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Dr Galluzzi is on the speakers bureaus of Eisai, Pfizer Inc, and Purdue Pharma LP.
Address correspondence to Katherine E. Galluzzi, DO, CMD, FACOFP dist, Professor and Chair, Department of Geriatric Medicine, Philadelphia College of Osteopathic Medicine, 4190 City Ave, Suite 315, Philadelphia, PA 19131-1633. E-mail: katherineg{at}pcom.edu
Pain may be the most common reason patients seek treatment from physicians. When persistent and unrelieved, pain can frustrate both the person suffering with this condition and the physician trying to alleviate it. Relief from such discomfort may be particularly difficult to achieve and fraught with misconceptions. Treatment usually requires trials of physical, pharmacologic, and surgical interventions to achieve resolution. In cases that remain insoluble, patients must accept partial relief and seek adaptive strategies.
Sources of persistent pain may be nociceptive or neuropathic. Both utilize the same nerve pathways for transmission, but significant physiologic differences exist in mechanisms through which these painful stimuli are biologically processed and resolved. Nociceptive pain resulting from a known or obvious source (eg, trauma, cancer metastasis, ischemia, arthritis) is often easy to identify. Neuropathic pain, however, may occur in the absence of an identifiable precipitating cause. Physicians must remain alert to differences in presentation and course of neuropathic pain syndromes, some of which may be subtle or unusual.
Bennett3 provided incidence estimates of common types of neuropathic pain and concluded that if neuropathic low back pain is included in the total, approximately 3.8 million individuals in the United States suffer from this disorder. Bowsher 4 calculated that as many as 1 million patients with PHN reside here. Such painful conditions are likely to increase as the population grows older and age-related disorders such as herpes zoster, diabetes mellitus, cerebrovascular accidents, Parkinson disease, and cancer—diseases of aging—develop.
Diabetic peripheral neuropathy, second only to low back pain–associated neuropathy, is estimated to account for 600 cases per 100,000 (Table 1); this disorder is certain to increase as the population of citizens with diabetes mellitus also continues to expand.
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Neuropathic Versus Nociceptive Pain |
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Information regarding intensity, quality, and location of pain is conveyed to the sensory cortex from the somatosensory thalamus. The central nervous system (CNS) utilizes descending inhibitory pathways via the dorsolateral fasciculus (Lissauer's tract) of the spinal cord and periaqueductal gray matter to modulate transmission of nociceptive stimuli.5,6 Namaka et al7 characterize this as a complex equilibrium of pain-signaling and pain-relieving pathways connecting peripheral and central nervous systems.
Efficient, rapid transmission of acute responses to a painful stimulus is a self-protection process. In general, acute pain provides an "alarm" that leads to subsequent protective responses; neuropathic pain, however, signals no imminent danger. The operative difference is that neuropathic pain represents a delayed, ongoing response to damage that is no longer acute but which continues to be expressed as painful sensations.
Sensory neurons damaged by injury, disease, or drugs produce spontaneous discharges leading to sustained levels of excitability. These ectopic discharges begin to "cross talk" with adjacent uninjured nerve fibers, resulting in amplification of pain impulses (peripheral sensitization). This hyperexcitability leads to greater transmitter release causing increased response by spinal cord neurons (central sensitization). This process, known as "windup," accounts for the fact that the level of perceived pain is far greater than what is expected based on what can be observed.8,9
Painful nerve stimulation leads to activation of N-methyl-D-aspartate (NMDA) receptors on postsynaptic membranes in the dorsal horn of the spinal cord. 6(pp207-228) Release of NMDA, a modulating neurotransmitter, is coupled with subsequent release of glutamate, an excitatory neurotransmitter. The resultant extended depolarization (influx of calcium and sodium and efflux of potassium) produces much larger than usual postsynaptic potentials, known as synaptic potentiation. Spinal windup has been described as "continuous increased excitability of central neuronal membranes with persistent potentiation."9,10 Neurons of peripheral and central nervous systems continue to transmit pain signals beyond an original injury, thus activating an ongoing, continuous central pain response (Figure 1). Devor et al11 presented evidence showing that damaged sensory fibers have a higher concentration of sodium channels, an alteration that would increase spontaneous firing.
