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Evidence-Based Reviews


Treating affective illness in patients with chronic pain

They resist psychiatric assessment, but you can change ‘patients with pain’ to ‘clients managing pain’

Vol. 3, No. 5 / May 2004

Ms. A, age 44, fell from a 3-foot stool while reaching for a high kitchen shelf and suffered severe neck flexion. Her initial pain persisted for weeks and then months, resulting in chronic neck pain aggravated by movement.

Over the past year, her doctor has prescribed numerous analgesics and muscle relaxants, including tramadol, hydrocodone, oxycodone, tizanidine, and nonsteroidal anti-inflammatory drugs (NSAIDs). Treatments at a pain clinic have included triggerpoint injections, cervical epidural corticosteroid injection, left-sided cervical medial branch blocks, transcutaneous electrical nerve stimulation, and physical therapy. None provided sustained relief.

During a pain clinic visit, Ms. A wept and said she was tired of living with pain. She acknowledged depression and agreed to psychiatric consultation.

As in Ms. A’s case, physicians often refer patients with chronic pain and affective symptoms for psychiatric evaluation. These patients are often fearful, angry, and suspicious of any suggestion that their physical discomfort has a psychiatric component. They typically believe their pain had a clear onset and therefore should have an end point. Many have experienced unproductive specialty evaluations and failed treatments.

To help you overcome these obstacles when treating patients with chronic pain and depression, we discuss:

  • strategies to gain patients’ trust and build a therapeutic alliance
  • how to assess their pain, depression, and suicide risk
  • the role of psychotherapy in treating chronic pain
  • and evidence for choosing effective, nonaddicting medications.

Psychiatric evaluation

Depression and pain are linked psychologically and biochemically, sharing neurotransmitters involved in both nociceptive pathways and mood, especially serotonin and norepinephrine. 1,2 One-third to one-half of patients with chronic pain report comorbid depression, 3 and more than one-half of depressed patients presenting to primary care physicians report only somatic symptoms—various pain complaints among the most common. 4,5

Primary care doctors tend to refer chronic pain and depression cases to psychiatrists when:

  • patients are preoccupied with medication, have not followed treatment recommendations, or do not respond to treatment as expected
  • extensive medical evaluations reveal few or equivocal findings
  • somatic complaints are vague and diffuse, or there is marked disparity between pain complaints/disability and objective findings. 6,7

Assessing pain. In the initial assessment, validate the patient’s pain experience by asking about the location, quality, and severity of pain. The visual analogue scale (VAS) is commonly used to measure pain severity. The patient marks a spot on a line from “no pain” to “worst possible pain,” or—on a numbered VAS—from 0 (no pain) to 10 (extreme pain). The least and most severe pain over the preceding month can be ranked as baseline values.8

Be sensitive to the patient’s fear that you will attribute the pain to psychosocial issues or imply that “the pain is in your head.” Emphasize that you intend to evaluate the “whole person,” not just the part that hurts. Focus on how the pain affects the patient’s lifestyle—rather than its cause—and explore medication use patterns.

Assessing depression. The word “depression” is emotionally charged for chronic pain patients, who view affective symptoms—if they acknowledge them at all—as secondary to pain. They may strongly resist treatment for anything but pain. One way to defuse this defensiveness is to avoid attributing the pain to stress or depression.

Begin by assessing vegetative symptoms, which overlap in chronic pain and depression. The Beck Depression Inventory-II (Beck-II) may be a useful screening tool in a busy practice; the short form (13 questions) takes about 5 minutes to complete. 9

Explore cognitive and behavioral symptoms such as concentration, pleasure and interest level, activity, and self-esteem. Review the chronology of pain onset, mood changes, and stressors (proximate, remote, and cumulative).

Seek clues to endogenous factors by asking about past affective episodes, response to antidepressants, and family history of psychopathology. Substances that may induce depression include reserpine, interferon, and antiparkinsonian agents. Screen for potential organic mood disorders, such as depression secondary to hypothyroidism, corticosteroid use, Parkinson’s disease, lupus, HIV infection, or cerebrovascular disease. Where appropriate, obtain collateral information from family or friends.

Assessing suicide risk. Chronic pain patients may be at greater risk of suicide than the general population. Besides pain, other risk factors for suicide—such as major depression, anxiety disorders, alcohol/substance abuse, sleep disturbances, male gender, diminished social support, and recent loss—are common among these patients. 10,11

Screen chronic pain patients with suicidal ideation for these risk factors. Interventions include:

  • aggressively treat associated depression, anxiety, or insomnia
  • elicit support from family or other caregivers
  • pay close attention to talk about suicide
  • hospitalize when necessary
  • and, of course, treat pain.

Case continued: No stranger to depression

Ms. A’s psychiatric assessments revealed a pain severity ranking of 9 on a 1-to-10 scale, frequent crying, hopelessness, disrupted sleep, low energy, limited ability to concentrate, and fleeting suicidal thoughts. Her history included counseling during her first marriage and severe depression after separation from her second husband 3 years ago. An 8-week trial of fluoxetine, 20 mg/d, did not improve her depression then.

On examination, she displayed obvious pain behavior, constantly shifting her neck position and moving about the room. Her affect was tearful and her mood depressed. She was taking the NSAID celecoxib, 100 mg bid, and the skeletal muscle relaxant tizanidine, 4 mg tid. She was no longer using opioids and had no history of alcohol or illicit drug abuse.

Based on this assessment, the psychiatrist diagnosed Ms. A as having pain disorder with medical and psychological features, including symptom amplification and depression.

Table 1

4 treatment goals for patients with chronic pain and depression

  • Identify and reduce suicide risk.
  • Simplify medications by eliminating as many as possible, while keeping those that are helpful.
  • Break the cycle of repetitive physician evaluations and testing.
  • Improve the patient’s attitude, activity level, and ability to focus on something other than pain.


Educating the patient

As part of your assessment, explain the reciprocal effects of depression and pain. Acknowledge that:

  • chronic pain is different from acute pain, although the patient’s pain experience is the same
  • treatment often becomes part of the problem in chronic pain.

Doctors tend to apply acute pain treatments chronically, risking long-term effects of polypharmacy to achieve short-term relief. Depressed patients may be more likely than nondepressed patients to receive opioids for chronic pain, 12 and opioids and benzodiazepines may have depressive effects, as reflected by DSM-IV-TR’s inclusion of criteria for “opioid-induced mood disorder” and “sedative-, hypnotic-, or anxiolytic-induced mood disorder.”

To reduce patients’ resistance to antidepressants, reiterate any history of cumulative stressors and affective episodes unrelated to pain. Try using an analogy, such as “stress and pain are like waves on a rock” that eventually damage mood and coping mechanisms, or depression complicating pain is like having “too much on one’s plate.”

Finally, help patients understand that chronic pain is managed, not cured. Encourage them to set treatment goals beyond reducing pain (Table 1) and to make the transition from “patient with pain” to “client managing pain.”

Table 2

Dosing antidepressants and anticonvulsants
for chronic pain and depression

Drug

Starting (mg/d)

Target (mg/d)

Administration tips

TCAs

 

 

Check serum levels for dosages ≥150 mg/d (nortriptyline 100 mg/d) to assess rapid metabolism, adherence, or toxic levels

Amitriptyline

10 to 25

75 to 300

Clomipramine

10 to 25

75 to 250

Desipramine

10 to 25

75 to 200

Doxepin

10 to 25

75 to 300

Imipramine

10 to 25

75 to 300

Nortriptyline

10 to 25

40 to 200

SNRI

Venlafaxine

37.5 to 75

75 to 375

Use XR form to minimize side effects and for once-daily dosing

SSRIs

Citalopram

10 to 20

40 to 60

 

Fluoxetine

10 to 20

20 to 80

May increase carbamazepine, TCA blood levels and inhibit efficacy of codeine, dihydrocodeine, and hydrocodone

Paroxetine

10 to 20

20 to 60

Same as fluoxetine

Anticonvulsants

Carbamazepine

200

800 to 1,200

Check blood levels; may increase clomipramine levels, reduce acetaminophen, contraceptive levels

Clonazepam

0.5

1 to 2

Habituating potential with chronic use

Gabapentin

300 to 900

3,600 to 4,800

Blood monitoring not necessary

Valproate

250

750 to 2,500 (maximum dosage 60 mg/kg/d)

Check blood levels (trough plasma level 50 to 100 μg/mL)

TCA: tricyclic antidepressant

SNRI: serotonin-norepinephrine reuptake inhibitor

SSRI: selective serotonin reuptake inhibitor

Prescribing principles

Before adding any new pain medications, consider reducing dosages or discontinuing opioids or benzodiazepines and other substances the patient may be taking. Opioid use is associated with risks of dependence, addiction, and side effects including somnolence, cognitive impairment, and reduced activity that amplify depressive symptoms.

