Chronic pain medical treatment guidelines
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- Biopsychosocial model of chronic pain
- Boswellia Serrata Resin (Frankincense) [DWC] Boswellia Serrata Resin (Frankincense) is not recommended for chronic pain. Botulinum toxin (Botox ®; Myobloc® )
- Bretylium See Biers block. Buprenorphine
- Capsaicin, topical [ODG]
- Carbamazepine (Tegretol®) See Anti-epilepsy drugs (AEDs) for general guidelines, as well as specific Carbamazepine listing. Carisoprodol (Soma®)
- Catapres® (Clonidine) See Clonidine, intrathecal. Celebrex®
- Cesamet® See Nabilone Chiropractic treatment See Manual therapy manipulation . Chondroitin sulfate
- Predictors of success and failure
Benzodiazepines Not recommended for long-term use because long-term efficacy is unproven and there is a risk of dependence. Most guidelines limit use to 4 weeks. Their range of action includes sedative/hypnotic, anxiolytic, anticonvulsant, and muscle relaxant. Chronic benzodiazepines are the treatment of choice in very few conditions. Tolerance to hypnotic effects develops rapidly. Tolerance to anxiolytic effects occurs within months and long-term use may actually increase anxiety. A more appropriate treatment for anxiety disorder is an antidepressant. Tolerance to anticonvulsant and muscle relaxant effects occurs within weeks. (Baillargeon, 2003) (Ashton, 2005) Bier's block Recommended as an option with bretylium for severe CRPS. Due to modest benefits and the invasiveness of the therapy, intravenous regional sympathetic block (Bier's block) with bretylium should be offered only after careful counseling, and should be followed by intensive physical therapy. For more information and references, see Regional sympathetic blocks; & CRPS, sympathetic and epidural blocks. Although there is very limited scientific evidence to support this treatment, it is recommended as an option in certain cases when there are no other alternatives. When the procedure is performed, it must be done in conjunction with a rehabilitation program. Any additional blocks must be based on objective evidence of improvement. Biofeedback Not recommended as a stand-alone treatment, but recommended as an option in a cognitive behavioral therapy (CBT) program to facilitate exercise therapy and return to activity. There is fairly good evidence that biofeedback helps in back muscle strengthening, but evidence is insufficient to demonstrate the effectiveness of biofeedback for treatment of chronic pain. Biofeedback may be approved if it facilitates entry into a CBT treatment program, where there is strong evidence of success. As with yoga, since outcomes from biofeedback are very dependent on the highly motivated self-disciplined patient, we recommend approval only when requested by such a patient, but not adoption for use by any patient. EMG biofeedback may be used as part of a behavioral treatment program, with the assumption that the ability to reduce muscle tension will be improved through feedback of data regarding degree of muscle tension to the subject. The potential benefits of biofeedback include pain reduction because the patient may gain a feeling that he is in control and pain is a manageable symptom. Biofeedback techniques are likely to use surface EMG feedback so the patient learns to control the degree of muscle contraction. The available evidence does not clearly show whether biofeedback's effects exceed nonspecific placebo effects. It is also unclear whether biofeedback adds to the effectiveness of relaxation training alone. The application of biofeedback to patients with CRPS is not well researched. However, based on CRPS symptomology, temperature or skin conductance feedback modalities may be of particular interest. (Keefe, 1981) (Nouwen, 1983) (Bush, 1985) (Croce, 1986) (Stuckey, 1986) (Asfour, 1990) (Altmaier, 1992) (Flor, 1993) (Newton-John, 1995) (Spence, 1995) (Vlaeyen, 1995) (NIH-JAMA, 1996) (van Tulder, 1997) (Buckelew, 1998) (Hasenbring, 1999) (Dursun, 2001) (van Santen, 2002) (Astin, 2002) (State, 2002) (BlueCross BlueShield, 2004) This recent report on 11 chronic whiplash patients found that, after 4 weeks of myofeedback training, there was a trend for decreased disability in 36% of the patients. The authors recommended a randomized-controlled trial to further explore the effects of myofeedback training. (Voerman, 2006). See also Cognitive behavioral therapy (Psychological treatment). ODG Screen for patients with risk factors for delayed recovery, as well as motivation to comply with a treatment regimen that requires self-discipline. Initial therapy for these “at risk” patients should be