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Characterization of Neuropathic Pain |
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Several types of abnormal sensations, or dysesthesias, may occur alone or in addition to other specific complaints in patients with neuropathic pain (Table 2). Unlike usual responses to such discomfort, these irritating or painful sensations occur in the absence of an apparent cause. A common example is the severe, aching, "toothache-like" response elicited by a cool draft of air on the cheek of a patient suffering from trigeminal neuralgia.
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Allodynia is a painful response to an otherwise benign stimulus. Taken to the extreme (eg, inability to remove the stimulus), this response can result in an agonizing neuropathic symptom known as hyperpathia. Another example of this condition is "touch sensitivity" of badly sunburned skin, where even light stroking of an inflamed area causes extreme discomfort; like neuropathic pain, this response seems out of proportion to the injury.
Pharmacologic induction of local anesthesia or hypoesthesia by lidocaine or transdermal fentanyl produces a predictable duration of action; this is not the case with neuropathic-induced anesthesia or hypoesthesia. The discomfort of one's foot "falling asleep" is a common paresthesia. That uncomfortable sensation is self-limiting and resolves spontaneously, unlike the continuous, self-perpetuating, and annoying sensation of pins and needles caused by neuropathic pain.
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Pain Scales for Assessing Neuropathic Pain |
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Examples of standardized scales used for pain assessment include:
One of the most widely used current evaluations is the 0-10 rating where "0" means "I have no pain" and "10" is "the worst pain I ever had." Investigators for the Shingles Prevention Trial devised a specific pain assessment tool for calculating a herpes zoster severity-of-illness score, the Zoster Brief Pain Inventory in which patients are asked questions to rate their pain and also are able to shade areas on a diagram to indicate the parts of their bodies that were most affected.21
These scales underscore the fact that it may be difficult for clinicians to assess or rate a patient's pain because the level of perceived discomfort may be much greater than what is observable. Pain scales provide useful, standardized, and validated tools for charting an individual's response to a pain-control intervention. In addition, detailed documentation utilizing accepted pain scales to assess a patient's level of discomfort provides protection from legal challenges regarding any prescribed pharmacotherapy.
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Treatment of Patients With Neuropathic Pain |
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Medications used to treat neuropathic pain include over-the-counter analgesics, anticonvulsants, tricyclic antidepressants (TCAs), and selective serotonin-norepinephrine reuptake inhibitors (SSNRIs), topical anesthetic agents, nonsteroidal anti-inflammatory drugs (NSAIDs), antiarrhythmics, non-narcotic analgesics, and opioids2,4,7 (Figure 2). This varied armamentarium reflects heterogeneity in this patient group and the different pathophysiologic mechanisms postulated to produce neuropathic pain. Seven agents (Figure 3) should be avoided (never used) in the treatment of patients with DPN.
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Recently, Hansson and Dickenson25 noted that treatment of patients with neuropathy may be based on "shared commonalities despite multiple etiologies." They concluded their review by stating that because there is little information on drugs affecting specific pain symptoms and no clear rationale for their use, treatment trials are warranted.25 This conclusion supports use of empiricism in selection of a treatment regimen for neuropathic pain.
Numerous treatment algorithms list trials of common analgesics such as ibuprofen or acetaminophen, topical treatment such as capsaicin cream or lidocaine patches, TCAs or other antidepressants (eg, amitriptyline hydrochloride, desipramine hydrochloride), and anticonvulsants (eg, carbamazepine, gabapentin, pregabalin, lamotrigine) as first-line therapy for neuropathic pain.5,7,9 These medications may be used alone or in combination. An example of clinical use of combination therapies is the pratice of initiating a neuroactive agent such as gabapentin concomitant with opioid analgesic (eg, oxycodone hydrochloride) for treatment of patient with postherpetic neuralgia. The choice of pharmacotherapy should be directed toward the type of painful symptom described.
