As it is clear that that there can be an enormous emotional, physical, and social impact of pain on a person’s daily life, any assessment of pain is not complete without an assessment of the numerous psychosocial factors and conditions that have been associated with pain-related distress and pain-related functional disability after SCI. It is important to obtain a psychosocial history that includes an assessment of present and past mental health history, as well as a more general understanding of the patient’s perception of pain, with specific focus on important coping strategies, such as pain catastrophizing. Furthermore, the assessment should seek to understand how environmental factors, such as the impact of the workplace or home environment, or social factors, such as interactions with family, friends, and coworkers when a person is in pain, contribute to the chronic pain experience. To aid in this assessment, clinicians may find it useful to use questionnaires to routinely screen for common difficulties, such as mood disorders. Measures like the Patient Health Questionnaire-9 (PHQ-9) or its 2-item form, the PHQ-2, are validated in SCI and can be quickly scored and interpreted.14
All of these psychosocial factors and conditions also referred to as yellow flags (Table 40.4
must be addressed if the treatment of pain is to be successful if they are contributing to ongoing or worsening pain. At an absolute minimum, pain interference with sleep, mood, and activities should always be evaluated and therefore are included in the ISCIPBDS (see Table 40.2
Musculoskeletal pain is nociceptive pain resulting from activation of nociceptors within musculoskeletal structures including muscles, tendons, ligaments, and bones within areas of at least partially retained sensation. In areas of apparent complete loss of sensation, nociceptors may be activated and can exacerbate at-level and below-level neuropathic pain as well as trigger autonomic dysreflexia (AD) and AD headache (see “Other Nociceptive Pain”
section). Musculoskeletal pain typically changes in intensity with movement or palpation of the responsible musculoskeletal structures in which the nociceptors are activated. Appropriate imaging (x-ray, magnetic resonance imaging [MRI], ultrasound) often shows musculoskeletal pathology consistent with the pain presentation. As might be expected after a traumatic SCI, musculoskeletal pain is common in the acute period related to acute fractures of the spine and other musculoskeletal trauma.16,17
Subsequently, this acute injury-related pain resolves, and other pains then begin to appear as individuals begin to function in new ways which predispose them to develop overuse injuries.
If it is unclear if a particular pain is nociceptive or neuropathic, as musculoskeletal pain typically responds better than other types of pain to rest, joint protection, anti-inflammatory medications, and physical measures such as stretching and massage, treatment of the pain using these specific interventions may be diagnostic. The converse may also be true in that many of the adjuvant medications recommended for the treatment of neuropathic pain such as those within the gabapentinoid and antidepressant classes may also be effective in ameliorating nociceptive pain.
Approximately one-half of individuals with SCI, including people with either paraplegia or tetraplegia and complete
or incomplete injuries who use all types of mobility devices ranging from wheelchairs to ambulatory assist devices, experience shoulder pain.18
In the acute period after SCI, shoulder pain is thought to develop due to the high demand on unconditioned muscles, whereas in the chronic phase, shoulder pain is thought to be related to overuse from repetitive motions and secondary degeneration of affected musculoskeletal structures.
TABLE 40.3 Cardinal Pain Attributes210
Examples of Usefulness for SCI Pain Classification
History of onset
Differentiates between subtypes, as nociceptive pain often is present only when there is stimulation of offending nociceptors, whereas neuropathic pain often may be more persistent due to damage related neuronal ectopy
Indicates subtype, especially if a few specific descriptors such as “burning,” “electric shock-like,” or “tender” are specified, as the first two descriptors are more commonly seen in neuropathic types, whereas the latter is commonly described for nociceptive pain
Ameliorating and exacerbating factors
Associated sensory disturbances
SCI, spinal cord injury.
Either global shoulder muscle weakness related to a high level cervical SCI or an imbalance of specific stabilizing muscles of the shoulder and scapula can be a factor in the development of pain in both acute and chronic phases for individuals with paraplegia or tetraplegia. This imbalance can develop insidiously through relative strengthening of certain muscles (e.g., shoulder abductors and flexors) with everyday activities such as transfers and wheelchair propulsion or through substitution of different muscles in those with cervical SCI if some of the usual shoulder stabilizers are not fully innervated and are therefore weak. Different activities stress different muscles; for example, in propelling a wheelchair up a ramp, the greatest activation is found in the shoulder flexors followed by the external rotators. This is in contrast to the greatest activation in the sternal pectoralis major muscle followed by the infraspinatus and supraspinatus muscles during push-up lift maneuvers.19,20
It has been shown that many individuals who develop shoulder pain have decreased muscle strength, particularly in the shoulder adductors, and lower levels of physical activity even before the onset of pain.21
TABLE 40.4 Yellow Flags: Psychosocial Factors and Conditions Associated with Pain-Related Distress and Functional Disability15
Psychosocial Factors and Conditions
Depression often manifesting with decreased appetite, poor sleep, and low energy and lack interest in activities
Poor motivation to complete daily activities or work because of pain
Decreased participation in valued activities
Avoidance of activities associated with pain
A history of preexisting pain problems
Poor coping especially with evidence of catastrophic thinking
Use and dependence on alcohol or illicit substances
Use and dependence on prescribed opioids, especially if there is evidence of misuse
Acquired tightness of the shoulder capsule and contracture of the scapular thoracic articulation caused by a lack of passive or active range of motion and underlying spasticity are also commonly associated with shoulder pain in individuals with tetraplegia, much less so in individuals with paraplegia. Individuals with tetraplegia are also more likely to have pain related to shoulder instability resulting from weakness of the muscles that stabilize the shoulder joint.
