Author(s): Surendra Barshikar, MD, MBA, Kacie Shannon, MS, Ellen Sloan, MD
Originally published: November 11, 2011 Last updated: January 15, 2026
Jump to:

Disease/Disorder

Definition

Persistent pain is a common physical sequela of spinal cord injury (SCI). It is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.1 Taxonomies classifying pain after SCI have evolved, more recently converging into the International Spinal Cord Injury Pain (ISCIP) Classification and further developed into the ISCIP Basic Data Set. SCI-related pain is broadly classified as nociceptive, neuropathic, other, or unknown. Nociceptive pain implies the stimulation of a peripheral nerve ending or sensory receptor that transduces noxious signals, and this can be further stratified into musculoskeletal and visceral subtypes. Neuropathic pain implies a pain generator within the somatosensory nervous system, which can be further classified by location with respect to the level (above, at, or below) of the SCI.2,3

Etiology

While the etiology for neuropathic pain following SCI is uncertain, evidence points toward the role of reorganization of the somatosensory cortex in regions responsible for transducing signals at and/or below the level of injury.4,5 Additionally, neuronal hyperexcitability secondary to inflammation and ion channel dysfunction and enhanced neural connectivity between regions influential in sensory processing may play a part.6,7 The etiology of nociceptive pain is often related to repetitive overuse of particular structures or bowel dysfunction, presenting as musculoskeletal or visceral pain.8 This article will focus on the most commonly encountered SCI-pain syndromes.

Epidemiology including risk factors and primary prevention

As many as 60-80% of patients with SCI suffer pain, with one-third of those individuals describing the pain as severe.9 Neuropathic pain is the most common type with around 50-60% of patients with SCI reporting this pain.10,11 The most severe pain is neuropathic pain below the level of injury.11 Older age at injury, bullet injury, and earlier onset of pain are risk factors for neuropathic pain, while a higher level of SCI and poor body mechanics are risk factors for musculoskeletal pain.12,13

Patho-anatomy/physiology

Due to various locations and types of pain from which patients with SCI suffer, the pathophysiology can vary. Acute traumatic SCI 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 extremities due to increased dependence on these regions for mobility and self-care activities.13,14 Common overuse injuries include rotator cuff injuries, wrist injuries such as median nerve entrapment (carpal tunnel syndrome) and De Quervain’s tenosynovitis, and myofascial pain of the neck and low back. Neuropathic pain may be attributable to degeneration of spinal segments adjacent to the original injury, syrinx formation, or focal nerve compression in the plexus or limbs. Additionally, neuropathic pain is postulated to be mediated by peripheral and central sensitization, with the latter playing a larger role in pain below the level of injury. Central sensitization is the dual process of hyperexcitability of ascending afferent pain signals and loss of inhibitory descending pathways from the spinal cord, thalamus, and supraspinal regions such as the periaqueductal grey and rostral ventromedial medulla. Neuronal hyperexcitability is thought to be mediated by modulating sodium and calcium channels, downregulation of potassium channels, and phosphorylation of glutamate channels, along with loss of inhibitory molecules including glycine and γ-aminobutyric acid (GABA). Neuroinflammatory signaling from cytokine/chemokine-releasing microglia and astrocytes also contributes. Collectively, these manifest as hyperalgesia, allodynia, pain amplification, and persistence or worsening pain below the level of injury over time. Furthermore, these processes may predispose patients to developing chronic pain syndromes long after the acute injury.6,7,15

