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Rehabilitation and Chronic Issues After Spinal Cord Injury

Pain and Spasticity After Spinal Cord Injury

Mechanisms and Treatment

Burchiel, Kim J. MD, FACS; K. Hsu, Frank P. MD, PhD

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Pain and spasticity are common sequelae of spinal cord injury (SCI). Many patients already burdened with the disability of paralysis, as well as the residua of emotional and physical trauma, must contend with these often-intolerable further functional impairments. Thus, an appreciation of these disorders and the therapeutic means to achieve functional restoration from these complications of SCI are particularly crucial to allow individuals with paraplegia and quadriplegia the opportunity to live a full, productive, and comfortable life. In this article we discuss each condition in turn.

Pain After Spinal Cord Injury

Clinical Features

Although loss of motor function is considered the most debilitating consequence of SCI, pain can represent the most pressing complaint of patients who have sustained a cord injury. In one British study in 11% of SCI patients, pain rather than loss of motor function was what prevented them from working. 133 In another study fully 37% of patients with cervical and high thoracic SCI and 23% of patients with lower thoracic or lumbosacral lesions would be willing to trade relief of pain for loss of bladder, bowel, or sexual function. 114

There is much discrepancy in the literature concerning the prevalence of SCI pain, in part because of the lack of a standardized scheme for classification of SCI pain types. 134 Recently, the Task Force on Pain Following Spinal Cord Injury of the International Association for the Study of Pain has introduced a taxonomy, which seeks to classify SCI pain based on presumed mechanism. 146

Epidemiology of Spinal Cord Injury Pain

Prevalence and Incidence of Spinal Cord Injury Pain.

In one decade-old review of “centrally” generated pain, a summary of 10 reports indicated that on average 69% of patients with SCI report pain and nearly one third rate their pain as severe. 19 This estimate has been confirmed in two more recent studies, in which a prevalence of 66% was established. 49,150 Two other prospective longitudinal studies revealed a prevalence of 64% at 6 months after SCI 143 and 63% at 12 months after discharge from their acute postinjury hospitalization.

Prevalence rates do vary considerably in the literature. Individual values from 34%104 to 90%20,116 have been reported, with the percentage of patients in severe pain ranging from 12%114 to 30%. 20

Variables that may influence the development of SCI pain are unclear. Factors that have been mentioned in the literature, including the level of the SCI 37,67 and cause of injury, 108,128 lack compelling evidence. 127,150,151 Clinical observations that patients with incomplete lesions are more likely to develop SCI pain 13,33 have been corroborated by autopsy findings. 72 Central SCIs are associated with spontaneous and evoked burning pain and hyperesthesia in the upper extremities. 48,69,93,146 Chronic SCI pain is associated with depressive symptoms and greater perceived stress. 132 Other studies have found an association between pain, spasticity, “abnormal nonpainful sensations,” and “sadness.”165

Classification of Spinal Cord Injury Pain Types

The lack of a universally recognized scheme for classification of SCI pain has clearly hampered research, communication, and the evaluation of treatments in this area. Comparison of epidemiologic studies has been difficult because of the lack of a widely accepted taxonomy. In part, the absence of an acceptable classification scheme is due to the dearth of fundamental data on the mechanisms of SCI pain, particularly those perceived pains generated in the central nervous system after a deafferenting cord injury. Numerous animal models of neuropathic pain after experimental SCI present a host of slightly different features. 26,57,86,142,158,170 This suggests that different clinical SCI pain syndromes may indeed stem from differences in their central mechanisms.

The concept that SCI pain is a monolithic entity should therefore be abandoned. The remaining challenge then will be to characterize the pain(s) in a “user friendly,” comprehensive, systematic, logical manner that is consistent with clinical use and with current concepts of pain types and terminology. The system should be based on mechanisms, as much as is currently feasible, and it should be consistently applied by clinicians that deal with SCI pain.

An International Association for the Study of Pain has proposed a scheme for characterizing SCI pain that attempts to meet these requirements. 146 The taxonomy broadly defines two types of SCI pain: nociceptive and neuropathic. Nociceptive pain is divided into musculoskeletal and visceral pain types, and neuropathic is divided into above-level, at-level, and below-level types, where level refers to the level of the spinal cord that was injured. Musculoskeletal pain is located in musculoskeletal structures and is usually described as dull, aching, movement-related, eased by rest, and is responsive to opioids and nonsteroidal anti-inflammatory drugs. Visceral pain is usually located in the abdominal region with preserved innervation and is dull and cramping. Dysreflexic headache (vascular) is considered to be part of this group. Neuropathic pain is usually described as sharp, shooting, burning, or electrical, and there is usually abnormal sensory responsiveness (hyperesthesia or hyperalgesia). Above-level neuropathic pain is located in the region of sensory preservation, at-level pain is located in a segmental pattern at the level of injury, and below-level pain is located diffusely below the level of injury. Although psychological factors play a role in all types of chronic pain, the drafters of this scheme did not attempt to add further complexity to an already three-tiered classification. Rather, they acknowledged that these factors can be superimposed on SCI pain of all types. Table 1 shows the entire proposed classification scheme. If adopted by the International Association for the Study of Pain, this taxonomy will represent a major step forward in the study of SCI pain and its treatments.

Table 1
Table 1:
Proposed IASP Classification of Pain Related to SCI

Animal Models of Spinal Cord Injury Pain

Vierck et al 160 have recently reviewed animal models of SCI with regard to potential mechanisms of chronic post-SCI pain. Evidence for at-level dysesthesia/pain and for enhancement of nocifensive reflex responses in dermatomes bordering spinal lesions has developed in SCI models involving excitotoxic damage to spinal gray matter (central cord) lesions. 168 Overgrooming/autotomy develops in adjacent ipsilateral dermatomes representing segments at and caudal to the lesion epicenter, particularly when the superficial dorsal horn remains outside the lesion. Also, nocifensive enhancement is seen for dermatomes near the level of ischemic spinal cord lesions that include the dorsal horn and dorsal spinal pathways. 166 Central cord lesions are clearly important to the development of at-level neuropathic pain, as has also been demonstrated by observations of lowered thresholds for nocifensive reflex responses from stimulation of the flank after thoracic contusion injury. 70,71,142 This hypersensitivity has been observed for lesions restricted to the central gray matter or the dorsal half of the spinal cord. 142 These findings are consistent with clinical reports that at-level SCI pain with allodynia/hyperalgesia is more common after central cord injuries than after complete lesions of the spinal cord. 143

Animal models of at-level neuropathic pain have suggested a complex sequence of anatomic, chemical, molecular, and physiologic changes triggered by SCI. This secondary injury likely has neurochemical, excitotoxic, and inflammatory components. As with other putative excitotoxic injuries, intraspinal release of glutamate may be a primary initiating event in this sequence of biochemical events. 153 Other factors implicated in the excitotoxic cascade include the production of inflammatory cytokines and prostanoids, breakdown of cytoskeletal proteins, and modulation of cellular messengers and transcription factors that might severely compromise both the anatomic and functional integrity of spinal neurons. 15,144,167 It appears that this spread of secondary injury to spinal cord segments rostral and caudal to the injury site is critical to the nature and distribution of SCI pain. 168

