As medical progress has given spinal cord injured individuals improved
health and life expectancy, chronic pain has emerged for some as a
significant challenge and the most difficult aspect with which they must
cope. Chronic pain is central neuropathic pain that requires
centrally-directed treatment. This review summarizes the treatment options
available that begin with conservative medical and physical therapy
progresses to neuroablative procedures, and finally narcotics as warranted.
Usually no single treatment
is efficacious and instead an eclectic program is needed. Multiple
treatments require a team of multi-disciplined professionals to provide the
appropriate combination of ongoing care that can reduce the hurt
of chronic spinal cord injury pain.
Introduction. Spinal cord injury (SCI) can cause paralysis, sensory
impairment, autonomic nervous system dysfunction, bowel, bladder, and sexual
dysfunction. These impairments may lead to immobility and physical
dependency that can alter lifestyle and self-esteem. The addition of
chronic, intractable pain to these impairments can be devastating. Chronic
pain superimposed on SCI can virtually drain the individual of strength,
motivation, and will. For the SCI survivor who already faces functional
loss, severe pain can further restrict the diversional activities that are
available, making it impossible for the individual to even temporarily
escape his or her pain.1
Chronic SCI pain is known to be variable and difficult to accurately measure
by any objective means. Over the last 40 years, the reported prevalence of
severe or disabling chronic pain in SCI has ranged from 18% to 63%.2 Medical
progress has given SCI patients greater longevity and improved overall
health, allowing chronic pain to emerge as a major complication in this
population. Lundquist et al3 reported severe pain to be the only
complication they tracked related to diminished quality of life. For many,
it is the most difficult problem with which they must cope.
Categorization. Pain of any origin is difficult to assess, categorize, and
treat because analysis relies on the patient’s own subjective and variable
perceptions. Chronic SCI pain is especially difficult to accurately measure.
Historically, it has been neither well investigated nor clearly understood.
These difficulties have led to limitations in study design that restrict the
validity of their conclusions. The lack of a widely accepted SCI pain
classification scheme has limited the comparability
of the pain interventions studied. Accordingly, many clinicians do not have
a clear idea of how to approach the problem diagnostically, or how to pursue
treatment. Tunks4 observed that, “We must not fool ourselves, we have many
impressions, but few facts regarding treatment of SCI pain.”
Over the past 40 years, investigators and clinicians have attempted to
categorize SCI pain using a variety of schemes. Classifications have usually
been based on the postulated origin, clinical features or localization of
the pain.5 For example, nociceptive pain localized above the level of spinal
cord injury can be contrasted to radiating neuropathic pain at the level of
injury, or to diffuse neuropathic pain below the level of injury. There is
very little evidence that characteristics of the injury itself, such as
level, completeness, or etiology, are associated with the development or
severity of pain. Distinguishing chronic SCI pain from acute or acute
persistent pain is vital in providing the most appropriate treatment for a
Acute Pain. Acute pain after SCI is usually nociceptive in origin and
localized above the injury level. It usually occurs from either the physical
or mechanical nature of the injury or some primary disease process. With
acute pain there is evidence of some peripheral source or exogenous source
of the noxious stimuli. Acute pain responds to an accurate clinical
diagnosis and treatment. If the medical, surgical, and physical problems can
be eliminated, so can the pain.
The initial differential diagnostic considerations in acute SCI pain include
spinal instability from fractured vertebrae or torn ligaments and localized
infection. Delayed acute pain problems include pseudoarthrosis, peripheral
bone and soft-tissue injury, peripheral nerve injury with neuritis, visceral
disorder, and heterotopic ossification.
Acute-persistent Pain and Cystic Myelopathy. Acute-persistent pain or
acute-recurrent pain tends to be localized in the injured area of the spine
and is frequently exacerbated by physical activity. It is often described as
a localized dull ache or a sharp, penetrating pain, and often occurs in the
setting of ongoing pathology. Sources of acute-persistent pain in SCI
include degenerative joint disease (DJD) of the spine, tumors, and nerve
root pain (radiculopathy).