Specific etiologies of shoulder pain related to all of the mentioned mechanisms include the rotator cuff impingement syndrome, subacromial bursitis, bicipital tendonitis, adhesive capsulitis, and osteoarthritis.22,23,24
Elbow and Wrist Pain
Musculoskeletal causes of elbow pain in persons with SCI include medial and lateral epicondylitis, triceps tendonitis, osteoarthritis, and olecranon bursitis. The latter often occurs in individuals who lean on their elbows for balance support or in those who push off with their elbows to assist with positioning and bed mobility.
Common musculoskeletal causes of wrist pain in adults include de Quervain tenosynovitis, inflammation/arthritis of the carpometacarpophalangeal joint of the thumb, and arthritis of the wrist. These typically are overuse injuries caused, for example, by repetitive grasping of a wheelchair push rim during wheelchair propulsion.
Musculoskeletal back pain in persons with SCI is common for a number of reasons, including a high prevalence of spinal surgeries, trunk muscle imbalances owing to spasticity and/or trunk weakness, kyphoscoliosis, and frequent dependence on wheelchairs. Structures in which nociceptors may be activated in and near the spine include muscles, tendons, and ligaments; the facet joint; the intervertebral disk; and the sacroiliac joint. Pain caused by spinal instability or spinal hardware failure is typically primarily nociceptive. After a portion of the spine is fused, the spinal segments adjacent to (above or below) the fusion often compensate for the lost motion of the fused segments and, over time, develop secondary degeneration and often pain. Sitting in a wheelchair, especially sitting in a kyphotic posture, can induce back pain in individuals with or without SCI.25
When an individual with limited hip flexion range (usually less than 90 degrees) is positioned for an extended period in a wheelchair with a seatback angle of 90 degrees, he or she
is at increased risk of acquiring back pain depending on the degree of at least partially preserved sensation. If the lack of hip flexion is unilateral, the individual will accommodate to leaning to the side opposite whenever sitting. If the lack of hip flexion is bilateral, the only way the individual will be able to “fit” within the chair is to have his or her ischial tuberosities (and sacrum) contact the seat more anteriorly than is optimal causing the lumbar spine to be unsupported and the thoracic spine to assume an exaggerated kyphotic posture.
Muscle Pain Related to Spasticity
Spasticity is a syndrome of different components, including a velocity-dependent increased resistance to passive motion, involuntary muscle contractions or spasms, and hyperreflexia. The involuntary muscle contractions result from different muscles acting synergistically, typically in a specific flexion or extension pattern. In someone with retained sensation, continuous or paroxysmal muscle spasms are often painful. Spasticity when significant and present to a greater degree on one side of the trunk as compared to the other often causes a coronal imbalance in spinal alignment (or a functional scoliosis) which can lead to musculoskeletal back pain especially in those with retained sensation in the spinal region of imbalance. Nociceptors activated through this coronal imbalance may arise not only from spastic muscles such as for instance the quadratus lumborum and thoracolumbar paraspinals but also from within the sacroiliac joint and lumbar facet joints on the side with more significant spasticity through the greater forces transmitted through these joints.
Visceral pain refers to pain located in the thorax, abdomen, or pelvis, which is believed to be primarily generated in visceral structures.10
Visceral pain of gastrointestinal system origin often is temporally related to food intake or bowel function and can be associated with symptoms of AD, anorexia, nausea, or vomiting as well, any of which can be more prominent than the pain itself. Tenderness to palpation of the abdomen is a common physical sign (in persons with some retained trunk sensation) as are the pain descriptors of “cramping,” “dull,” or “tender.” The characteristics of chronic abdominal pain in SCI are very similar to those of chronic constipation,26
and appropriate imaging often shows visceral pathology consistent with the pain presentation (e.g., colonic distension by stool). Abdominal visceral pain has a late onset being relatively uncommon during the first 5 years after SCI and increasing in prevalence afterward with approximately one-fifth of those at 10 years and one-third of those at 20 years reporting it; the prevalence does not seem to increase after 20 years, however.27
Other less common causes of visceral pain include bowel obstruction, bowel infarction, bowel perforation, cholecystitis, choledocholithiasis, pancreatitis, appendicitis, splenic rupture, bladder perforation, pyelonephritis, urinary tract infection, or superior mesenteric syndrome. As individuals with limited somatic sensation in the abdominal wall may experience only dull or aching pain, even with serious intra-abdominal emergencies such as acute appendicitis, cholecystitis, peritonitis, bowel obstruction, or mesenteric artery thrombosis, a degree of suspicion for these other causes should always be maintained.