Cellular electrophysiologic recordings from spinal projection neurons and interneurons in segments in the vicinity of experimental SCIs have revealed substantial functional changes, including a shift in neuronal stimulus–response functions toward increasing responsiveness, an increase in level of spontaneous neuronal background activity, increased numbers of “wide dynamic range” neurons, and an increased duration of after-discharge responses. 59,71,169 These manifestations of pathologic hyperexcitability are reminiscent of abnormal functional characteristics of neurons recorded in patients with chronic pain after SCI. 88

Neuroprotective and anti-inflammatory strategies that suppress abnormal hyperactivity of neurons in the vicinity of a lesion should inhibit the development of hypersensitivity after both experimental and clinical SCI. In the laboratory setting, administration of an N-methyl-D-aspartate (NMDA) antagonist can reduce secondary ischemic damage and prevent the development of hypersensitivity. 10,59 Similar strategies have reduced chronic pain from SCI in humans. 44 Gabapentin, an anticonvulsant, can alleviate chronic hypersensitivity in spinally injured rats. 58,71

After acute ischemic injury to the spinal cord, there are several periods during which cutaneous hypersensitivity can be inferred from responses to stimulation within dermatomes adjacent to the injury. An acute period of hypersensitivity (1–5 days) is associated with reduced γ-aminobutyric acid (GABA) immunoreactivity and is attenuated by activation of GABAB receptors. 166 Acute hypersensitivity after ischemic spinal damage also seems to be insensitive to intrathecal application of morphine at a time when μ-opioid receptor immunoreactivity in the region of injury is reduced. 174

Almost an inverse profile of GABA and opioid expression/sensitivity is present after the acute phase of central cord injury. Chronic enhancement of nocifensive behaviors after ischemic damage to the spinal cord does not appear to depend on GABAergic mechanisms. 166 Enhanced nocifensive responses have been observed after intrathecal injection of naloxone in rats that did not spontaneously develop hypersensitivity after ischemic spinal injury. 166 These observations suggest that endogenous opioid activity influences the development and incidence of more chronic dysesthesia/pain.

Models of Below-Level Neuropathic Pain.

The clinical literature on SCI pain suggests that interruption of the spinothalamic tract with deafferentation of its rostral targets is integral to the development of below-level SCI pain. 21 Experimental lesions of the anterolateral column of the spinal cord in monkeys and rats have been shown to produce overgrooming/autotomy caudal to the lesion. 86,100 Furthermore, it is well known that allodynia and hyperalgesia can occur after “recovery” from anterolateral cordotomy in humans, monkeys, and rats. 159,161 Abnormal spontaneous and evoked firing patterns are observed in rostral projection targets (e.g., in the ventrobasal thalamus) after spinothalamic tractotomy. 163 This abnormal activity alone is not evidence of pain or allodynia. It is likely that the neuronal activity patterns that signal pain are complex and distributed at multiple levels of the nervous system.

Involvement of dorsal spinal pathways in the SCI may also contribute to the establishment of bilateral below-level phenomena. An investigation of humans with below-level neuropathic pain after SCI implicated the dorsal columns, 113 and pain associated with syringomyelia is reported to be more prevalent when a central cavity expands to include dorsal pathways. 99

Spinal cord injury pain is not a static entity. In the chronic phase after SCI, at-level, below-level, or both categories of pain may be present. 12 There may be a temporal progression in that they tend to occur in sequence (at-level, followed by below-level pain, with or without a continuance of at-level phenomena), suggesting the existence of an interaction in the mechanisms of each type of pain. Abnormal neuronal activity associated with at-level pain may predispose an individual toward later development of below-level pain.

In addition to a variable onset and incidence, below-level neuropathic SCI pain is highly labile and may be, in part, under stimulus control. Once established, below-level neuropathic pain and related allodynia/hyperalgesia in humans with SCI is not constant but typically is episodic, 21 as is overgrooming/autotomy seen in monkeys after anterolateral cordotomy. 86 In some cases below-level pain is triggered by deep visceral and somatic input, such as from bladder filling. 37 This may be related to the dynamic balance between the degree of rostral deafferentation and the stimulation of deafferented neurons from remaining incontinuity spinal cord pathways. This may be exemplified by the predilection of central cord injuries to be associated with upper extremity pain. Incomplete iatrogenic disruption of the spinal cord can also produce the same result. Historically, the SCI attendant to anterolateral cordotomy, performed to produce caudal contralateral analgesia from cancer pain, extended medial to the anterolateral column, resulting in damage to the anterior horn and central gray of the spinal cord. 42 This often resulted in signs of below-level neuropathic pain, or “postcordotomy dysesthesias,” in a proportion of cases with extended survival. 86,161 Interestingly, when central damage to the spinal cord is minimized by making superficial lesions of one anterolateral column, the desired prolonged contralateral analgesia is produced, without the development of postcordotomy chronic pain or dysesthesias. 112,159

Pharmacologic Treatment of Spinal Cord Injury Pain

Initial pharmacologic treatment of SCI pain often relies on the mainstays of therapy for neuropathic pain, in general, antidepressants and anticonvulsants. Unfortunately, neither of these two classes of drugs is highly effective for SCI pain. Recent reports indicate that opioids and α-adrenergic antagonists may play an important role in the future. A GABAB agonist, baclofen, may also be considered, particularly when symptoms of painful spasticity dominate the patient’s clinical syndrome. There are still relatively few data on NMDA receptor antagonists for the treatment of SCI pain. As with surgical therapies for this entity, no one agent has emerged as producing consistently beneficial results.


There is only one Class I study on the effect of antidepressants on SCI. 33 In this work trazodone hydrochloride, a presynaptic serotonin reuptake blocker, was not more effective in the treatment of diffuse burning and tingling sensations after traumatic SCI than placebo. The most common side effects were drowsiness, dry mouth, dizziness, increased spasticity, and urinary retention. In an uncontrolled study by Heilporn, 63 8 of 11 SCI patients with diffuse pain responded to a combination of melitracen 150 mg by mouth and flupenthixol 3 mg by mouth daily, but in this study the authors did not use standard outcome measurement scales. In a report by Fennolosa et al, 49 25 of 33 SCI patients with various types of pain obtained “satisfactory” pain relief with amitriptyline and clonazepam in combination with a nonsteroidal anti-inflammatory drug or 5-OH-tryptophan and transcutaneous electrical nerve stimulation or spinal cord stimulation (SCS). Two articles reported the effect of a combination of an antidepressant and an antiepileptic on neuropathic SCI pain. 24,137


Only one Class I study has been published regarding the effects of anticonvulsants on SCI pain. Drewes et al 39 studied the effect of valproate for treatment of pain after SCI. They found no significant analgesic effect, but a trend toward improvement was observed in most pain measurements. Gibson and White 53 reported on the effect of carbamazepine on SCI pain in two patients with traumatic complete paraplegia. Zachariah et al 175 described two of three patients who had a beneficial effect of valproate on both spasticity and pain. In a case of SCI pain, Ness et al 115 described the marked effect of gabapentin on episodic unilateral pain.

