of randomized controlled trials. Front Pharmacol. 2022;13:866235. PMID: 35571093. DOI: 10.3389/fphar.2022.866235
- Norrbrink C, Lundeberg T. Tramadol in neuropathic pain after spinal cord injury: a randomized, double-blind, placebo-controlled trial. Clin J Pain. 2009;25(3):177-184. DOI: 10.1097/AJP.0b013e31818a744d
- Widerstrom-Noga E, et al. Development of a pain education resource for people with spinal cord injury. Front Public Health. 2023;11:1197944. PMID: 37554730. DOI: 10.3389/fpubh.2023.1197944
- Widerstrom-Noga E, et al. Perspectives of people with spinal cord injury on a pain education resource. Front Public Health. 2024;12:1385831. PMID: 38962773. DOI: 10.3389/fpubh.2024.1385831