AT- AND BELOW-LEVEL SPINAL CORD INJURY PAIN
At-level SCI pain is neuropathic pain perceived within the dermatome of the NLI and/or a maximum of three dermatomes below this level. It must be attributed to damage to the spinal cord or nerve roots.11
Pain thought due to injury to the cauda equina is always classified as at-level SCI pain. One-third of individuals with SCI report at-level SCI pain soon after injury, and its prevalence over time does not seem to change.16,17
At-level SCI pain is suggested by altered sensation within the painful area, especially allodynia or hyperalgesia, and the descriptors of “hot,” “burning,” “tingling,” “pricking,” “pins and needles,” “sharp,” “shooting,” “squeezing,” “painful cold,” or “electric shock-like.”10
It is usually difficult to distinguish between the two subcategories of at-level SCI pain, spinal cord pain and radicular pain, because both are typically involved in any traumatic SCI and may have the exact same clinical presentation. However, radicular pain is generally, although not always, unilateral and radiating in a dermatomal pattern. When at-level SCI pain is associated with spinal instability where spinal movement exacerbates the pain especially if there is evidence of nerve root traction or compression, the pain is presumably more likely to be radicular in etiology. Neuropathic pain in this location at or inferiorly adjacent to the NLI that is not attributed to either spinal cord or nerve root damage should be classified as other neuropathic pain and not as at-level SCI pain. One example of other neuropathic pain is focal peripheral nerve compression (e.g., symptomatic carpal tunnel syndrome in a person with a lower cervical SCI).
Below-level SCI pain refers to neuropathic pain perceived more than three dermatomes below the NLI, with or without extension up to the NLI, that is attributed to damage to the spinal cord.10
If a pain that occurs within the NLI and the three dermatomes immediately below the NLI is considered by the individual experiencing it to be the same pain that is experienced distal to those three dermatomes adjacent to the NLI, this pain should be classified as a single below-level pain and not as at-level and below-level pain.
The pain distribution of below-level spinal cord pain should be thought of, not as dermatomal, but regional, enveloping large areas such as the anal region, the bladder, the genitals, the legs, or commonly the entire body below the NLI. It is usually continuous in presence, although the intensity of the pain can fluctuate in response to yellow flag factors and conditions (see Table 40.4
), fatigue, smoking, noxious stimuli below the level of injury, and weather changes.
Less than one-fifth of individuals report below-level SCI pain in the first year after injury, but its prevalence increases to approximately one-third after the first year and beyond.16,17,30
Below-level SCI pain can occur in persons with complete or incomplete SCI, and its descriptors are the same as those listed for at-level SCI pain.10
Allodynia or hyperalgesia can be present within the pain distribution for persons with incomplete injuries. In fact, sensory hypersensitivity (particularly cold-evoked dysesthesia) at 1 month postinjury seems to be a predictor for
the development of below-level SCI pain at 1 year.16
Similar to at-level SCI pain, neuropathic pain that occurs in this distribution that cannot be attributed to spinal cord damage should be classified as other neuropathic pain and not as below-level SCI pain.
FIGURE 40.1 Algorithm for assessing and treating nociceptive pain after spinal cord injury. (From Chhabra HS. ISCoS Text Book on Comprehensive Management of Spinal Cord Injuries. 1st ed. New Delhi: Wolters Kluwer; 2015. Figure 55.3.)
An evaluation including search for potentially treatable causes of neuropathic pain, such as nerve root or spinal cord compression, tethering, or posttraumatic syringomyelia (PTS), should be initiated when the cause is not clearly apparent.
There are three scenarios where worsening of already established neuropathic pain can be seen (Fig. 40.2
). In the first, the worsening is due to the natural history of the pain related to ongoing neuroplastic changes occurring within the nervous system during that first year after SCI. In the second, there is progression of the neurologic injury (nerve root or spinal cord) due to changes in degree of nerve root or spinal cord compression, tethering, or PTS. In the third and probably most common scenario, there is the development of a red flag condition
) that may aggravate neuropathic pain.15
A thorough history and physical exam is the first step needed to determine to which of the three scenarios the worsening of pain can be attributed. For evidence of the first, which we can call natural pain evolution, improvements in other neurologic findings such as improved sensation and motor strength on examination (or at least no signs of neurologic deterioration) can be reassuring. In contrast, concurrent worsening of other neurologic findings such as loss of sensation, strength, and deep tendon reflexes indicates that the neurologic decline is likely due to changes in or development of nerve root or cord compression, tethering, or PTS or other structural change, and a diagnostic workup in most cases should be begun.
