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One of the most frequently occurring physical sequelae following spinal cord injury (SCI) is persistent pain. Taxonomies for pain after spinal cord injury are available.1,2 These taxonomies have commonality, defining pain by location with respect to the level of spinal cord injury (above, at, and below) and classifying pain as nociceptive or neuropathic. Nociceptive pain implies a peripheral pain generator that is not part of the nervous system, while neuropathic pain implies a pain generator within the somatosensory nervous system.


The etiology for neuropathic pain after SCI is uncertain. However, emerging evidence demonstrates the role of cortical reorganization in neuropathic pain at and/or below the level of injury,3,4 as well as central sensitization.5 The etiology of musculoskeletal pain, a subset of nociceptive pain, is related to repetitive overuse of the particular structure involved. Although other subtypes of pain occur, the focus of this article is the most commonly encountered SCI-pain syndromes.

Epidemiology including risk factors and primary prevention

Across studies, two-thirds to three-quarters of persons with SCI report pain, with one-third of those individuals describing the pain as severe. The most common pain is musculoskeletal pain above the level of injury.6 Neuropathic pain following SCI is most commonly categorized into pain at and pain below the level of the lesion. Over 50% of patients with SCI report neuropathic pain.7 The most severe pain is neuropathic pain below the level of injury.6


Due to the varying locations and types of pain from which spinal cord injured patients suffer, the pathophysiology can vary.  Acute traumatic spinal cord injury and subsequent surgery often lead to severe nociceptive pain related to local inflammation. Long-term, patients can develop musculoskeletal pain due to overuse injuries, particularly in the upper limbs due to increased dependence on the upper limbs for mobility and self-care activities.8 Neuropathic pain can be due to degeneration of spinal segments adjacent to their original injury, syrinx formation, or focal nerve compression in the plexus or limbs, but is postulated to be mediated by peripheral and central sensitization. While both peripheral and central ectopic neuronal activity may cause pain at the level of injury, it is thought that central sensitization plays a larger role in pain below level of injury.5 Central sensitization is the dual process of hyperexcitability of ascending afferent pain signals and loss of inhibitory descending pathways from the spinal cord and thalamus that reduce hypersensitivity. Neuronal hyperexcitability is presumed to be mediated by modulating sodium and calcium channels, down-regulating potassium channels and phosphorylating glutamate channels, along with this loss of inhibitory molecules including glycine and γ-aminobutyric acid (GABA). This often manifests as hypersensitivity, hyperalgesia, allodynia or worsening pain below level of injury over time. These processes may predispose patients with spinal cord injury to later on developing chronic pain syndromes.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Pain after spinal cord injury is common in the acute phase. As patients acquire new skills for mobility and self- care, patients can develop musculoskeletal pain from post-injury remobilization and overuse while in therapies focusing on improving function and self-care. Persistent or recurrent musculoskeletal pain is more common among patients who use their upper body for transfers and mobility. Neuropathic pain at the level of injury develops most commonly in the acute stage of SCI, whereas neuropathic pain below the level of injury begins to increase 1 year after SCI. Neuropathic pain overall is more prevalent after 6 months of injury in comparison to acute SCI.7

Specific secondary or associated conditions and complications

Numerous complications are seen secondary to SCI pain. Pain can disrupt mood and psychosocial functioning,9,10 occupational activities,11 and basic needs, such as sleep.12 Persistent pain is associated with lower quality of life post-injury.13

Essentials of Assessment


The history should start with the date and mechanism of spinal cord injury. Pain history including time course, location, quality, and quantity (e.g., visual analogue scale) should be obtained. Information on alleviating and aggravating factors, past evaluations and treatments (including effectiveness) and pharmacological assessment should be obtained. Obtaining this information will allow the examiner to begin to formulate a differential diagnosis based on pain location and type and thereby guide additional work up. Conditions that may cause or aggravate pain should be evaluated. This may include fractures, spasticity, heterotopic ossification, infections, visceral disorders, cardiovascular issues, gastrointestinal diseases, and malignancy. Social, functional, occupational, and leisure history should be obtained as well as the impact of pain on these activities. Psychological assessment should include history and symptoms of depression, anxiety, catastrophizing, readiness for change, substance use, secondary gain issues, patient perception of cause of injury and treatment goals.

Physical examination

The physical examination should include an International Standards for Neurological Classification of SCI (ISNCSCI) evaluation, and further neurological testing, including reflex testing and evaluation of spasticity. Observation of pain behavior and palpation of the painful area is important. Evaluation of active and passive range of motion and abnormalities of posture or gait/mobility and their impact on pain should be noted.

Functional assessment

Functional assessment should be done as it relates to current pain complaints. Changes in function or deviation from expected level of function with current neurological level of injury should be noted.

