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Mrs. A, age 50, reports recurrent headaches and neck pain from a motor vehicle accident in 1999. At the time, MRI revealed degenerative changes at the C5-C6 vertebrae without bony stenosis or spinal injury. Treatment consisted of conservative measures and physical therapy; she was not a candidate for surgical intervention.
Although Mrs. A can manage activities of daily living, pain prevents her from pastimes she previously enjoyed, including painting and pottery, and is causing problems in her marriage.
Mrs. A’s pain became much worse approximately 1 year ago. In the past year, its severity has lead to multiple clinical presentations and consultations. She uses transdermal fentanyl, 75 mcg/hr every 72 hours, and acetaminophen/ hydrocodone, 5 mg/500 mg every 4 hours up to 6 times a day for breakthrough pain. Even so, she still rates her pain as 7 on a 10-point scale.
Pain is a complex perception with psychological and sensory components. It is the most common reason patients seek treatment at ambulatory medical settings.1 Most pain remits spontaneously or responds to simple treatment, but up to 25% of symptoms remain chronic.1
Chronic pain—defined as pain at ≥1 anatomic sites for ≥6 months—can substantially impair adaptation and vocational and interpersonal functioning. Treatments that focus solely on analgesics are shortsighted and often of limited benefit. Patients with chronic pain need a rehabilitative approach that incorporates psychiatric and psychological intervention.
Complex chronic pain
Most individuals with chronic pain can maintain basic functioning, work, relationships, and interests. They work with healthcare providers and obtain relief from medications or other interventions.
Some, however, are preoccupied with—and entirely debilitated by—their pain. For them, life revolves around the pain and perceived disability. Many if not all aspects of this patient’s life are contingent on pain and fears it might worsen.2 Preoccupation with pain can profoundly affect social activities and prevent employment. The patient may become dependent on others, and being a patient can become a primary psychosocial state. A chronic pain patient also may become increasingly preoccupied with medication use and possibly abuse.
- a general medical condition
- psychological factors
- both.
Pain disorder criteria often are perceived as insufficiently operationalized—there is no checklist of symptoms that collectively define the syndrome.5,6 The clinician must infer whether—and to what extent—psychological factors are involved in the pain.5 There are no guidelines to help psychiatrists ascertain whether psychological factors “have an important role” in pain (criteria C) or if pain is “not better accounted for” by a mood disorder (criteria E).6 This distinction can be indecipherable because of frequent comorbidity of mood disturbances with pain.7,8 Some clinicians have suggested that pain disorder be removed from the somato-form disorder classification and instead confined to Axis III.9
Table 1
DSM-IV-TR diagnostic criteria for pain disorder
A. Pain in ≥1 anatomical sites |
B. Produces distress or impairs social, occupational, or other functioning |
C. Psychological factors have an important role in pain onset, severity, exacerbation, or maintenance |
D. Not intentionally produced or feigned (as in factitious disorder or malingering) |
E. Not better accounted for by a mood, anxiety, or psychotic disorder and does not meet criteria for dyspareunia |
Subtypes |
Pain disorder associated with psychological factors, which are judged to have the major role in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with both psychological factors and a general medical condition, which are judged to have important roles in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with a general medical condition.* If psychological factors are present, they do not have a major role in pain onset, severity, exacerbation, or maintenance |
* Not considered a mental disorder (encoded on Axis III) Source: Adapted from Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
What are the risk factors?
Psychological and social covariates play a substantial role in the chronic pain experience (Table 2). How patients experience chronic pain also is influenced by personality and premorbid, semi-dormant characteristics that become activated by the stress of unremitting pain.7
- mood
- thought patterns
- perceptions
- coping abilities
- personality.
Table 2
Patient factors that contribute to or perpetuate chronic pain
Poor modulation of emotions (anger, depression, anxiety) |
Somatization (using pain to avoid confl icts, express anger, or punish others) |
Problematic cognitive styles (catastrophizing, perceived loss of control) |
Poor coping skills |
Psychiatric comorbidities |
Social/interpersonal variables:
|
Reinforcement for remaining sick and/or disabled:
|
Source: Adapted from reference 3 |
CASE CONTINUED: Underlying causes
Psychological and psychosocial factors appear to play an important role in Mrs. A’s pain. After her husband’s job was restructured, the couple moved away from Mrs. A’s mother, which she found distressing. Additionally, Mrs. A reports that her son has incurred substantial gambling debt.
Mrs. A admits she has “a hard time” accepting these events, but she cannot acknowledge anger or frustration. She avoids questions about such feelings and focuses on her pain. She reports, “The pain is always there and ruins my entire life. Absolutely nothing gives me relief.”
She does not endorse depressive or psychotic symptoms. She sometimes has passive thoughts of death when she feels hopeless about her persistent pain, but she vehemently denies suicidal ideas, intent, or plans. She has smoked 1 pack of cigarettes per day for 12 years but denies alcohol abuse or use of illicit substances.
Biopsychosocial assessment
Assessing a chronic pain patient includes evaluating somatic, psychological, and social factors (Table 3).3 A biopsychosocial approach recognizes that the patient’s experience of pain, presentation, and response to treatment are determined by the interaction of:
- biological factors
- the patient’s psychological makeup
- psychological comorbidities
- the extent of social support
- extenuating environmental circumstances.3,10
A thorough psychiatric assessment may reveal psychiatric comorbidity and psychological conditions that mediate pain.8 Recognizing and treating coexisting psychiatric disorders often will enhance effective pain management.
Subsyndromal psychological factors—such as troubling affective states, problematic cognitive styles,14 and ineffective coping strategies and interpersonal skills—can accompany pain. If unattended, such factors can heighten the patient’s pain awareness and compromise rehabilitation.
For example, patients such as Mrs. A can aggravate pain by catastrophizing.15 Having a tendency to exaggerate pain and the significance of related life events interferes with their ability to attend to matters within their control and pursue productive activities.16 Catastrophizing is associated with increased pain and perceived disability, poor adjustment to pain, and marked emotional distress.17,18
How pain shapes beliefs. Pain can shape the manner with which patients make sense of events in their lives by altering the way they perceive themselves and the world. Problematic beliefs of the self (inadequacy and helplessness), of the world (dangerousness), and of the future (hopelessness) can produce significant distress. A patient with such beliefs may experience a loss of self-esteem, self-efficacy, and connections with others and may experience marked disappointment and disillusionment.
- substance abuse
- nonadherence with treatment
- withdrawal from support systems
- incapacitating emotional states, such as marked dysphoria, anger, or anxiety.
Table 3
Biopsychosocial assessment of chronic pain patients: 3 components
Somatic factors |
Determine pain onset/duration, location, quality, intensity, associated features, aggravating and alleviating factors |
Single-dimension pain rating scales, such as Numeric Rating Scale or Visual Analog Scale |
Review prescribed and over-the-counter analgesic use (adherence, excess use, impact on functional adaptation) |
Psychological factors |
Mood and affect, cognitive content and processes, coping skills |
Psychiatric comorbidities (substance abuse/dependence; anxiety, sleep, and somatoform disorders; delirium; depression; sexual dysfunction) |
Suicide risk assessment |
Multidimensional pain rating scales, such as Coping Strategies Questionnaire or Multidimensional Pain Inventory |
Social factors |
Impact on relationships, including capacity for intimacy, mutuality, and sexuality |
Impact on activities of daily living, vocational and recreational functioning |
Determine functions patient can perform despite pain |
Source: Adapted from reference 3 |
CASE CONTINUED: Multifaceted treatment
You prescribe amitriptyline, 20 mg at bed-time, for pain and refer Mrs. A for cognitive-behavioral therapy (CBT). The emphasis of therapy is to identify affective states and cognitive distortions that are temporally related to pain exacerbations, to develop coping skills to deal with stressors, and to effectively express her anger. Mrs. A learns relaxation techniques and self-hypnosis to reduce distress. These measures help reduce her pain severity ratings to 3 on a 10-point scale. She also participates in physical therapy and yoga classes, which increase her endurance.