Cystic myelopathy is a common source of acute-persistent pain in SCI caused
by the development of cystic changes in the spinal cord which ascend from
the zone of injury. Arachnoiditis and tethering of the cord to the spinal
canal are important predisposing factors. Destruction of spinal cord tissue
from gradually increasing cystic pressure, especially in the dorsal horn
region, can cause increasing pain. Other signs and symptoms suggesting
cystic myelopathy include progressive motor/sensory losses, exacerbating
spasticity, autonomic hyperreflexia, hyperhidrosis, and Horners1 Syndrome. A
thorough history and physical examination coupled with a magnetic resonance
imaging of the spinal cord provides the most accurate diagnosis of cystic
myelopathy. Treatment of cystic myelopathy is well described later in this
Chronic Pain. Chronic pain after SCI is most often neuropathic in origin,
experienced below the level of injury. It occurs equally with complete and
incomplete lesions, and tends not to follow a dermatomal distribution. It is
most frequently perceived as a burning, tingling, electric-like, or aching
sensation. This neuropathic pain is generated within the central nervous
system and continues long after exogenous or peripheral sources of acute
pain have resolved. It may be the most difficult of the SCI pain syndromes
The central nervous system focus of chronic neuropathic SCI pain occurs from
the deafferented zone of the injury, the area exhibiting impaired sensory
input from the peripheral nervous system. Scarring, arachnoiditis, abnormal
axonal sprouting, and cord tethering in the dorsal horn region may have
developed. These anatomical changes may cause alterations in the normal
physiology of the cord, including abnormal burst firing, altered
neuropeptide concentrations, ephaptic spread from sympathetic fibers to pain
fibers, and altered function of descending inhibitory pain pathways that
terminate in the dorsal root entry zone (DREZ) of the spinal cord.4 Normal
concentrations of opioid peptides and GABA-like substances in the substantia
gelatinosa of the spinal cord may be reduced. Neurons within the spinal cord
that normally carry pain impulses may be subjected to increased facilitation
or reduced inhibition that allows painful stimuli to spread to supra-spinal
Abnormal burst firing from dorsal horn cells rostral to an area of spinal
cord trauma has been demonstrated by Loeser, et al.6 Abnormal electrical
activity of secondary interneurons in the substantia gelatinosa was noted
after deafferentation on experimental animals by Nashold, et al.7 This
uncontrolled repetitive neuronal firing in the spinal cord has been
described as “central neurophysiologic epileptiform activity” by Crue,8
and likened to a convulsive syndrome of the spinal cord by Fibson and White.9 At the cortical level, the existence of a “neuromatrix” has been
described which may act as the substrate of sensory experiences which can be
modified by afferent stimuli or their absence. Cortical memory of body parts
may generate the perception of pain where afferent stimuli are totally
absent after SCI.10
Treatment of Chronic SCI Pain. Chronic SCI pain is central neuropathic pain
that requires centrally directed treatment.8 Treatment options begin with
conservative pharmacological, medical and physical therapies, progress
through neuroablative procedures, and finally utilize narcotics if
warranted. In general, treatment involves attempts to resolve abnormal
central nervous system activity with centrally acting medications or
centrally directed neurosurgical procedures. Although peripherally directed
treatments are not definitive, they may be used to help reduce noxious
stimuli that act as exacerbating factors of central pain.
Chronic SCI pain is often recalcitrant and refractory to non-surgical
procedures.11 Nonetheless, when considering treatment options it is best to
start conservatively and only use more invasive surgical procedures as
dictated by continuing complaints. This approach should be attempted with
all patients, as a small number will experience satisfactory relief
following conservative measures. In addition, it may be psychologically
important for patients to know they have tried all the less “risky”
treatments before proceeding with surgery.
Usually, a multidisciplinary program is needed for effective treatment of
chronic SCI pain. The team usually consists of physicians with experience in
pain management, rehabilitation nursing staff, psychologists, and physical,
occupational, and recreational therapists. An eclectic program incorporating
all the options provided by a comprehensive pain clinic is required to
optimize outcome. Treatment options for chronic SCI pain fall into the
following categories: 1) general health promotion and relief from
exacerbating factors, 2) non-narcotic pharmacologic, 3) physical, 4)
surgical, and 5) narcotic pharmacologic.