physical Possibly consider biofeedback referral in conjunction with CBT after 4 weeks: - Initial trial of 3-4 psychotherapy visits over 2 weeks - With evidence of objective functional improvement, total of up to 6-10 visits over 5-6 weeks (individual sessions) - Patients may continue biofeedback exercises at home Biopsychosocial model of chronic pain See Chronic pain programs (functional restoration programs), which are recommended where there is access to programs with proven successful outcomes, for patients with conditions that put them at risk of delayed recovery, including the detailed "Criteria for use of multidisciplinary pain management programs" highlighted in blue. These treatment programs are based on the biopsychosocial model, one that views pain and disability in terms of the interaction between physiological, psychological and social factors. Bisphosphonates Recommend treatment of bone resorption with bisphosphonate-type compounds as an option for patients with CRPS Type I. Not recommended for other chronic pain conditions. Signifcant improvement has been found in limited studies of intravenous clodronate and intravenous alendronate. Alendronate (Fosamax®) given in oral doses of 40 mg a day (over an 8 week period) produced improvements in pain, pressure tolerance and joint moblity. The effects may potentially involve avenues other than inhibition of bone resorption. (Manicourt, 2004) See also CRPS, medications. Bisphosphonates are a class of drugs that inhibit osteoclast action and the resorption of bone. Alendronate (Fosamax®) is in this class. Boswellia Serrata Resin (Frankincense) [DWC] Boswellia Serrata Resin (Frankincense) is not recommended for chronic pain. Botulinum toxin (Botox®; Myobloc®) Not generally recommended for chronic pain disorders, but recommended for cervical dystonia. See more details below. Not recommended for the following: tension-type headache; migraine headache; fibromyositis; Several recent studies have found no statistical support for the use of Botulinum toxin A (BTX-A) for any of the following: - The evidence is mixed for migraine headaches. This RCT found that both botulinum toxin type A (BoNTA) and divalproex sodium (DVPX) significantly reduced disability associated with migraine, and BoNTA had a favorable tolerability profile compared with DVPX. (Blumenfeld, 2008) In this RCT of episodic migraine patients, low-dose injections of BoNTA into the frontal, temporal, and/or glabellar muscle regions were not more effective than placebo. (Saper, 2007) Botulinum neurotoxin is probably ineffective in episodic migraine and chronic tension-type headache (Level B). (Naumann, 2008) - Myofascial analgesic pain relief as compared to saline. (Qerama, 2006) - Use as a specific treatment for myofascial cervical pain as compared to saline. (Ojala, 2006) (Ferrante, 2005) (Wheeler, 1998) - Injection in myofascial trigger points as compared to dry needling or local anesthetic injections. (Kamanli, 2005) (Graboski, 2005). Recent systematic reviews have stated that current evidence does not support the use of BTX-A trigger point injections for myofascial pain. (Ho, 2006) Or for mechanical neck disease (as compared to saline). (Peloso-Cochrane, 2006) Recommended: cervical dystonia, a condition that is not generally related to workers’ compensation injuries (also known as spasmodic torticolis), and is characterized as a movement disorder of the nuchal muscles, characterized by tremor or by tonic posturing of the head in a rotated, twisted, or abnormally flexed or extended position or some combination of these positions. When treated with BTX-B, high antigenicity limits long-term efficacy. Botulinum toxin A injections provide more objective and subjective benefit than trihexyphenidyl or other anticholinergic drugs to patients with cervical dystonia. Recommended: chronic low back pain, if a favorable initial response predicts subsequent responsiveness, as an option in conjunction with a functional restoration program. Some additional new data suggests that it may be effective for low back pain. (Jabbari, 2006) (Ney, 2006) Botulinum neurotoxin may be considered for low back pain (Level C). (Naumann, 2008) Bretylium See Bier's block. Buprenorphine Recommended for treatment of opiate addiction. Also recommended as an option for chronic pain, especially after detoxification in patients who have a history of opiate addiction (see below for specific recommendations). A schedule-III controlled substance, buprenorphine is a partial agonist at the mu-receptor (the classic morphine receptor) and an antagonist at the kappa-receptor (the receptor that is thought to produce