Pain Following Spinal Cord Injury

Kevin N. Alschuler

Maria Regina Reyes

Thomas N. Bryce

Pain following spinal cord injury (SCI) is common and includes a spectrum of pain types which can impact function across the physical, psychological, and social domains. This chapter provides an overview of SCI-related pain, including the extent and impact, assessment and classification, psychosocial aspects, and treatment.

Extent and Impact of the Problem

Four out of five individuals with SCI report pain, defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage¹ as an ongoing problem.² Many individuals with SCI and pain do not have just one pain but experience at least two different distinct types of pain with many reporting three or more.³^,⁴ In the same person, this might, for example, include shoulder pain from overuse and neuropathic pain related to SCI or spinal cord disease.

In more than half of individuals who report ongoing pain, the ongoing pain interferes with activities of daily living and work,² whereas one out of every five individuals with SCI who is unemployed reports that it is pain rather than loss of function that prevents them from working.⁵ One out of every four people with SCI and significant pain note they would be willing to trade a chance of recovery of bowel, bladder, or sexual function for relief from the pain.⁶

Pain prevalence does not differ among those with different levels of injury nor degree of completeness of injury.⁷ The same holds for men and women with SCI with neither group being more likely to report pain.⁷

Assessment and Classification of Pain Following Spinal Cord Injury

Most pains after SCI are either nociceptive or neuropathic. Nociceptive pain occurs when intact peripheral nerve sensory receptors capable of transducing and encoding noxious stimuli (also known as nociceptors) are activated within an intact somatosensory nervous system, whereas neuropathic pain occurs when a lesion or disease of the somatosensory nervous system activates the somatosensory nervous system.¹^,⁸

The International Spinal Cord Injury Pain (ISCIP) Classification was developed to organize the different types of pain seen after SCI in to an easily understandable framework (Table 40.1).⁹^,¹⁰ Within this framework, in addition to the nociceptive and neuropathic pain types, there is a third type of pain, labeled as “other” pain, for which no identifiable noxious stimulus nor any inflammation or damage to the nervous system responsible for the pain can be identified. Pain syndromes of unknown etiology such as fibromyalgia and complex regional pain syndrome type I fall into this category.

TABLE 40.1 The International Spinal Cord Injury Pain Classification¹⁰

Tier 1: Pain Type	Tier 2: Pain Subtype	Tier 3: Primary Pain Source and/or Pathology (Examples of)
Nociceptive pain	Musculoskeletal pain	Lateral epicondylitis, comminuted femur fracture, muscle spasm
	Visceral pain	Abdominal pain owing to bowel impaction, cholecystitis
	Other nociceptive pain	Migraine headache, surgical skin incision
Neuropathic pain	At-level SCI pain	Spinal cord compression, nerve root compression
	Below-level SCI pain	Spinal cord ischemia, spinal cord compression
	Other neuropathic pain	Carpal tunnel syndrome
Other pain		Fibromyalgia, complex regional pain syndrome type I, interstitial cystitis, irritable bowel syndrome
Unknown pain
SCI, spinal cord injury.

The ISCIP Classification is an integral part of the International Spinal Cord Injury Pain Basic Data Set (ISCIPBDS) (Table 40.2),¹¹ one of more than 20 data sets which have been developed to standardize clinical data collection related to SCI throughout the world.¹²

In determining where a particular pain that a person describes fits within the ISCIP Classification, it is helpful for clinicians to elicit the seven cardinal pain attributes described in Table 40.3 through the completion of a thorough history and physical examination. This physical examination should include a neurologic examination which incorporates the International Standards for the Neurological Classification of SCI as a correct neurologic classification of the SCI and is essential in order to correctly differentiate between at-level and below-level SCI pain and to provide insight into the likelihood of nociceptive pains being perceived in relation to retained sensation.¹³

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)¹⁵ 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).¹¹

TABLE 40.2 International Spinal Cord Injury Pain Basic Data Set (Complete for Each Different Pain)¹¹

MUSCULOSKELETAL PAIN

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.

Shoulder 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

Pain Attribute	Examples of Usefulness for SCI Pain Classification
History of onset	Links the SCI to a specific pain Indicates a pain generator through the mechanism of inciting event
Pain location	Indicates a neuropathic type when occurring at or below the level of injury in a specific pattern Indicates pain generator through its specific location
Temporal pattern	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
Pain quality	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	Differentiates nociceptive and neuropathic subtypes, especially if movement is involved, as a pain generator can often be localized by replicating exacerbating factors
Associated sensory disturbances	Allodynia or hyperpathia, either noted on history or on physical examination, are highly suggestive of neuropathic subtypes.
Pain intensity	Intensity is an accepted proxy for severity of pain and is the most commonly used measure of the effectiveness of treatment.
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

Anxiety

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.

Back Pain

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

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.