Table 1: Summary of Neuropathic versus Nociceptive Pain in SCI

FeatureNociceptive PainNeuropathic Pain
Primary SourceTissue damage, inflammation, or musculoskeletal overuseInjury or dysfunction of somatosensory nervous system
Common Causes in SCIAcute trauma, postoperative inflammation, shoulder/upper-extremity overuse injuriesSCI itself, adjacent segment degeneration, syrinx formation, plexus or peripheral nerve compression
MechanismActivation of peripheral nociceptorsPeripheral and central sensitization, channel dysregulation, impaired inhibitory pathways, neuroinflammation
Clinical FeaturesPain that is aching, throbbing, sharp. Usually localized to area of tissue injury. May be associated with local tenderness, swelling, mechanical provocation of pain.Pain that is burning, shooting, electric, tingling. Can occur at-, above-, or below-level of injury; often diffuse or radiating. May be associated with allodynia, hyperalgesia, pain amplification, dysesthesia
Impact on FunctionLimits mobility or activity due to mechanical painImpairs sleep, mood, and participation; often persistent and debilitating
Response to TreatmentTypically improves with NSAIDs, rest, PT, or addressing mechanical sourceOften require multimodal therapy; responds variably to anticonvulsants, antidepressants, neuromodulation

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 while undergoing therapies targeted on improving mobility, function, and self-care, they can develop musculoskeletal pain from post-injury remobilization and overuse. 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 one year after SCI. Overall, neuropathic pain is more prevalent after six months of injury in comparison to acute SCI.10 The prevalence of neuropathic pain tends to increase over time, while musculoskeletal pain slightly decreases.16

Specific secondary or associated conditions and complications

Numerous psychological and physical complications are observed secondary to SCI pain. Patients may experience disruptions in psychosocial functioning, mental wellbeing, feelings of anger, isolation, sleep, and suicidal ideation.17 An example of potential mechanisms mediating these disturbances is nighttime neuropathic pain and musculoskeletal pain from frequent turning and joint loading disrupting quality sleep.18 Beyond these associations, there is also evidence for a reciprocal, synergistic relationship between chronic SCI pain and post-traumatic stress disorder symptomology.19 Physical complications may also manifest, with secondary health conditions such as spasticity, pressure ulcers, and autonomic dysfunction posing long-term challenges that necessitate intensive rehabilitation to optimize function. Overall, persistent pain is associated with a lower quality of life post-injury.20

Essentials of Assessment

History

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 documented. Information on alleviating and aggravating factors, past evaluations and treatments (including effectiveness), and pharmacological assessment should be obtained. Gathering this information enables the examiner to formulate a differential diagnosis based on pain location and type, thereby guiding next steps. Pain generators frequently seen in SCI patients include fractures, spasticity, heterotopic ossification, infections, visceral disorders, cardiovascular issues, gastrointestinal diseases, genitourinary issues, and malignancy. Social, functional, occupational, and leisure history should also be obtained given 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 the cause of injury, support system, 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, abnormalities of posture, abnormalities of gait/mobility, and their impact on pain should be noted.

Functional assessment

Functional assessment should be completed as it relates to current pain complaints. Tools such as the Barthel Index or Functional Independence Measure can be useful in determining a patient’s ability to complete their activities of daily living (ADLs). 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 or other symptomology, specific laboratory evaluation is recommended. Some possibilities include urinalysis for urinary tract infection, liver function tests for gallbladder disease, amylase/lipase for pancreatitis given bodily stasis, and cardiac enzymes for suspected symptomatic coronary artery disease. Inflammatory markers such as erythrocyte sedimentation rate, C-reactive protein, and procalcitonin are nonspecific but may be helpful.

Imaging

Imaging will be dependent on the pain complaint, physical examination, and differential diagnosis. Plain x-ray or computed tomography (CT) of the skeletal system is appropriate within the context of the history and physical exam to evaluate for structural abnormalities, fractures, or degenerative changes. Spinal magnetic resonance imaging (MRI) to assess soft tissue structures may help identify degenerative disease, syrinx, or compressive lesions causing neuropathic symptoms. Neuromuscular ultrasound (NMUS) and musculoskeletal ultrasound (MSK US) play increasingly important roles in visualizing neuropathic and nociceptive pain generators. NMUS can help visualize focal nerve entrapments or compressions, assess nerve morphological changes consistent with neuropathy, and evaluate for signs of brachial plexus and/or peripheral nerve trauma following high-energy SCI or even traction related injuries from spinal stabilization. In a similar fashion, MSK US may also help identify sources of nociceptive pain. Ultrasound enables real-time assessment of impingement, subluxation, tendon glide, or instability. It can aid in diagnosing overuse injuries that are common in users of wheelchairs, such as rotator cuff tendinopathy or tears, subacromial bursitis, impingement syndromes, acromioclavicular joint degeneration, lateral/medial epicondylitis, De Quervain’s tenosynovitis, and carpal tunnel syndrome.

