The Psychiatrist/Psychologist as Pain Manager

From the 14th Annual Psychopharmacology Update, presented by the University of Nevada School of Medicine and the Nevada Psychiatric Society

Educational Objectives

The goals of this program are to encourage psychiatrists and psychologists to participate in pain management, and to improve the diagnosis and treatment of fibromyalgia. After hearing and assimilating this program, the clinician will be better able to:

1.   State the contributions psychiatrists and psychologists can make to the field of pain management.

2.   Describe the pathophysiology of chronic pain.

3.   Discuss methods for managing chronic pain.

4.   Define fibromyalgia using the American College of Rheumatology criteria.

5.   Diagnose and treat fibromyalgia.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the plan­ning committee to disclose relevant financial relationships within the past 12 months that might create any personal con­flicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in heath care and not a proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Cole is a consultant to Eli Lilly, King Pharmaceuticals, NeurogesX, and Meda; he is also on the Speaker’s Bureau for Eli Lilly. Dr. Horne receives grant/research support from Abbott, AstraZeneca, Corcept Therapeutics, Eli Lilly, Pfizer, Janssen, Organon, sanofi-aventis, and Dainippon Sumitomo Pharma, and is a consultant for Abbott, AstraZeneca, Eli Lilly, Janssen, and Pfizer. He is on the Speaker’s Bureaus for Abbott, AstraZeneca, Cephalon, Eli Lilly, Janssen, Pfizer, Sepracor, and Takeda. Both speakers presented information related to off-label or investigational use of medications. The planning committee re­ported nothing to disclose.

Acknowledgments

Drs. Cole and Horne were recorded at The 14th Annual Psychopharmacology Update, held February 12-14, 2009, in Las Vegas, NV, and sponsored by the University of Nevada School of Medicine and the Nevada Psychiatric Society. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

Treatment of Chronic Pain: Psychiatrists and Psychologists Must Get Involved

Barry Eliot Cole, MD, MPA, Executive Director, American Society of Pain Educators, and Vice-President for Medical and Scientific Services, Aventine HealthServices, Montclair, NJ

Introduction: “psychiatry is such a natural for pain management”; historically, psychiatrists at core of pain manage­ment until 1980s, when anesthesiologists began to have more influence; speaker opines that psychiatrists (and psy­chologists) should reclaim role as pain managers

Problems encountered by patients with chronic pain: access to medical care; practitioners reluctant to deal with chronic pain; comorbid depression and/or anxiety; deconditioning due to inactivity; complications of medications; job loss; work restrictions; loss of medical coverage; cost of care; litigation; workers’ compensation issues; disabil­ity issues; loss of customary role in family; difficulties maintaining activities of daily living

Pain in society: in developed countries, high economic costs associated with chronic pain; physicians charged with diagnosis and treatment of disease and with relief of pain and suffering; more people in pain today than in past be­cause population now larger; barriers to pain relief  —  poor coverage by health insurance; failure of clinicians to identify pain relief as priority; insufficient training of clinicians in pain assessment and treatment; fear (on the parts of clinicians and patients) about regulatory scrutiny

1978 composite model for understanding pain: early approach to study of pain that integrated pathophysiologic and psychiatric factors; attempted to identify differences between acute and chronic pain; sensory gate screens out minor unimportant pain information; after long period of bombardment with pain, system overwhelmed, leading to awareness of pain and changes in affective display due to anxiety and depression; once pain becomes chronic, it “becomes all-consuming,” and drains patients of adaptive capability; some individuals able to accept chronicity of pain and adapt accordingly; others develop infantile dependent modes of behavior over time, with loss of self-es­teem; patients often take multiple medications for pain

Nerve blocks: provided by anesthesiologists; represent only one aspect of pain management; aneshesia cannot be permanent; psychiatrists and psychologists can provide another approach by “looking at the whole patient”

Differentiating chronic pain from other types of pain: several systems available for classifying pain; speaker uses temporal classification

Acute pain: experienced during first 30 days after initiating event (although some extend category to 90  or even 180 days); useful for survival (ie, inhibits potentially harmful behaviors); allows healing to occur; source of pain usually obvious; psychologic factors may become issue if pain persists beyond 30 days; historically, treatment focused on getting to origin of pain or interrupting neurotransmission pathways