Commonalities in presentation may influence the clinician's choice of pain medication. For example, PHN and DPN may produce spasms, burning, and tingling characteristic of neuronal hyperexcitability. Nervous system excitability can produce seizure activity. Thus, anticonvulsants are used with reasonable efficacy to treat patients with neuropathic pain.7,8
Anticonvulsants
Neuropathic pain sufferers may respond to gabapentin, which is structurally
related to 
-aminobutyric acid (GABA), a pain-modulating
neurotransmitter. Gabapentin readily crosses the blood-brain barrier and has
been studied for treatment of patients with DPN; pain relief efficacy was
similar to that of TCAs except for a shorter onset of action. In a study of
gabapentin as monotherapy, Backonja et
al23 noted that
relatively high doses were needed (3600 mg/d was the forced maximum dose, ie,
the target maximum dose). Higher doses, however, limited upward titration
because of adverse effects, most common being dizziness and somnolence; weight
gain, nausea, abdominal pain, asthenia, and other symptoms were also
reported.
Pregabalin is a member of the gabapentinoid family that binds to
-2-
subunit of the voltage-gated calcium channel with
a higher binding affinity than
gabapentin.26
Several studies have shown favorable effects in patients with painful diabetic
neuropathy, and dose titration may be easier for pregabalin. The European
Federation of Neurological Societies (EFNS) Task Force guidelines on
pharmacologic treatment of patients with neuropathic pain note that titration
with gabapentin should be slow and individualized with initial dosages of 300
mg/d (less in geriatric patients); pregabalin titration can occur more rapidly
and has a shorter onset of action (<1
week).27
Additionally, pregabalin may be dosed twice a day, whereas gabapentin must be
taken three times daily.
Recently, pregabalin received US Food and Drug Administration (FDA) approval for treatment of patients with pain due to fibromyalgia, which is considered to be another centrally mediated pain syndrome. In a 14-week, randomized double-blind placebo-controlled trial, patients received pregabalin twice daily in doses ranging from 300 mg to 600 mg.28 Clinically significant reductions in pain scores were noted as early as week one, and efficacy was also shown for improvement in global assessment, functional status and sleep, compared with placebo.28
Other anticonvulsants have been used for both PHN and DPN; eg, patients with trigeminal neuralgia have been treated for decades with carbamazepine, a sodium-channel blocker. Oxcarbazepine, a successor to carbamazepine, has shown limited efficacy in clinical trials and will not be marketed in the United States, though the EFNS guidelines support its use at initially low doses with slow upward titration and careful monitoring for hyponatremia.22,27
A study of divalproex sodium for PHN noted subjective improvement in the treatment group compared with the group receiving placebo and found clinically significant adverse effects in only one patient.29 Trials of other anticonvulants (eg, lamotrigine) may be indicated in patients with neuropathic pain refractory to alternatives. To minimize the occurrence of rash (a major adverse effect), lamotrigine must be titrated very slowly and should not be used in combination with valproate.27
Topical Anesthetic Agents
Patients with PHN or other localized regions of peripheral neuropathy may
respond well to topical 5% lidocaine patches, especially if the region of pain
is relatively small and circumscribed. Studies have demonstrated efficacy of
topical lidocaine either as monotherapy or in combination with oral agents
used to treat patients with neuropathic pain; it was safe, easily
administered, and had minimal side
effects.30,31
Capsaicin cream has also been used effectively in patients with PHN but must
be carefully applied because of its powerful irritating effects (which are
related to the degree of subsequent analgesia).
Antidepressants
Tricyclic antidepressants have been used for treatment of patients with DPN
since the 1970s. These agents have documented pain-control
efficacy32 but are
limited by a slow onset of action (analgesia in days to weeks),
anticholinergic side effects (eg, dry mouth, blurred vision,
confusion/sedation, and urinary retention), and potential cardiac toxicity.
Amitriptyline hydrochloride is the most extensively studied at oral doses of
10 mg to 25 mg at bedtime. This dose can be slowly titrated with escalating
amounts every 4 to 7 days. Frail and elderly patients may be unable to
tolerate therapeutic doses of amitriptyline because of sedation. Desipramine
hydrochloride and nortriptyline are less-sedating alternatives to
amitriptyline; plasma drug levels are available for the latter.