Psychiatrists’ role in treatment
Many chronic nonmalignant pain syndromes—including arthritic conditions, back pain, and fibromyalgia—are tenacious and not easily cured. Treatment goals are to relieve pain and maximize the patient’s functioning and quality of life while minimizing risks of iatrogenic harm. As part of a biopsychosocial approach to care:
- diagnose and treat psychiatric comorbidities
- assess responses to treatment interventions
- refine treatment measures when patients do not achieve functional and adaptational goals
- initiate pharmacologic interventions for pain
- address subsyndromal emotional and cognitive impediments to functional restoration.
In initial CBT sessions, the goal is to elicit the patient’s:
- perception of pain
- life situations
- beliefs about his or her life, relationships, and the future
- coping measures.
Self-regulatory techniques—including relaxation training, biofeedback, and hypnosis—can facilitate relaxation and “turn down” the physiologic triggers that cause and perpetuate pain.25,26 Hypnosis can lead to dissociative states that modify how a patient experiences pain. There is modest evidence that self-regulatory techniques are effective for treating pain.27,28
Pharmacotherapy. Multiple pathophysiologic mechanisms—including ion channel up-regulation, spinal hyperexcitability, and descending neurotransmitter pathway impairment—play a role in chronic pain states. Several classes of psychoactive agents can mitigate pain (Table 4), and some psychotropics are FDA-approved for specific pain conditions (Table 5).
Individualize medication selection, considering:
- cost
- ease of use
- tolerability
- interactions with coadministered medications
- clinical comorbidities.
- opioid therapy fails
- patients become dependent on escalating doses of opioids.
Antidepressants influence pain by blocking monoamine reuptake. Those that influence noradrenergic and serotonergic transmission may have greater analgesic effects than those that affect serotonin or norepinephrine reuptake alone.31-33
Anticonvulsants mitigate pain by influencing sodium or calcium channel regulation, GABA activity, or combinations of the 3.
In randomized controlled trials that included patients with diabetic and postherpetic neuropathies:
- one-third of patients achieved ≥50% pain relief with tricyclic antidepressants (TCAs) or anticonvulsants
- adverse effects were slightly more common with TCAs.34,35
Because antidepressants and anticonvulsants have different presumed mechanisms of action for pain relief, anticonvulsants might be useful for patients whose pain persists despite optimal antidepressant dosing or for whom antidepressants are in-tolerable. Alternately, coadministering antidepressants and anticonvulsants might capitalize on complimentary mechanisms of action. With coadministration, lower doses may be sufficiently analgesic and avoid adverse effects.
Benzodiazepines have been used short-term to mitigate muscle spasm pain as in fibromyalgia, phantom limb pain, and restless legs syndrome.36,37 Long-term benzodiazepine use can lead to low activity levels, high use of ambulatory medical services, and high disability levels, however.38 if required for muscle spasm or restless legs syndrome, benzodiazepines may best be confined to short-term use.
Antipsychotics. Limited studies have evaluated antipsychotics’ efficacy for chronic pain.39,40 Some have been found to be useful in neuropathic pain.40 Antipsychotics are seldom used to treat pain because of limited efficacy data, potential side effects, and an abundance of alternate agents. Because risks—most notably extrapyramidal side effects and tardive dyskinesia—appear to outweigh analgesic efficacy, I would confine antipsychotics to pain patients with delirium or psychosis. Antipsychotics’ potential role in treating refractory pain might warrant further investigation.40
Stimulants may reduce sedation, dysphoria, and cognitive inefficiency that can accompany opioid use.
Table 4
Uses of psychotropics in patients with chronic pain
Class/drug | Uses | Limitations |
---|---|---|
Antidepressants | Neuropathic pain, tension and migraine headache, FM, functional GI disorders, pain comorbid with depression/anxiety | NE/5-HT reuptake inhibitors are most effective for analgesia; side effects (TCAs may be least tolerable); drug interactions |
Anticonvulsants | Neuropathic pain, migraine headache, central pain, phantom limb pain | Side effects (sedation, motor and GI effects, rash); drug interactions |
Benzodiazepines | Muscle relaxation, restless legs syndrome, anxiety, insomnia | Abuse/dependence potential; sedation |
Lithium | Cluster headache prophylaxis | Not effective for episodic cluster headache; risk of toxicity if dehydration occurs or with certain drug combinations |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Antipsychotics | Neuropathic pain, migraine, cancer pain, delirium | Limited data; risks such as EPS and TD may outweigh benefi ts |
EPS: extrapyramidal symptoms; FM: fibromyalgia; GI: gastrointestinal; NE: norepinephrine; 5-HT: serotonin; TCAs: tricyclic antidepressants; TD: tardive dyskinesia | ||
Source: Adapted from reference 3 |
Table 5
Psychotropics approved for managing pain
Drug | Indication |
---|---|
Carbamazepine | Trigeminal neuralgia |
Divalproex | Migraine prophylaxis |
Duloxetine | Diabetic neuropathy |
Gabapentin | Postherpetic neuralgia |
Pregabalin | Postherpetic neuralgia, diabetic neuropathy, fibromyalgia |
Source: Adapted from reference 3 |
- International Association for the Study of Pain. www.iasp-pain.org.
- Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
- Loeser JD, Butler SH, Chapman CR, Turk DC. Bonica’s management of pain. 3rd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2001.
- Acetaminophen/hydrocodone • Lortab, others
- Amitriptyline • Elavil, Endep
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Duloxetine • Cymbalta
- Fentanyl transdermal • Duragesic
- Gabapentin • Neurontin
- Lithium • Eskalith, Lithobid
- Pregabalin • Lyrica
Dr. Leo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Schappert SM. National Ambulatory Medical Care Survey: 1989 summary. Vital Health Stat 13 1992;(110):1-80.
2. Sternbach RA. Pain patients: traits and treatment. New York, NY: Academic Press; 1974.
3. Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
4. Aigner M, Bach M. Clinical utility of DSM-IV pain disorder. Compr Psychiatry 1999;40(5):353-7.
5. Boland RJ. How could the validity of the DSM-IV pain disorder be improved in reference to the concept that it is supposed to identify? Curr Pain Headache Rep 2002;6(1):23-9.
6. Sullivan MD. DSM-IV pain disorder: a case against the diagnosis. Int Rev Psychiatry 2000;12:91-8.
7. Dersh J, Polatin PB, Gatchel RJ. Chronic pain and psychopathology: research findings and theoretical considerations. Psychosom Med 2002;64:773-86.
8. Fishbain DA. Approaches to treatment decisions for psychiatric comorbidity in the management of the chronic pain patient. Med Clin North Am 1999;83:737-60.