alterations in the perception of pain, including emotional response). In recent years, buprenorphine has been introduced in most European countries as a transdermal formulation ("patch") for the treatment of chronic pain. Proposed advantages in terms of pain control include the following: (1) No analgesic ceiling; (2) A good safety profile (especially in regard to respiratory depression); (3) Decreased abuse potential; (4) Ability to suppress opioid withdrawal; & (5) An apparent antihyperalgesic effect (partially due to the effect at the kappa-receptor). (Kress, 2008) (Heit, 2008) (Johnson, 2005) (Landau, 2007) Available formulations: Buprenorphine hydrochloride: Buprenex®: Supplied as an injection solution; Subutex®: Supplied as a sublingual tablet in 2 daily dosage strengths (2 mg or 8 mg). Buprenorphine hydrochloride and naloxone hydrochloride: Suboxone®: Also supplied as a sublingual tablet in 2 dosage strengths (2/0.5 mg or 8/2 mg). Developed to have a lower intravenous (IV) misuse potential. When injected IV, naloxone is intended to cause withdrawal effects in individuals who are opiate-dependent, and to prevent the “high-effect” related to opioids such as euphoria. Pharmacokinetics: After sublingual administration the onset of effect occurs in 30 to 60 minutes. Peak blood levels are found at 90 to 100 minutes, followed by a rapid decline until 6 hours, and then a gradual decline over more than 24 hours. (Helm, 2008) (Koppert, 2005) Indications: Treatment of opiate agonist dependence (FDA Approved indication includes sublingual Subutex® and Suboxone®): Recommended. When used for treatment of opiate dependence, clinicians must be in compliance with the Drug Addiction Treatment Act of 2000. (SAMHSA, 2008) Buprenorphine’s pharmacological and safety profile makes it an attractive treatment for patients addicted to opioids. Buprenorphine’s usefulness stems from its unique pharmacological and safety profile, which encourages treatment adherence and reduces the possibilities for both abuse and overdose. Studies have shown that buprenorphine is more effective than placebo and is equally as effective as moderate doses of methadone in opioid maintenance therapy. Few studies have been reported on the efficacy of buprenorphine for completely withdrawing patients from opioids. In general, the results of studies of medically assisted withdrawal using opioids (e.g., methadone) have shown poor outcomes. Buprenorphine, however, is known to cause a milder withdrawal syndrome compared to methadone and for this reason may be the better choice if opioid withdrawal therapy is elected. (McNicholas, 2004) (Helm, 2008) Bupropion (Wellbutrin®) Recommended as an option after other agents. While bupropion has shown some efficacy in neuropathic pain there is no evidence of efficacy in patients with non-neuropathic chronic low back pain. Furthermore, bupropion is generally a third-line medication for diabetic neuropathy and may be considered when patients have not had a response to a tricyclic or SNRI. See Antidepressants for Calcitonin Recommended as a treatment option for patients with CRPS Type I with a contraindication for treatment of bone resorption with a bisphosphonate. Not recommended for other chronic pain conditions. Signifcant improvement has been found in limited studies of intravenous clodronate and intravenous alendronate. Alendronate (Fosamax®) given in oral doses of 40 mg a day (over an 8 week period) produced improvements in pain, pressure tolerance and joint moblity. (Manicourt, 2004) Mixed results have been found with intranasal calcitonin (Miacalcin®). (Sahin, 2005) (Appelboom, 2002) (Rowbathan, 2006) (Sharma, 2006) See also CRPS, medications. Calcitonin is a hormone known to participate in calcium and phosphorus metabolism. Cannabinoids Not recommended. In total, 11 states have approved the use of medical marijuana for the treatment of chronic pain, but there are no quality controlled clinical data with cannabinoids. Restricted legal access to Schedule I drugs, such as marijuana, tends to hamper research in this area. It is also very hard to do controlled studies with a drug that is psychoactive because it is hard to blind these effects. At this time it is difficult to justify advising patients to smoke street-grade marijuana, presuming that they will experience benefit, when they may also be harmed. (Mackie, 2007) (Moskowitz, 2007) One of the first dose-response studies of cannabis in humans has found a window of efficacy within which healthy volunteers experienced relief from experimentally induced pain. But although mid-range doses provided some pain relief, high doses appeared