Sodium Channel Blockers.

It has been suggested that sodium channel blockers reduce central neuropathic pain by reduction of ectopic discharge from peripheral injured afferents by blocking voltage-gated sodium channels. The exact mechanism by which lidocaine may reduce central pain is not known. Lidocaine is not available in an oral formulation, and its oral analog, mexiletine, is often not well tolerated. Three controlled trials on lidocaine or mexiletine have been published. Attal et al 2 studied the effects of intravenously administered lidocaine on different components of neuropathic pain in 16 patients with chronic post stroke (n = 6) or SCI (n = 10) related pain. Lidocaine significantly reduced spontaneous ongoing pain and brush-induced allodynia and mechanical hyperalgesia but was no better than placebo against thermal allodynia and hyperalgesia. Six SCI patients receiving lidocaine showed a significant reduction (≥50%) in spontaneous pain compared with four with placebo, and three of five showed reduction in brush-evoked allodynia after lidocaine compared with one of five after placebo. In a study by Loubser and Donovan, 91 21 patients with constant (most often burning) or stabbing, paroxysmal pain secondary to traumatic SCI at or below the level of the lesion underwent subarachnoid injection of placebo and lidocaine. The pain response to subarachnoid lidocaine differed significantly from placebo. Spinal anesthesia was also associated with changes in pain distribution and altered sensation. Chiou-Tan et al 25 examined the effects of mexiletine on SCI and showed no significant effect of mexiletine on SCI pain measured on visual analog scales and the McGill Pain Questionnaire. Pollock et al 119 described the effect of intrathecal tetracaine hydrochloride in four cases of SCI pain. Distal pain disappeared and returned at a time compatible with the patients’ recovery from anesthesia. 119


Although neuropathic pains may be relatively less responsive to opioids than nociceptive pains, the commonly held belief that opiate narcotics are completely ineffective in the treatment of central pain 120 is contradicted by numerous lines of evidence. Two placebo-controlled trials have been published regarding opioids in the treatment of SCI pain. In a trial by Eide et al, 44 the effects of intravenous infusion of alfentanil, ketamine, or placebo on continuous, intermittent, and evoked pain in nine SCI patients were studied. The study showed an effect of the μ-opioid receptor agonist alfentanil as well as ketamine on both continuous and evoked pain. Six patients reported side effects after treatment with alfentanil and five after treatment with ketamine. Siddall et al 145 found that a combination of intrathecal morphine and clonidine produced significant relief of neuropathic SCI pain compared with saline placebo. Either morphine or clonidine alone did not produce significant pain relief. In this study the concentration of morphine in the cervical cerebrospinal fluid and the degree of pain relief correlated significantly. In a nonrandomized, single-blind study by Glynn et al, 54 epidural morphine had an analgesic effect in five of 14 patients with neuropathic pain after SCI. In a study on one patient, 5 mg Δ-9-tetrahydrocannabinol and 50 mg codeine had an analgesic effect on painful post-SCI dysesthesias in comparison with placebo. 94 Pain and spasticity improved in eight of 12 SCI patients given continuous intrathecal infusion of morphine (0.3–1.0 mg/d). Six patients were alive after 3 years of follow-up, and none of these developed dependence or a significant degree of tolerance. 45


There are only a few reports on clonidine, an α2-adrenergic agonist, for the treatment of SCI pain. In the controlled study by Siddall et al, 145 a combination of intrathecal clonidine and morphine had an analgesic effect. In the study by Glynn et al, 54 10 of 15 patients receiving epidural clonidine (150 μg) for neuropathic pain after SCI had pain relief. Petros and Wright 118 described a patient with paraplegia, who had good relief of pain after epidural clonidine and moderate relief with oral clonidine. Intrathecal infusion of morphine in combination with clonidine had an analgesic effect on continuous and shooting central pain in a patient with SCI pain, 141 and a combination of intrathecal baclofen and clonidine had an effect on painful anal spasms in a patient with anterior cord syndrome. 98

Potassium Channel Blockers.

There are a number of studies on the effect of the potassium channel blocking drug 4-aminopyridine (4-AP) on transient recovery of neurologic function in SCI patients. Some of these reports also commented on the effects of 4-AP on pain. In a randomized double-blind dose–titration crossover trial of oral fampridine-SR (sustained release 4-AP) in 26 SCI patients with incomplete lesions, there were no statistically significant benefits of the drug on pain (present pain intensity, McGill Pain Questionnaire). 121 In a randomized, double-blind study the effect of intravenous infusion of 4-AP on neurologic status was studied in eight SCI patients. Standardized pain scales were not used, but the authors concluded that the improvement seen in neurologic status included the reduction of chronic pain and spasticity. 56 In another investigation of six SCI patients, 4-AP reduced spasticity in two patients and reduced pain in one patient. 62

N-methyl-d-aspartate Receptor Agonists.

Central NMDA receptors that modulate the binding site for the excitatory amino acid glutamate are involved in central sensitization seen in neuropathic pain. 138 Almost no interpretable studies have been performed on these agents. In one controlled trial by Eide et al, 44 ketamine had an effect on both continuous and evoked SCI pain.

γ-Aminobutyric AcidB Receptor Agonists.

Existing evidence from experimental animal studies of neurogenic pain supports the role of decreased inhibitory influence of GABAergic neurotransmission in neuropathic pain. 169 The effect of baclofen, an agonist of the GABA receptor, on SCI pain has been assessed in one controlled trial and several uncontrolled trials. Herman et al 64 assessed the effect of acute intrathecal baclofen (50 μg) on seven patients with spinal spasticity, i.e., multiple sclerosis, SCI, and transverse myelitis. Baclofen significantly suppressed central neuropathic pain and spasm-related pain but did not influence pinch-induced and musculoskeletal (low back) pain. Contrary results were found in the uncontrolled study by Loubser and Akman 90; 12 patients with spasticity and pain (six with neuropathic pain, three with musculoskeletal pain, and three with both pain components) secondary to SCI were assessed before intrathecal baclofen pump implantation and again 6 and 12 months after surgery. After surgery (at both 6- and 12-month intervals) seven patients with neurogenic pain (78%) demonstrated no significant change in pain severity, whereas in five patients (83%) musculoskeletal pain decreased significantly. In the pilot study by Taira et al, the effect of an intrathecal bolus injection of baclofen was investigated in 14 patients with neuropathic pain due to a stroke (eight cases) or SCI (six cases). 152 Nine patients reported “substantial” pain relief. The effect appeared 1–2 hours after the injection and persisted for 10–24 hours. Allodynia and hyperalgesia, if present, were relieved as well. One case report suggested that a combination of intrathecal baclofen and clonidine had an effect on painful anal spasms in a patient with anterior cord syndrome. 98

Surgical Treatment of Spinal Cord Injury Pain

Despite increasing knowledge of the pathophysiology of SCI pain, treatment of chronic neuropathic pain from SCI remains a frustrating experience for many patients. Treatment of SCI pain often devolves to an iterative series of ineffective medical and surgical treatments. No one therapy is consistently effective. In the following paragraphs we describe the available evidence on various methods now used in an attempt to alleviate this difficult problem.