9. Mayou R, Kirmayer LJ, Simon G, et al. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162(5):847-55.
10. Gallagher RM. Treatment planning in pain medicine—integrating medical, physical, and behavioral therapies. Med Clin North Am 1999;83(3):823-49.
11. Jensen MP, Karoly P, Braver S. The measurement of clinical pain intensity: a comparison of six methods. Pain 1986;27:117-26.
12. Rosenstiel AK, Keefe FJ. The use of coping strategies in chronic low back pain patients: relationship to patient characteristics and current adjustment. Pain 1983;17:33-44.
13. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale multidimensional pain inventory (WHYMPI). Pain 1985;23:345-56.
14. Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: a critical review. Pain 1991;47:249-83.
15. Sullivan MJL, Stanish W, Waite H, et al. Catastrophizing, pain, and disability in patients with soft-tissue injuries. Pain 1998;77:253-60.
16. Crombez G, Eccleston C, Baeyens F, et al. When somatic information threatens, catastrophic thinking enhances attentional interference. Pain 1998;75:187-98.
17. Hasenbring M, Hallner D, Klasen B. Psychological mechanisms in the transition from acute to chronic pain: over-or underrated? Schmerz. 2001;15:442-7.
18. Sullivan MJ, Thorn B, Haythornthwaite JA, et al. Theoretical perspectives on the relation between catastrophizing and pain. Clin J Pain 2001;17:52-64.
19. Arnstein P. The mediation of disability by self efficacy in different samples of chronic pain patients. Disabil Rehabil 2000;22(17):794-801.
20. Fishbain DA. The association of chronic pain and suicide. Semin Clin Neuropsychiatry 1999;4(3):221-7.
21. Astin JA, Beckner W, Soeken K, et al. Psychological interventions for rheumatoid arthritis: a meta-analysis of randomized controlled trials. Arthritis Rheum 2002;47:291-302.
22. Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292(19):2388-95.
23. Morley S, Eccleston C, Williams A. Systematic review and meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999;80:1-13.
24. Hoffman BM, Papas RK, Chatkoff DK, Kerns RD. Meta-analysis of psychological interventions for chronic low back pain. Health Psychol 2007;26(1):1-9.
25. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, II: operant conditioning, hypnosis, and cognitive-behavioral therapy. Pain 1982;12:23-46.
26. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, I: relaxation training and biofeedback. Pain 1982;12:1-21.
27. Carroll D, Seers K. Relaxation for the relief of chronic pain: a systematic review. J Adv Nurs 1998;27:476-87.
28. Keel PJ, Bodoky C, Gerhard U, et al. Comparison of integrated group therapy and group relaxation training for fibromyalgia. Clin J Pain 1998;14:232-8.
29. Eriksen J, Sjogren P, Bruera E, et al. Critical issues on opioids in chronic non-cancer pain: an epidemiological study. Pain 2006;125:172-9.
30. Ballantyne JC, Mao J. Opioid therapy for chronic pain. N Engl J Med 2003;349:1943-53.
31. Lynch ME. Antidepressants as analgesics: a review of randomized controlled trials. J Psychiatry Neurosci 2001;26(1):30-6.
32. McQuay HJ, Tramer M, Nye BA, et al. A systematic review of antidepressants in neuropathic pain. Pain 1996;68:217-27.
33. Sussman N. SNRI’s versus SSRI’s: mechanisms of action in treating depression and painful physical symptoms. Prim Care Companion J Clin Psychiatry 2003;5(suppl 7):19-26.
34. Collins SL, Moore RA, McQuay HJ, et al. Antidepressants and anticonvulsants for diabetic neuropathy and postherpetic neuralgia: a quantitative systematic review. J Pain Symptom Manage 2000;20:449-58.
35. McQuay HJ. Neuropathic pain: evidence matters. Eur J Pain 2002;6(suppl A):11-8.
36. Bartusch SL, Sanders BJ, D’Alessio JG, et al. Clonazepam for the treatment of lancinating phantom limb pain. Clin J Pain 1996;12:59-62.
37. Dellemijn PL, Fields HL. Do benzodiazepines have a role in chronic pain management? Pain 1994;57:137-52.
38. Ciccone DS, Just N, Bandilla EB, et al. Psychological correlates of opioid use in patients with chronic nonmalignant pain: a preliminary test of the downhill spiral hypothesis. J Pain Symptom Manage 2000;20:180-92.
39. Gomez-Perez FJ, Rull JA, Dies H, et al. Nortriptyline and fluphenazine in the symptomatic treatment of diabetic neuropathy: a double-blind cross-over study. Pain 1985;23:395-400.
40. Fishbain DA, Cutler RB, Lewis J, et al. Do the second-generation “atypical neuroleptics” have analgesic properties? A structured evidence-based review. Pain Med 2004;5:359-65.
Mrs. A, age 50, reports recurrent headaches and neck pain from a motor vehicle accident in 1999. At the time, MRI revealed degenerative changes at the C5-C6 vertebrae without bony stenosis or spinal injury. Treatment consisted of conservative measures and physical therapy; she was not a candidate for surgical intervention.
Although Mrs. A can manage activities of daily living, pain prevents her from pastimes she previously enjoyed, including painting and pottery, and is causing problems in her marriage.
Mrs. A’s pain became much worse approximately 1 year ago. In the past year, its severity has lead to multiple clinical presentations and consultations. She uses transdermal fentanyl, 75 mcg/hr every 72 hours, and acetaminophen/ hydrocodone, 5 mg/500 mg every 4 hours up to 6 times a day for breakthrough pain. Even so, she still rates her pain as 7 on a 10-point scale.
Pain is a complex perception with psychological and sensory components. It is the most common reason patients seek treatment at ambulatory medical settings.1 Most pain remits spontaneously or responds to simple treatment, but up to 25% of symptoms remain chronic.1
Chronic pain—defined as pain at ≥1 anatomic sites for ≥6 months—can substantially impair adaptation and vocational and interpersonal functioning. Treatments that focus solely on analgesics are shortsighted and often of limited benefit. Patients with chronic pain need a rehabilitative approach that incorporates psychiatric and psychological intervention.
Complex chronic pain
Most individuals with chronic pain can maintain basic functioning, work, relationships, and interests. They work with healthcare providers and obtain relief from medications or other interventions.
Some, however, are preoccupied with—and entirely debilitated by—their pain. For them, life revolves around the pain and perceived disability. Many if not all aspects of this patient’s life are contingent on pain and fears it might worsen.2 Preoccupation with pain can profoundly affect social activities and prevent employment. The patient may become dependent on others, and being a patient can become a primary psychosocial state. A chronic pain patient also may become increasingly preoccupied with medication use and possibly abuse.
- a general medical condition
- psychological factors
- both.