Recurrent acute pain: pain recurs repeatedly, but each episode discrete (eg, migraine headaches); recovery complete after each episode; treated with 1 to 3 days of medication; when recurrences frequent, may require management resembling that of chronic pain (integrative approach)

Subacute pain: experienced for 31 to 89 days (or £179 days, according to some); “golden 100 days”  —  if pain re­versed in first 100 days, chances of complete pain relief good, but after 100 days, complete relief unlikely; justi­fies aggressive and comprehensive treatment; often requires management with approaches for both acute and chronic pain

Chronic pain: after 89 days; no biologic utility; complete freedom from pain unlikely; associated with anxiety, de­pression, substance abuse, disability, and failed relationships; pathophysiology different from that of acute pain and therefore requires different treatment; interventions may play role in pain relief, but rehabilitation usually needed

Understanding chronic pain: “it’s not just changes in wiring”; complex process that starts with chronic pain as ad­aptation of nervous system, but eventually results in calcium channels fused in open position; wide-dynamic-range (WDR) neurons respond only to pain (reasons unknown); leads to central sensitization

Suffering and pain: not same thing; suffering goes beyond physical pain, and disrupts function and living; accom­panies not only pain, but many disease states as well; unknown why some people suffer with pain and some do not (possibly learned helplessness)

Disruptions caused by pain: changes lives due to disability and impairment; associated with diminished ability to walk, socialize, do household chores, sleep, concentrate, and function independently; patient becomes concerned about taking medicines properly, having side effects, feeling disbelieved, and experiencing dissatisfaction with treatment; “go withs” include depression, helplessness, loneliness, and feeling that no one else shares this condi­tion

Cognitive distortions with chronic pain: catastrophizing; magnification of significance; helplessness; overgeneral­ization; personalization; labeling; selective abstraction; support groups helpful to patient and family in resolving some of these issues

Treatment of chronic pain: includes pharmacologic, nonpharmacologic, and integrative approaches

Pharmacology: nonopioids  —  include acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and COX-2 inhibitors; opioids  —  immediate-release or controlled-release; can be administered orally, transdermally, or neuraxially; potential adjuvant medications  —  anticonvulsants, mood stabilizers, antidepressants, anxiolytics, atypical antipsychotics, botulinum toxin, central nervous system (CNS) stimulants, and skeletal muscle relax­ants; others  —  calcium channel blockers; sodium channel blockers

Nonpharmacologic methods: physical therapy; occupational therapy; implanted devices

Integrative options: dietary and nutraceutical therapies; magnet therapy; meditation; prayer; touch therapy; yoga; traditional Chinese medicine (including acupuncture); Ayurvedic medicine; chiropractic; homeopathy

Role for psychiatrists and psychologists in pain management: thorough assessment of complex people (ie, not simply mind or body, but totality of both); improvement of medication management; setting realistic expectations (eg, helping patients to accept unlikelihood of complete pain relief); letting patients tell their stories; helping pa­tients to find alternatives; advocating for patients; performing thorough pain assessments (eg, rating scales, ques­tionnaires, pain diaries); speaker recommends becoming familiar with operant-behavioral model of pain

Moral imperative: “we need to do more for our patients in pain; we need to learn more about pain; we need to be­come leaders in the field of pain management”

Optimal Therapy for Fibromyalgia

Robert Lynn Horne, MD, Professor of Psychiatry, University of Nevada School of Medicine, Reno

What is fibromyalgia (FM)? chronic condition characterized by widespread pain; patients often have heightened sensitivity to pain (hyperalgesia); non-noxious stimuli may result in pain (allodynia)

American College of Rheumatology criteria: widespread bilateral pain, above and below waist, and in axial skele­ton (cervical spine, anterior chest, thoracic spine, or low back); duration ³3 mo; presence of pain on application of pressure (by patient or clinician) of »4 kg at ³11 of 18 specific muscle-tendon sites

