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
|
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.