FIGURE 40.2 Algorithm for evaluating an exacerbation of at-level or below-level spinal cord injury pain.
Evidence for the third scenario, aggravation of existing neuropathic pain by a red flag condition, is bolstered by a stable neurologic exam and the presence of signs and symptoms pointing to changes in other organ systems. It is not uncommon that associated changes in severity of at-level or below-level neuropathic pain can even be more prominent than those other signs and symptoms of a potential red flag condition. These red flag conditions presumably cause ascending noxious stimuli which provide feedback onto existing pain pathways (not necessarily perceived as such in a person with impaired or absent sensation), although the exact pathophysiologic mechanisms for the worsening pain are not clear. Red flag conditions typically require additional diagnostic evaluation and medical intervention.
TABLE 40.5 Red Flag Conditions that May Cause, Aggravate, or Mimic Neuropathic Pain and that Require Further Investigation and Prompt Medical Review15
Red Flag Indicators
Red Flag Conditions
Recent trauma, new deformity, changes in range of motion, new-onset localized swelling, and warmth
Fracture or dislocation, heterotopic ossification
Pressure injury, ingrown nail
Chest pain, shortness of breath, fevers, chills or sweats, autonomic symptoms, new limb swelling
Abdominal aortic aneurysm, aortic dissection, myocardial infarction, deep vein thrombosis
Chest pain, shortness of breath
Pulmonary embolism, pneumonia
Changes in urine appearance or smell, pain over kidneys, new incontinence, leakage between catheterizations, a history of renal or bladder calculi, scrotal or testicular swelling
Lower urinary tract infection, pyelonephritis, renal or bladder calculi, urinary retention, testicular torsion, epididymitis
Relation of pain to menstruation
Ovarian cysts, endometriosis and other genitourinary conditions
Changes in bowel habit, distended abdomen
Stool impaction, constipation, volvulus, appendicitis, cholecystitis
One specific cause of late-onset spinal cord pain worthy of further mention is PTS. Although it is common to find evidence of a cyst within the spinal cord at the level of the injury using appropriate imaging (MRI or computed tomography [CT] myelogram), only 2% to 5% of all people with SCI develop PTS.31,32,33
The hallmark of PTS is the new onset of signs and symptoms of neurologic decline which may include pain, sensory loss, weakness, altered muscle tone, and various autonomic symptoms presumably caused by expansion of the cyst and compression of the residual spinal cord at the level of the cyst leading to these signs and symptoms.
A delayed onset of pain after SCI, especially beginning after 1 year, should strongly raise the suspicion of PTS as the cause of pain.32,33,34,35
Bulbar signs and symptoms, especially facial pain, associated with at-level pain of late onset, are rare but virtually diagnostic of PTS. The most commonly reported initial symptom of PTS is pain, either unilateral or bilateral,32,36
whereas pain presenting only with cough is not an uncommon initial presentation historically.34
“Burning,” “dull,” and “aching” are the most commonly reported descriptors reported in several large series, although “sharp,” “electrical,” and “stabbing” have been reported as well.32,33,37
FIGURE 40.3 Algorithm for assessing and treating neuropathic pain. (From Chhabra HS. ISCoS Text Book on Comprehensive Management of Spinal Cord Injuries. 1st ed. New Delhi: Wolters Kluwer; 2015. Figure 55.4.)
MRI is the diagnostic study of choice in the evaluation of PTS, although a CT myelogram with up to 24-hour delayed imaging often will show contrast dye within a syrinx cavity in those for whom an MRI is unobtainable.
Another late cause of neuropathic pain is spinal cord or nerve root tethering. Tethering of the spinal cord is a result of meningeal or arachnoid scar formations that can occur after SCI and prevent normal rostrocaudal sliding of the cord within the spinal canal. Tethering of the cord in the cervical spine can generate enough cord traction with flexion of the neck to cause cord or brainstem displacement and neurologic symptoms, including pain, weakness, and sensory deficits. Tethering of the thoracic and lumbar spine often also includes changes in bowel and bladder function. MRI is the diagnostic study of choice for the evaluation of tethering.
At-level spinal cord and nerve root and below-level SCI can result from late compression of the spinal cord or nerve roots by progressive spondylosis, progressive spinal deformity caused by posttraumatic or surgical destabilization, intervertebral disk herniation, or hardware failure. Nociceptive musculoskeletal pain is typically experienced concurrently. X-rays, CTs, and MRIs are the diagnostic studies of choice.
An algorithm for the assessment of neuropathic pain developed by Siddall and Middleton29
is outlined in Figure 40.3