Transcutaneous Electrical Nerve Stimulation.

Reports on the use of transcutaneous electrical nerve stimulation in SCI patients are limited, and controlled trials are not available. Patients with muscular pain or at-level pain may obtain some pain relief. At present there is little evidence that transcutaneous electrical nerve stimulation is useful for the treatment of central neurogenic pains secondary to SCI. 4,9,36,45,55,63

Spinal Cord Stimulation.

Spinal cord stimulation appears to be most effective in patients with incomplete and in patients with postcordotomy pain. Poor results have been reported in patients with complete lesions. Most studies agree that the therapeutic effect declines with time. Spinal cord stimulation occasionally is effective for the so-called “end zone” pains that occur after SCI. There is no evidence of its effectiveness for the “central dysesthetic” pains that project diffusely into insensate areas below an SCI patient’s absolute sensory level. 23,27,38,84,95,96,100,130,155,164

Deep Brain Stimulation.

The number of studies on deep brain stimulation (DBS) for treatment of chronic pain peaked in the 1970s and 1980s. Over the last decade, reports on the use of DBS for chronic pain diminished sharply, in part because of the lack of FDA approval for the procedure for any pain indication. In the studies that are available for review, DBS was used in patients who had failed all other conventional treatment methods. The areas targeted for DBS were the periaqueductal gray/periventricular gray, thalamic nuclei (ventroposterolateral [VPL] and ventroposteromedial [VPM]), and the internal capsule. Periventricular gray/periaqueductal gray stimulation has generally been recommended for nociceptive pain, and thalamic stimulation has generally been used for treatment of deafferentation pain. However, these recommendations have not been strictly followed.

Although studies on DBS espouse some optimism for treatment of chronic intractable pain due to SCI, none of these studies has a consistent and adequate follow-up period. Richardson et al 130 published a study in which six of 19 patients (32%) with paraplegia had good results with DBS after a 1-year follow-up. Young et al 168 described one of six patients who had excellent results and three of six who had partial response to DBS. The mean follow-up for patients in this study was 20 months (range 2–60 months). Yezierski 168 conducted a study that included four patients with “paraplegic pain.” These patients underwent DBS of thalamic nuclei (specifically VPL), and their response was assessed (follow-up ranged from 6 months to 6 years). Two (50%) of these patients had excellent results to the therapy, and the other two patients also showed an improvement in their pain profile. Levy et al 87 also published a study on DBS for chronic intractable pain, which included 11 patients with SCI. Even though four of the 11 patients had an initial response to DBS (6 weeks), none of the 11 patients had long-term results. The mean follow-up for this study was substantial (80 months), and these patients received a combination of periaqueductal gray/periventricular gray and thalamic electrodes; three of the patients stimulating both thalamic and periaqueductal gray/periventricular gray electrodes. This study created some doubt regarding the long-term effectiveness of DBS for paraplegia pain. Kumar et al reported that two of two patients with “trauma to cord/peripheral nerves” had long-term benefit with a follow-up ranging 6 months to 10 years. 81 Kumar et al 80 later published another study in which none of the three patients with “traumatic SCI” had long-term relief of pain. If all cases of long-term follow-up with DBS for SCI pain are compiled, no patient with SCI pain has achieved long-term pain relief with DBS.

Cordotomy, Cordectomy, and Myelotomy.

It appears that cordotomy and cordectomy may be mostly effective for spontaneous lancinating or shooting pain, or evoked pain. Cord section does not seem to be as effective for constant, dysesthetic, burning, or aching pain. 5 Complications from these ablative procedures include intractable contralateral pain and dysesthesias, bladder dysfunction, loss of pre-existing sexual function, and development of muscle spasms. The further impairment of residual nervous function below the lesion or the permanent limitation of neurologic recovery presents substantial physical and psychological barriers to patients.

Several authors have suggested that cordotomies should be performed bilaterally because unilateral cordotomy leads to a high incidence of intractable contralateral pain and dysesthesias. When pain recurs, attempts to re-establish analgesia by secondary or tertiary tractotomy nearly always end in failure after a year or more. 166 Melzack and Loeser described five patients in whom cordectomy was performed. 97 One of their patients with shooting pain in the back and legs had complete pain relief after a spinal cordotomy for 11.5 years. After this time he had recurrence of pain, which was the exact same type and distribution as 12 years earlier. Level of operation also seems to be very important. In another case report 40 an SCI patient with pain after a traumatic L1 lesion first underwent bilateral section of the eleventh and twelfth thoracic dorsal roots, then cordectomy through the injured eleventh thoracic segment, both with only temporary relief of pain. Eventually, he had a transection done through apparently normal adjacent cord segment at the junction of the tenth and eleventh thoracic segments with lasting relief of pain (follow-up 18 months). 40

In light of evidence that spread of neuronal injury rostrally is important in the development of SCI pain and data that dorsal root entry zone (DREZ) lesions at and just above the damaged segment can relieve not only “end-zone” at-level pains as well as, less commonly, below-level neuropathic pains, suggests that favorable results with cordectomy may due to ablation of adjacent rostral cord segments that are partially damaged. Cordectomy at and slightly above the injury level in patients with thoracic SCI may be effective for the same reasons that DREZ is hypothesized to work, namely, by elimination of an ectopic generator of centrally propagating nociceptive impulses at and just above the injury level. Raising the sensory level one thoracic dermatome in a patient with SCI pain and paraplegic is usually an acceptable trade-off to achieve pain relief. Obviously, this approach would not be applicable in the cervical spinal cord because of the likelihood of further impairment of the patient’s functional sensorimotor level.

Dorsal Root Entry Zone Operation.