The advent of selective serotonin reuptake inhibitors (SSRIs) gave hope that they could be used for chronic pain without the concerns of cardiotoxicity and anticholinergic adverse effects. However, pain control results have been disappointing; they may be useful adjuncts to treat patients who have pain with depression when TCAs are contraindicated. Duloxetine hydrochloride and venlafaxine hydrochloride are SSNRIs that have received FDA approval for the PHN indication.
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Antiarrythmics
Neuronal hyperexcitability resulting from nerve damage may respond to
therapy with antiarrythmic medications. A randomized trial of amitriptyline
and mexiletine in a group of patients with painful distal sensory neuropathy
due to HIV infection showed that dosages of amitriptyline hydrochloride up to
100 mg/d and mexiletine hydrochloride up to 60 mg/d were generally well
tolerated.33
However, there was no evidence of significant pain relief for this
indication.
Anti-Inflammatory Agents
The usefulness of NSAIDs such as aspirin and ibuprofen for neuropathic pain
is limited. Use of NSAIDs for DPN should be discouraged because of the adverse
effects of these drugs on renal function. Selective cyclooxygenase-2 (COX-2)
inhibitors have been under scrutiny for adverse cardiovascular events, and
rofecoxib has lost FDA approval. Celecoxib, the remaining agent, cannot be
recommended for the long-term administration needed to treat patients with
neuropathic pain syndromes.
Opioid Analgesics
In response to severe or persistent pain, interneurons in the dorsal horn
release endogenous opioids that reduce perceived pain. These endogenous
substances (enkephalins, endorphins, and dynorphins) play a major role in
mechanisms of pain reduction and modulation by preventing transmission of pain
signals to higher centers. Exogenously administered opioids mimic physiologic
effects of enkephalin and dynorphin at µ-type opioid receptors, which occur
throughout the brain and spinal
cord.6(pp207-228)
This mechanism accounts for opioid efficacy in neuropathic pain syndromes.
Tramadol, a semisynthetic opioid analgesic, may also affect neuropathic pain by low-affinity binding to µ receptors as well as weak inhibition of norepinephrine and serotonin reuptake, mirroring mechanism of actions of both opioids (former action) and TCAs (latter effect). One trial suggests that tramadol may be better tolerated than TCAs in some individuals with DPN or other neuropathic pain syndromes.34
Because of concerns about tolerance, abuse, and addiction, prescribing opioids for nonmalignant pain was formerly considered controversial. In recent years, however, much research has supported use of these agents. Opioids are now commonly and effectively prescribed to treat patients for neuropathic pain.7,24,32,35,36
A double-blind, dose-response study reported in 2003 used levorphanol tartrate (3 mg equivalent to 45 mg to 90 mg of oral morphine sulfate or 30 mg to 45 mg of oral oxycodone hydrochloride) and showed a 48% overall reduction in pain and moderate or better pain relief in 66% of patients.35 These researchers noted that higher doses are more effective in reducing the intensity of chronic neuropathic pain. They also demonstrated that tolerance was not a clinically significant problem as only 4 (9%) of the 43 patients in the high-strength group ever reached the maximal allowed dose. Further, they noted no addictive behavior.35
Raja et al32 studied pain intensity, pain relief, cognitive and physical functioning, sleep, mood, side effects, and treatment preference in a group of patients with PHN. They compared responses to TCA therapy with those to opioids, noting that both agents act via independent mechanisms and varied individual effects. This investigation observed that patients who completed all three treatments (including placebo) preferred opioids to TCAs; it was concluded that opioids effectively treat patients with PHN without impairment of cognition.32
NMDA-Receptor Antagonists
Nerve injury results in upregulation of NMDA receptors through repeated
firing of peripheral afferent fibers and release of glutamate. This results in
greater-than-expected peripheral
pain.6(pp207-228)
NMDA-receptor blockers have been studied for their efficacy in chronic pain.
Currently available agents include dextromethorphan hydrobromide, memantine
hydrochloride, and
ketamine.10,37
NMDA receptors have been studied for their role in opioid tolerance. Adjuvant use of ketamine may reduce morphine requirements and cause improvement in analgesia, as noted in case reports by Bell.38 A larger study showed that ketamine improves morphine analgesia in difficult pain syndromes (neuropathic pain caused by cancer); however, adverse CNS effects such as psychomimetic effects were noted.39 The authors state that future studies must address treatments to prevent or reduce these adverse central effects of ketamine.
| Patient Perspectives on
Pain In preparing to write this overview of neuropathic pain, the author initiated conversations with several of her patients to elicit descriptions of how their individual pain symptoms feel and how it has affected their lives. Their responses follow.