General Health Promotion and Relief From Exacerbating Factors.
Rehabilitation physicians and nursing staff provide the care and education
needed to improve the patients general health and reduce factors that
exacerbate chronic SCI pain. The physician is responsible for treating
general medical problems including those complications common to patients
with spinal injuries, such as pulmonary and genitourinary infections,
autonomic hyperreflexia, spasticity, and heterotopic ossification. The
nursing staff assesses the patient’s skin, bowel, and bladder management,
and recommends programs to prevent urinary tract infections, decubiti, and
bladder or bowel distention. Educating the patient in proper self-management
techniques and general health maintenance instills a feeling of well being
and heightened confidence. An improved attitude can reduce stress and
anxiety, and may help to increase levels of natural opiates.
Non-narcotic Pharmacologic Treatment. The most commonly used centrally
acting non-narcotic medications for the treatment of chronic SCI pain
include antidepressants, anticonvulsants, and antipsychotics. There
has been a lack of scientifically designed, controlled, double-blind studies
adequate follow-up that show these medications are consistently reliable in
providing permanent relief of chronic SCI pain. Hence, many pain experts
believe these medications are ineffective in providing pain relief.12
Nevertheless, numerous less rigorous studies suggest patients have
experienced subjective pain reduction when using these medications. They
appear to be especially effective in combination, presumably due to
complimentary mechanisms of action.13 The ease of administration, relative
lack of side effects, and low cost of these medications usually warrant a
trial for efficacy.
Antidepressants. The most commonly used antidepressants for neuropathic
pain, including chronic SCI pain, are tertiary amines. Commonly referred to
as tricyclic antidepressants, these include amitriptyline, nortriptyline,
doxepin, and imipramine.14 The exact mechanism of actual pain relief is
believed to involve interference with the synaptic reuptake of the
neurotransmitters dopamine, norepinephrine, and serotonin. This may reduce
activity in afferent pain pathways with serotonergic synapses, and to make
large quantities of norepinephrine available in the descending pain
inhibitory pathways that terminate in the substantia gelatinosa of the
dorsal spinal cord where hyperexcitable neurons may exist.13, 14
Interestingly, the analgesic benefits of antidepressants do not seem to be
mediated by an antidepressant effect. Atkinson15 notes that maximum pain
relief from antidepressant medications for diabetic neuropathy occurred
within 2 weeks and was achieved at half the drug concentrations usually
required for antidepressant activity. No positive correlation exists between
improving chronic pain symptoms and drug concentration levels. However,
obtaining pain relief at lower serum concentrations decreases the
possibility of adverse effects, which includes sedative, anticholinergic,
orthostative, sexual dysfunction, and weight gain.
Choosing of the most appropriate antidepressant for a particular patient is
largely empirical. Amitriptyline is usually
the first choice for a majority of physicians, but proceeding from there
remains a trial
and error method.
Anticonvulsants. Chronic central neuropathic pain was described earlier as
epileptiform activity of uncontrolled hyperactive neurons, or a convulsive
syndrome of the spinal cord.8,9 If this is the case, then treatment with
anticonvulsants certainly seems appropriate. The 2 most favored
anticonvulsants are carbamazephine and phenytoin. More recently approved by
the FDA, gabapentin (Neurontin), has been gaining wider use for neurogenic
pain with anecdotal clinical success.
The mechanism of action for central pain relief probably involves
stabilizing the threshold of hyperexcitablilty of neurons and inhibiting the
spread of “central neurophysiologic epileptiform” activity in second
order neurons involved in nociception.16 Hitchcock, et al,17 suggest that
activation of inhibitory pain pathways in the central nervous system may
play a role.
Results using single anticonvulsant therapy in SCI pain have been
inconclusive.18 Better results have occurred using a combination therapy of
carbamazepine and an antidepressant.19 Again, efficacy of anticonvulsant
treatment, either alone or in combination with antidepressants, requires
approximately 2 weeks of administration. Adverse reactions may be serious
and routine blood count tests are warranted.