OTHER NOCICEPTIVE PAIN

Other (nociceptive) pain refers to a nociceptive pain that does not fall into either the musculoskeletal or visceral categories.¹⁰ These pains may be indirectly related to the SCI (e.g., pain from nociceptor activation within the disrupted integument due to pressure injury) or may be unrelated to SCI (e.g., migraine headache).²⁸

One particular other nociceptive pain worthy of special mention is headache pain due to AD. It can be severe and usually is described as “pounding.” It is most common in a person with a neurologic level of injury (NLI) at or above T6. AD headache is associated with an elevated blood pressure and often with diaphoresis, piloerection, cutaneous vasodilatation above the level of injury, bradycardia or tachycardia, nasal stuffiness, conjunctival congestion, and mydriasis. AD is usually triggered by a noxious stimulus caudal to the NLI, usually related to the bowel or bladder (e.g., bowel impaction or urinary tract infection).

An algorithm for the assessment of nociceptive pain developed by Siddall and Middleton²⁹ is outlined in Figure 40.1.

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
(Table 40.5) 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

System	Red Flag Indicators	Red Flag Conditions
Musculoskeletal	Recent trauma, new deformity, changes in range of motion, new-onset localized swelling, and warmth	Fracture or dislocation, heterotopic ossification
Dermatologic	Redness, ulceration	Pressure injury, ingrown nail
Cardiovascular	Chest pain, shortness of breath, fevers, chills or sweats, autonomic symptoms, new limb swelling	Abdominal aortic aneurysm, aortic dissection, myocardial infarction, deep vein thrombosis
Respiratory	Chest pain, shortness of breath	Pulmonary embolism, pneumonia
Genitourinary	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
Pelvic	Relation of pain to menstruation	Ovarian cysts, endometriosis and other genitourinary conditions
Gastrointestinal	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.

OTHER NEUROPATHIC PAIN

Other neuropathic pain refers to neuropathic pain that is present above, at, or below the NLI but is not directly related to the SCI.¹⁰ Compressive neuropathy pain fits within this category and occurs in a specific peripheral nerve distribution distal to the root level and is attributed to compression of a specific peripheral nerve or plexus of nerves, most commonly affecting not only the median nerve at the wrist but also the ulnar, radial, and axillary nerves. The signs and symptoms of carpal tunnel syndrome include numbness or tingling of thumb, index, or middle fingers; abnormal sensation on testing; or numbness or tingling with provocative tests. This syndrome is thought to result from a combination of repetitive trauma, as occurs with propulsion of manual wheelchairs, and ischemia from repetitive marked increases in carpal canal pressures, as occurs with push-up pressure reliefs or transfers from one seating surface to another.³⁸ A higher risk for developing pain has been shown in those who are overweight or use improper wheelchair propulsion biomechanics.³⁹

PSYCHOSOCIAL ASPECTS OF PAIN AFTER SPINAL CORD INJURY

Psychosocial factors are understood to play a significant role in the chronic pain experience. In contrast to past generations of medicine where the mind-body dualistic perspective resulted in medically unexplained pain being labeled psychogenic, the modern biopsychosocial approach suggests that few patients—if any—should be classified in such a manner. In addition to being inaccurate, the diagnosis is also often counterproductive to successful pain management.⁴⁰ However, one must always be attentive to the psychosocial factors that may have a significant impact on pain intensity, function, and quality of life.

Psychological Factors

A growing body of research suggests a strong relationship between pain and psychological factors. Indeed, some have suggested that psychosocial rather than biologic factors are more closely associated with the presence and severity of pain.⁴^,⁶ Broadly, research on psychology and pain can be summarized in two areas.

The first explores the association between pain (primarily pain intensity) and psychological factors (primarily mood), through cross-sectional research. These studies have consistently identified strong relationships between psychological symptoms (depression, anxiety, and/or posttraumatic stress disorder [PTSD] and pain intensity.⁴¹^,⁴²^,⁴³^,⁴⁴^,⁴⁵^,⁴⁶^,⁴⁷ The few longitudinal studies have highlighted potential causal relationships, with one study supporting a likely bidirectional relationship, such that the presence of either pain or mood difficulties may make higher levels of the other more likely⁴⁸; in contrast, another study more specifically highlighted the ways in which chronic pain contributes to depressed mood.⁴⁹ Furthermore, a longitudinal study assessing mood trajectories in people with SCI suggested that having greater pain intensity is associated with a moderate to severe depression trajectory.⁵⁰ As with much of the chronic pain experience, though, it is important to note that stronger relationships may be present between pain interference and mood rather than pain intensity and mood.⁵¹

The second broad area of pain psychology research refers to the ways in which a person copes with pain, including his or her thoughts, beliefs, and pain-related behaviors. Although these are generally factors that emerge once a person already has pain, it is important to recognize that how individuals approach their pain at onset may influence the evolution of their pain and function over time. The most commonly studied pain coping construct is pain catastrophizing, a maladaptive and disproportionate worry about chronic pain, which has consistently been associated with greater pain intensity and pain interference in persons with SCI.⁵²^,⁵³ Important implications also exist for other coping strategies, with task persistence repeatedly demonstrated as an adaptive approach, but guarding (e.g., tensing muscles for self-protection or avoiding engaging affected muscles) and resting (e.g., avoiding activity) have been found to be maladaptive approaches.⁵³ More generally, active coping strategies (e.g., those that promote engagement with the world) have more positive impacts on outcomes relative to passive coping strategies (e.g., those that cause an individual to withdraw from the world around them).⁵³^,⁵⁴ Finally, more recent research has emphasized the relationship of pain acceptance with pain-related outcomes, such that being willing to experience pain and/or engaging with valued life activities despite pain is associated with greater function and quality of life.⁵⁵^,⁵⁶

