Abnormal Psychology, 18th Ed (Jim M. Hooley, Matthew K. Nock etc.)

264 Chapter 7
For most patients who are moderately to seriously
depressed, including those with persistent depressive disor-
der, the drug treatment of choice from the 1960s to the early
1990s was tricyclic antidepressants (TCAs; called this
because of their chemical structure) such as imipramine.
TCAs increase neurotransmission of the monoamines, pri-
marily norepinephrine and to a lesser extent serotonin
(Thase & Denko, 2008). The ecacy of TCAs in significantly
reducing depressive symptoms has been demonstrated in
hundreds of studies where the response of patients with
depression who were given these drugs has been compared
with the response of patients given a placebo. However,
only about 50 percent show what is considered clinically
significant improvement, and many of these patients still
have significant residual depressive symptoms. Fortunately,
about 50 percent of those who do not respond to an initial
trial of medication will show a clinically significant response
when switched to a dierent antidepressant or to a combi-
nation of medications (Hollon, Thase, & Markowitz, 2002).
Unfortunately, TCAs have unpleasant side eects for
some people (e.g., dry mouth, constipation, sexual dys-
function, and weight gain). Although these side eects
often diminish over time, they are so unpleasant to many
patients that they stop taking their medications before the
side eects go away. In addition, because these drugs are
highly toxic when taken in large doses, there is some risk in
prescribing them for suicidal patients, who might use them
for an overdose.
The side eects and toxicity of TCAs have led physi-
cians to increasingly prescribe selective serotonin reup-
take inhibitors (SSRIs) (Olfson & Marcus, 2009). SSRIs are
generally no more eective than the tricyclics; indeed some
findings suggest that TCAs are more eective than SSRIs
for severe depression. However, the SSRIs tend to have
many fewer side eects and are better tolerated by patients,
as well as being less toxic in large doses. The primary nega-
tive side eects of the SSRIs are problems with orgasm and
psychosocial risk factors for mood disorders operate across
cultures, and there is some initial evidence that factors like
rumination, hopelessness, and pessimistic attributional
style (Abela et al., 2011) are associated with risk for depres-
sion in other countries, such as China (Hong et al., 2010).
Treatments and Outcomes
7.7 Describe and distinguish between dierent
treatments for mood disorders.
Many patients with mood disorders (especially unipolar
disorders) never seek treatment. Even without formal
treatment, the great majority of individuals with mania and
depression will recover (often only temporarily) within less
than a year. However, given the enormous amount of personal
suering and lost productivity that these individuals endure,
and given the wide variety of treatments that are available
today, more and more people who experience these disorders
are seeking treatment. There was a rapid increase in the
treatment of depression from 1987 to 1997, and there has been
a more modest increase since 1998 (Marcus & Olfson, 2010).
Interestingly, between 1998 and 2007, there was a decline in
the reported use of psychotherapy, although the use of
antidepressant medication remained relatively stable. These
changes are happening in an era in which there is greatly
increased public awareness of the availability of eective
treatments and during a time in which significantly less
stigma is associated with experiencing a mood disorder.
Nevertheless, only about 40 percent of people with mood
disorders receive minimally adequate treatment, with the
other 60 percent receiving no treatment or inadequate care
(Wang, Lane, et al., 2005). Fortunately, the probability of
receiving treatment is somewhat higher for people with
severe unipolar depression and with bipolar disorder than for
those with less severe depression (Kessler et al., 2007).
Pharmacotherapy
Antidepressant, mood-stabilizing, and antipsychotic drugs
are all used in the treatment of unipolar and bipolar disor-
ders (see Chapter 16 for further information about these
medications). The first category of antidepressant medica-
tions—developed in the 1950s—is the monoamine oxidase
inhibitors (MAOIs) because they inhibit the action of mono-
amine oxidase, the enzyme responsible for the breakdown
of norepinephrine and serotonin once released. The MAOIs
can be as eective in treating depression as other categories
of medications, but they have potentially dangerous (even
potentially fatal) side eects if certain foods rich in the amino
acid tyramine are consumed (e.g., red wine, beer, aged
cheese, salami). Thus, they are not used very often today
unless other classes of medication have failed. Depression
with atypical features is the one subtype of depression that
seems to respond preferentially to the MAOIs. Illustration of serotonin.