Supplemental assessment tools

Electromyography for the evaluation of radiculopathies or plexopathies is appropriate, and this study can be combined with NMUS to identify peripheral nerve involvement.  Psychiatric or psychological assessment for psychiatric, mood, and behavioral dysfunction is appropriate in chronic SCI–related pain. A pain assessment scale developed specifically for assessing pain in SCI is the International Spinal Cord Injury Basic Pain Data Set (ISCIPBDS).3

Early predictions of outcomes

Individuals who experience neuropathic pain in the weeks or first few months after injury are more likely to suffer from chronic neuropathic pain, and this can occur in individuals with either complete or incomplete injuries.20 Early sensory hypersensitivity one month after traumatic SCI, particularly dysesthesia in response to cold sensation, is a predictor for neuropathic pain below the level of injury.16 Tetraplegia and age greater than fifty are also risk factors for the development of neuropathic pain.10 Decreased pinprick and light touch scores on the International Standards for Neurological Classification of Spinal Cord Injury (SC-ISNCSCI) upon admission are clinical findings that can reliably predict later development of central neuropathic pain.21 Compared to the more predictable trajectory of neuropathic pain, chronic visceral and musculoskeletal pain is not well-predicted by pain during the first few months after injury, as the latter often arises with overuse during the rehabilitation and mobility phases.22 Long periods of unstable employment have also been associated with persistent pain.23

Professional issues

While the professional burden of SCI-related pain has not been readily quantified, the multifaceted effects are logically ascertained. Chronic pain may result in reduced work capacity, lost productivity, and disability leave, and thereby exacerbate economic burden for individuals and society. One study estimates that an additional $22,545 in annual medical expenses are incurred by individuals with SCI and neuropathic pain compared to those with SCI alone.24 Overall, mental and physical health challenges can be expected for individuals and caregivers alike.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The ISCIPBDS establishes a standardized method of defining pain conditions after SCI. This offers the examiner a detailed, metric assessment tool to catalogue and quantify pain complaints, and to qualify each pain as nociceptive, neuropathic, other, or unknown.3

At different disease stages

  • Acute pain management for nociceptive pain occurs with opiate and non-opiate pain relievers. Neuropathic pain is treated with anticonvulsants, with gabapentin and pregabalin often used as first-line therapy. Antidepressant medications such as amitriptyline and duloxetine can also be helpful for neuropathic pain and associated depressive symptoms.25 
  • Subacute management includes anti-inflammatory agents, non-opioid pain relievers, and physical modalities including exercise for nociceptive pain management. Addressing cognitive, emotional, and social issues is also important in providing holistic care.
  • Chronic pain management requires a multidisciplinary approach that includes physical and occupational therapy, psychology, physiatry, and pain subspecialists. In addition to therapies utilized in the acute and subacute phases, individuals may wish to trial other modalities for pain relief. It must be noted that the role of opiates in chronic pain management after spinal cord injury remains unclear and even discouraged. If prescribed, caution and special attention must be given to their impact on secondary conditions (i.e. bowel management, biliary stasis, respiratory drive) and function. More recently, transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) have demonstrated analgesic benefits on neuropathic pain, but consensus regarding optimal delivery methods is still in the nascent stages.25 Electroacupuncture (EA) has shown efficacy in treating neuropathic pain, although the underlying mechanism has yet to be elucidated.25 Surgical options also represent an emerging area, with spinal cord stimulation (SCS) showing some promise for relief of neuropathic pain and reduction of opioid utilization.26 Intrathecal analgesic agents such as baclofen and ziconotide administered via pumps may provide pain control, but there is no proven efficacy in their modulation of underlying pathogenesis.27