"You know, you'd have to have a complete injury not to feel pain. Not all quads and paras have complete injuries; we do have pain. The worst pain kind of starts like a pressure, like from an overworked muscle. Then it progresses into a burning, like a heat you can't make stop. It gets to the point where—honestly, doc—you don't want to live anymore. "You know, you get a few days of bad weather and the pain starts up, and you're stuck in bed 3 or 4 days, it's rough. "I haven't had a full night's sleep since 1997. [Motor vehicle accident in 1997 caused spinal cord injury.] "Don't forget to tell your readers that chronic pain destroys relationships. It can destroy friendships and social life. Friends call to ask me to go down the shore and sit on the beach; I can't do that! Fifteen minutes in the car and I have to turn around and go back so I can lie down." [Patient has symptoms of autonomic dysfunction, such as sweating and tachycardia, that are the cause.]
"The pain in my hands is so bad sometimes, it feels like my hands are stuffed too tightly into the skin and they are going to explode. It keeps me awake at night. And my feet don't feel like feet. Half the time they are numb blocks, and the other half they're burning. "My family is going to Europe this summer, and I decided to stay home. I just can't sit that long on a plane without being in extreme pain. "I guess you can tell that my mood is affected by this." [Nonetheless, this patient refuses antidepressant therapy on the grounds that he already takes too many medications.]
"I know you doctors try to help us, but you can't know how it feels. When I try to move sometimes, it's like someone is jabbing me with a hot poker. My muscles jump, and it feels like the nerves are being shocked. You know, this is just miserable. "I hate to let my daughter see me when I'm in pain, because I look and feel like a witch. I think it scares her, and that's why she doesn't come to visit me very often. I miss being able to watch her grow up." [The patient has lived in a nursing facility for more than 10 years; she is wheelchair bound and unable to perform self-care.]
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Cannabinoids
Administration of cannabinoids for central neuropathic pain is not approved
by the FDA. However, several European studies exploring their use in patients
with chronic pain indicated efficacy in patients with multiple sclerosis in
treatment of spasticity and pain, and have shown decreases in allodynia or
hyperalgesia in various animal models.
A Danish study tested use of synthetic -9-tetrahydrocannabinol
(dronabinol) and showed a modest but clinically relevant effect on central
pain in patients with multiple
sclerosis.40
Central, neuropathic pain in patients with multiple sclerosis was also studied
using a whole plant cannabis–based medicine containing
-9-tetrahydrocannabinol and cannabidiol (CBM). This investigation
documented reductions in pain using a visual analog scale and increases in
quality of life measures such as sleep. Although treatment group subjects
reported more side effects than those in the nontreatment group, it was
concluded that CBM was effective in reducing pain and sleep disturbance in
patients with multiple sclerosis–related central
pain.40
Combined Analgesic Therapy
Clinical experience supports the use of more than one agent for patients
with refractory neuropathic pain. Because physiologic mechanisms causing pain
can be different, use of more than one type of medication may be necessary.
Monotherapy may be desirable for both ease of administration and reduction of
potential side effects, but this approach may not achieve satisfactory pain
relief. A strategy of using two or more agents with different mechanims of
action at lower doses to achieve synergistic pain efficacy is not uncommon.
Several studies have evaluated effectiveness of this
strategy.32,33,41
Gilron et al41 used a four-period crossover trial to assess efficacy of morphine and gabapentin alone, these drugs in combination, and active placebo (in the form of low-dose lorazepam). They concluded that gabapentin substantially enhanced morphine efficacy (P=.03), and suggested that further studies of combination drug trials are warranted.
Osteopathic physicians are trained to treat the whole person, and, with this goal in mind, it must be remembered that side effects of medications may pose limitations to their use. Skillful and judicious use of adjuvants, here defined as any agent that enables the use of a primary medication to its full dose potential, is mandated. An obvious example of this practice is the customary use of laxatives in combination with opioids.
