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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 nervous system.


Etiology is uncertain; however, emerging evidence demonstrates the role of cortical reorganization in neuropathic pain at and/or below the level of injury.3,4 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 nociceptive pain above the level of injury. The most severe pain is neuropathic pain below the level of injury.5


Due to the varying locations and types of pain from which spinal cord injured patients suffer, the pathophysiology can vary. Patients can have musculoskeletal pain in the upper body from using the upper limbs both for mobility and for self-care activities, with local injury–mediated and inflammation-mediated pain processes (i.e. nociceptive). 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. Persistent pain may be due to peripheral or central/cortical reorganization. Acute spinal cord injury is also thought to enhance spinal cord excitability possibly predisposing this population to chronic pain syndromes. O

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

Pain during disease progression: Pain after spinal cord injury is common in the acute phase. As patients acquire new skills for mobility and self- care, musculoskeletal pain in the early training periods of inpatient and early outpatient rehabilitation is common. Persistent or recurrent musculoskeletal pain is more common among patients who use their upper body for transfers and mobility. Neuropathic pain can occur early in the course of injury, especially as it relates to pain at the level of injury, where local root and cord injury can result in the sensation of persistent, aberrant pain. Late onset neuropathic pain can be due to degenerative spine processes, syrinx, or focal neuropathies. Persistent pain after spinal cord injury typically starts in the first year post injury.

Specific secondary or associated conditions and complications

Numerous complications are seen secondary to SCI pain. Pain can disrupt mood and psychosocial functioning,6,7 occupational activities,8 and basic needs, such as sleep.9 Persistent pain is associated with lower quality of life postinjury.10



The history should start with the date and mechanism of spinal cord injury. Pain history including time course, location, quality, and quantity (e.g. VAS) 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, thereby narrowing the associated diagnostic investigation needed. 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, and patient perception of cause of injury and treatment goals.

Physical examination

The physical examination should include an American Spinal Injury Association (ASIA) Impairment Scale evaluation, further neurological testing, including reflex testing and evidence of abnormalities in sensation (allodynia, hyperalgesia, hyperpathia) and evaluation of spasticity and other muscle overactivity. 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

This should be done as it relates to current pain complaints. Assessment of a change 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. 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 a 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.

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. 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.12,13

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.


Available or current treatment guidelines

The International Spinal Cord Injury Basic Pain Data Set and Extended Set were 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.11

At different disease stages

  1. 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. Alternative anticonvulsants (oxcarbazepine, lamotrigine, and lacosamide) were not recommended. Antidepressants (amytriptyline, 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. P
  2. 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.
  3. Chronic pain management requires multidisciplinary management that includes physical and occupational therapy, psychology, physiatry, and pain physician. The role of opiates in chronic pain management after spinal cord injury is not clear. Their use should be with caution and with special attention to their impact on secondary conditions (bowel management, biliary stasis) and function. The use of centrally active agents, including anticonvulsants and pregabalin, is considered standard of care although evidence for all except pregabalin is lacking.14 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.
  4. Pre-terminal N/A

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 were 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.11


Cutting edge concepts and practice

  1. Dorsal root entry zone stimulation techniques
  2. Role of neuromodulation in chronic pain management


Gaps in the evidence-based knowledge

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


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  2. Bryce T, Ragnarsson KT.Epidemiology and classification of pain after spinal cord injury. Top SCI Rehabil. 2001;7:1-17.
  3. Wrigley PJ, Press SR, Gustin SM, et al. Neuropathic pain and primary somatosensory cortex reorganization following spinal cord injury. 2009;141:52-59.
  4. Duggal N, Rabin D, Bartha R, et al. Brain reorganization in patients with spinal cord compression evaluated using fMRI. 2010;74:1048-1054.
  5. 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. 2003;103:249-57.
  6. Richards JS, Meredith RL, Nepomuceno C, Fine PR, Bennett G. Psychosocial aspects of chronic pain in spinal cord injury. 1980;8:355-366.
  7. Elliot TR, Harkins SW. Psychosocial concomitants of persistent pain among persons with spinal cord injuries. 1991;1:7-16.
  8. Rose M, Robinson J, Ells P, Cole J. Pain following spinal cord injury: results from a postal survey. 1988;34:101-102.
  9. 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.
  10. Putzke JD, Richards JS, Hicken BL, DeVivo MJ. Interference due to pain following spinal cord injury: important predictors and impact on quality of life. 2002;100:231-242.
  11. 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.
  12. 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. 2003;103:249-257.
  13. 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.
  14. 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. 67:1792-1800.
  15. Huang YJ, Lee KH, Murphy L, Garraway SM, Grau JW. Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization. Experimental Neurology. 2016 Nov;285(Pt A): 82-95.
  16. Evidence-based guideline: treatment of painful diabetic neuropathy. Report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. 2011 May 17.

Original Version of the Topic

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

Author Disclosure

Paolo Mimbella, MD
Nothing to Disclose

Argyrios Stampas, MD
Nothing to Disclose