TABLE 2 Key messages for patient education about depression
Antidepressants work only if taken every day
Antidepressants are not addictive
Benefits from medication appear slowly over several weeks
Continue antidepressants even after you feel better
Mild side effects are common and usually improve with time
If you are thinking of stopping the medication, call your physician first
The goal of treatment is compete remission, but this sometimes takes several medication adjustments
Counseling
Patients often benefit from counseling regarding sleep, exercise, and substance use. Many patients with depression experience early morning awakening. Those with agitated depression also often experience delayed sleep onset associated with worry. Providing the patient with information on basic sleep hygiene, exercise, and encouraging abstinence from or moderation in consumption of alcohol might all help.28-30 Additionally, sleep disturbances can indicate the possibility of comorbid disorders. A report that a patient fears going to sleep because of nightmares suggests posttraumatic stress disorder.
For some patients, counseling by the family physician or through referral may be a helpful treatment adjunct. Often depressed patients have deficient coping mechanisms and need assistance in developing strategies to resolve issues in their life. Principles used in cognitive behavioral therapy might be helpful in patient education and counseling.31 These include problem-solving strategies to resolve stressful concerns and cognitive techniques to identify and correct distorted or maladaptive thought patterns.29
As patients respond to depression treatment, an additional component of primary-care-based counseling should target reinvolvement with pleasurable social and physical activities. This may simply involve identifying activities the patient enjoyed prior to the onset of depression but has since stopped, and focusing on the steps required to reactivate these interests.
Shared decision-making with regard to treatment will improve subsequent patient adherence.27 Treatment options include psychotherapy, particularly cognitive behavioral therapy, pharmacotherapy, and electroconvulsive therapy. The latter should be considered for severely depressed patients, particularly persons with few social supports who are at significant risk of suicide.25
Cognitive behavioral therapy and other psychotherapies can show effectiveness equal to that of pharmacotherapy, although response usually lags by a month to 6 weeks compared with that attained by pharmacotherapy.32 For moderately to severely depressed patients, pharmacotherapy is the treatment of choice in part because of its more rapid onset of action.25
Pharmacotherapy
Pharmacotherapy, most often in the form of an SSRI, is the treatment of choice for depression as a result of patient preference, insurance coverage limitations, or time constraints. In choosing an anti-depressant, the family physician should be guided by effectiveness and potential for drug–drug interactions and for both short-and long-term side effects.33
Tricyclics, the SSRIs, and other newer antidepressants offer similar efficacy.34 While efficacy assesses outcome under ideal treatment conditions, the primary care physician is more concerned with effectiveness, defined as the proportion of patients started on an antidepressant during routine clinical practice who attain lasting benefit. Effectiveness includes consideration of patients who discontinue treatment because of side effects or drug–drug interactions, as well as those who do not obtain adequate therapeutic response. Since about 25% of patients discontinue SSRIs because of side effects, this is an important concern.24 Few studies have been conducted comparing the effectiveness of antidepressants.
Drug–drug interactions are mediated predominately by the cytochrome P450 isoenzymes responsible for drug metabolism in the liver.35-37 The 2D6 isoenzyme is responsible for 50% of drug metabolism in the liver; the 3A4 isoenzyme is responsible for another 30%.38 As a clinical example of the importance of such inhibition, codeine requires 2D6-mediated metabolism to become morphine and is ineffective for pain in many patients who are prescribed a 2D6 inhibitor. Patients receiving such agents also can have a 300% to 400% increase in blood levels of previously stable ß-blockers. Paroxetine and fluoxetine, the two SSRIs that strongly inhibit the 2D6 isoenzyme, cause clinically significant interactions; fluoxetine is also a moderate inhibitor of the 3A4 isoenzyme.35 Because of the number of potential drug–drug interactions through these isoenzymes, physicians must check for interactions before prescribing these medications or adding other new medications in patients already receiving these agents. This also is a consideration for patients who might require additional medications acutely, for instance in response to a cardiac or other emergency.
Side effects of concern include gastrointestinal effects, particularly nausea, and central nervous system (CNS) effects, including anxiety and agitation, sleep disturbance, and tremor. When these occur, they often decrease rapidly over the first 1 to 3 weeks. If severe, they can be managed by a temporary dosage decrease. For patients with significant CNS side effects, altering the timing of the daily dose might provide relief from daytime somnolence or agitation or from nighttime insomnia.