The first published report of a DREZ operation was in 1976 on a patient with arm pain after a brachial plexus avulsion. 111 Since then, many patients have undergone the DREZ procedure for treatment of pain in SCI. 43,47,51,79,109,110,122,123,126,131,135,136,165,173 Patients with pain confined to dermatomes at or just below the level of spinal injury (at-level pain), pain extending caudally from the level of the injury, and patients with unilateral pain have been reported to have good results after DREZ lesions, but results have not been as good in patients with sacral pain (below-level pain). Complications include cerebrospinal fluid leaks, new weakness or sensory loss, new paresthesias or dysesthesias, exacerbation of bowel bladder and sexual dysfunction, and epidural/subcutaneous hematomas. The effectiveness of DREZ lesions is thought to be destruction of abnormal activity in pain neurons in the dorsal horn rostral to the level of injury (epileptiform “pain-generating centers”), interruption of ascending pain pathways, or rebalancing of inhibitory and excitatory inputs within a damaged sensory network. 109,122

Dorsal root entry zone can be performed using a radiofrequency technique or microsurgical dissection and coagulative ablation of the superficial lamina of the DREZ and dorsal horn. Dorsal root entry zone lesions are usually performed from one or two dermatomal segments above the level of injury down to and including the level of the lesion. However, no widely accepted method has been established to determine the extent of rostral DREZ lesion necessary to provide adequate analgesia in each case. The Craig Institute group has described computer-assisted DREZ microcoagulation, in which recordings in the DREZ area at and above the injury level were made and analyzed. Areas with “abnormal focal hyperactivity” were ablated. In 39% of the cases areas of focal hyperactivity were found higher than three levels above the injury site. They have claimed that this technique had a higher success rate (even though 93% of their patients had diffuse and/or sacral pain, normally not being very responsive to standard DREZ operations) and also claimed fewer complications than standard DREZ operations. Falci et al described a new technique utilizing spontaneous intramedullary recordings to guide DREZ lesioning. 47 Using spontaneous intramedullary recordings alone, seven of 11 patients achieved 100% pain relief and nine of 11 achieved 50–100% pain relief. Using both techniques 21 of 25 patients achieved 50–100% pain relief.


Two thirds of patients with SCI report pain, and in one third of those the pain is severe and debilitating. Animal models indicate that at-level neuropathic pain probably results from damage to the spinal gray and white matter one or more segments above the injury site. These models have identified putative mechanisms for generation of at-level pain and have suggested a number of potential therapeutic approaches. Current evidence also suggests that restricting the extent of excitotoxicity/ischemia after traumatic SCI might prevent the development of below-level neuropathic pain, both by reducing excitatory influences and by limiting the extent of white matter damage. Below-level neuropathic pain results not only from interruption of spinothalamic projections pathways, but also appears to be potentiated by interruption and/or activation of other pathways in the central spinal cord, including central propriospinal systems of diffuse conduction. Further examination of interactions between at-level and below-level phenomena should provide new insights into mechanism(s) and therapies for SCI pain.

Currently, oral pharmacologic therapy for severe SCI pain is relatively ineffective. Intrathecal drug therapy holds considerable promise, through combinations of agents such as morphine, clonidine, and baclofen. The promise of innovative agents, such as intrathecal gabapentin, or a new class of analgesics, the conotoxins, has yet to be realized in patients. Surgical therapy can help patients with “end-zone” pains and in some patients with diffuse below-level pain. The possible improved efficacy of physiologically guided DREZ will have to be demonstrated through wider application.

With an improved taxonomy, research on SCI pain will be facilitated. There are ample opportunities for research progress in this area, both in the laboratory and in the clinic.

Recommendations for treatment of SCI pain were made using aspects of a recently developed analytic method. 60 Evidence was categorized by evaluating individual studies, their linkage to and consistency with other studies in the field, and the quality of the evidentiary linkage to the framework of other studies in the field. Based on this analysis, an evidence table on the treatment of SCI pain was developed (Table 2).

Table 2
Table 2:
Treatment of SCI Pain

Spasticity After Spinal Cord Injury

Spasticity is an unfortunate and inevitable sequela of brain or SCI. Spasticity is defined as both abnormal increase in tone (hypertonus) and velocity-dependent increased resistance to muscle stretch. The patients with post-traumatic spasticity have high incidence of problems such as flexion contractures, decubitus ulcers, and poor perineal hygiene because of adductor spasms. Patients with spasticity are in general difficult to treat. In treating patients with severe spasticity, realistic goals should be set to improve the quality of life. These goals include the ability to sit in a wheelchair and accomplish a pivot transfer. Neurosurgical treatments remain viable and important options in treating patients with post-traumatic spasticity.

Mechanisms of Post–Spinal Cord Injury Spasticity

The exact mechanisms underlying the development of spasticity are not fully understood. Studies of patients with central paresis (upper motor neuron syndromes) and spasticity indicate that the monosynaptic reflex response to stretch is enhanced, whereas the long-latency (polysynaptic) stretch reflex appears to be reduced in strength. 22

It was long thought that the increased gain of stretch reflexes in spasticity resulted from hyperactivity of the γ motor neurons. Recent experiments, however, have cast doubt on this explanation. Although γ overactivity may be present in some cases, changes in the background activity of motor neurons and interneurons are probably a more important factor. 73

Several factors may contribute to a decreased inhibition of α motor neurons, so that they react with abnormal firing frequency and duration to an excitatory stimulus. 22,73,140,171 The change in the spinal cord may be the most important factor. The loss of descending corticospinal fibers most likely results in decreased activity of inhibitory interneurons. There is some evidence that the activity of the inhibitory interneurons activated from tendon organs (Ib afferents) is reduced. Therefore, the normal inhibition of certain α motor neurons from tendon organs when the muscular tension increases may be missing in spastic patients. There is also evidence of reduced activity of GABAergic interneurons mediating presynaptic inhibition of Ia afferent terminals. This would lead to a stronger excitatory effect of muscle stretch than normal (particularly rapid stretch) on the α motor neurons. Another possible factor may be reduced recurrent inhibition of α motor neurons in spastic patients. The Renshaw cells, mediating the recurrent inhibition, are known to be under supraspinal control. Thus, Renshaw cells acting on the motor neurons of the antagonists of a working muscle are excited by corticospinal fibers. There is evidence that the activity of interneurons mediating reciprocal inhibition, controlled by descending supraspinal pathway, is reduced. The passive viscoelastic properties change in spastic muscles. Thus, the resistance to stretching (the stiffness) can be increased even when no reflex contraction is elicited.

Pharmacologic Treatment of Post–Spinal Cord Injury Spasticity

Whatever the precise mechanism that produces spasticity, the effect is a strong facilitation of transmission in the monosynaptic reflex pathway from Ia sensory fibers to α motoneurons. Indeed, this has been the basis for therapeutic treatment. Disruption of the myotatic reflex decreases the output of α motoneurons. The most effective agents for control of spasticity include two that act predominantly within the central nervous system (baclofen and diazepam) and one (dantrolene) that acts directly on skeletal muscle. Newer agents such as tizanidine and botulinum toxin have also been tried with success. Table 2 summarizes the clinical trials of the pharmacologic treatment for spasticity.