Other Treatment Modalities
Osteopathic manipulative treatment (OMT) should be offered to all patients
with neuropathic or other chronic pain syndromes as primary or adjunctive
therapy, or both (Figure
4) Myofascial trigger point release for carpal or
tarsal tunnel syndrome pain is an example of an effective primary technique.
Indirect or passive myofascial techniques may be used to address all regions
of tissue texture change. Adjunctively, educating patients with neuropathic
pain about the importance of postural influence and functional movement can
enhance their sense of well-being and maintain or improve physical
functioning. Prescribing flexion/stretching exercises for neuropathic low back
pain assures that patients maintain active range of motion and ambulatory
function. (See
http://www.spinalinjuryfoundation.org/101_new/williams.htm
and
http://www.catmanor.com/moonbeam/back/flexion.html.)
As previously noted, drug treatment of patients with neuropathic pain lacks a standardized rationale and relies on clinical empiricism. Despite best efforts at treatment trials, some patients may continue to suffer. In these cases, referral to pain specialists is essential. Surgical interventions such as motor cortex stimulation,42 transcutaneous electrical nerve stimulation (TENS) units, and other peripheral stimulation43 have been shown to be helpful in patients with pain refractory to pharmacotherapy.
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Prophylaxis |
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A large prospective, randomized placebo-controlled double-blind study was recently completed by the Shingles Prevention Study Group.21 This investigation included 38,546 adults aged 60 years or older and used a highly potent zoster vaccine (several times the concentration of that used for primary vaccination against chickenpox in children). Vaccine recipients showed reduced burden of illness (incidence and severity) by greater than half (61.1%; P<.001). The incidence of herpes zoster was reduced by 51.3%, and, most significantly, incidence of PHN was reduced by 66.5% (P<.001). These authors suggest that decreases in PHN morbidity more than adequately offset costs of large-scale immunization of individuals aged 60 years or older.21 This vaccine was approved by the FDA in May 2006.
The Advisory Committee on Immunization
Practices44
currently recommends immunization with the zoster vaccine, live for all
individuals aged 60 or older who have not had herpes zoster. Contraindications
to vaccine administration include history of anaphylactic reaction to any
product component, serious current illness (or temperature 
38.5° C
[101.3°F]), immunodeficiency states (eg, lymphoma, leukemia, or malignant
neoplasm affecting the bone marrow or lymphatic system), AIDS or other
clinical manifestations of HIV, immunosuppressive therapy including high-dose
corticosteroids, untreated tuberculosis, or patients who may be pregnant.
Following is an anecdotal description of a patient who is typically seen in primary care with the chief complaint of pain.
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Case Presentation |
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Patient Approach and Considerations |
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Of the following options, which is the most appropriate initial treatment strategy for the patient at this visit?
The best plan for adjunctive therapy for this patient will include
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Discussion |
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Long-acting opioid analgesia may be helpful in patients in whom other modalities have proven unsuccessful. Long-acting agents are best initiated only in patients who have had their dosage requirement carefully titrated using short-acting "immediate release" agents. In such patients, a long-acting/split-dose regimen with short-acting "breakthrough" doses as needed may be beneficial.
Pregabalin has shown efficacy in controlling diabetic peripheral neuropathic pain, is easily administered in twice-daily doses, and does not require protracted up-titration schedule. Thus, it is a good first choice. An alternative would be an SSNRI (duloxetine or venlafaxine) to address the painful symptoms and possibly improve mood, sleep, and general quality of life. The SSNRI could be initiated as monotherapy, or adjunctive to other pain medication that Harry is using.
Osteopathic physicians are trained and motivated to treat the whole patient. The holistic approach to Harry would include referrals to other appropriate disciplines such as psychology or physical therapy, pain specialists, and endocrinologists as indicated. Osteopathic manipulative treatment, especially myofascial release technique, remains a mainstay as valuable adjunctive treatment to improve Harry's range of motion, muscle relaxation, ambulation, and sense of well-being.
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Comment |
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References |
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From a 34-year-old man with T10 paraplegia: