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Anesth Analg 2007; 105:1462-1473
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000282804.25682.0f
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PAIN MEDICINE

Pain Management in a Patient With Intractable Spinal Cord Injury Pain: A Case Report and Literature Review

Jocelyn C. Que, MD, MMed (Pain Mgt), DPBA, FFPMANZCA, FIPP*, Philip J. Siddall, MBBS, MMed (Pain Mgt), PhD, FFPMANZCA{dagger}, and Michael J. Cousins, AM, MD, DSc, FANZCA, FRCA, FFPMANZCA, FAChPM (RACP){dagger}

From the *Pain Management Unit, University of Santo Tomas Faculty of Medicine and Surgery, University of Santo Tomas Hospital, Manila, Philippines; and {dagger}Pain Management Research Institute, University of Sydney, Royal North Shore Hospital, Sydney, Australia.

Address correspondence to Michael J. Cousins, AM, MD, DSc, FANZCA, FRCA, FFPMANZCA, FAChPM (RACP), Pain Management Research Institute, Royal North Shore Hospital, St. Leonards, 2065 Sydney, Australia. Address e-mail to mcousins{at}nsccahs.health.nsw.gov.au.


   Abstract
Top
 Abstract
Introduction
 CASE HISTORY
 DISCUSSION
 REFERENCES
 
Chronic pain is one of the more disturbing sequelae of spinal cord injury, often interfering with the basic activities, effective rehabilitation, and quality of life of the patient. Pain in the cord-injured patient is often recalcitrant to treatment. This dilemma is amplified by the limited availability of effective pharmacological and nonpharmacological treatment options. We identified relevant articles regarding pain after spinal cord injury from the Medline database from 1975 to 2005 using the search terms "spinal cord injury" or "spinal cord injuries" and "pain" or "spasticity or "muscle spasms." We also searched by hand the review articles in a recently published book from the International Association for the Study of Pain Press on spinal cord injury pain, and identified relevant articles through reference lists. We present a patient with intractable spinal cord injury pain who was successfully treated with a pain management plan that addressed the various aspects of spinal cord injury pain. The evidence for treatment options is reviewed.


   Introduction
Top
 Abstract
 Introduction
CASE HISTORY
 DISCUSSION
 REFERENCES
 

"As you ought not to attempt to cure eyes without head, or head without body, so you ought not to treat body without mind."

Socrates, Ca. 400 B.C.

Spinal cord injury (SCI) is a life-changing event with disturbing complications. The presence of pain, particularly severe pain, not only interferes with the basic activities and effective rehabilitation, but also disrupts the psychological functioning and social integration of the person (1). Unfortunately, reliable and effective treatment options for SCI pain remain disappointing, with controlled trials focused on pharmacological approaches only (2).

This case presents a multidisciplinary approach to the management of a patient with intractable SCI pain. Pharmacotherapy with intrathecal combination analgesic therapy and physiotherapy had been essential components of our patient's rehabilitation, and yet had provided suboptimal relief of his pain and spasms. A practical three-step approach to developing an interdisciplinary pain management plan involving the various domains of SCI pain management allowed our patient to live independently, and, most importantly, return to work.


   CASE HISTORY
Top
 Abstract
 Introduction
 CASE HISTORY
DISCUSSION
 REFERENCES
 
Mr. H is a 51-yr-old gentleman who presented with generalized body pain from the shoulders to both feet. The pain began after he fell from a rope swing into shallow water on his own property on January 1991. He sustained a SCI at the C3/4 level that initially resulted in tetraplegia. Mr. H underwent a posterior spinal fusion and wiring procedure in January 1991. Several months later, he underwent an anterior spinal fusion at C5 level to provide stability. After about 3 mo, there was remarkable recovery, and Mr. H. was able to stand and swim laps in the pool, although the pain and spasms were still present in both legs.

In 1994, his condition deteriorated, with spreading stiffness and cramp-like sensations in the lower back and across the chest, sharp, stabbing pain in the neck and right shoulder, and increasing weakness in both arms. A syrinx was identified by magnetic resonance imaging (MRI) in the cervical spinal cord. A shunt was inserted, which prevented further loss of function. In 1996, a spinal cord detethering procedure was done to release cord adhesions causing pain and limitation of mobility. However, the pain and spasms persisted.

The pain was diffusely located over his entire body from the shoulders to the feet except the buttock area. Pain descriptors were throbbing, burning, stabbing, and cramp-like. The pain was extremely tiring and debilitating. His pain was constant with fluctuations in intensity relative to movement and muscle spasms. At rest, the pain was 5/10, but increased to 9–10/10 with activity. It was markedly increased with stress and physical activity and was reduced by lying prone.