Baclofen is a derivative of the inhibitory neurotransmitter GABA. It is an agonist to GABAB receptors. It targets at enhancing the inhibitory effects of the interneurons. Binding of GABA to these receptors decreases the influx of calcium into the presynaptic terminals and hence reduces the amount of transmitter release. 73 Baclofen is particularly useful to reduce the frequency and severity of flexor or extensor spasms and to reduce increased flexor tone. Because it is effective in patients with complete spinal transactions, its primary site of action appears to be in the spinal cord. 16 Baclofen is absorbed rapidly after oral administration, and it has a half-life in plasma of about 3–4 hours. It is largely excreted unchanged by the kidney. The use of baclofen may be limited by its adverse effects, which include drowsiness, insomnia, dizziness, weakness, ataxia, and mental confusion. Sudden withdrawal of baclofen after chronic administration may cause auditory and visual hallucinations, anxiety, and tachycardia. Coma, respiratory depression, and seizures have been reported after significant overdosage. The threshold for initiation of seizure may be lowered in patients with epilepsy. 16

Baclofen is available in 10- and 20-mg tablets. Determination of optimal dosage in individual patients requires careful titration. Treatment is initiated with an oral dose of 5 mg, given two or three times daily, and after 3 days the individual dose is increased to 10 mg. The usual maximal dosage is 20 mg, four times daily. Occasionally, total doses of 100–150 mg per day may be beneficial. Abrupt withdrawal of the drug should be avoided. Baclofen should be administered cautiously and in decreased dosage to patients with impaired renal function. 16,172 Baclofen is most effective in the treatment of spasticity caused by multiple sclerosis or other diseases of the spinal cord, particularly traumatic lesions. Similar to other muscle relaxants, it may impair the ability of the patient to walk or stand.


Diazepam belongs to the class of benzodiazepines. The presumed mechanism of action of the benzodiazepines is to enhance the efficiency of GABAergic transmission. 61 At the level of spinal cord, this may be manifest by enhancement of presynaptic inhibition of afferent neuronal terminals in the primary reflex arc. Diazepam is particularly useful for the treatment of patients with spinal cord lesions, although it is probably not as effective as baclofen in relieving intermittent flexor spasms. 172 Sedation can limit the efficacy of diazepam as a muscle relaxant, although its sedative and anxiolytic properties may be of value in certain patients. 89 The dose of diazepam should be titrated upward gradually to minimize unwanted effects, particularly sedation. 61


Dantrolene is unique in comparison with baclofen and diazepam, in that it exerts its effect by direct actions on skeletal muscle. 32,157 Dantrolene reduces contraction of skeletal muscle by a direct action on excitation–contraction coupling, apparently by decreasing the amount of calcium released from the sarcoplasmic reticulum. In patients with upper motoneuron lesions, spasticity is generally diminished by treatment with dantrolene, and functional spasticity is often improved. Placebo-controlled trials of dantrolene have demonstrated effective reduction of muscle tone and hyper-reflexia. 75 Unfortunately, the drug also tends to cause a generalized muscle weakness that negates the functional improvement. Absorption of dantrolene from the gastrointestinal tract is slow and incomplete but sufficiently consistent to provide dose-related concentrations in plasma. The median half-life of the drug in adults is about 9 hours after a 100-mg dose. It is slowly metabolized by the liver, and the 5-hydroxy and acetamido metabolites are excreted with unchanged drug in the urine.

Dantrolene has a serious potential to cause hepatotoxicity, and hepatic function should be monitored. The most common side effect is weakness, an extension of its effect on skeletal muscle. Although weakness may be transient or mild, its persistence in some ambulatory patients may compromise therapeutic benefit. The starting dose of 25 mg once a day is gradually increased by increments of 25 mg every 4 to 7 days to a maximal dose of 400 mg/d, given in four divided doses. 16

Dantrolene can relieve spasticity, but the weakness it produces may handicap the patient more than the spasticity it relieves. It provides sustained reduction of spasticity and improves functional capacity for the majority of paraplegic and hemiparaplegic patients; clonus, mass reflex movements, and abnormal resistance to passive stretch are reduced. 16


Tizanidine is an imidazole derivative and is a centrally acting α2-adrenergic agonist that inhibits the release of excitatory amino acids in spinal interneurons. It may also act by facilitating the action of glycine. 30,78 Tizanidine has demonstrated potent muscle-relaxing properties in animal models of spasticity, and it was found to suppress the polysynaptic reflex in the spinal transected cat. 34,35 In placebo-controlled trials tizanidine has been shown to reduce muscle tone and frequency of muscle spasms in both patients with multiple sclerosis and SCIs. 83,107,156 Nance et al reported the results from a multicenter, randomized, double-blind, and placebo-controlled study on the efficacy and safety of tizanidine in the treatment of spasticity in patients with SCI. 107 Of the 124 patients admitted to this study, 78 completed it. Tizanidine was titrated to an optimized dosage in each patient to a maximum of 36 mg/d. Muscle tone, assessed by Ashworth score, was significantly reduced by tizanidine treatment in comparison with placebo. No significant alterations in muscle strength or vital signs were noted in either treatment group. The most common adverse events during tizanidine treatment were somnolence, xerostomia, and fatigue. In the double-blind, placebo-controlled study of tizanidine used for patients with multiple sclerosis, performed by the United Kingdom Tizanidine Study Group, it was found to reduce spasticity without altering muscle strength as well. However, it has not been shown to have consistent positive effects on the functional status of patients. 156 Several studies compared the efficacy of zanitidine and baclofen or diazepam. Tizanidine demonstrated similar efficacy in reducing spasticity and better tolerability. 8,14,46,68,83,148,162 When compared with baclofen, night-time insomnia was reported more frequently with tizanidine, and weakness was reported less compared with baclofen. 14,78

Tizanidine is cleared by both liver and kidney. It undergoes first-pass hepatic metabolism and is subsequently eliminated by the kidney. Liver function test should be checked periodically. Treatment is initiated at 2 to 4 mg/d, increasing every 3 days by 2 to 4 mg/d. 78 The total dosage should not exceed 36 mg/d in three divided doses. Adverse effects include dry mouth, drowsiness, and dizziness and were seen primarily when dosage exceeded 24 mg/d. Visual hallucinations and elevated liver function tests were reversible with dosage reduction. 78,156 Tizanidine has not been found to have consistent effects on blood pressure, but because of its central α2-adrenergic activity and risk of hypotension, concomitant use of antihypertensives, especially clonidine, should be avoided.


Clonidine is a centrally acting α2-adrenergic agonist that has been shown to decrease the vibratory inhibition index in patients with SCI. 105,106 Clonidine is rarely used as a single agent in the treatment of spasticity. 78 It is available in 0.1-mg tablets, but the patch formulation (0.1 mg and 0.2 mg) is designed to deliver the specified dose daily and must be changed after every 7 days. Adverse effects include bradycardia, hypotension, dry mouth, drowsiness, constipation, dizziness, and depression.


