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.
Case continued: A bump in the road
The psychiatrist saw Ms. A 18 months later. Interim history revealed that her pain and mood improved on nortriptyline, 100 mg at bedtime. When she stopped taking nortriptyline 5 months earlier, her neck pain increased and she experienced a “deep blue mood.” Her physician restarted the nortriptyline.
At follow up, Ms. A reported no depressive symptoms and very little neck pain. The psychiatrist discussed with her depression’s relapse rate and the importance of continuing antidepressant therapy. As Ms. A was feeling much better and functioning normally, the psychiatrist decided additional psychotherapeutic intervention was not necessary.
Antidepressant options
TCAs provide analgesia via descending regulatory pathways by inhibiting serotonin and norepinephrine reuptake.17 When using TCAs for chronic pain, start with 10 to 25 mg at bedtime and increase by 10 to 25 mg every 3 to 7 days as tolerated. Increase incrementally until the pain responds or to the full antidepressant dosage (Table 2). Drug levels (when available) can help you provide an appropriate trial and monitor the patient’s adherence.
If the pain does not respond after 6 to 8 weeks, consider switching to another dual-action agent such as venlafaxine or to an SSRI.
SNRIs. Venlafaxine is a serotonin and norepineph-rine reuptake inhibitor (SNRI) with less-troublesome side effects than TCAs. It is structurally similar to tramadol18 and has combined serotonin and norepinephrine inhibition at dosages >75 mg/d. Although venlafaxine is not indicated for chronic pain, some studies have suggested possible benefits, including long-term analgesia, reduced polyneuropathic pain, and migraine prophylaxis.19-21 Venlafaxine may be a reasonable first or second choice for treating depression in patients with chronic pain, especially headache.14
Duloxetine—another SNRI—awaits FDA approval. Some studies have suggested that duloxetine improves painful physical symptoms as well as mood and functioning in major depression.22
SSRIs may be effective for certain types of pain, but the evidence is conflicting. Results of 41controlled trials support TCAs’ analgesic efficacy for neuropathic pain, headache, and central and post-stroke pain, whereas SSRIs’ analgesic efficacy varies from study to study. Comparisons of TCAs and SSRIs as analgesics uniformly show TCAs to be more effective, with the SSRIs often showing no analgesic effect.
Of three controlled trials of SSRIs for diabetic neuropathy, one showed fluoxetine similar to placebo, and two smaller studies showed paroxetine and citalopram more effective than placebo. Fluoxetine has shown analgesic effect for fibromyalgia in one study, but no effect in another. Citalopram showed no analgesic effect for fibromyalgia in another study.23
A prospective, double-blind study comparing fluoxetine, sertraline, paroxetine, and venlafaxine for migraines reported moderate to significant improvement in less than one-half of SSRI-treated patients vs two-thirds of venlafaxine-treated patients.21 SSRIs are no longer recognized by the International Headache Society as primary preventative medications for migraine.