continuation period, somatic therapy is usually discon-tinued in the patient
with a single episode of major depression. Before discontinuing, however, it is
important to remember that depression is often a lifelong disease with a
chronic course. One should always weigh the benefits of discontinuance against
the risks of recurrent depression.
past, a distinction between exogenous and endog-enous depression was used to
predict the risk of recurrence. Infer-ences about etiology, however, are not an
accurate predictor of recurrence. More useful information are the age of onset
during the initial episode and the number of episodes. Patients with a sin-gle episode
of acute depression, who have an onset before age 50 years, are the best
candidates for discontinuance (Greden, 1993).
TCAs, the usual strategy is to taper the medications at a rate of 25 to 50
mg/day every 2 to 3 days. Too rapid a discon-tinuation may produce symptoms of
cholinergic “rebound” or supersensitivity. Such a rebound includes severe
gastrointestinal symptoms (nausea, vomiting and cramping), other signs of
auto-nomic hyperactivity (diaphoresis, anxiety, agitation, headaches) and
insomnia (often with vivid nightmares). In severe cases, a full delirium may
result. Cholinergic rebound may occur as early as 48 hours or as late as 2
weeks after discontinuation. These symptoms may account for some cases of presumed
early relapse from antidepressant discontinuation.
also have a withdrawal syndrome, including symptoms of psychosis, on abrupt
withdrawal; however, this syn-drome is rarer than that seen with TCAs.
has a long half-life, and abrupt discontinuation should be permissible.
Sertraline, citalopram and paroxetine, with shorter half-lives of around a day,
may require a 7- to 10-day taper. With the shorter-acting agents, a withdrawal
syndrome in-cluding symptoms of fatigue, insomnia, abdominal distress and
influenza-like symptoms have been reported when they are too abruptly
discontinued. The same may be true for venlafaxine.
investigators question current tapering schedules, which are based on
pharmacokinetic rather than pharmacody-namic (i.e., receptor) effects. Given an
antidepressant’s long-term effects, they suggest that receptors will “need”
more time to readjust to a new medication-free environment. Greden (1993), for
instance, recommended a one-fourth reduction in dose every third month for
tricyclic medication. For fluoxetine, he recom-mended slowly increasing the
dosing interval: from daily to every other day for 3 months, then every third
day for 3 months. After 3 months of dosing every 3 days, he recommended
switch-ing to a liquid form to permit 25% dose reductions each quarter year.
Obviously, such a strategy would dramatically increase the taper period from
several weeks to approximately a year. It will be interesting to see whether
studies support the contention that extended tapers are more likely to prevent
discontinuance, the goal is to enable early intervention should symptoms recur.
A first episode of depression has a high risk of recurrence, and the risk of
recurrence is even higher in pa-tients who show only partial response to
medication. The patient should be educated to recognize symptoms of depression.
The patient’s own history suggests which symptoms were prodromal to the
patient’s full depressive episode.