Pain disorder criteria often are perceived as insufficiently operationalized—there is no checklist of symptoms that collectively define the syndrome.5,6 The clinician must infer whether—and to what extent—psychological factors are involved in the pain.5 There are no guidelines to help psychiatrists ascertain whether psychological factors “have an important role” in pain (criteria C) or if pain is “not better accounted for” by a mood disorder (criteria E).6 This distinction can be indecipherable because of frequent comorbidity of mood disturbances with pain.7,8 Some clinicians have suggested that pain disorder be removed from the somato-form disorder classification and instead confined to Axis III.9
Table 1
DSM-IV-TR diagnostic criteria for pain disorder
A. Pain in ≥1 anatomical sites |
B. Produces distress or impairs social, occupational, or other functioning |
C. Psychological factors have an important role in pain onset, severity, exacerbation, or maintenance |
D. Not intentionally produced or feigned (as in factitious disorder or malingering) |
E. Not better accounted for by a mood, anxiety, or psychotic disorder and does not meet criteria for dyspareunia |
Subtypes |
Pain disorder associated with psychological factors, which are judged to have the major role in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with both psychological factors and a general medical condition, which are judged to have important roles in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with a general medical condition.* If psychological factors are present, they do not have a major role in pain onset, severity, exacerbation, or maintenance |
* Not considered a mental disorder (encoded on Axis III) Source: Adapted from Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
What are the risk factors?
Psychological and social covariates play a substantial role in the chronic pain experience (Table 2). How patients experience chronic pain also is influenced by personality and premorbid, semi-dormant characteristics that become activated by the stress of unremitting pain.7
- mood
- thought patterns
- perceptions
- coping abilities
- personality.
Table 2
Patient factors that contribute to or perpetuate chronic pain
Poor modulation of emotions (anger, depression, anxiety) |
Somatization (using pain to avoid confl icts, express anger, or punish others) |
Problematic cognitive styles (catastrophizing, perceived loss of control) |
Poor coping skills |
Psychiatric comorbidities |
Social/interpersonal variables:
|
Reinforcement for remaining sick and/or disabled:
|
Source: Adapted from reference 3 |
CASE CONTINUED: Underlying causes
Psychological and psychosocial factors appear to play an important role in Mrs. A’s pain. After her husband’s job was restructured, the couple moved away from Mrs. A’s mother, which she found distressing. Additionally, Mrs. A reports that her son has incurred substantial gambling debt.
Mrs. A admits she has “a hard time” accepting these events, but she cannot acknowledge anger or frustration. She avoids questions about such feelings and focuses on her pain. She reports, “The pain is always there and ruins my entire life. Absolutely nothing gives me relief.”
She does not endorse depressive or psychotic symptoms. She sometimes has passive thoughts of death when she feels hopeless about her persistent pain, but she vehemently denies suicidal ideas, intent, or plans. She has smoked 1 pack of cigarettes per day for 12 years but denies alcohol abuse or use of illicit substances.
Biopsychosocial assessment
Assessing a chronic pain patient includes evaluating somatic, psychological, and social factors (Table 3).3 A biopsychosocial approach recognizes that the patient’s experience of pain, presentation, and response to treatment are determined by the interaction of:
- biological factors
- the patient’s psychological makeup
- psychological comorbidities
- the extent of social support
- extenuating environmental circumstances.3,10
A thorough psychiatric assessment may reveal psychiatric comorbidity and psychological conditions that mediate pain.8 Recognizing and treating coexisting psychiatric disorders often will enhance effective pain management.
Subsyndromal psychological factors—such as troubling affective states, problematic cognitive styles,14 and ineffective coping strategies and interpersonal skills—can accompany pain. If unattended, such factors can heighten the patient’s pain awareness and compromise rehabilitation.
For example, patients such as Mrs. A can aggravate pain by catastrophizing.15 Having a tendency to exaggerate pain and the significance of related life events interferes with their ability to attend to matters within their control and pursue productive activities.16 Catastrophizing is associated with increased pain and perceived disability, poor adjustment to pain, and marked emotional distress.17,18
How pain shapes beliefs. Pain can shape the manner with which patients make sense of events in their lives by altering the way they perceive themselves and the world. Problematic beliefs of the self (inadequacy and helplessness), of the world (dangerousness), and of the future (hopelessness) can produce significant distress. A patient with such beliefs may experience a loss of self-esteem, self-efficacy, and connections with others and may experience marked disappointment and disillusionment.
- substance abuse
- nonadherence with treatment
- withdrawal from support systems
- incapacitating emotional states, such as marked dysphoria, anger, or anxiety.
Table 3
Biopsychosocial assessment of chronic pain patients: 3 components
Somatic factors |
Determine pain onset/duration, location, quality, intensity, associated features, aggravating and alleviating factors |
Single-dimension pain rating scales, such as Numeric Rating Scale or Visual Analog Scale |
Review prescribed and over-the-counter analgesic use (adherence, excess use, impact on functional adaptation) |
Psychological factors |
Mood and affect, cognitive content and processes, coping skills |
Psychiatric comorbidities (substance abuse/dependence; anxiety, sleep, and somatoform disorders; delirium; depression; sexual dysfunction) |
Suicide risk assessment |
Multidimensional pain rating scales, such as Coping Strategies Questionnaire or Multidimensional Pain Inventory |
Social factors |
Impact on relationships, including capacity for intimacy, mutuality, and sexuality |
Impact on activities of daily living, vocational and recreational functioning |
Determine functions patient can perform despite pain |
Source: Adapted from reference 3 |
CASE CONTINUED: Multifaceted treatment
You prescribe amitriptyline, 20 mg at bed-time, for pain and refer Mrs. A for cognitive-behavioral therapy (CBT). The emphasis of therapy is to identify affective states and cognitive distortions that are temporally related to pain exacerbations, to develop coping skills to deal with stressors, and to effectively express her anger. Mrs. A learns relaxation techniques and self-hypnosis to reduce distress. These measures help reduce her pain severity ratings to 3 on a 10-point scale. She also participates in physical therapy and yoga classes, which increase her endurance.
Psychiatrists’ role in treatment
Many chronic nonmalignant pain syndromes—including arthritic conditions, back pain, and fibromyalgia—are tenacious and not easily cured. Treatment goals are to relieve pain and maximize the patient’s functioning and quality of life while minimizing risks of iatrogenic harm. As part of a biopsychosocial approach to care:
- diagnose and treat psychiatric comorbidities
- assess responses to treatment interventions
- refine treatment measures when patients do not achieve functional and adaptational goals
- initiate pharmacologic interventions for pain
- address subsyndromal emotional and cognitive impediments to functional restoration.
In initial CBT sessions, the goal is to elicit the patient’s:
- perception of pain
- life situations
- beliefs about his or her life, relationships, and the future
- coping measures.
Self-regulatory techniques—including relaxation training, biofeedback, and hypnosis—can facilitate relaxation and “turn down” the physiologic triggers that cause and perpetuate pain.25,26 Hypnosis can lead to dissociative states that modify how a patient experiences pain. There is modest evidence that self-regulatory techniques are effective for treating pain.27,28
Pharmacotherapy. Multiple pathophysiologic mechanisms—including ion channel up-regulation, spinal hyperexcitability, and descending neurotransmitter pathway impairment—play a role in chronic pain states. Several classes of psychoactive agents can mitigate pain (Table 4), and some psychotropics are FDA-approved for specific pain conditions (Table 5).
Individualize medication selection, considering:
- cost
- ease of use
- tolerability
- interactions with coadministered medications
- clinical comorbidities.
- opioid therapy fails
- patients become dependent on escalating doses of opioids.
Antidepressants influence pain by blocking monoamine reuptake. Those that influence noradrenergic and serotonergic transmission may have greater analgesic effects than those that affect serotonin or norepinephrine reuptake alone.31-33
Anticonvulsants mitigate pain by influencing sodium or calcium channel regulation, GABA activity, or combinations of the 3.