Neuroleptics. The use of neuroleptics
for chronic SCI pain is more limited,20
perhaps due to physicians desire to avoid the devastating side effects of
tardive dyskinesias or neuroleptic malignant syndrome (NMS). Fluphenazine is
the most commonly used for treatment of chronic SCI pain. The exact
mechanism whereby its therapeutic action is exerted is unknown, but
proposals have included an antagonistic effect to dopamine and a
potentiation of antidepressant effects.16,20 Combining fluphenazine with an
antidepressant has been recommended with anecdotal reports of good pain
This combined therapy has demonstrated efficacy in treating postherpetic
neuralgia, which is somewhat analogous to chronic SCI pain.16, 20 Treatment
is best instituted with a low initial dose. As with all medications, the
smallest amount that produces the desired result must be carefully determined.
Physical Treatment. This category involves the treatment of chronic SCI pain
mainly by mechanical and other physical methods. Physicians, physical,
occupational, and recreational therapists provide most of
this type of care. Therapists evaluate and treat the patient for mechanical,
musculoskeletal, and functional problems that can act as exacerbating
factors of chronic SCI pain.
Daily focused range of motion and stretching exercises help reduce
spasticity and prevent joint contractures, adhesive capsulitis, and reflex
sympathetic dystrophy (RSD). Changes in wheelchairs and seating cushions
help prevent decubiti, scoliosis, joint contractures, and inefficient
propulsion. Recreational therapy exposes patients to a variety of
diversional activities of which they may be capable. These are especially
important as resources of modifying pain behavior. In addition, physical
therapists administer various modality treatments, such as transcutaneous
electrical nerve stimulation (TENS), warm and cool modalities.
Although some researchers have found TENS ineffective in relieving pain,22
some success has been reported in treating chronic SCI pain in patients with
TENS, especially those with sensory incomplete injuries.13, 23 This modality
appears to work on the gate control theory of pain proposed by Melzack and
Wall.24 Skin surface electrodes stimulate peripheral sensory input through
large diameter A fibers, activating pain inhibitory interneurons in the
substantia gelatinosa or dorsal root entry zone of the spinal cord. This
sensory input essentially “closes the gate” of the secondary neuron in
pain transmission. Although this may make sense for an intact spinal cord,
it raises theoretical questions about effectiveness in a damaged cord.
Nonetheless, a trial of TENS therapy is often felt justified because of its
possible efficacy, relative lack of adverse side effects, and low cost.
Thermal modalities include superficial warm and cool packs and deep heat
with ultrasound. However, none of these are considered definitive treatment
for permanent relief of pain because of their peripherally directed
mechanism of action, but may reduce other sources of nociceptive input.
Various types of nerve blocks have been tried in treating chronic SCI pain.
Peripheral, epidural, and sympathetic nerve blocks have all been in
effective in treating this type of pain mainly because of their inability to
affect central mechanisms of pain. They can, however, be used as a
diagnostic tool for distinguishing peripheral from central pain. They may
also be used as a therapeutic tool by reducing peripheral noxious stimuli
that can exacerbate central pain.
Dorsal Root Entry Zone Lesions. The zone of dorsal root entry (DREZ) is the
substantia gelatinosa of Rolando, a column of small neurons at the apex of
the dorsal gray horns throughout the length of the spinal cord. The
transmission of messages from peripheral pain receptors is subject to
alteration or “editing” in the substantia gelatinosa. In the uninjured
state, data for pain is received by the substantia gelatinosa from primary
sensory neurons where it may be modified when transferred to secondary pain
neurons or tract cells. In the injured or deafferented state, this modifying
influence is lost, allowing hyperexcitability and abnormal neurochemistry of
secondary pain neurons to develop.7, 25
DREZ surgery is a limited ablative procedure with a high success rate in
relieving chronic SCI pain. The effectiveness of creating a DREZ lesion is
thought to be due to the destruction of these abnormal secondary neurons in
the dorsal horn.7 The surgical procedure involves a laminectomy for exposure
of the spinal cord, direct examination and multiple radio frequency lesions
for destruction of the DREZ. It is common for lesions to be performed
approximately 2 dermatomal levels above and 1 dermatomal level below the
level of injury, which implies the possible loss of several sensory levels.
Since the first DREZ surgery was performed in 1975 at Duke University
Medical Center, hundreds of subsequent procedures
have been performed for deafferentation pain at Craig Hospital and various
other centers. Successful pain relief based on specific neurosurgical
criteria has been reported at approximately 60% to 90%.26,27 Nashold26
reported better success with patients who had pain in dermatomes just caudal
to the level of injury or unilateral pain in comparison to patients with
diffuse or burning pain. Edgar27 initially reported greater success on lower
thoracic level injuries but more recent experience has demonstrated nearly
equal improvement with higher level injuries.
If conservative management has failed to provide a patient with satisfactory
pain relief and other causes of chronic pain have been ruled out,
neurosurgical treatment should be considered. Neurosurgical treatments
consist of neuroablative, and neuroaugmentative procedures. Neuroablative
refers to the surgical production of a neurologic lesion that blocks
afferent nociceptive pathways, whereas neuroaugmentative refers to
procedures that stimulate physiologic activity of pain inhibitory pathways
or the production of naturally occurring analgesic substances, such as
Prior to the development of DREZ surgery, neuroablative procedures usually
failed to relieve chronic SCI pain and frequently produced a higher level of
neurological loss and deafferentation. Examples of these procedures include
sympathectomy, peripheral neurolysis, dorsal rhizotomy, cordectomy,
anterolateral cordotomy, mesencephalotomy, and cingulotomy. Although useful
in other settings, these neuroablative procedures failed to provide
substantial or long lasting relief in SCI. Ineffectiveness was due in part
to their inability to destroy abnormal electrical activity in secondary
interneurons and their connections in the damaged spinal cord, as well as
the post-lesion augmentation of auxiliary nociceptive pathways.
Patients who are at least 1 year past their date of injury and have tried
conservative treatments provided by a comprehensive pain clinic without
success should consider this treatment. Complications of this procedure
include cerebrospinal fluid leaking, loss of motor/sensory functions,
exacerbation of bowel, bladder and sexual dysfunction, and
epidural/subcutaneous hematomas. Persistent pain may be due to thalamic
imprinting from the hyperexcitable secondary pain neurons.
Dorsal Column Stimulation. This is a neuroaugmentative surgical procedure in
which electrodes used to stimulate the dorsal columns of the spinal cord are
implanted epidurally to treat chronic pain. Its proposed mechanism of action
involves blocking ascending pain pathways and stimulating the production and
release of endorphins.28 Theoretically, the electrode leads must be placed
where an intact afferent pathway exists to be effective. Before the 1980’s,
many technical problems plagued this procedure. There was a very high
complication rate of stimulator migration and breakage. Many patients also
reported that the vibratory feeling the stimulators produced in their chest
or abdomen was uncomfortably intense.30
Improved equipment and implantation techniques, including percutaneous
implantation, have reduced the technical problems, but skepticism regarding
the procedure s efficacy in reducing chronic pain remains. The best pain
reduction results have occurred in cases of failed back surgery syndrome (FBSS),
vasculopathic pain, and postherpetic neuralgia.29, 30 At present, it appears
to have limited clinical usefulness in central neuropathic pain.30, 31
Narcotics. Opioid treatment for nonmalignant chronic SCI pain should be
considered as part of a multidisciplinary pain treatment program in those
patients who have not obtained satisfactory relief from either conservative
or surgical treatment. Traditionally, opioid use for chronic nonmalignant
pain was felt to be unacceptable and many physicians and patients alike
reluctant to use such drugs for nonterminal conditions.32,33 This reluctance
stems from fear of side effects that include impaired function and
motivation, the potential for accelerated tolerance, dependency and
addiction, peer criticism, and DEA scrutiny. Consequently, when an opioid is
finally utilized to treat chronic SCI pain, it is usually too little, too
late. Thus, it is important to keep in mind that although these concerns are
legitimate and do warrant a healthy respect for narcotics, an unquestioning
fear of their usage is not justified.