Timonina/Shutterstock
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Mood Disorders and Suicide 265
medication because about 50 percent of those who do not
respond to the first drug prescribed do respond to a second
one. Also, discontinuing the drugs when symptoms have
remitted may result in relapse. Recall that the natural
course of an untreated depressive episode is typically 6 to 9
months. Thus, when depressed patients take drugs for 3 to
4 months and then stop because they are feeling better, they
are likely to relapse because the underlying depressive epi-
sode is actually still present, and only its symptomatic
expression has been suppressed (Gitlin, 2002; Hollon,
Thase, & Markowitz, 2002; Hollon et al., 2006). Because
depression is often a recurrent disorder, physicians have
increasingly recommended that patients continue for very
long periods of time on the drugs (ideally at the same dose)
in order to prevent recurrence (Nutt, 2010). Thus, these
medications can often be eective in prevention, as well as
treatment, for patients subject to recurrent episodes (Hollon
et al., 2006; Thase & Denko, 2008). Nevertheless, approxi-
mately 25 percent of patients continuing to receive medica-
tion during the maintenance phase of treatment show
recurrence of MDD (Solomon et al., 2005). Patients showing
residual symptoms are most likely to relapse, indicating the
importance of trying to treat the patient to full remission of
symptoms (Keller, 2004; Thase & Denko, 2008).
LITHIUM AND OTHER MOOD-STABILIZING DRUGS
Lithium therapy has now become widely used as a mood
stabilizer in the treatment of both depressive and manic
lowered interest in sexual activity, although insomnia,
increased physical agitation, and gastrointestinal distress
also occur in some patients (Thase, 2009b).
SSRIs are used not only to treat severe depression but
also to treat people with mild depressive symptoms (Git-
lin, 2002). Importantly, recent research has shown that anti-
depressant medication is superior to placebo only for
patients with very severe depressive symptoms, with neg-
ligible treatment eects observed for those with less severe
symptoms (Fournier et al., 2010; see Figure 7.9).
In the past decade, several new atypical antidepres-
sants (neither tricyclics nor SSRIs) have also become
increasingly popular, each with its own advantages
( Marcus & Olfson, 2010). For example, bupropion
( Wellbutrin) does not have as many side eects (especially
sexual side eects) as the SSRIs and, because of its activat-
ing eects, is particularly good for depression involving
significant weight gain, loss of energy, and oversleeping. In
addition, venlafaxine (Eexor) seems superior to the SSRIs
in the treatment of severe or chronic depression, although
the profile of side eects is similar to that for the SSRIs.
Several other atypical antidepressants have also been
shown to be eective (see Chapter 16).
THE COURSE OF TREATMENT WITH ANTIDEPRESSANT
DRUGS Antidepressant drugs usually require at least 3 to
5 weeks to take eect. Generally, if there are no signs of
improvement after about 6 weeks, physicians try a new
HRSD change
0
810121416182022242628303234363840
4
8
12
16
20
24
28
32
HRSD scores at intake
Observed placebo change
Observed ADM change
Estimated placebo change
Estimated ADM change
Figure 7.9 Eectiveness of Antidepressants Based on Severity of Depression
This figure shows the amount of change in depressive symptoms, as measured by the Hamilton Rating
Scale for Depression (HRSD), from treatment intake to the end of treatment for those receiving antidepres-
sant medication (ADM; dark circles) relative to placebo (light circles). The size of the circle represents the
number of data points that contributed to that mean. The two lines represent the estimated change in
depressive symptoms. Note that the circles (and lines) are overlapping for those with low and moderate
depressive symptoms at intake (the left half of the figure), and a dierence between ADM and placebo
only emerges for those with high depressive symptoms at intake (the right half of the figure). The take-
home message: Antidepressants appear to be most eective for severe depression, but are no more
eective than placebo for mild or moderate depression.