Laboratory studies

If occult organ dysfunction is suspected as a cause of pain, specific laboratory evaluation is recommended. Examples include urinalysis for urinary tract infection or sign of hematuria in the presence of kidney stones, liver function tests for gallbladder disease, white blood cell count for suspected appendicitis, and cardiac enzymes for suspected symptomatic coronary artery disease are just some of the multitude of possibilities. Inflammatory markers such as Westergren method sedimentation rate, C-reactive protein, and procalcitonin are nonspecific and not generally helpful.


Imaging will be dependent on the pain complaint, physical examination, and the differential diagnosis that was generated. Spine magnetic resonance imaging (MRI) for degenerative disease or syrinx causing neuropathic symptoms would be appropriate. Plain x-ray or ultrasound of the skeletal system would be appropriate within the context of the history and physical exam.

Supplemental assessment tools

Electromyography for the evaluation of radiculopathies, plexopathies or focal nerve impingement/injury would be appropriate. Neuropsychological assessment for psychiatric, mood, and behavioral dysfunction would be appropriate in chronic spinal cord injury–related pain. Pain assessment scales developed specifically for assessing pain in SCI include a modified version of the West Haven-Yale Multidimensional Pain Inventory (MPI), known as the MPI-SCI and the International Spinal Cord Injury Basic Pain Data Set (ISCIPDS:B).14,15

Early predictions of outcomes

Individuals who have neuropathic pain early after injury are likely to experience ongoing pain; chronic musculoskeletal pain is not predicted by pain during the first few months after injury.16 Hypersensitivity one month after traumatic SCI is a predictor for neuropathic pain below the level of injury.17 Tetraplegia and age greater than 50 are also risk factors for the development of neuropathic pain.7 Unemployment at the time of injury has been associated with persistent pain. The relationship between chronic neuropathic pain and incomplete injury has not been firmly established.7,13

Professional Issues

Disability due to spinal cord related pain has not yet been quantified, but such disability would be reasonable to expect, considering reports of the negative impact and interference attributed to pain experienced by people with SCI. In some states, medical cannabinoids are available by law to patients with physician endorsement, despite the limitations in the available evidence of efficacy in SCI-related pain.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The International Spinal Cord Injury Basic Pain Data Set and Extended Set was developed to have a standardized method of defining pain conditions after SCI. This pain set gives the examiner a detailed, metric assessment tool to catalogue each pain complaint that a patient has, to qualify each pain as nociceptive or neuropathic, and to quantify each pain.15

At different disease stages

  • Acute pain management for nociceptive pain occurs with opiate and non-opiate pain relievers. Neuropathic pain is treated with anticonvulsants and antidepressant medications. AAN, AAPMR, and AANEM have published recommendations for neuropathic pain, although specific for ‘Painful Diabetic Neuropathy.’ Major recommendations include pregabalin and/gabapentin for treatment of neuropathy. Weaker evidence was found for valproic acid. Evidence for alternative anticonvulsants (oxcarbazepine, lamotrigine, and lacosamide) were inconclusive. Antidepressants (amitriptyline, venlafaxine, and duloxetine) ‘should be considered.’ Clinicians should always be aware of potential adverse effects of these medications (e.g., valproate is potentially teratogenic). Physical modalities such as transcutaneous electrical nerve stimulation (TENS) should also be strongly considered for neuropathic pain.18,19
  • Subacute management promotes the use anti-inflammatory agents, non-opioid pain relievers and physical modalities including exercise for nociceptive pain management. Use of complementary and alternative methods, such as massage and acupuncture, do not have a defined role.18
  • Chronic pain management requires a multidisciplinary approach that includes physical and occupational therapy, psychology, physiatry, and pain subspecialists. The role of opiates in chronic pain management after spinal cord injury is not clear. They should be used with caution and with special attention to their impact on secondary conditions (bowel management, biliary stasis) and function. Surgical options, including intrathecal medication (baclofen, opiates, ziconotide), spinal and cortical stimulators, ablation and decompression have been trialed but do not have proven efficacy at this time.

Coordination of care

(See Management at Different Stages, above.)

Emerging/unique interventions

Impairment Based Measurements

The International Spinal Cord Injury Basic Pain Data Set and Extended Set was developed to have a standardized method of defining pain conditions after SCI. This pain set gives the examiner a detailed, metric assessment tool to catalogue each pain complaint that a patient has, to qualify each pain as nociceptive or neuropathic, and to quantify each pain.15

Cutting Edge/ Emerging and Unique Concepts and Practice

  • Transcranial magnetic stimulation (rTMS)20,21 and transcranial direct current stimulation (tDCS)21
  • Botulinum toxin type A injections22

Gaps in the Evidence-Based Knowledge

  • Medication effectiveness of neuropathic pain medications for SCI-related pain (see Management at Different Stages, above)
  • Interventional effectiveness (including neuromodulation that includes intrathecal medication)
  • Surgical effectiveness for pain, including spine decompression and cord de-tethering
  • Complementary and alternative interventions, including medical marijuana.