to exacerbate pain. (Wallace, 2007) Results of a double-blind crossover study suggest that smoked cannabis may reduce pain intensity for patients with neuropathic pain, although the Food and Drug Administration (FDA), Substance Abuse and Mental Health Services Administration (SAMHSA), and the National Institute for Drug Abuse (NIDA) report that no sound scientific studies support the medicinal use of cannabis. Psychoactive effects were also seen, including feeling high, although these were less apparent at the lower dose. Of more concern, were effects on cognitive performance, which in this chronic pain population was at or below the threshold for impairment already at baseline. Cannabis use was associated with modest declines in cognitive performance, particularly learning and recall, especially at higher doses. The finding necessitates caution in the prescribing of medical marijuana for neuropathic pain, especially in instances in which learning and memory are integral to a patient's work and lifestyle. (Wilsey, 2008) Capsaicin, topical Recommended only as an option in patients who have not responded or are intolerant to other treatments. Formulations: Capsaicin is generally available as a 0.025% formulation (as a treatment for osteoarthritis) and a 0.075% formulation (primarily studied for post-herpetic neuralgia, diabetic neuropathy and post-mastectomy pain). There have been no studies of a 0.0375% formulation of capsaicin and there is no current indication that this increase over a 0.025% formulation would provide any further efficacy. Indications: There are positive randomized studies with capsaicin cream in patients with osteoarthritis, fibromyalgia, and chronic non-specific back pain, but it should be considered experimental in very high doses. Although topical capsaicin has moderate to poor efficacy, it may be particularly useful (alone or in conjunction with other modalities) in patients whose pain has not been controlled successfully with conventional therapy. The number needed to treat in musculoskeletal conditions was 8.1. The number needed to treat for neuropathic conditions was 5.7. (Robbins, 2000) (Keitel, 2001) (Mason-BMJ, 2004) Mechanism of action: Capsaicin, which is derived from chili peppers, causes vasodilation, itching, and burning when applied to the skin. These actions are attributed to binding with nociceptors, which causes a period of enhanced sensitivity followed by a refractory period of reduced sensitivity. Topical capsaicin is superior to placebo in relieving chronic neuropathic and musculoskeletal pain. Capsaicin produces highly selective regional anesthesia by causing degeneration of capsaicin-sensitive nociceptive nerve endings, which can produce significant and long lasting increases in nociceptive thresholds. (Maroon, 2006) Adverse reactions: Local adverse reactions were common (one out of three patients) but seldom serious (burning, stinging, erythema). Coughing has also been reported. . See also CRPS, medications; Topical analgesics. Carbamazepine (Tegretol®) See Anti-epilepsy drugs (AEDs) for general guidelines, as well as specific Carbamazepine listing. Carisoprodol (Soma®) Not recommended. This medication is not indicated for long-term use. Carisoprodol is a commonly prescribed, centrally acting skeletal muscle relaxant whose primary active metabolite is meprobamate (a schedule-IV controlled substance). Carisoprodol is now scheduled in several states but not on a federal level. It has been suggested that the main effect is due to generalized sedation and treatment of anxiety. Abuse has been noted for sedative and relaxant effects. In regular abusers the main concern is the accumulation of meprobamate. Carisoprodol abuse has also been noted in order to augment or alter effects of other drugs. This includes the following: (1) increasing sedation of benzodiazepines or alcohol; (2) use to prevent side effects of cocaine; (3) use with tramadol to produce relaxation and euphoria; (4) as a combination with hydrocodone, an effect that some abusers claim is similar to heroin (referred to as a “Las Vegas Cocktail”); & (5) as a combination with codeine (referred to as “Soma Coma”). (Reeves, 1999) (Reeves, 2001) (Reeves, 2008) (Schears, 2004) There was a 300% increase in numbers of emergency room episodes related to carisoprodol from 1994 to 2005. (DHSS, 2005) Intoxication appears to include subdued consciousness, decreased cognitive function, and abnormalities of the eyes, vestibular function, appearance, gait and motor function. Intoxication includes the effects of both carisoprodol and meprobamate, both of which act on different