Benzodiazepines can generally be tapered by 10% per day, although you may need to extend the final taper over 3 to 4 days or longer, depending upon chronicity of use. Opioids may be tapered by 20% over 5 to 7 days. Breakthrough doses may be needed for marked withdrawal symptoms. Converting to longer half-life agents—such as clonazepam for benzodiazepines or methadone for opioids—often aids tapering, although other agents and strategies exist. 13

To gauge patient attempts at self-medication, monitor use of alcohol or illicit drugs with urine screening. For patients with a substantial history of substance abuse or positive toxicology screens, monitor randomly every 2 to 4 weeks.

On the other hand, undertreated pain also may impair mood and function. 1 If pain and mood improve and problematic drug-related behaviors resolve with increased opioid analgesia, consider maintaining opioids with regular re-evaluation of mood, coping, and medication adherence. 11 Transfer from immediate-release to controlled-release opioids to reduce dosing frequency, clockwatching, and the likelihood of inter-dose pain escalation. In general, maintain and optimize the dosage of nonaddictive analgesics such as NSAIDs, anticonvulsants, or antidepressants.

Case continued: Switching medication

The psychiatrist started Ms. A on nortriptyline, 25 mg at bedtime, to be increased after 3 nights to 50 mg at bedtime. Tizanidine, which had been ineffective, was discontinued to reduce the risk of xerostomia and oversedation in combination with nortriptyline. If tolerated, nortriptyline was to be further increased by 25 mg every 3 days to an initial target dosage of 100 mg at bedtime. The psychiatrist explained to Ms. A that it might take 4 to 6 weeks to gauge the medication’s efficacy.

Psychoeducation addressed the importance of stress reduction, prioritizing commitments, and setting limits on other people’s expectations. The door was left open to future psychotherapeutic exploration of past cumulative stressors.

Because antidepressants may provide an analgesic effect, 6,14 they are often used to treat affective symptoms in chronic pain. Headache and neuralgia tend to respond to antidepressants more robustly than do arthritis and low-back pain. Although some patients respond to low-dose antidepressants, a definitive trial requires full doses for 6 to 8 weeks (Table 2).

Matching a patient’s symptoms with medication side effects is useful when choosing antidepressants (Table 3). So-called “adverse” effects may have a corresponding benefit, depending on the clinical presentation. For example, a moreactivating antidepressant—such as the selective serotonin reuptake inhibitor (SSRI) fluoxetine—may help a patient with fatigue, whereas a moresedating agent—such as a tricyclic antidepressant (TCA) or mirtazapine—may improve sleep for a patient with insomnia.

Psychosocial therapies such as cognitive-behavioral therapy (CBT) or relaxation training (Table 4) may help patients with chronic pain to:

  • process covert emotions such as fear and anger as well as guilt, loss, and disability
  • reduce somatic preoccupation that is aggravating the pain
  • adhere to treatment.

Evidence strongly supports using relaxation techniques to reduce chronic pain in many medical conditions and hypnosis to ameliorate cancer pain. CBT and biofeedback appear moderately effective in relieving chronic pain. 15 CBT is significantly more effective than waiting list control conditions for relieving chronic nonheadache pain in measures of pain experience, mood/affect, cognitive coping and appraisal, pain behavior and activity level, and social role functioning. 16

Pain and opioid medications can impair concentration and affective processing, so initial psychotherapy may need to be supportive while you provide other treatments and simplify medication regimens. Eventually the patient may be ready to address underlying issues that may be contributing to the pain syndrome, such as a history of abuse. However, it is important to address this potentially destabilizing subject only after carefully gauging a patient’s defenses and readiness.

Continued...
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