In randomized controlled trials that included patients with diabetic and postherpetic neuropathies:
- one-third of patients achieved ≥50% pain relief with tricyclic antidepressants (TCAs) or anticonvulsants
- adverse effects were slightly more common with TCAs.34,35
Because antidepressants and anticonvulsants have different presumed mechanisms of action for pain relief, anticonvulsants might be useful for patients whose pain persists despite optimal antidepressant dosing or for whom antidepressants are in-tolerable. Alternately, coadministering antidepressants and anticonvulsants might capitalize on complimentary mechanisms of action. With coadministration, lower doses may be sufficiently analgesic and avoid adverse effects.
Benzodiazepines have been used short-term to mitigate muscle spasm pain as in fibromyalgia, phantom limb pain, and restless legs syndrome.36,37 Long-term benzodiazepine use can lead to low activity levels, high use of ambulatory medical services, and high disability levels, however.38 if required for muscle spasm or restless legs syndrome, benzodiazepines may best be confined to short-term use.
Antipsychotics. Limited studies have evaluated antipsychotics’ efficacy for chronic pain.39,40 Some have been found to be useful in neuropathic pain.40 Antipsychotics are seldom used to treat pain because of limited efficacy data, potential side effects, and an abundance of alternate agents. Because risks—most notably extrapyramidal side effects and tardive dyskinesia—appear to outweigh analgesic efficacy, I would confine antipsychotics to pain patients with delirium or psychosis. Antipsychotics’ potential role in treating refractory pain might warrant further investigation.40
Stimulants may reduce sedation, dysphoria, and cognitive inefficiency that can accompany opioid use.
Table 4
Uses of psychotropics in patients with chronic pain
Class/drug | Uses | Limitations |
---|---|---|
Antidepressants | Neuropathic pain, tension and migraine headache, FM, functional GI disorders, pain comorbid with depression/anxiety | NE/5-HT reuptake inhibitors are most effective for analgesia; side effects (TCAs may be least tolerable); drug interactions |
Anticonvulsants | Neuropathic pain, migraine headache, central pain, phantom limb pain | Side effects (sedation, motor and GI effects, rash); drug interactions |
Benzodiazepines | Muscle relaxation, restless legs syndrome, anxiety, insomnia | Abuse/dependence potential; sedation |
Lithium | Cluster headache prophylaxis | Not effective for episodic cluster headache; risk of toxicity if dehydration occurs or with certain drug combinations |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Antipsychotics | Neuropathic pain, migraine, cancer pain, delirium | Limited data; risks such as EPS and TD may outweigh benefi ts |
EPS: extrapyramidal symptoms; FM: fibromyalgia; GI: gastrointestinal; NE: norepinephrine; 5-HT: serotonin; TCAs: tricyclic antidepressants; TD: tardive dyskinesia | ||
Source: Adapted from reference 3 |
Table 5
Psychotropics approved for managing pain
Drug | Indication |
---|---|
Carbamazepine | Trigeminal neuralgia |
Divalproex | Migraine prophylaxis |
Duloxetine | Diabetic neuropathy |
Gabapentin | Postherpetic neuralgia |
Pregabalin | Postherpetic neuralgia, diabetic neuropathy, fibromyalgia |
Source: Adapted from reference 3 |
- International Association for the Study of Pain. www.iasp-pain.org.
- Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
- Loeser JD, Butler SH, Chapman CR, Turk DC. Bonica’s management of pain. 3rd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2001.
- Acetaminophen/hydrocodone • Lortab, others
- Amitriptyline • Elavil, Endep
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Duloxetine • Cymbalta
- Fentanyl transdermal • Duragesic
- Gabapentin • Neurontin
- Lithium • Eskalith, Lithobid
- Pregabalin • Lyrica
Dr. Leo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Mrs. A, age 50, reports recurrent headaches and neck pain from a motor vehicle accident in 1999. At the time, MRI revealed degenerative changes at the C5-C6 vertebrae without bony stenosis or spinal injury. Treatment consisted of conservative measures and physical therapy; she was not a candidate for surgical intervention.
Although Mrs. A can manage activities of daily living, pain prevents her from pastimes she previously enjoyed, including painting and pottery, and is causing problems in her marriage.
Mrs. A’s pain became much worse approximately 1 year ago. In the past year, its severity has lead to multiple clinical presentations and consultations. She uses transdermal fentanyl, 75 mcg/hr every 72 hours, and acetaminophen/ hydrocodone, 5 mg/500 mg every 4 hours up to 6 times a day for breakthrough pain. Even so, she still rates her pain as 7 on a 10-point scale.
Pain is a complex perception with psychological and sensory components. It is the most common reason patients seek treatment at ambulatory medical settings.1 Most pain remits spontaneously or responds to simple treatment, but up to 25% of symptoms remain chronic.1
Chronic pain—defined as pain at ≥1 anatomic sites for ≥6 months—can substantially impair adaptation and vocational and interpersonal functioning. Treatments that focus solely on analgesics are shortsighted and often of limited benefit. Patients with chronic pain need a rehabilitative approach that incorporates psychiatric and psychological intervention.
Complex chronic pain
Most individuals with chronic pain can maintain basic functioning, work, relationships, and interests. They work with healthcare providers and obtain relief from medications or other interventions.
Some, however, are preoccupied with—and entirely debilitated by—their pain. For them, life revolves around the pain and perceived disability. Many if not all aspects of this patient’s life are contingent on pain and fears it might worsen.2 Preoccupation with pain can profoundly affect social activities and prevent employment. The patient may become dependent on others, and being a patient can become a primary psychosocial state. A chronic pain patient also may become increasingly preoccupied with medication use and possibly abuse.
- a general medical condition
- psychological factors
- both.
Pain disorder criteria often are perceived as insufficiently operationalized—there is no checklist of symptoms that collectively define the syndrome.5,6 The clinician must infer whether—and to what extent—psychological factors are involved in the pain.5 There are no guidelines to help psychiatrists ascertain whether psychological factors “have an important role” in pain (criteria C) or if pain is “not better accounted for” by a mood disorder (criteria E).6 This distinction can be indecipherable because of frequent comorbidity of mood disturbances with pain.7,8 Some clinicians have suggested that pain disorder be removed from the somato-form disorder classification and instead confined to Axis III.9
Table 1
DSM-IV-TR diagnostic criteria for pain disorder
A. Pain in ≥1 anatomical sites |
B. Produces distress or impairs social, occupational, or other functioning |
C. Psychological factors have an important role in pain onset, severity, exacerbation, or maintenance |
D. Not intentionally produced or feigned (as in factitious disorder or malingering) |
E. Not better accounted for by a mood, anxiety, or psychotic disorder and does not meet criteria for dyspareunia |
Subtypes |
Pain disorder associated with psychological factors, which are judged to have the major role in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with both psychological factors and a general medical condition, which are judged to have important roles in pain onset, severity, exacerbation, or maintenance |
Pain disorder associated with a general medical condition.* If psychological factors are present, they do not have a major role in pain onset, severity, exacerbation, or maintenance |
* Not considered a mental disorder (encoded on Axis III) Source: Adapted from Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
What are the risk factors?
Psychological and social covariates play a substantial role in the chronic pain experience (Table 2). How patients experience chronic pain also is influenced by personality and premorbid, semi-dormant characteristics that become activated by the stress of unremitting pain.7
- mood
- thought patterns
- perceptions
- coping abilities
- personality.