Gabapentin is structurally similar to GABA, exerting GABAergic activity by binding receptors in the neocortex and hippocampus. However, it does not bind conventional GABAA, GABAB, glycine, glutamate, benzodiazepine, or NMDA receptors. 78 It is easily absorbed, reaching peak plasma concentration in 2–3 hours, it is not protein bound, it dose not undergo metabolism, and it is excreted unchanged in the urine. It is well tolerated in doses up to 3600 mg/d. 124 Recent studies suggested its usefulness in treating spasticity, but further investigation is required to confirm its efficacy. 124

Table 3 classifies the available evidence on the pharmacologic treatment of post-SCI spastici-ty. 3,8,14,29,41,46,52,66,68,75,83,107,139,148,149,156,162

Table 3
Table 3:
Summary of Clinical Trials of Various Pharmacologic Agents for the Treatment of Spasticity


Botulinum blocks presynaptic release of acetylcholine from the nerve terminal. Botulinum, when injected intramuscularly, spreads through muscles and fascia approximately 30 mm, binding presynaptic cholinergic nerve terminals, resulting in a chemical denervation. Botulinum toxin injection has been examined as a treatment for severe spasticity. 1,65,147 Snow et al studied botulinum toxin A in nine patients with advanced multiple sclerosis in a randomized, crossover double-blind study. Muscle tone, frequency of spasms, and hygiene/self-care scores were used to assess efficacy. Botulinum toxin injection produced a significant reduction in spasticity and improvement in ease of nursing care, with no adverse effects. 149 Botulinum toxin injection is off-label for treatment of spasticity. It may be used to treat patients with severe localized spasms. 78 Onset of muscle fiber paralysis begins in 24 to 72 hours with a maximal effect seen at 5 to 14 days. The paralysis is transient, lasting 12 to 16 weeks. Localizing specific muscles with electromyographic guidance may be necessary to produce optimal effects. Because delivery of toxin is not entirely contained, the paralysis of muscles may not be exact. Excessive weakness may result from the injections.

Surgical Treatment of Post–Spinal Cord Injury Spasticity

Surgical procedures can be classified into ablative procedures and neuromodulation procedures. Ablative procedures involve destruction or lesioning of anatomic structures, whereas neuromodulation procedures involve implantation of systems to deliver electrical stimulation or pharmacologic agent.

Ablative Procedures.

Disruption of the reflex arc serves as the basis of the ablative procedures. The reflex arc can be disrupted at the level of posterior or anterior nerve roots or in the spinal cord. Thus, posterior and anterior rhizotomies had been attempted. Myelotomy had been used to interrupt the spinal reflex as well.


Interruption of the peripheral reflex arc by cutting the posterior roots had been complicated by a high rate of failure in reducing spasticity. 50 Anterior root section improved the duration of spasticity reduction, but it resulted in severe muscle atrophy in the lower limbs. 103

Kennemore was the first to describe the methodology for performing percutaneous radiofrequency rhizotomy. He reported a procedure in which a rhizotomy electrode was introduced to the neural foramen under fluoroscopic guidance. 76,77 With the stimulation mode, each root was stimulated and the electrode was positioned such that motor activity was obtained in the appropriate muscle groups with a stimulation threshold of <0.5 V. Lesions were made in most roots at 90 C for 120 seconds. After the electrode returned to body temperature, repeat stimulation threshold was tested. An adequate lesion was considered to have been made when an increase in stimulation threshold of at least 0.2 V was achieved. Kasdon and Lathi performed a prospective study of radiofrequency rhizotomy in the treatment of post-traumatic spasticity in 25 patients. 74 All or most of the prospectively identified goals were accomplished in 24 of the 25 patients, with improvement persisting during an average follow-up period of 12 months. The improvement due to decreased tone was much greater than the improvement due to increased range of motion. No patient had a change in prerhizotomy bowel, bladder, or sexual function.


Bischof myelotomy. In 1951, Bischof first described interruption of the reflex pathways between the anterior and posterior horns by means of a lateral longitudinal incision of the spinal cord from L1 to S2 roots. 17 The spinal cord was bisected from both sides, and the myelotomy separated the dorsal half of the cord from the ventral half. The operation is performed through a laminectomy of T11, T12, and L1 to expose the lumbar segments and the conus medullaris. After the dura is opened, the lumbar and sacral segments should be identified with a nerve stimulator. The largest root is usually S1. Localization may be confirmed by electrical stimulation. After identification of the other appropriate nerve roots and related segments, the cord is rotated slightly and an incision is made in a longitudinal plane from the T12 to S1 segments, approximately in line with the attachment of the dentate ligaments.

In 1962, Tönnis and Bischof reported their results with 20 cases. 154 All patients had initial relief of spasticity, but the spasticity recurred in five cases. It was considered that 17 of the 20 patients experienced successful reduction in spasticity. Of the 20 patients, 18 had been confined to bed before operation; only three remained bed ridden after surgery. Residual neurologic function was not preserved. Tönnis and Bischof 154 also pointed out that it is usually difficult to assess the amount of potential voluntary movement in the presence of severe spasticity so that relief of spasticity may indicate greater motor function than had been anticipated. Nevertheless, they did not think that this myelotomy should be carried out on a patient who could walk at all. In 1969, Moyes reported 21 cases of Bischof myelotomy for severe intractable flexor spasms performed by nine Canadian neurosurgeons. 101 Of the 21 patients, 19 had good results. Two patients were improved, but not completely relieved of their flexor spasms. They had some reservations about carrying out the procedure on patients with incomplete cord lesions but thought that it was the best procedure at the time for patients with complete cord lesions.

T-myelotomy. Because the residual neurologic function was not always preserved in the classic Bischof myelotomy, the operation was revised by Bischof in 1967 to entail a dorsal midline myelotomy with lateral extension to protect any preserved bladder and motor function. 18 Laitinen and Singounas reported good results with the procedure in nine patients. 82 Cusick et al used the T-myelotomy with evoked potential response to delineate the limits of myelotomy. 31 After the conus was exposed, a bipolar platinum disc electrode was placed over the dorsal surface of the spinal cord at the superior limits of the laminectomy. A ring electrode about one small toe and a cutaneous electrode were used to record from the nerve roots near the conus medullaris. The root from which the maximal reproducible response at the proper latency was recorded was considered to be the L5 or S1 root. The site at which this root left the conus marked the inferior extent of the myelotomy. They reported that 12 patients who underwent this operation had excellent relief from spasticity in the lower limbs. 31 Averaged evoked potential recording helped delineate the limits of the myelotomy and were useful for evaluation of injury to the dorsal columns. Although preservation of any residual motor function is unlikely after T-myelotomy, the risk of permanent loss of preserved sensory, bladder, or sexual function was not great. In 1991, Putty and Shapiro reported their experience using T-myelotomy in treating spasticity in 20 patients. 125 All 20 patients enjoyed immediate complete relief of their painful spasms, although two (10%) eventually experienced return of their spasms and were thus classified as long-term failures. A total of 17 patients succeeded in markedly reducing, or being completely weaned from, their antispasmodic medications. In 11 of 14 patients, nonhealing decubitus ulcers subsequently healed with treatment. Bladder function was unchanged from the preoperative status in all patients. 125

Peripheral Neurectomy and Myotomy.