He had muscle spasms in all four extremities, but they were worse in both lower limbs and, when severe, would keep his legs in flexion (modified Ashworth spasticity scale 3–4) and interfere with his walking. He also experienced intermittent diffuse allodynia, most marked in the shoulders and arms, and worsening generalized weakness. He had moderate control of his bladder and bowels, and often required intermittent self-catheterization and a second daily enema.

Impact of Pain on Function
The increasing pain and spasm interfered with walking and eating. He had to be assisted by his 11-yr-old daughter to eat and get dressed. Because of the pain and spasms, he had to stop working as a journalist, being unable to type on the computer keyboard. His cognitive abilities, particularly the ability to concentrate and focus attention, were affected by the amount of medication he had been taking to control his pain and spasms, making him drowsy and unable to work. Despite all these limitations, he managed to drive a car and to write two books.

His sleep was significantly disrupted, which worsened his mood and made him tire more easily. He had become irritable and found his worsening pain and spasms frustrating. He had become significantly depressed, though he did not have any suicidal ideation.

Medications
At the time of assessment, his medications included: baclofen 25 mg qid, diazepam 2 mg qid, and tramadol sustained release 100 mg once in the morning, all of which made him drowsy but did not significantly relieve his pain and spasms. He had tried gabapentin 300 mg bid a few weeks before the initial consultation. It reduced his pain by 30%, but he had to stop using it because of the expense. He had never been prescribed antidepressants.

He consulted a practitioner of osteopathic and chiropractic treatment who used massage, manipulation, and bioflavinoids in the early phase of his injury. He also consulted a spine rehabilitation specialist, a physiotherapist, a spine surgeon, and a neurologist.

His Medical History
He had hypersensitivity to monosodium glutamate. Before the SCI, he was a healthy individual.

Patient's Cognitions Regarding His Pain
The patient believed that his pain and spasms were caused by the injury to his spinal cord, and that these were interfering with his resumption of usual activities and his return to work. When the pain and spasms became severe, he would cease all activity and lie down. He considered a 50%–75% reduction in the painful spasms would be necessary to enable him to resume activities of daily living and return to work. He was keen to try new therapeutic options to manage his pain and spasms, but preferred nonpharmacological alternatives to avoid the sedating effects of medications.

Premorbid Personality, Including Coping Strategies
Having been a top-ranking television station executive, he was a determined and well-respected journalist. At the time of presentation, he had not developed effective coping strategies to help him accept his loss of control and his functional limitations.

Physical Examination
He walked with a shuffling gait and a pronounced limp, tending to veer to his left. He avoided flexing forward on undressing due to poor balance. He could sit and stand without any difficulty, stand on his toes and heels and on the insides and outsides of his feet, but could not squat. He was unsteady when standing on either leg. There was good range of lumbar mobility, whereas the cervical spine was mildly restricted. Upper limb mobility was limited to 90° shoulder flexion and abduction, internal and external rotation half range and slightly reduced arm strength. Straight leg raising was limited to 30° (active) and to 75° (passive) on the left.

Neurological examination revealed hyperactive reflexes in all four extremities but no significant clonus, with modified Ashworth spasticity score of 2. Touch and vibration sensations were preserved, but hot and cold sensation and position sense were absent in all limbs. Motor power in all four limbs was almost normal.

Psychosocial Assessment
The patient was resistant to accepting assistance or directions from others. Loss of control of some of his bodily functions made him feel helpless. Loss of his identity as breadwinner of the family and his position at work had made him feel frustrated and depressed. He had to go to Social Security to apply for unemployment benefits, which he found very degrading. Added to this was his anger at the shortcomings of health professionals and facilities during his previous prolonged hospitalizations. He used this as justification for his doubts and rejections of medical advice. He had even written a book chronicling his experiences after his injury. He was well motivated and tended to overdo things, which worsened his pain and spasms and further added to his frustration.

He had supportive friends and family, especially during the most difficult phase of his recovery, which had helped sustain his desire to recover. However, his reliance on his wife and daughter, particularly for feeding and dressing, was a constant source of frustration and depression. He is now divorced and lives with his 11-yr-old daughter.

Investigations
MRI of the cervical spine in 1993 showed evidence of posterior spinal fusion at the C3/4 level and anterior vertebral body fusion at the C5/6 level. There was a 2-cm cystic region within the cervical cord at C3/4 level. MRI of the cervical spine in 1994 reported a 7-mm syrinx at the C3/4 level.

MRI of the cervical spine in 2002 showed the presence of metallic artifact at the level of C2/3 intervertebral disk. There was atrophy of the cervical cord and thoracic cord with no visible evidence of cord tethering.

Diagnostic Formulation
In summary, Mr. H presented with C3/4 incomplete tetraplegia due to cord trauma treated with posterior spinal fusion at C3/4 level, anterior spine fusion at C5 level, shunting and spinal cord detethering procedures. A number of specific issues contributing to his problem were identified:

  1. Biological issues: at-level neuropathic SCI pain due to partially resolved syrinx and segmental deafferentation; below-level neuropathic SCI pain due to spinal cord trauma, muscle spasm pain, constipation, and reflex bladder.
  2. Psychological issues: loss of control and self-efficacy, resistance to accepting assistance, depression, poor coping strategies, and poor pacing.
  3. Social and environmental issues: anger and frustration at the health care system and health professionals, separation and divorce from his wife, loss of work with concomitant loss of economic independence, and loss of personal identity as breadwinner of the family.

The limitations imposed by his physiological dysfunction (i.e., pain and spasticity), psychological distress, and social isolation contributed to his chronic pain condition and experience, and interfered with his recovery and rehabilitation.

Multidisciplinary Management Plan
The effect of gabapentin at therapeutic doses could not be explored due to cost concerns, and because further dose escalations caused unwanted side effects. Therefore, our multidisciplinary team, after a neurosurgical review of his spine, recommended that the main option for this patient was intrathecal delivery of baclofen for spasticity, combined with an opioid and clonidine for pain. A spinal rehabilitation team assessment was organized to address the problems of constipation and reflex bladder, and thus reduce the factors that may exacerbate his pain and facilitating overall rehabilitation.

Although Mr. H presented with depressive symptoms, these did not satisfy the criteria for a major depressive disorder. A psychiatric review to address his depression was advised. The team recommended that, once his pain was better controlled and he was able to return to activity, he might benefit from a cognitive-behavioral pain management program to teach him nonpharmacological strategies of coping with his chronic pain condition. Involvement of a social worker was organized to assist with home care and family education.

Progress
The patient was admitted to the hospital and intrathecal testing was done as follows: First dose, hydromorphone 0.05 mg with clonidine 25 mcg, after which pain was assessed. Second dose, baclofen 50 mcg, after which spasm was assessed. Third dose, a combination of hydromorphone, clonidine, and baclofen, with doses adjusted according to the responses to the first two doses. Overall, he had a positive response to the intrathecal testing with loss of all pain, and he could mobilize with decreased spasms. At the time, he was receiving his usual oral pain spasm medications of baclofen 25 mg qid, diazepam 2 mg qid, gabapentin 300 mg bid, and tramadol SR 100 mg bid.

In view of the favorable outcome of the intrathecal testing, an intrathecal pump was inserted and an intrathecal infusion mixture of hydromorphone, clonidine, and baclofen was started. He subsequently developed postural hypotension and motor weakness despite dose adjustments, leading to elimination of clonidine from the intrathecal solution. He was then maintained on an intrathecal infusion of hydromorphone and baclofen, which reduced his pain and spasms.

Three months later, despite some initial skepticism and uneasiness, he participated in a 3-wk cognitive behavioral pain management program modified for SCI patients. With the objective of reducing the impact of pain on Mr. H and his activities of daily living, cognitive behavioral therapy was applied to alter his unhelpful thoughts and feelings (loss of independence, external locus of control, and anger toward health care professionals) and maladaptive behavior patterns (overdoing, depression) that interfered with his ability to rehabilitate himself. Involvement of his significant other and his daughter in the program helped facilitate both Mr. H's and his daughter's adaptation to the circumstances. Adjustments to his workplace at home enhanced his working tolerance.

Outcome of Pain Management Program
Eighteen months after completion of the interdisciplinary pain management program, Mr. H's background pain (2/10) and spasm (Ashworth score 1) were reduced substantially by the intrathecal hydromorphone and baclofen, but pain relief remained suboptimal (5/10), especially when the spasms were severe, requiring further increments of his daily intrathecal infusion doses. Nevertheless, he was able to increase his ability to perform various activities, was walking without assistance, was feeding and dressing himself, was working 4–6 h a day, and was pacing himself so as not to overdo. He was no longer taking any oral analgesics or antispastic medication, thus avoiding the sedating and constipating effects of these drugs. His mood had markedly improved, although he was frustrated occasionally because he was unable to type; nevertheless, he managed not to get depressed. He felt more in control than before and has achieved his ultimate goal, to live independently and to return to work part-time as a journalist.


   DISCUSSION
Top
 Abstract
 Introduction
 CASE HISTORY
 DISCUSSION
REFERENCES
 
Epidemiology and Taxonomy
Chronic pain is one of the more frequent and troublesome sequelae of SCI, often interfering with the effective rehabilitation of the patient. In addition to the chronic pain syndromes seen in the non-SCI population, e.g., migraine and postherpetic neuralgia, patients with SCI may also suffer from pain syndromes unique to SCI. The reported prevalence of chronic SCI pain varies between 25% and 94%, with almost one-third of these patients experiencing severe pain (3–5). The wide disparity in the prevalence of SCI pain among studies is due to differences in study design, factors such as subject recruitment, time and duration of assessment after injury, assessment procedure, and lack of consistent terminology and taxonomy of SCI pain.

The lack of a comprehensive taxonomy was addressed by the International Association for the Study of Pain Task Force on Pain after SCI, which developed a three-tiered classification (Table 1) (6). Based on this taxonomy, several studies have reported the prevalence of the various types of SCI pain presented in Tier 2. Musculoskeletal pain was the most common type experienced at 6 mo after injury (40%) (4) and at 5 yr after SCI (59%) (7). An increase in the prevalence of at-level and below-level neuropathic pain has likewise been observed more than 5 yr after SCI (4,7).


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  		Table 1. International Association for the Study of Pain Classification of Pain Related to Spinal Cord Injury

 

Variables that influence the development of SCI pain remain unclear. Factors such as the level of the injury, completeness of the injury, cause of injury, and psychosocial factors have been considered (8). Musculoskeletal pain was more common in patients with thoracic level injuries and was reported to be more prevalent in those who had surgical intervention 2 wk after SCI (9). Neuropathic pain that was associated with allodynia was observed to be more common in patients with incomplete spinal cord lesions, in cervical than thoracic cord injuries, and in central cord syndrome (4). This was evident in our patient who developed incomplete cervical cord injury and experienced neuropathic pain and allodynia within the first 6 mo after injury. Below-level neuropathic pain was more common in patients with anterior cord lesions with relative preservation of dorsal column function (10).

Despite these studies suggesting that certain physical factors contribute to post-SCI pain, other investigations have reported that psychosocial rather than physical factors were major determinants of the experience or severity of pain after injury (11,12). This will be discussed later.

Post-SCI Pain Types
In addition to the four major types of SCI pain under Tier 2, there are other recognized pain conditions, most of which are under Tier 3 in the International Association for the Study of Pain Taxonomy (6). These need to be clinically identified so that appropriate treatment may be instituted. Of these pain conditions, our patient presented with mechanical instability of the spine, muscle spasm pain, at-level neuropathic pain due to segmental deafferentation and a syrinx, and below-level neuropathic pain.

Musculoskeletal Pain
Mechanical instability of the spine: This type of pain is brought about by disruption of ligaments/joints or fractures of bone, resulting in instability of the spine. As observed in our patient, it occurs early after injury and is located in the region of the spine close to the site of SCI. It is related to position, worsened by activity and decreased by rest (8). Diagnosis is aided by radiographs, computerized tomography or MRI to identify the nature and site of pathology.

Muscle spasm pain: Spasticity is defined as a motor disorder characterized by a velocity-dependent increase in the tonic stretch reflexes (muscle tone) with exaggerated tendon reflexes, resulting from hyperexcitability of the stretch reflex (13). An imbalance in any of the numerous excitatory and inhibitory modulatory synaptic influences on the {alpha} motor neuron and muscle results in hyperactivity of the stretch reflex arc. Although this pain type usually occurs late after SCI, our patient developed spasms within 6 mo post-SCI. Muscle spasm pain is often seen in people with incomplete SCI (6), as evident in Mr. H.

At-Level Neuropathic Pain
Segmental deafferentation/Girdle or Border or transitional zone pain: This pain was experienced early after SCI by Mr. H who initially reported cramp-like pain in the neck and shoulders with intense allodynia to light touch and hyperalgesia of the affected region, and has gradually resolved with time. This is a variation of at-level neuropathic pain that occurs within a band of two to four segments above or below the level of SCI. It often occurs on the border of normal sensation and anesthetic skin (8).

Syringomyelia: Pain due to a syrinx (i.e., an abnormal cyst in the spinal cord) often occurs with a delayed onset, a mean of 6 yr. The damage to the central part of the spinal cord with cervical injuries results in the central cord syndrome characterized by pain and weakness of the arms and relatively strong but spastic leg function. Mr. H presented with the characteristic spreading stiffness, spastic legs, and increasing weakness and constant sharp stabbing pain in the arms 3 yr post-SCI. The pain of syringomyelia is sometimes described as a constant burning pain with allodynia (8,14).

Below-Level Neuropathic Pain
Central dysaesthesia syndrome/central pain/deafferentation pain: Our patient presented with constant throbbing, burning, and stabbing pain diffusely located caudal to the level of SCI (C3/4), i.e., over his entire body from the shoulders to the feet, typical of below-level neuropathic pain. The pain was associated with hyperalgesia and gradually worsened over time. It occurs with spontaneous and/or evoked episodes, and is often worsened by infections, sudden noise, and jarring movements (8).

Pathophysiology and Mechanisms of SCI Pain
Pain associated with SCI is a consequence of both injury characterized by pathological changes from mechanical trauma and vascular compromise of the cord parenchyma. It is influenced by the nature of the lesion, the neurological structures damaged, and the secondary pathophysiological changes of the surviving tissue (15). There are at least three proposed basic mechanisms underlying SCI pain: increased neuronal hyperexcitability, reduced inhibition, and neuronal reorganization or plasticity.

Increased Neuronal Hyperexcitability
An initial consequence of SCI after traumatic or ischemic SCI is the brief but dramatic increase of excitatory amino acids, which triggers an injury cascade of secondary pathological changes. The major components of this spinal "central injury cascade" include anatomical, neurochemical, excitotoxic, and inflammatory events that collectively interact to increase the responsiveness of the neurons at the level of injury, resulting in the generation of the clinical symptoms of allodynia and hyperalgesia (16).

Reduced Inhibition
Damage to the ascending and descending pathways in the spinal cord results in deafferentation of supraspinal structures due to damage to ascending pathways, disruption of local inhibitory interneurons, and loss or decreased influence of supraspinal and propriospinal inhibitory pathways (16). This disruption of local and descending inhibition may allow for an increased excitability of projection neurons in the spinal cord and thus increased responsiveness and spontaneous pain (15).

Clinical investigations on SCI pain suggest that interruption of the spinothalamic tract (17) or the dorsal columns (18) with deafferentation of its rostral targets contributes to the development of neuropathic SCI pain. Pain associated with syringomyelia is believed to result from irritation of the cord at the rostral end of the cyst (19), and has been reported to be more prevalent after central cord injuries extending to the dorsal pathways (20). However, although much of the evidence highlights the importance of the spinothalamic tract in the development of neuropathic pain (10,17,21), the role of the relative preservation of the dorsal column pathways continues to be a matter of contention.

Neuronal Reorganization/Plasticity
The emergence of spinal and supraspinal generators or amplifiers and their involvement in SCI pain has been supported by the demonstration of abnormal bursting activity of thalamic neurons after SCI that is most pronounced after complete cord transection (22–24) and by the development of abnormal responses and prolonged afterdischarges of spinal sensory neurons after experimental SCI (25). The nature of the influence of the thalamus and other supraspinal and spinal structures on SCI pain awaits further investigation.

SCI pain is a dynamic entity with complex neuronal activity patterns that are distributed at different levels of the nervous system. Although at-level pain occurs most often early after injury, there may be a progression to below-level pain, with or without continuation of at-level neuropathic pain. This temporal progression suggests an interaction in the mechanisms of each type of pain (26). At-level and below-level SCI pain seem to present with anatomical differences where cellular or central gray loss is observed with at-level pain and axonal or peripheral white matter loss is seen with below-level pain (16). Deep visceral and somatic input, such as from bladder filling and pressure sores, can trigger below-level neuropathic pain. This has been attributed to the dynamic balance between the degree of rostral deafferentation and the inputs from remaining preserved spinal cord pathways (26). This underscores the importance of controlling the factors that may exacerbate pain and spasms in the SCI patient which, in Mr. H's case, included constipation and reflex bladder.

Psychosocial Aspects of SCI Pain
Often persistent and refractory to treatments, SCI pain amplifies the burdens imposed by SCI on a person's ability to perform and participate in activities of daily living (27,28). A study of 217 persons with chronic SCI pain reported that chronic pain frequently interfered with common activities such as sleep, household chores, exercise, work, and other activities of daily living. High pain intensity was one of the most significant factors related to frequent pain interference (28), contributing to a decreased quality of life. Chronic pain can negatively influence a person's ability to cope with the consequences of SCI, and negative coping after SCI is associated with depression (29). However, several psychosocial factors determine the association between pain and depression and how SCI patients adapt to SCI pain.

In a case comparison study of a community sample of 62 individuals with paraplegia or lower limb amputation, Rudy et al. (30) found a strong association between physical performance and psychosocial factors which included perceptions of self-efficacy (i.e., belief in one's ability to perform tasks), fear of movement-related pain, cognitive coping (e.g., avoiding catastrophic thoughts about patient's condition), and depression. Perceptions of self-efficacy were the strongest predictors of performance outcome, whereas significant-other support and demographic measures of age, sex, and duration of chronic pain condition were not significantly associated with performance outcome (30). McColl et al. (31) found that the relationship between support from significant others and coping with SCI changed over time. Support can be a double-edged sword where, on the one hand, it has been demonstrated to moderate depression early after injury but, on the other, it can reinforce dependence and disability later after injury (32).

An important determinant for quality of life after SCI is successful independent living, which may include the perception of having control over one's life, having a satisfying social function such as being employed, and being minimally dependent on others for activities of daily living (33). Because chronic pain interferes with activities of daily living such as work and social activities, patients who experience chronic SCI pain are at high risk of having diminished quality of life and developing psychosocial problems (e.g., divorce, suicide, drug abuse, and self-neglect). The adaptation and coping skills of SCI patients are crucial to achieving satisfactory quality of life (33). Thus, successful psychosocial adjustment to SCI is an individual response influenced by various psychosocial, physical, financial, and other variables (34).

Evaluation of the Patient With SCI
As it is with chronic pain of any etiology, a patient with SCI pain requires a multidisciplinary assessment. The initial step is a detailed history of pain, including an inventory of pain characteristics, such as onset, quality, distribution, factors affecting pain (and spasms), interventions and treatments received, problems encountered (e.g., spasms, infections, pressure sores), and the level of daily function of the patient. A thorough physical examination with a neurological examination oriented toward identifying possible causes of pain and the presence of abnormal sensations and movements is required. Evaluation of spasticity includes investigating factors that exacerbate the spasticity such as bladder infection, constipation, pressure ulcers, poor fit in a brace or a wheelchair, and assessing the severity of spasticity and the range of movement of the spastic joints (35). A widely accepted assessment tool for severity of spasticity is the modified Ashworth spasticity scale (Table 2) (36).


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  		Table 2. Modified Ashworth Spasticity Scale

 

Ancillary tests such as electrodiagnostic studies, imaging, and urodynamic testing may be done to further determine the cause of pain, level and extent of injury, and presence of specific pain syndromes. MRI is warranted for syringomelia diagnosis and can provide useful information regarding the cord below the level of the lesion such as cord atrophy, myelomalacia, and cord tethering (37). Quantitative sensory testing, somatosensory evoked potentials, and motor evoked potentials may be necessary to document extent of injury and to delineate different degrees of dissociated sensory loss.

Assessments by physiotherapists and rehabilitation specialists are important in planning rehabilitation programs for the SCI patient. Evaluation of psychological and social factors that may affect the pain and the adaptation and function of the patient and family by a psychologist who understands chronic pain and SCI is critical to developing an appropriate treatment program.

Management of SCI Pain
The heterogeneity of SCI pain conditions and the potential influence of a number of diverse factors underscore the need for an interdisciplinary approach that tailors treatment to the needs of individual patients. Treatment tailoring enhances patient motivation and participation in treatment, and allows clinicians to streamline treatment, reduce costs, and make treatments more accessible to patients who need them (38).

Certain factors need to be considered in developing a realistic, relevant, and rational treatment plan for the person with SCI pain. These are the patient's medical condition and goals of treatment, and the available support and resources. Table 3 presents a practical three-step approach to formulating a rational management plan. The first step involves the determination of existing biological, psychological, and social or environmental contributors to the patient's SCI pain, and the potential adverse sequelae that may ensue. These include the level of injury, types of SCI pain, and presence of comorbidities and psychosocial issues, as well as the influence of these factors on the individual's pain experience, level of functioning, and adjustment to SCI. This information is best obtained from the diagnostic formulation of a patient's pain condition after a thorough multidimensional assessment. The second step requires identifying the patient's specific goals of treatment. Consideration of the severity of SCI pain and the limitations imposed by impairment and disability ensures realistic and relevant goals, which heightens motivation and commitment and encourages the person's active involvement in treatment. Common goals of SCI patients include: relief of pain and spasms, and improvement of function to achieve independent living and return to work. The third step entails the development of a comprehensive interdisciplinary pain management plan that considers the treatment modalities appropriate for the SCI patient and the availability of support and resources.


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  		Table 3. Three-Step Approach to Tailoring Treatment Plan for Patients With Spinal Cord Injury (SCI) Pain

 

The management of SCI pain involves four domains: pain management (i.e., pharmacological, neuroaugmentative, and neurosurgical treatments), spinal rehabilitation, psychological treatment, and social or environmental modification (Fig. 1). Of these domains, the reduction of pain, particularly severe pain, is the prerequisite for all interventions, as the overall rehabilitation and adjustment process are more readily achieved in an individual with tolerable pain, if not in a pain-free state. The relative contribution of each domain in the management plan is dependent on the patient's injury, response, and progress.


Figure 148
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  		Figure 1. Proposed multidisciplinary treatment algorithm in the management of SCI pain. UTI = urinary tract infection; AED = antiepileptic drug; TCA = tricyclic antidepressant; SSRI = selective serotonin reuptake inhibitor; 5-HT = 5-hydroxytryptamine or serotonin; NA = noradrenaline; DREZ = dorsal entry zone; SCI = spinal cord injury. aBased on treatment algorithm proposed by Siddall and Middleton (39). bIn acute, inpatient setting. cIn subacute or chronic setting. dCombination more effective than either drug alone. eFor at-level neuropathic pain.

 

Pharmacological Treatment
A treatment algorithm predicated on current available evidence, recently proposed by Siddall and Middleton (39), emphasizes the need for identifying the most likely underlying contributors of pain so that appropriate treatment may be applied. For pain conditions that are not amenable to treatment, particularly at-level and below-level neuropathic pain, management becomes largely symptomatic. Management of SCI at-level and below-level neuropathic pain remains a challenge, with effective treatment options being limited in number and efficacy (2). Randomized controlled trials of various treatments specifically for at-level and below-level neuropathic pain are limited and have been summarized in two reviews (2,40). An update of this summary on randomized controlled trials of pharmacological treatment of SCI pain is presented in Table 4.


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  		Table 4. RCTs of Pharmacologic Treatment of SCI Pain

 

Acknowledging the limitations of these studies and the various factors that may influence choice of treatment, Siddall and Middleton (39) proposed a three-tiered approach to the pharmacological treatment of SCI pain based on existing levels of evidence. A treatment algorithm that includes some of the recommendations from their approach is presented in Figure 1.

The first-line medications include systemic lidocaine, gabapentin, and pregabalin. Second-line medications include tricyclic antidepressants, alone or in combination with antiepileptic drugs. Third-line medications include ketamine, opioids, selective serotonin reuptake inhibitors, other antiepileptic drugs, intrathecal morphine with clonidine, and intrathecal baclofen.

Patients with localized pain symptoms may respond to topical lidocaine therapy. In diffuse and complex syndromes, initial drug therapy with gabapentin or nortriptyline is commenced at the lowest dose and then titrated gradually to desired analgesic effect with the least adverse effects. Incomplete or partial response to a drug after an adequate trial may be augmented by the addition of another drug with a different mechanism of action, but evidence for duration of adequate drug trials for SCI pain is lacking. Dworkin et al. (58) proposed that the duration of an adequate trial for antineuropathic drugs varies with each drug, such that an adequate trial for topical lidocaine should last 2 wk, 4–6 wk for opioid analgesics and tramadol, and 6–8 wk titration with at least 1–2 wk at maximum tolerated dosage for gabapentin and tricyclic antidepressants.

The treatment of muscle spasm pain needs special mention. Muscle spasm pain or pain from spasticity is often difficult to treat, as in our patient, particularly where no underlying pathology can be addressed. Because spasticity is a component of the upper motor neuron syndrome that is manifested by both positive and negative symptoms (Table 5) (35), treating spasticity will unmask the negative symptoms which have a significant impact on a patient's level of function. Thus, spasticity should be treated only when it interferes with function or puts the individual at risk (35).


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  		Table 5. Features of the Upper Motor Neuron Syndrome

 

Oral baclofen, a {gamma}-amino-butyric acidB receptor-agonist, is the first line of drug recommended for spasticity (26). Oral diazepam, which enhances presynaptic inhibition of afferent neuronal terminals in the primary reflex arc, is an alternative treatment for spasticity (2). When oral administration of baclofen is ineffective in controlling spasticity probably due to poor passage across the blood-brain barrier, intrathecal administration allows effective delivery of baclofen directly to the spinal cord (59).

Gradual titration of different combinations of Mr. H's analgesic and antispastic drugs failed to achieve a good balance between satisfactory analgesia and spasm control.

Because of the concerns of partial response to, disturbing adverse effects from, and expense of these oral medications, Mr. H received an intrathecal infusion of hydromorphone and baclofen that provided significant reduction of his pain and spasms and eliminated the need for oral drugs.

Intrathecal drug administration for SCI pain and spasticity: The seminal discovery of opioid receptors in the dorsal horn of the spinal cord heralded the advent of intrathecal delivery of opioid drugs. Intrathecal drug infusions overcame many of the obstacles presented by systemic drug therapy (60). Drug delivery into the subarachnoid space eliminated the influence of the blood-brain barrier and delivered the analgesics directly to opioid receptors, requiring significantly lower doses. This limited systemic exposure and reduced side effects that often complicate the use of oral medications. In an effort to gain better control of pain, spinal administration of opioid and nonopioid drugs has evolved from monodrug spinal therapy to the coadministration of two or three drugs intrathecally, which reduces the development of opioid tolerance by decreasing opioid requirements (60). An algorithm based on the current best available evidence and expert opinion for the use of intraspinal drug infusions in pain management was developed in 2003. It updated the clinical guidelines released by the Polyanalgesic Consensus Conference 2000 (61).