Table 2
Patient factors that contribute to or perpetuate chronic pain
Poor modulation of emotions (anger, depression, anxiety) |
Somatization (using pain to avoid confl icts, express anger, or punish others) |
Problematic cognitive styles (catastrophizing, perceived loss of control) |
Poor coping skills |
Psychiatric comorbidities |
Social/interpersonal variables:
|
Reinforcement for remaining sick and/or disabled:
|
Source: Adapted from reference 3 |
CASE CONTINUED: Underlying causes
Psychological and psychosocial factors appear to play an important role in Mrs. A’s pain. After her husband’s job was restructured, the couple moved away from Mrs. A’s mother, which she found distressing. Additionally, Mrs. A reports that her son has incurred substantial gambling debt.
Mrs. A admits she has “a hard time” accepting these events, but she cannot acknowledge anger or frustration. She avoids questions about such feelings and focuses on her pain. She reports, “The pain is always there and ruins my entire life. Absolutely nothing gives me relief.”
She does not endorse depressive or psychotic symptoms. She sometimes has passive thoughts of death when she feels hopeless about her persistent pain, but she vehemently denies suicidal ideas, intent, or plans. She has smoked 1 pack of cigarettes per day for 12 years but denies alcohol abuse or use of illicit substances.
Biopsychosocial assessment
Assessing a chronic pain patient includes evaluating somatic, psychological, and social factors (Table 3).3 A biopsychosocial approach recognizes that the patient’s experience of pain, presentation, and response to treatment are determined by the interaction of:
- biological factors
- the patient’s psychological makeup
- psychological comorbidities
- the extent of social support
- extenuating environmental circumstances.3,10
A thorough psychiatric assessment may reveal psychiatric comorbidity and psychological conditions that mediate pain.8 Recognizing and treating coexisting psychiatric disorders often will enhance effective pain management.
Subsyndromal psychological factors—such as troubling affective states, problematic cognitive styles,14 and ineffective coping strategies and interpersonal skills—can accompany pain. If unattended, such factors can heighten the patient’s pain awareness and compromise rehabilitation.
For example, patients such as Mrs. A can aggravate pain by catastrophizing.15 Having a tendency to exaggerate pain and the significance of related life events interferes with their ability to attend to matters within their control and pursue productive activities.16 Catastrophizing is associated with increased pain and perceived disability, poor adjustment to pain, and marked emotional distress.17,18
How pain shapes beliefs. Pain can shape the manner with which patients make sense of events in their lives by altering the way they perceive themselves and the world. Problematic beliefs of the self (inadequacy and helplessness), of the world (dangerousness), and of the future (hopelessness) can produce significant distress. A patient with such beliefs may experience a loss of self-esteem, self-efficacy, and connections with others and may experience marked disappointment and disillusionment.
- substance abuse
- nonadherence with treatment
- withdrawal from support systems
- incapacitating emotional states, such as marked dysphoria, anger, or anxiety.
Table 3
Biopsychosocial assessment of chronic pain patients: 3 components
Somatic factors |
Determine pain onset/duration, location, quality, intensity, associated features, aggravating and alleviating factors |
Single-dimension pain rating scales, such as Numeric Rating Scale or Visual Analog Scale |
Review prescribed and over-the-counter analgesic use (adherence, excess use, impact on functional adaptation) |
Psychological factors |
Mood and affect, cognitive content and processes, coping skills |
Psychiatric comorbidities (substance abuse/dependence; anxiety, sleep, and somatoform disorders; delirium; depression; sexual dysfunction) |
Suicide risk assessment |
Multidimensional pain rating scales, such as Coping Strategies Questionnaire or Multidimensional Pain Inventory |
Social factors |
Impact on relationships, including capacity for intimacy, mutuality, and sexuality |
Impact on activities of daily living, vocational and recreational functioning |
Determine functions patient can perform despite pain |
Source: Adapted from reference 3 |
CASE CONTINUED: Multifaceted treatment
You prescribe amitriptyline, 20 mg at bed-time, for pain and refer Mrs. A for cognitive-behavioral therapy (CBT). The emphasis of therapy is to identify affective states and cognitive distortions that are temporally related to pain exacerbations, to develop coping skills to deal with stressors, and to effectively express her anger. Mrs. A learns relaxation techniques and self-hypnosis to reduce distress. These measures help reduce her pain severity ratings to 3 on a 10-point scale. She also participates in physical therapy and yoga classes, which increase her endurance.
Psychiatrists’ role in treatment
Many chronic nonmalignant pain syndromes—including arthritic conditions, back pain, and fibromyalgia—are tenacious and not easily cured. Treatment goals are to relieve pain and maximize the patient’s functioning and quality of life while minimizing risks of iatrogenic harm. As part of a biopsychosocial approach to care:
- diagnose and treat psychiatric comorbidities
- assess responses to treatment interventions
- refine treatment measures when patients do not achieve functional and adaptational goals
- initiate pharmacologic interventions for pain
- address subsyndromal emotional and cognitive impediments to functional restoration.
In initial CBT sessions, the goal is to elicit the patient’s:
- perception of pain
- life situations
- beliefs about his or her life, relationships, and the future
- coping measures.
Self-regulatory techniques—including relaxation training, biofeedback, and hypnosis—can facilitate relaxation and “turn down” the physiologic triggers that cause and perpetuate pain.25,26 Hypnosis can lead to dissociative states that modify how a patient experiences pain. There is modest evidence that self-regulatory techniques are effective for treating pain.27,28
Pharmacotherapy. Multiple pathophysiologic mechanisms—including ion channel up-regulation, spinal hyperexcitability, and descending neurotransmitter pathway impairment—play a role in chronic pain states. Several classes of psychoactive agents can mitigate pain (Table 4), and some psychotropics are FDA-approved for specific pain conditions (Table 5).
Individualize medication selection, considering:
- cost
- ease of use
- tolerability
- interactions with coadministered medications
- clinical comorbidities.
- opioid therapy fails
- patients become dependent on escalating doses of opioids.
Antidepressants influence pain by blocking monoamine reuptake. Those that influence noradrenergic and serotonergic transmission may have greater analgesic effects than those that affect serotonin or norepinephrine reuptake alone.31-33
Anticonvulsants mitigate pain by influencing sodium or calcium channel regulation, GABA activity, or combinations of the 3.
In randomized controlled trials that included patients with diabetic and postherpetic neuropathies:
- one-third of patients achieved ≥50% pain relief with tricyclic antidepressants (TCAs) or anticonvulsants
- adverse effects were slightly more common with TCAs.34,35
Because antidepressants and anticonvulsants have different presumed mechanisms of action for pain relief, anticonvulsants might be useful for patients whose pain persists despite optimal antidepressant dosing or for whom antidepressants are in-tolerable. Alternately, coadministering antidepressants and anticonvulsants might capitalize on complimentary mechanisms of action. With coadministration, lower doses may be sufficiently analgesic and avoid adverse effects.
Benzodiazepines have been used short-term to mitigate muscle spasm pain as in fibromyalgia, phantom limb pain, and restless legs syndrome.36,37 Long-term benzodiazepine use can lead to low activity levels, high use of ambulatory medical services, and high disability levels, however.38 if required for muscle spasm or restless legs syndrome, benzodiazepines may best be confined to short-term use.
Antipsychotics. Limited studies have evaluated antipsychotics’ efficacy for chronic pain.39,40 Some have been found to be useful in neuropathic pain.40 Antipsychotics are seldom used to treat pain because of limited efficacy data, potential side effects, and an abundance of alternate agents. Because risks—most notably extrapyramidal side effects and tardive dyskinesia—appear to outweigh analgesic efficacy, I would confine antipsychotics to pain patients with delirium or psychosis. Antipsychotics’ potential role in treating refractory pain might warrant further investigation.40
Stimulants may reduce sedation, dysphoria, and cognitive inefficiency that can accompany opioid use.
Table 4
Uses of psychotropics in patients with chronic pain
Class/drug | Uses | Limitations |
---|---|---|
Antidepressants | Neuropathic pain, tension and migraine headache, FM, functional GI disorders, pain comorbid with depression/anxiety | NE/5-HT reuptake inhibitors are most effective for analgesia; side effects (TCAs may be least tolerable); drug interactions |
Anticonvulsants | Neuropathic pain, migraine headache, central pain, phantom limb pain | Side effects (sedation, motor and GI effects, rash); drug interactions |
Benzodiazepines | Muscle relaxation, restless legs syndrome, anxiety, insomnia | Abuse/dependence potential; sedation |
Lithium | Cluster headache prophylaxis | Not effective for episodic cluster headache; risk of toxicity if dehydration occurs or with certain drug combinations |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Stimulants | Opioid analgesia augmentation, opioid-induced fatigue and sedation | Abuse/dependence potential; overstimulation, anorexia, insomnia |
Antipsychotics | Neuropathic pain, migraine, cancer pain, delirium | Limited data; risks such as EPS and TD may outweigh benefi ts |
EPS: extrapyramidal symptoms; FM: fibromyalgia; GI: gastrointestinal; NE: norepinephrine; 5-HT: serotonin; TCAs: tricyclic antidepressants; TD: tardive dyskinesia | ||
Source: Adapted from reference 3 |
Table 5
Psychotropics approved for managing pain
Drug | Indication |
---|---|
Carbamazepine | Trigeminal neuralgia |
Divalproex | Migraine prophylaxis |
Duloxetine | Diabetic neuropathy |
Gabapentin | Postherpetic neuralgia |
Pregabalin | Postherpetic neuralgia, diabetic neuropathy, fibromyalgia |
Source: Adapted from reference 3 |
- International Association for the Study of Pain. www.iasp-pain.org.
- Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
- Loeser JD, Butler SH, Chapman CR, Turk DC. Bonica’s management of pain. 3rd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2001.
- Acetaminophen/hydrocodone • Lortab, others
- Amitriptyline • Elavil, Endep
- Carbamazepine • Tegretol
- Divalproex • Depakote
- Duloxetine • Cymbalta
- Fentanyl transdermal • Duragesic
- Gabapentin • Neurontin
- Lithium • Eskalith, Lithobid
- Pregabalin • Lyrica
Dr. Leo reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Schappert SM. National Ambulatory Medical Care Survey: 1989 summary. Vital Health Stat 13 1992;(110):1-80.
2. Sternbach RA. Pain patients: traits and treatment. New York, NY: Academic Press; 1974.
3. Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
4. Aigner M, Bach M. Clinical utility of DSM-IV pain disorder. Compr Psychiatry 1999;40(5):353-7.
5. Boland RJ. How could the validity of the DSM-IV pain disorder be improved in reference to the concept that it is supposed to identify? Curr Pain Headache Rep 2002;6(1):23-9.
6. Sullivan MD. DSM-IV pain disorder: a case against the diagnosis. Int Rev Psychiatry 2000;12:91-8.
7. Dersh J, Polatin PB, Gatchel RJ. Chronic pain and psychopathology: research findings and theoretical considerations. Psychosom Med 2002;64:773-86.
8. Fishbain DA. Approaches to treatment decisions for psychiatric comorbidity in the management of the chronic pain patient. Med Clin North Am 1999;83:737-60.
9. Mayou R, Kirmayer LJ, Simon G, et al. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162(5):847-55.
10. Gallagher RM. Treatment planning in pain medicine—integrating medical, physical, and behavioral therapies. Med Clin North Am 1999;83(3):823-49.
11. Jensen MP, Karoly P, Braver S. The measurement of clinical pain intensity: a comparison of six methods. Pain 1986;27:117-26.
12. Rosenstiel AK, Keefe FJ. The use of coping strategies in chronic low back pain patients: relationship to patient characteristics and current adjustment. Pain 1983;17:33-44.
13. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale multidimensional pain inventory (WHYMPI). Pain 1985;23:345-56.
14. Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: a critical review. Pain 1991;47:249-83.
15. Sullivan MJL, Stanish W, Waite H, et al. Catastrophizing, pain, and disability in patients with soft-tissue injuries. Pain 1998;77:253-60.
16. Crombez G, Eccleston C, Baeyens F, et al. When somatic information threatens, catastrophic thinking enhances attentional interference. Pain 1998;75:187-98.
17. Hasenbring M, Hallner D, Klasen B. Psychological mechanisms in the transition from acute to chronic pain: over-or underrated? Schmerz. 2001;15:442-7.
18. Sullivan MJ, Thorn B, Haythornthwaite JA, et al. Theoretical perspectives on the relation between catastrophizing and pain. Clin J Pain 2001;17:52-64.
19. Arnstein P. The mediation of disability by self efficacy in different samples of chronic pain patients. Disabil Rehabil 2000;22(17):794-801.
20. Fishbain DA. The association of chronic pain and suicide. Semin Clin Neuropsychiatry 1999;4(3):221-7.
21. Astin JA, Beckner W, Soeken K, et al. Psychological interventions for rheumatoid arthritis: a meta-analysis of randomized controlled trials. Arthritis Rheum 2002;47:291-302.
22. Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292(19):2388-95.
23. Morley S, Eccleston C, Williams A. Systematic review and meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999;80:1-13.
24. Hoffman BM, Papas RK, Chatkoff DK, Kerns RD. Meta-analysis of psychological interventions for chronic low back pain. Health Psychol 2007;26(1):1-9.
25. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, II: operant conditioning, hypnosis, and cognitive-behavioral therapy. Pain 1982;12:23-46.
26. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, I: relaxation training and biofeedback. Pain 1982;12:1-21.
27. Carroll D, Seers K. Relaxation for the relief of chronic pain: a systematic review. J Adv Nurs 1998;27:476-87.
28. Keel PJ, Bodoky C, Gerhard U, et al. Comparison of integrated group therapy and group relaxation training for fibromyalgia. Clin J Pain 1998;14:232-8.
29. Eriksen J, Sjogren P, Bruera E, et al. Critical issues on opioids in chronic non-cancer pain: an epidemiological study. Pain 2006;125:172-9.
30. Ballantyne JC, Mao J. Opioid therapy for chronic pain. N Engl J Med 2003;349:1943-53.
31. Lynch ME. Antidepressants as analgesics: a review of randomized controlled trials. J Psychiatry Neurosci 2001;26(1):30-6.
32. McQuay HJ, Tramer M, Nye BA, et al. A systematic review of antidepressants in neuropathic pain. Pain 1996;68:217-27.
33. Sussman N. SNRI’s versus SSRI’s: mechanisms of action in treating depression and painful physical symptoms. Prim Care Companion J Clin Psychiatry 2003;5(suppl 7):19-26.
34. Collins SL, Moore RA, McQuay HJ, et al. Antidepressants and anticonvulsants for diabetic neuropathy and postherpetic neuralgia: a quantitative systematic review. J Pain Symptom Manage 2000;20:449-58.
35. McQuay HJ. Neuropathic pain: evidence matters. Eur J Pain 2002;6(suppl A):11-8.
36. Bartusch SL, Sanders BJ, D’Alessio JG, et al. Clonazepam for the treatment of lancinating phantom limb pain. Clin J Pain 1996;12:59-62.
37. Dellemijn PL, Fields HL. Do benzodiazepines have a role in chronic pain management? Pain 1994;57:137-52.
38. Ciccone DS, Just N, Bandilla EB, et al. Psychological correlates of opioid use in patients with chronic nonmalignant pain: a preliminary test of the downhill spiral hypothesis. J Pain Symptom Manage 2000;20:180-92.
39. Gomez-Perez FJ, Rull JA, Dies H, et al. Nortriptyline and fluphenazine in the symptomatic treatment of diabetic neuropathy: a double-blind cross-over study. Pain 1985;23:395-400.
40. Fishbain DA, Cutler RB, Lewis J, et al. Do the second-generation “atypical neuroleptics” have analgesic properties? A structured evidence-based review. Pain Med 2004;5:359-65.
1. Schappert SM. National Ambulatory Medical Care Survey: 1989 summary. Vital Health Stat 13 1992;(110):1-80.
2. Sternbach RA. Pain patients: traits and treatment. New York, NY: Academic Press; 1974.
3. Leo RJ. Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing; 2007.
4. Aigner M, Bach M. Clinical utility of DSM-IV pain disorder. Compr Psychiatry 1999;40(5):353-7.
5. Boland RJ. How could the validity of the DSM-IV pain disorder be improved in reference to the concept that it is supposed to identify? Curr Pain Headache Rep 2002;6(1):23-9.
6. Sullivan MD. DSM-IV pain disorder: a case against the diagnosis. Int Rev Psychiatry 2000;12:91-8.
7. Dersh J, Polatin PB, Gatchel RJ. Chronic pain and psychopathology: research findings and theoretical considerations. Psychosom Med 2002;64:773-86.
8. Fishbain DA. Approaches to treatment decisions for psychiatric comorbidity in the management of the chronic pain patient. Med Clin North Am 1999;83:737-60.
9. Mayou R, Kirmayer LJ, Simon G, et al. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162(5):847-55.
10. Gallagher RM. Treatment planning in pain medicine—integrating medical, physical, and behavioral therapies. Med Clin North Am 1999;83(3):823-49.
11. Jensen MP, Karoly P, Braver S. The measurement of clinical pain intensity: a comparison of six methods. Pain 1986;27:117-26.
12. Rosenstiel AK, Keefe FJ. The use of coping strategies in chronic low back pain patients: relationship to patient characteristics and current adjustment. Pain 1983;17:33-44.
13. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale multidimensional pain inventory (WHYMPI). Pain 1985;23:345-56.
14. Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: a critical review. Pain 1991;47:249-83.
15. Sullivan MJL, Stanish W, Waite H, et al. Catastrophizing, pain, and disability in patients with soft-tissue injuries. Pain 1998;77:253-60.
16. Crombez G, Eccleston C, Baeyens F, et al. When somatic information threatens, catastrophic thinking enhances attentional interference. Pain 1998;75:187-98.
17. Hasenbring M, Hallner D, Klasen B. Psychological mechanisms in the transition from acute to chronic pain: over-or underrated? Schmerz. 2001;15:442-7.
18. Sullivan MJ, Thorn B, Haythornthwaite JA, et al. Theoretical perspectives on the relation between catastrophizing and pain. Clin J Pain 2001;17:52-64.
19. Arnstein P. The mediation of disability by self efficacy in different samples of chronic pain patients. Disabil Rehabil 2000;22(17):794-801.
20. Fishbain DA. The association of chronic pain and suicide. Semin Clin Neuropsychiatry 1999;4(3):221-7.
21. Astin JA, Beckner W, Soeken K, et al. Psychological interventions for rheumatoid arthritis: a meta-analysis of randomized controlled trials. Arthritis Rheum 2002;47:291-302.
22. Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA 2004;292(19):2388-95.
23. Morley S, Eccleston C, Williams A. Systematic review and meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 1999;80:1-13.
24. Hoffman BM, Papas RK, Chatkoff DK, Kerns RD. Meta-analysis of psychological interventions for chronic low back pain. Health Psychol 2007;26(1):1-9.
25. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, II: operant conditioning, hypnosis, and cognitive-behavioral therapy. Pain 1982;12:23-46.
26. Turner JA, Chapman CR. Psychological interventions for chronic pain: a critical review, I: relaxation training and biofeedback. Pain 1982;12:1-21.
27. Carroll D, Seers K. Relaxation for the relief of chronic pain: a systematic review. J Adv Nurs 1998;27:476-87.
28. Keel PJ, Bodoky C, Gerhard U, et al. Comparison of integrated group therapy and group relaxation training for fibromyalgia. Clin J Pain 1998;14:232-8.
29. Eriksen J, Sjogren P, Bruera E, et al. Critical issues on opioids in chronic non-cancer pain: an epidemiological study. Pain 2006;125:172-9.
30. Ballantyne JC, Mao J. Opioid therapy for chronic pain. N Engl J Med 2003;349:1943-53.
31. Lynch ME. Antidepressants as analgesics: a review of randomized controlled trials. J Psychiatry Neurosci 2001;26(1):30-6.
32. McQuay HJ, Tramer M, Nye BA, et al. A systematic review of antidepressants in neuropathic pain. Pain 1996;68:217-27.
33. Sussman N. SNRI’s versus SSRI’s: mechanisms of action in treating depression and painful physical symptoms. Prim Care Companion J Clin Psychiatry 2003;5(suppl 7):19-26.
34. Collins SL, Moore RA, McQuay HJ, et al. Antidepressants and anticonvulsants for diabetic neuropathy and postherpetic neuralgia: a quantitative systematic review. J Pain Symptom Manage 2000;20:449-58.
35. McQuay HJ. Neuropathic pain: evidence matters. Eur J Pain 2002;6(suppl A):11-8.
36. Bartusch SL, Sanders BJ, D’Alessio JG, et al. Clonazepam for the treatment of lancinating phantom limb pain. Clin J Pain 1996;12:59-62.
37. Dellemijn PL, Fields HL. Do benzodiazepines have a role in chronic pain management? Pain 1994;57:137-52.
38. Ciccone DS, Just N, Bandilla EB, et al. Psychological correlates of opioid use in patients with chronic nonmalignant pain: a preliminary test of the downhill spiral hypothesis. J Pain Symptom Manage 2000;20:180-92.
39. Gomez-Perez FJ, Rull JA, Dies H, et al. Nortriptyline and fluphenazine in the symptomatic treatment of diabetic neuropathy: a double-blind cross-over study. Pain 1985;23:395-400.
40. Fishbain DA, Cutler RB, Lewis J, et al. Do the second-generation “atypical neuroleptics” have analgesic properties? A structured evidence-based review. Pain Med 2004;5:359-65.