Other features of FM: pain with heat, cold, or electrical stimulation; cognitive complaints, including impairment of working and/or recognition memory, and/or recall; sleep disturbance characterized by nonrestorative sleep and increased awakenings; fatigue throughout day

Pathophysiology: believed to be central pain mechanism; increased levels of excitatory neurotransmitters (ie, gluta­mate and substance P) may contribute to neuronal hyperactivity and central sensitization; compared with normal controls, levels of substance P in cerebrospinal fluid (CSF) 3-fold higher in patients with FM; functional magnetic resonance imaging (fMRI) data provide supporting evidence that FM involves altered central pain processing

Precipitants of FM syndrome (FMS): often “nothing that we know of”; physical and emotional trauma; infection, especially viral; hypothyroidism (measure thyroid hormone levels, not thyrotropin); autoimmune diseases, includ­ing rheumatoid arthritis, systemic lupus erythematosus, and osteoarthritis

Common comorbidities: chronic fatigue syndrome (treat with modafinil, 200 mg every morning); migraine head­aches (treat with divalproex extended-release [ER], not delayed-release [DR], 500 to 1000 mg every night, or topiramate titrated from 25 to 400 mg daily); other comorbidities include muscle contraction headaches, irritable bowel syndrome, and psychiatric illnesses

Psychiatric comorbidities: lifetime prevalence of mood disorders, 74.4%, with major depressive disorder (61.5%) and bipolar disorder (12.8%) being most common; lifetime prevalence of anxiety disorders, 60.3%, most com­monly panic disorder (28.2%) and posttraumatic stress disorder (23.1%)

Genetic basis: 32.1% of first-degree relatives of patients with FM have mood disorder, 29.5% have major depressive disorder, and 2.6% have bipolar disorder (compared to first-degree relatives of patients with rheumatoid arthritis [mood disorder, 19.1%; major depressive disorder, 18.3%; bipolar disorder, 0.8%])

Outcome studies: with continuing treatment,  25% of participants in remission at 1 yr, and  65% in remission at 2 yr, without complaints of widespread pain

Pharmacologic treatment: only pregabalin and duloxetine have Food and Drug Administration (FDA) approval for treatment of FM; have different mechanisms of action and safe to combine if necessary; efficacy of other drugs in same classes not supported by research

Pregabalin: structure differs from g-aminobutyric acid (GABA) and gabapentin; indications include management of FM, neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, and adjunctive ther­apy for adults with partial-onset seizures; modulates influx of calcium into hyperexcited neurons; does not alter vascular or cardiac function; pharmacokinetics better than those of gabapentin; rapidly absorbed; bioavailability >90%; serum levels proportional to dose; no food effect; rapid dose increase possible without side effects; 90% unchanged upon excretion; no protein binding, so low potential for pharmacokinetic drug interactions; study data  —  14-wk fixed-dose double-blind trial of monotherapy with pregabalin found significant results with 450-mg dose for improvement in pain, response rates, and number of patients (75%) reporting global improvement; durability study found 68% of patients on pregabalin maintained response over 6-mo period; most common ad­verse events in trials included dizziness, somnolence, headache, dry mouth, peripheral edema, and infection

Duloxetine: selective serotonin-norepinephrine reuptake inhibitor; approved for treatment of FM, major depressive disorder, generalized anxiety disorder, and management of neuropathic pain associated with diabetic peripheral neuropathy; in monotherapy trials, significant number of patients (30%) reported >50% pain relief and signifi­cantly improved pain scores (based on Fibromyalgia Impact Questionnaire, and particularly for 120-mg dose); adverse events included nausea, dry mouth, constipation, decreased appetite, somnolence, insomnia, and head­ache

Not approved by FDA: 3 double-blind, placebo-controlled trials of tramadol showed superiority to placebo; weak opiate-receptor agonist; weak inhibitor of serotonin and norepinephrine reuptake (unrelated to mechanism of pain relief); can be used alone or in combination with acetaminophen; side effects include sedation, dizziness, nausea, and vomiting

Contraindicated for fibromyalgia: antidepressants (tricyclic antidepressants [TCAs] and SSRIs); anticonvulsants other than pregabalin or gabapentin; opioid analgesics