The under utilization of long-term narcotic use for chronic, nonmalignant
pain has been referred to as the “tragedy of needless pain” by Melzack.35 Unfortunately, as with the non-narcotic pharmacologic treatments,
a review of the literature gives no evidence of scientifically designed,
controlled, double blind studies with follow-up demonstrating narcotic
medication as being consistently reliable in providing relief of chronic SCI
pain. Generally, both proponents and opponents of long term opioid use in
central neuropathic pain have submitted anecdotal data in support of their
respective viewpoints. Proponents1 research has suggested that the use of
low dose narcotics can provide pain relief without causing serious side
effects and without needing to continually escalate the dosage.35, 36
Opponents1 research questions the utilization of long term opioids in
treating pain without demonstrable organic pathology, such as neuropathic
central pain.37-39 As the controversy awaits declaration based on future
controlled, prospective, double blind studies, the use of opioid therapy
should not be abandoned.
Methadone is the narcotic of choice for treating chronic SCI pain. It is a
synthetic narcotic analgesic with multiple actions quantitatively similar to
morphine. It is nearly equipotent with parenterally administered
intramuscular morphine. Its relative oral effectiveness is rated as 3 times
that of pentazocine, oxycodone, meperidine, codeine, and morphine.35 The
advantages of oral methadone include a relatively long half-life with
prolonged effectiveness, minimal cognitive dulling as compared to shorter
acting opioids, and relative low cost. Adverse reactions, as with other
are dose-related and include respiratory depression, sedation, constipation,
antidiuretic effect, and reduced libido and/or potency. Interestingly, Foley
and Portenoy36 found no clinically significant side effects in 19 patients
who had undergone years of methadone or oxycodone therapy for nonmalignant
Methadone can produce dependency of the morphine-type and has the potential
for being abused, although only 4% to 9% of all narcotic addicts began using
narcotics as “naive patients” treated for pain.35, 36 Tennant, et al40
noted a 5% iatrogenic addiction rate and 17% drug abuse rate. Morgan and
Penovich41 noted the drug s prolonged effect produces a mild withdrawal or
abstinence syndrome that may pass unnoticed.
Tricyclic antidepressants are frequently used as adjunctive medications to
potentiate narcotic analgesia, perhaps by increasing opiate receptor
sensitivity. Anecdotal reports suggest a synergistic benefit from combining
amitriptyline with a narcotic analgesic for chronic pain relief.15
Before the first dose of methadone a formal contract should be reviewed and
signed by the patient and the prescribing physician. Although each patient’s
treatment program is designed to meet individual needs, certain guidelines
should be standard for all contracts.13, 35, 42
- Patient enrollment in a multi-disciplinary pain treatment program
- Educating the patient in the use of methadone, its potential risks and
- Single physician prescribing responsibility with dispensing limited to a
- Constant monthly visits with careful overall monitoring of the patient
- Intolerance of abuse behavior
- Periodic tapering of drug to assess the patient’s current therapeutic
status and response
Hopefully, participation in a supervised narcotic pain treatment program
will break the pain behavior cycle. If a patient experiences enough physical
and psychological pain relief from narcotics, he or she is more likely to
increase physical activity and participation in other treatments. As general
health, function, and behavior improve, narcotics may be tapered.
Conclusion. Both pain and its relief
are relative and abstract concepts that are influenced by psychological and
environmental factors.11, 43 Therefore, evaluating and quantifying the
benefits of any single or combined treatment is difficult. We know that
treatment is helping when a SCI pain patient states that he is not “hurting”
as much as before. Pain relief is usually accompanied by improvement in both
function and behavior, but these remain subjective and unreliable,
especially in patients with higher levels of SCI. Curing chronic SCI pain is
not always possible, but reducing it is. Any reduction in this type of pain
increases the possibility of greater participation in daily activities,
escape from pain, and improved self-esteem.
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