Benzel et al presented an operative technique for making a suprapubic incision for an infraperitoneal approach to a femoral and obturator neurectomy and an incision of the iliacus and psoas muscles bilaterally. 11 This was proposed as an alternative method for treating severe spasticity resistant to other surgical options.

Neuromodulation Procedures.

Unlike the ablative procedures, neuromodulation procedures offer the advantage of minimal invasiveness, nondestructiveness, and potential reversibility. These procedures include spinal cord or peripheral nerve stimulation and intrathecal drug delivery systems.

Spinal Cord Stimulation.

Spinal cord stimulation is a well-established method for treating chronic neuropathic pain syndromes. Clinical reports provided evidence that SCS may be of benefit in ameliorating spasms resulting from SCI. 7,129 Despite theoretic promise, SCS has not enjoyed widespread use in the management of intractable spasms and spasticity in traumatic myelopathy. The possible reason for this is that perhaps new antispasm medications have been introduced and in part because of the continued use of neuroablative procedures. Barolat et al reported their experience with 16 patients. 6 All patients had previously undergone extensive trials with oral medications and physical therapy. All 14 subjects in whom a satisfactory placement of the electrode could be obtained had a reduction in the severity of the spasms. In six patients the spasms were almost abolished. Extremity, truncal, and abdominal spasms were affected. Clonus in the upper extremities was consistently reduced. Marked improvement in bladder and bowel function was observed in each of two subjects. In more than 1 year of follow-up, five subjects showed persistence of the results, with less stimulation required to maintain the therapeutic effects. Complications included one system infection, one electrode migration, one wire breakage and skin breakdown at a connector site, development of high impedance in one electrode, and one skin breakdown over the lead.

Maiman et al performed animal studies in cats to examine the effect of SCS on post-traumatic spasticity. 92 After SCI was induced in cats at T8 and spasticity was allowed to develop, SCS was applied to the level above and below injury level. Electromyogram changes in hamstring and quadriceps muscles were monitored. The authors found that spasticity was aggravated by SCS delivered above the level of the lesion. Spasms were markedly suppressed by monopolar stimulation delivered below the level of the lesion. Effects were maximal with the negative electrode applied to the cord and were slightly less with reversal of polarity. These results suggested that SCS activates local inhibitory processes or depolarizes local excitatory pathways.

Intrathecal Baclofen Administration.

Baclofen is an agonist of GABA. Müller et al demonstrated that a reduction in electromyographic activity associated with clinical improvement in spasticity was observed with intrathecal baclofen infusion. 102 Many investigators also reported favorable outcome in reducing spasticity with intrathecal baclofen infusions. 85,176 Penn et al performed a randomized double-blind crossover study on the effect of the intrathecal baclofen infusion on abnormal muscle tone and spasms associated with spinal spasticity. 117 Twenty patients with spinal spasticity caused by multiple sclerosis or SCI who had no response to treatment with oral baclofen received an intrathecal infusion of baclofen or saline for 3 days. The infusions were administered by means of a programmable pump implanted in the lumbar subarachnoid space. Muscle tone decreased in all 20 patients. The Ashworth score for rigidity and spasms was decreased in 18 of 19 patients who had spasms. All patients were then entered in an open long-term trial of continuous infusion of intrathecal baclofen. During a mean follow-up period of 19.2 months, muscle tone has been maintained with the normal range and spasms reduced to a level that does not interfere with activities of daily living. No drowsiness or confusion occurred, one pump failed, and two catheters became dislodged and had to be replaced. No infection was observed. The authors suggested that intrathecal baclofen is an effective long-term treatment for spinal spasticity that has not responded to oral baclofen. Coffey et al reported the long-term results from a multicenter study. 28 A total of 93 patients were entered into a randomized double-blind placebo-controlled study screening protocol of intrathecal baclofen test injections. Of the 88 responders, 75 underwent implantation of a programmable pump system for chronic therapy. Patients were observed for 5–41 months after surgery (mean 19 months). Rigidity was reduced from a mean preoperative Ashworth scale score of 3.9 to a mean postoperative score of 1.7. Muscle spasms were reduced from a mean preoperative score of 3.1 to a mean postoperative score of 1.0. Although the dose of intrathecal baclofen required to control spasticity increased with time, drug tolerance was not a limiting factor in this study. Only one patient withdrew from the study because of a late surgical complication (pump pocket infection). Another patient received an intrathecal baclofen overdose because of a human error in programming the pump. The result of this study indicated that intrathecal baclofen infusion can be safe and effective for long-term treatment of intractable spasticity in patients with SCI or multiple sclerosis.


Surgery remains a viable option in the treatment of intractable post-traumatic spasticity. Although many surgical procedures are available, intrathecal programmable delivery of baclofen seems to enjoy the most success currently. The main contributing factor for this success is that intrathecal baclofen pump implantation is a neuromodulation procedure. The implantation technique is minimally invasive and straightforward. Second, many recent and well-performed clinical studies provided adequate evidence that intrathecal baclofen is effective in spasticity reduction. However, the intrathecal baclofen system is costly and requires a certain level of maintenance as well as patient commitment. It should be kept in mind that the ablative procedures, although technically more challenging, are still effective procedures to consider when treating patients with severe spasticity. Data on the pharmacologic and surgical treatment of spasticity were analyzed by the method discussed above for SCI pain treatment. 60Table 4 presents an evidence table on the treatment of post-SCI spasticity.

Table 4
Table 4:
Treatment of Post-SCI Spasticity


Considerable progress has been made in the medical and surgical therapy of spasticity from SCI. Most patients who do not get relief from either oral baclofen or tizanidine can be helped by intrathecal baclofen. Percutaneous radiofrequency rhizotomy, an underutilized procedure, can be useful in patients with spastic complete paraplegia in whom their increased tone is completely nonfunctional. Currently, rhizotomies and myelotomies are rarely necessary.

The development of effective treatments for SCI pain is an evolving story. However, this is one area where sequential basic research development may prevail over the serendipitous clinical breakthrough. The unraveling of the physiology of the animal model of SCI pain will surely foster the development of new and more effective therapies. More aggressive treatment of secondary injury in the first few hours after SCI may reduce the prevalence of the problem. Reconstruction of damaged spinal cords, even partial, may eventually help to defeat the pathophysiology of the disorder. Fundamental improvement in the prevention and treatment of SCI pain will certainly occur within the next decade.

Key Points

  • Pain after SCI is often difficult to treat, but recent advances in pharmacology and treatment have improved the prognosis for pain relief.
  • Spasticity after SCI can be successfully managed with oral medication, but in a minority of cases, intrathecal baclofen or ablative surgery may be indicated.


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