neurotransmitters. (Bramness, 2007) (Bramness, 2004) A withdrawal syndrome has been documented that consists of insomnia, vomiting, tremors, muscle twitching, anxiety, and ataxia when abrupt discontinuation of large doses occurs. This is similar to withdrawal from meprobamate. (Reeves, 2007) (Reeves, 2004) There is little research in terms of weaning of high dose carisoprodol and there is no standard treatment regimen for patients with known dependence. Most treatment includes treatment for symptomatic complaints of withdrawal. Another option is to switch to phenobarbital to prevent withdrawal with subsequent tapering. A maximum dose of phenobarbital is 500 mg/day and the taper is 30 mg/day with a slower taper in an outpatient setting. Tapering should be individualized for each patient. (Boothby, 2003) For more information and references, Catapres® (Clonidine) See Clonidine, intrathecal. Celebrex® Celebrex® is the brandname for celecoxib, and it is produced by Pfizer. Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) that is a COX-2 selective inhibitor, a drug that directly targets COX-2, an enzyme responsible for inflammation and pain. See Anti-inflammatory medications. See NSAIDs (non-steroidal anti-inflammatory drugs) for specific patient decision-making criteria. Unlike other NSAIDs, celecoxib does not appear to interfere with the antiplatelet activity of aspirin and is bleeding neutral when patients are being considered for surgical intervention or interventional pain procedures. Cesamet® See Nabilone Chiropractic treatment See Manual therapy & manipulation. Chondroitin sulfate See Glucosamine (and Chondroitin Sulfate). Chronic pain programs (functional restoration programs) Recommended where there is access to programs with proven successful outcomes, for patients with conditions that put them at risk of delayed recovery. Patients should also be motivated to improve and return to work, and meet the patient selection criteria outlined below. Also called Multidisciplinary pain programs or Interdisciplinary rehabilitation programs, these pain rehabilitation programs combine multiple treatments, and at the least, include psychological care along with physical therapy & occupational therapy (including an active exercise component as opposed to passive modalities). While recommended, the research remains ongoing as to (1) what is considered the “gold-standard” content for treatment; (2) the group of patients that benefit most from this treatment; (3) the ideal timing of when to initiate treatment; (4) the intensity necessary for effective treatment; and (5) cost-effectiveness. It has been suggested that interdisciplinary/multidisciplinary care models for treatment of chronic pain may be the most effective way to treat this condition. (Flor, 1992) (Gallagher, 1999) (Guzman, 2001) (Gross, 2005) (Sullivan, 2005) (Dysvik, 2005) (Airaksinen, 2006) (Schonstein, 2003) (Sanders, 2005) (Patrick, 2004) (Buchner, 2006) Unfortunately, being a claimant may be a predictor of poor long-term outcomes. (Robinson, 2004) These treatment modalities are based on the biopsychosocial model, one that views pain and disability in terms of the interaction between physiological, psychological and social factors. (Gatchel, 2005) There appears to be little scientific evidence for the effectiveness of multidisciplinary biopsychosocial rehabilitation compared with other rehabilitation facilities for neck and shoulder pain, as opposed to low back pain and generalized pain syndromes. (Karjalainen, 2003) Types of programs: There is no one universal definition of what comprises interdisciplinary/multidisciplinary treatment. The most commonly referenced programs have been defined in the following general ways (Stanos, 2006): (1) Multidisciplinary programs: Involves one or two specialists directing the services of a number of team members, with these specialists often having independent goals. These programs can be further subdivided into four levels of pain programs: (a) Multidisciplinary pain centers (generally associated with academic centers and include research as part of their focus) (b) Multidisciplinary pain clinics (c) Pain clinics (d) Modality-oriented clinics (2) Interdisciplinary pain programs: Involves a team approach that is outcome focused and coordinated and offers goal-oriented interdisciplinary services. Communication on a minimum of a weekly basis is emphasized. The most intensive of these programs is referred to as a Functional Restoration Program, with a major emphasis on maximizing function versus minimizing pain. See Functional restoration programs.
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