Of the first-line intrathecal analgesics, hydromorphone has been preferred over morphine in some cases, primarily because of its greater potency and solubility. Whereas morphine is stable at a maximum concentration of 30 mg/mL, hydromorphone allows higher concentration in solution with its potency being five times that of morphine. This permits longer periods between pump refills (61).

The efficacy of intrathecal baclofen treatment for spasticity has been well substantiated in the literature (59,62), with the majority of patients experiencing good long-term relief of spasticity and pain. However, the potential for tolerance to intrathecal baclofen may become an issue with long-term treatment (59,63,64).

Neuroaugmentative Treatment
Neuroaugmentative treatment options for SCI pain include transcutaneous electric nerve stimulation, spinal cord stimulation, and deep brain stimulation, all of which have little evidence of efficacy (65), except for at-level neuropathic pain and incomplete lesions (66) such as Brown-Sequard syndrome, where some sensation is preserved in painful areas.

Surgical Treatment
Of the many types of SCI pain, only a few can be successfully ameliorated with surgery. These include spinal fusion for stabilization of the spine, surgical decompression of nerve root compression, and drainage and shunting for syrinx, which may require subsequent detethering of the spinal cord. Other surgical treatments, including cordotomy, cordectomy, myelotomy, and dorsal root entry zone lesion (particularly for at-level neuropathic pain), have limited evidence of efficacy (65,67).

The successful rehabilitation and social reintegration of a patient with SCI pain does not rest solely on the control of pain and spasms. Despite the substantial reduction in pain and spasms, Mr. H continued to be depressed and frustrated with his functional limitations and isolated himself socially, hindering the attainment of his goals of independent living and returning to work. His case highlights the contributions of the other components of an interdisciplinary pain management plan that are fundamental to the successful rehabilitation and adjustment of the SCI patient. These domains include spinal rehabilitation, psychological therapy, and social or environmental modification, as presented in Figure 1.

Spinal Rehabilitation
Rehabilitation therapy is one of the principal components of treatment to restore functional independence and improve the quality of life of patients with SCI. Yet there is very limited evidence demonstrating the efficacy of various rehabilitative treatments (68). Physical treatment includes exercise and hydrotherapy, postural reeducation, pressure relief, use of physical aids, such as crutches, orthotics and wheelchairs, and other physical modalities. Unfortunately, physical therapy does not help reduce neuropathic SCI pain.

Psychological Therapy
The focus of psychological treatment for SCI pain is on the reduction of the psychological distress experienced by SCI patients, improvement of quality of life and facilitation of social reintegration. These are achieved by interventions that include development of pain-coping skills, cognitive behavioral therapy, exposure to social, sexual, and communication skill training, and involvement of individuals who may otherwise interfere with the patient's treatment progress.

As a guide for designing treatment programs tailored to the individual psychosocial characteristics of SCI patients, the adaptational pattern of each patient is identified based on response to the Multidimensional Pain Inventory (69). For people with low levels of pain, affective distress and life interference and high sense of control and activity (Adaptive Copers), only support, and education in the use of additional coping skills may be required along with physical and pharmacological modalities. In contrast, those with high levels of pain, affective distress and perceived activity interference, and low levels of perceived control (dysfunctional) and those with high levels of pain and low levels of social and emotional support (interpersonally distressed) are more likely to benefit from an interdisciplinary approach that combines pharmacotherapy and physiotherapy with cognitive behavioral therapy (70).

There are many cognitive-behavioral pain management programs for individuals with various chronic pain conditions, however, few are available for SCI individuals with chronic neuropathic pain, and hence the paucity of data on the effectiveness of such programs in cord-injured patients (71). A recent study performed in patients with SCI suggests that although cognitive behavioral approaches may not produce significant reductions in pain, they can provide improvements in other aspects of function such as mood (72).

Social or Environmental Modification
With chronicity, SCI pain may be amplified and perpetuated by biological, psychological, and environmental factors as patients struggle to adapt to their condition and to return to function and employment (12). To reduce SCI pain and facilitate adjustment to SCI and social reintegration, certain environmental factors need to be addressed. These include the need for homecare, family education, availability of employment opportunities appropriate to the patient's functional abilities and workplace adjustment.


   ACKNOWLEDGMENTS
 
We acknowledge and appreciate the support and valuable input of Ms Kathryn Nicholson Perry and the staff of the Pain Management Research Institute, Royal North Shore Hospital, Sydney, Australia.


   Footnotes
 
Accepted for publication July 10, 2007.

Reprints will not be available from the authors.

This work has not been funded by any source including nonprofit foundations.

Conflict of Interest: No conflict of interest to disclose.


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Top
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 Introduction
 CASE HISTORY
 DISCUSSION
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