TCAs: advantages  —  inexpensive; may be somewhat effective for pain; probably helpful for insomnia; disadvantages  —many side effects, especially at doses used for depression; lethal in overdose; high risk for car­diac arrhythmias; American Geriatric Society recommendations state TCAs contraindicated for treatment of FM in patients >65 yr of age

SSRIs: in only double-blind, placebo-controlled trial, no difference between 20-mg fluoxetine and placebo; 80 mg superior to placebo for pain, fatigue, and depression, but not for tender points; 2 double-blind, placebo-controlled trials of citalopram showed no difference between 20- or 40- mg doses and placebo

Recommendations for combination pharmacotherapy: start with pregabalin daily, 75 mg bid for 1 wk; increase to 150 mg bid for 1 wk; if tolerated, increase to £225 mg bid; if side effects prevent increase to effective dose, cross-taper by 50 mg of pregabalin for 300 mg of gabapentin per day (some patients tolerate gabapentin better than pre­gabalin); 75% of patients require second medication to achieve remission; add duloxetine 30 mg daily for 1 wk, then 60 mg daily; after 4 wk, increase to 90 mg per day for 1 wk, then 120 mg per day, if needed; if side effects prevent increase to effective dose, cross-taper 30 mg of duloxetine for 75 mg venlafaxine per day (up to 225 mg); add modafinil, 200 mg once daily, if needed for fatigue; use celecoxib, 200 mg once or bid, or tramadol, up to 100 mg bid, for residual pain

Opiates: speaker strongly recommends against their use “unless and until you’ve done every other possible thing for your patient with fibromyalgia”

Suggested Reading

Acuna C: Duloxetine for the treatment of fibromyalgia. Drugs Today (Barc) 44:725, 2008; Apkarian AV: Pain and brain changes. In: Benzon HT et al eds: Raj’s Practical Management of Pain, 4th Ed. Philadelphia: Mosby-Elsevier, 2008; Arnold LM: Pain and the brain: chronic widespread pain. J Clin Psychiatry 70:e10, 2009; Cole BE: Resources for education on pain and its management: a practitioner’s compendium. Curr Pain Headache Rep 13:110, 2009; Crofford LJ et al: Pregabalin 1008-105 Study Group. Pre­gabalin for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebo-controlled trial. Arthritis Rheum 52:1264, 2005; Fink K et al: Inhibition of neuronal Ca(2+) influx by gabapentin and pregabalin in the human neocortex. Neuropharmacology 42:229, 2002; Harris RE, Clauw DJ: Newer treatments for fibromyalgia syndrome. Ther Clin Risk Manag 4:1331, 2008; Henriksson KG: Fibromyalgia  —  from syndrome to disease. Overview of pathogenetic mechanisms. J Rehabil Med 41(Suppl):89, 2003; Leo RJ: Clinical Manual of Pain Management in Psychiatry. Washington, D.C.: American Psychiatric Publi­cations, 2007; McCracken LK: Psychological effects of chronic pain: an overview. In Rice A et al eds: Clinical Pain Manage­ment: Chronic Pain, 2nd Edition. London, UK: Hodder Arnold, 2008; Mease PJ et al: Long-term safety, tolerability, and efficacy of duloxetine in the treatment of fibromyalgia. Semin Arthritis Rheum Jan 17, 2009. [Epub ahead of print]; Morris DB, Wilson PR: The challenges of pain and suffering. In Rice A et al eds: Clinical Pain Management: Chronic Pain, 2nd Edition. London, UK: Hodder Arnold, 2008; Otis JD et al: The influence of family and culture on pain. In: Dworkin RH, Breitbart WS, eds: Psychoso­cial Aspects of Pain: A Handbook for Health Care Providers. Seattle, WA: IASP Press, 2004; Rich B: Pain in society: ethical and legal perspectives. In Rice A et al eds: Clinical Pain Management: Chronic Pain, 2nd Edition. London, UK: Hodder Arnold, 2008; Staud R, Rodriguez ME. Mechanisms of disease: pain in fibromyalgia syndrome. Nat Clin Pract Rheumatol 2:90, 2006.