Social and Environmental Factors

Research also suggests a strong association of social and environmental factors with the pain experience. In general, greater social support is associated with greater function in persons with chronic pain and disabilities, including SCI.⁵⁷ However, functioning is greater in individuals who receive social support without solicitous responses relative to those who receive solicitous support.⁵³ Furthermore, perceived negative responses from friends, caregivers, and relatives may have a negative effect. For example, punishing responses have been shown to have a negative impact on pain severity.⁵⁸

Management of Pain in People with Spinal Cord Injury

Effective management of chronic pain after SCI remains a clinical challenge. Although some types of nociceptive pain may respond to commonly used interventions, neuropathic SCI pain has been a poorly understood entity that is largely resistant to a variety of interventions.⁵⁹^,⁶⁰ Treatment approaches attempt to address the growing but incomplete body of knowledge regarding the multiple potential mechanisms underlying the development of neuropathic pain. Variable responses are common, and many interventions found to be successful in the treatment of non-SCI neuropathic pain have had disappointing results when applied to SCI neuropathic pain. The experience of pain must be considered and treated in the context of psychosocial factors. This section reviews existing literature for available interventions for chronic SCI pain.

NOCICEPTIVE PAIN

Musculoskeletal Pain

The principles of care used in the general population to treat degenerative and inflammatory musculoskeletal conditions may be applied to people with SCI, although there are specific therapeutic considerations.⁶¹ For example, complete or even relative rest of a painful overused upper extremity can be difficult to implement in a person who is reliant on the upper extremities for all mobility. Activity restrictions may result in the need for additional caregiver or transportation services, new equipment such as power mobility, or modifications to transfer techniques. Surgery may not always result in good functional long-term outcomes due to the overuse of the repaired structures necessitated by the intrinsic limitations in functional mobility caused by SCI. Because of this impact, knowledgeable and timely treatment of such pain is critical to preserving independence. Physical and occupational therapy play a key role in appropriately adapting musculoskeletal care principles to those with impaired mobility, or utilizing SCI-specific protocols for addressing common musculoskeletal problems, such as shoulder impingement and dysfunction.⁶²^,⁶³

The primary treatment strategy to address chronic nociceptive musculoskeletal pain after SCI is focused on addressing the established or probable etiologic condition and its root cause. Short-term and occasional long-term pharmacologic management may be required if nonpharmacologic interventions fail to sufficiently improve function and quality of life.

Nonpharmacologic Management

Factors that may lead to chronic inflammatory musculoskeletal pain include abnormal posture, altered gait or upper limb biomechanics, and the cumulative effects of repeated transfers and wheelchair or assistive device use. Correcting or reducing excessive mechanical stresses is a fundamental and key principle in the treatment of musculoskeletal SCI pain and can be addressed by appropriate education, retraining, and equipment modifications. Seating in wheelchair users influences not only trunk position but also shoulder position and biomechanical forces during wheelchair propulsion, transfer activities, and activities of daily living. Optimizing seated position is the foundation for long-term protection of upper limbs in wheelchair users. Comprehensive guidelines to address the highly prevalent problem of upper limb musculoskeletal SCI pain are available.⁶²

Pharmacologic Management

Pharmacologic interventions for inflammatory musculoskeletal pain are often indicated. Options include the use of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), local corticosteroid injections, and antispasticity medications.

Acetaminophen is preferable over NSAIDs as the first-line analgesic for musculoskeletal pain, due to the risk for NSAIDrelated gastric erosion and the potential for poor clinical detection of gastrointestinal bleeding in people with high SCI levels. However, cautious use of NSAIDs may be considered as the next option, in the absence of other contraindications, and preferably outside the acute period following SCI when the risk for gastritis is at its peak. If NSAIDs and acetaminophen are not appropriate or effective, opioids with relatively weak opioid activity, such as tramadol, would be reasonable. Rarely, “stronger” opioids may be necessary for short-term management of severely limiting pain such as might occur after surgery. However, the use of “stronger” opioids, as a treatment in chronic, noncancer pain is discouraged due to inconclusive or weak evidence in support of this practice⁶⁴^,⁶⁵ and high rates of adverse effects including tolerance, dependence (both physical and psychological), and opioid-induced hyperalgesia.⁶⁶ Specific considerations for longterm use of opioids in people with SCI, if they are used at all, include the potential for these drugs to exacerbate bowel or bladder dysfunction, contribute to cardiovascular and respiratory compromise, osteoporosis, and hypogonadism.⁶⁷^,⁶⁸^,⁶⁹ Case-by-case consideration for long-term opioid therapy should strictly follow published clinical and regulatory guidelines.⁷⁰^,⁷¹^,⁷²^,⁷³

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