Coordination of care

A multidisciplinary team may include physiatrists, pain management specialists, physical therapists, occupational therapists, psychologists, and social workers. A thorough assessment of the patient’s pain, functional abilities, psychological state, and social circumstances is indicated, including how it impacts their overall quality of life. Educating patients and their families about pain management options, self-care strategies, and the importance of adherence to a treatment plan with adequate follow-up is key. Additionally, connecting patients with community resources and support services such as a personal care attendant can facilitate a smoother reintegration from the acute care setting back into the community, as well as aid in goal setting of realistic expectations.28

Emerging/unique interventions

N/A

Cutting Edge/Emerging and Unique Concepts and Practice

Emerging, multidisciplinary approaches are beginning to reshape treatment of SCI-related pain. Alterations in the gut microbiome following SCI influence systemic inflammation and neuroimmune signaling via the gut-spinal axis, making microbiome modulation a potential adjuvant strategy to reduce neuroinflammation and pain25. Botulinum toxin type A injections, which are a well-established treatment for focal spasticity, have demonstrated analgesic effects in neuropathic pain syndromes following SCI.29

Immunology-targeted therapies are also advancing: extracellular vesicles from stem cells can deliver anti-inflammatory microRNAs and proteins to injured spinal tissue, while stromal cell therapies can modulate microglial cell activation and secrete trophic factors that dampen neuroinflammation and promote healing.30,31 Lastly, regenerative medicine and gene therapy offer potential to restore neural circuitry and alter maladaptive pain signaling via gene delivery, reprogramming, and genome-editing strategies 32

Gaps in the Evidence-Based Knowledge

  • Practical integration of evidence-based practices into real-world settings given resource, logistical, and financial constraints
  • Mechanisms underlying the efficacy of rTMS, tDCS, EA, and SCS
  • Interventional effectiveness of spinal cord stimulation for chronic pain, particularly regarding patient selection and long-term efficacy
  • Surgical effectiveness for pain, including spine decompression and cord de-tethering
  • Complementary and alternative interventions, including medical marijuana.