  1. Siddall PJ, Taylor DA, Cousins MJ. Classification of pain following spinal cord injury. Spinal Cord. 1997;35(2):69-75.
  2. Bryce T, Ragnarsson KT. Epidemiology and classification of pain after spinal cord injury. Top SCI Rehabil. 2001;7(2):1-17.
  3. Wrigley PJ, Press SR, Gustin SM, et al. Neuropathic pain and primary somatosensory cortex reorganization following spinal cord injury. Pain. 2009;141(1-2):52-59.
  4. Duggal N, Rabin D, Bartha R, et al. Brain reorganization in patients with spinal cord compression evaluated using fMRI. Neurology. 2010;74:1048-1054.
  5. Attal N. Spinal cord injury pain. Revue Neurologique. 2021;177(5): 606-612.
  6. Siddall PJ, McClelland JM, Rutkowski SB, Cousins MJ. A longitudinal study of the prevalence and characteristics of pain in the first five years after spinal cord injury. Pain. 2003;103(3):249-57.
  7.  Burke D, Fullen BM, Stokes D, Lennon O. Neuropathic pain prevalence following spinal cord injury: a systematic review and meta-analysis. European Journal of Pain. 2017;21:29-44.
  8. Alvarado J, Felix E, Gater D. Upper extremity overuse injuries and obesity after spinal cord injury. Top Spinal Cord Inj Rehabil. 2021;27(1):68-74.
  9. Richards JS, Meredith RL, Nepomuceno C, Fine PR, Bennett G. Psychosocial aspects of chronic pain in spinal cord injury. Pain. 1980;8(3):355-366.
  10. Elliot TR, Harkins SW. Psychosocial concomitants of persistent pain among persons with spinal cord injuries. Spinal Cord Injury. 1991;1(4):7-16.
  11. Rose M, Robinson J, Ells P, Cole J. Pain following spinal cord injury: results from a postal survey. Pain. 1988;34:101-102.
  12. Budh CN, Hultling C, Lundeberg T. Quality of sleep in individuals with spinal cord injury: a comparison between patients with and without pain. Spinal Cord. 2005;43:85-95.
  13. Putzke JD, Richards JS, Hicken BL, DeVivo MJ. Interference due to pain following spinal cord injury: important predictors and impact on quality of life. Pain. 2002;100(3):231-242.
  14. Widerström-Noga EG, Cruz-Almeida Y, Martinez-Arizala, A. Internal consistency, stability, and validity of the spinal cord injury version of the Multidimensional Pain Inventory. Archives of Physical Medicine and Rehabilitation. 2006;87(4):516–523. https://doi.org/10.1016/j.apmr.2005.12.036
  15. Widerström-Noga E, Biering-Sørensen F, Bryce T, et al. The international spinal cord injury basic pain data set. Spinal Cord. 2008;46:818-23.
  16. 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;103:249-257.
  17. Finnerup, NB., Norrbrink C, Trok K. Phenotypes and predictors of pain following traumatic spinal cord injury: A prospective study. The Journal of Pain. 2014;15(1): 40–48. (15)
  18. Cardenas, DD, Felix, ER. Pain after spinal cord injury: a review of classification, treatment approaches, and treatment assessment. Phys Med Rehabil. 2009;1:1077-1090.
  19. Finnerup N, et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14:162-173.
  20. Awad BI, Carmody MA, Zhang X, Lin VW, Steinmetz MP. Transcranial magnetic stimulation after spinal cord injury. World Neurosurg. 2015 Feb;83(2):232-5. doi: 10.1016/j.wneu.2013.01.043. Epub 2013 Jan 12. PMID: 23321378.
  21. Boldt I, Eriks-Hoogland I, Brinkhof MW, 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 Nov 28;(11):CD009177. doi: 10.1002/14651858.CD009177.pub2. PMID: 25432061.
  22. Han ZA, Song DH, Oh HM, Chung ME. Botulinum toxin type A for neuropathic pain in patients with spinal cord injury. Ann Neurol. 2016 Apr;79(4):569-78. doi: 10.1002/ana.24605. Epub 2016 Feb 16. PMID: 26814620; PMID: PMC4825405.

Original Version of the Topic

Anthony Chiodo, MD. Spinal Cord Injury – Related Pain. 12/27/2012

Previous Revision(s) of the Topic

Paolo Mimbella, MD, Argyrios Stampas, MD. Spinal Cord Injury – Related Pain. 3/29/2017

Author Disclosure

Audrey Leung, MD
Nothing to Disclose

Daniel Nguyen, MD
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David Pilkington, DO
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Albert Chang, MD
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Barbara Kozminski, MD
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