References

  1. Raja SN, Carr DB, Cohen M, Finnerup NB, Flor H, Gibson S, Keefe FJ, Mogil JS, Ringkamp M, Sluka KA, Song XJ, Stevens B, Sullivan MD, Tutelman PR, Ushida T, Vader K. The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain. 2020 Sep 1;161(9):1976-1982. doi: 10.1097/j.pain.0000000000001939. PMID: 32694387; PMCID: PMC7680716.
  2. Bryce, T., Biering-Sørensen, F., Finnerup, N. et al. International Spinal Cord Injury Pain Classification: part I. Background and description. Spinal Cord 50, 413–417 (2012). https://doi.org/10.1038/sc.2011.156
  3. Widerström-Noga E, Biering-Sørensen F, Bryce TN, Cardenas DD, Finnerup NB, Jensen MP, Richards JS, Rosner J, Taylor J. The international spinal cord injury pain basic data set (version 3.0). Spinal Cord. 2023 Oct;61(10):536-540. doi: 10.1038/s41393-023-00919-w. Epub 2023 Jul 25. PMID: 37491608.
  4. 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.
  5. Jutzeler CR, Freund P, Huber E, Curt A, Kramer JLK. Neuropathic Pain and Functional Reorganization in the Primary Sensorimotor Cortex After Spinal Cord Injury. J Pain. 2015 Dec;16(12):1256-1267. doi: 10.1016/j.jpain.2015.08.008. Epub 2015 Sep 21. PMID: 26392031.
  6. Kang J, Cho SS, Kim HY, Lee BH, Cho HJ, Gwak YS. Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury. Cell Mol Neurobiol. 2020 Aug;40(6):861-878. doi: 10.1007/s10571-020-00785-7. Epub 2020 Jan 18. PMID: 31955281; PMCID: PMC11448802.
  7. Huynh V, Lütolf R, Rosner J, Luechinger R, Curt A, Kollias S, Hubli M, Michels L. Supraspinal nociceptive networks in neuropathic pain after spinal cord injury. Hum Brain Mapp. 2021 Aug 15;42(12):3733-3749. doi: 10.1002/hbm.25401. Epub 2021 Jun 16. PMID: 34132441; PMCID: PMC8288099.
  8. Franz, S., Finnerup, N.B. (2017). Diagnostics and Treatment of Pain in Spinal Cord Injury. In: Weidner, N., Rupp, R., Tansey, K. (eds) Neurological Aspects of Spinal Cord Injury. Springer, Cham. https://doi.org/10.1007/978-3-319-46293-6_12
  9. Masri R, Keller A. Chronic pain following spinal cord injury. Adv Exp Med Biol. 2012;760:74-88. doi: 10.1007/978-1-4614-4090-1_5. PMID: 23281514; PMCID: PMC3560294
  10. 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.
  11. Ivolgin, Aleksander & Mazur, Andrey & Litvinenko, Igor & Tsygan, Nikolay & Avseitseva, Tatyana & Yakovleva, Viktoriya. (2023). Epidemiology of pain in spinal cord injury. Russian Military Medical Academy Reports. 42. 369-375. 10.17816/rmmar611165.
  12. Margot-Duclot A, Tournebise H, Ventura M, Fattal C. What are the risk factors of occurence and chronicity of neuropathic pain in spinal cord injury patients? Ann Phys Rehabil Med. 2009 Mar;52(2):111-23. doi: 10.1016/j.rehab.2008.12.003. Epub 2009 Jan 22. PMID: 19909702.
  13. Figoni, Steve. (2009). Overuse shoulder problems after spinal cord injury: A conceptual model of risk and protective factors. Clinical Kinesiology. 63. 12-22.
  14. 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.
  15. Attal N. Spinal cord injury pain. Revue Neurologique. 2021;177(5): 606-612.
  16. Finnerup NB, Norrbrink C, Trok K, Piehl F, Johannesen IL, Sørensen JC, Jensen TS, Werhagen L. Phenotypes and predictors of pain following traumatic spinal cord injury: a prospective study. J Pain. 2014 Jan;15(1):40-8. doi: 10.1016/j.jpain.2013.09.008. Epub 2013 Oct 1. PMID: 24268112.
  17. Mashola MK, Korkie E, Mothabeng DJ. Exploring the Experience of Living with Pain after Spinal Cord Injury: A Qualitative Study. Behav Neurol. 2024 Feb 2;2024:9081530. doi: 10.1155/2024/9081530. PMID: 38343899; PMCID: PMC10857878.
  18. Aydin T, Öneş K, Kesiktaş FN, Corum M, Kalaoğlu E, Karacan I. Sleep quality in individuals with short-duration chronic spinal cord injury. Int J Rehabil Res. 2020 Dec;43(4):369-375. doi: 10.1097/MRR.0000000000000436. PMID: 32947351.
  19. Ginzburg K, Greener H, Bondi M, Zeilig G, Defrin R. Predicting chronic pain two years following a spinal cord injury: Longitudinal study on the reciprocal role of acute pain and PTSD symptoms. J Spinal Cord Med. 2025 May;48(3):405-414. doi: 10.1080/10790268.2024.2361552. Epub 2024 Jun 24. PMID: 38913447; PMCID: PMC12035952.
  20. Lee S, Zhao X, Hatch M, Chun S, Chang E. Central Neuropathic Pain in Spinal Cord Injury. Crit Rev Phys Rehabil Med. 2013;25(3-4):159-172. doi: 10.1615/CritRevPhysRehabilMed.2013007944. PMID: 25750485; PMCID: PMC4350234.
  21. Levitan Y, Zeilig G, Bondi M, Ringler E, Defrin R. Predicting the Risk for Central Pain Using the Sensory Components of the International Standards for Neurological Classification of Spinal Cord Injury. J Neurotrauma. 2015 Nov 1;32(21):1684-92. doi: 10.1089/neu.2015.3947. Epub 2015 Aug 5. PMID: 26244708.
  22. 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.
  23. Macchia L, Daly M, Delaney L. The effect of adverse employment circumstances on physical pain: Evidence from Australian panel data. Prev Med. 2023 Aug;173:107574. doi: 10.1016/j.ypmed.2023.107574. Epub 2023 Jun 17. PMID: 37331489.
  24. Margolis JM, Juneau P, Sadosky A, Cappelleri JC, Bryce TN, Nieshoff EC. Health care resource utilization and medical costs of spinal cord injury with neuropathic pain in a commercially insured population in the United States. Arch Phys Med Rehabil. 2014 Dec;95(12):2279-87. doi: 10.1016/j.apmr.2014.07.416. Epub 2014 Aug 24. PMID: 25159715.
  25. Li J, Kang W, Wang X, Pan F. Progress in treatment of pathological neuropathic pain after spinal cord injury. Front Neurol. 2024 Nov 11;15:1430288. doi: 10.3389/fneur.2024.1430288. PMID: 39606699; PMCID: PMC11600731
  26. Huang XL, Chen YC, Kuo CC, Tsai ST. Potential benefits of spinal cord stimulation treatment on quality of life for paralyzed patients with spinal cord injury. Tzu Chi Med J. 2022 Nov 7;35(2):131-136. doi: 10.4103/tcmj.tcmj_102_22. PMID: 37261296; PMCID: PMC10227680.
  27. Karri J, Doan J, Vangeison C, Catalanotto M, Nagpal AS, Li S. Emerging Evidence for Intrathecal Management of Neuropathic Pain Following Spinal Cord Injury. Front Pain Res (Lausanne). 2022 Jul 28;3:933422. doi: 10.3389/fpain.2022.933422. PMID: 35965596; PMCID: PMC9371595.
  28. Klebine P, Azuero C, Arthur K, Zanca J. Personal Care Attendants and Spinal Cord Injury. Model Systems Knowledge Translation Center; 2020. Accessed November 15, 2025. https://msktc.org/sci/factsheets/personal-care-attendants-and-spinal-cord-injury
  29. Lakra C, Cohen H. A clinical review of the use of Botulinum Toxin type A in managing central neuropathic pain in patients with spinal cord injury. J Spinal Cord Med. 2022 Sep;45(5):651-655. doi: 10.1080/10790268.2020.1848278. Epub 2020 Dec 2. PMID: 33263489; PMCID: PMC9542712.
  30. Lim YJ, Seo MS, Park WT, Park S, Lee GW. Extracellular vesicle-derived MicroRNAs as potential therapies for spinal cord and peripheral nerve injuries. RNA Biol. 2025 Dec;22(1):1-9. doi: 10.1080/15476286.2025.2512618. Epub 2025 May 30. PMID: 40448270; PMCID: PMC12128652.
  31. Zheng B, Kuang Y, Yuan D, Huang H, Liu S. The research landscape of immunology research in spinal cord injury from 2012 to 2022. JOR Spine. 2023 May 9;6(3):e1261. doi: 10.1002/jsp2.1261. PMID: 37780822; PMCID: PMC10540832.
  32. Kalashnikova IV, Farmer MA, Shea LD, Park J. Gene therapy of neuropathic pain after spinal cord injury. In: Sang CN, Hulsebosch CE, eds. Spinal Cord Injury Pain. Academic Press; 2022:423-441. doi:10.1016/B978-0-12-818662-6.00017-0

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

Albert Chang, MD, Daniel Nguyen, MD, David Pilkington, DO, Barbara Kozminski, MD, Audrey Leung, MD. Spinal Cord Injury – Related Pain. 9/1/2022

Author Disclosure

Surendra Barshikar, MD, MBA
Nothing to Disclose

Kacie Shannon, BS
Nothing to Disclose

Ellen Sloan, MD
Nothing to Disclose