(Based on Fournier J. C., DeRubeis R. J., Hollon S. D., Dimidjian S., Amsterdam J. D., Shelton R. C., and Fawcett J.
(2010). Antidepressant drug eects and depression severity: A patient-level meta-analysis. JAMA, 303, 47-53.)
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266 Chapter 7
signs of psychosis (hallucinations and delusions) may also
receive treatments with antipsychotic medications (see
Chapters 13 and 16) in conjunction with their antidepres-
sant or mood-stabilizing drugs (Keck & McElroy, 2002;
Rothschild et al., 2004).
Alternative Biological Treatments
In addition to the use of pharmacotherapy, there are sev-
eral other biologically oriented approaches to the treat-
ment of mood disorders. These approaches have been the
subject of empirical study in recent years, and they appear
to be promising treatment options.
ELECTROCONVULSIVE THERAPY Because antidepres-
sants often take 3 to 4 weeks to produce significant
improvement, electroconvulsive therapy (ECT) is often
used with patients who are severely depressed (especially
among the elderly) and who may present an immediate
and serious suicidal risk, including those with psychotic or
melancholic features (Goodwin & Jamison, 2007). It is also
used in patients who cannot take antidepressant medica-
tions or who are otherwise resistant to medications
(Heijnen et al., 2010; Mathew et al., 2005). When selection
criteria for this form of treatment are carefully observed, a
complete remission of symptoms occurs for many patients
after about 6 to 12 treatments (with treatments adminis-
tered about every other day). This means that a majority of
patients with severe depression can be vastly better in 3 to
5 weeks (George et al., 2013). The treatments, which induce
seizures, are delivered under general anesthesia and with
muscle relaxants. The most common immediate side eect
is confusion, although there is some evidence for lasting
adverse eects on cognition, such as amnesia and slowed
response time (Sackeim et al., 2007). Maintenance dosages
of an antidepressant and a mood-stabilizing drug such as
lithium are then ordinarily used to maintain the treatment
gains achieved until the depression has run its course
(Mathew et al., 2005; Sackeim et al., 2009). ECT is also very
useful in the treatment of manic episodes; reviews of the
evidence suggest that it is associated with remission or
marked improvement in 80 percent of patients with mania
(Gitlin, 1996; Goodwin & Jamison, 2007). Maintenance on
mood-stabilizing drugs following ECT is usually required
to prevent relapse.
TRANSCRANIAL MAGNETIC STIMULATION Although
transcranial magnetic stimulation (TMS) has been available
as an alternative biological treatment for some time now,
only in the past decade has it begun to receive significant
attention. TMS is a noninvasive technique allowing focal
stimulation of the brain in patients who are awake. Brief but
intense pulsating magnetic fields that induce electrical
activity in certain parts of the cortex are delivered (Goodwin
& Jamison, 2007; Janicak et al., 2005). The procedure is
episodes of bipolar disorder. The term mood stabilizer is
often used to describe lithium and related drugs because
they have both antimanic and antidepressant eects—that
is, they exert mood-stabilizing eects in either direction.
Lithium has been more widely studied as a treatment of
manic episodes than of depressive episodes, and estimates
are that about three-quarters of those in a manic episode
show at least partial improvement. In the treatment of
bipolar depression, lithium may be no more eective than
traditional antidepressants (study results are inconsistent),
but about three-quarters show at least partial improve-
ment (Keck & McElroy, 2007). However, treatment with
antidepressants is associated with significant risk of pre-
cipitating manic episodes or rapid cycling, although the
risk of this happening is reduced if the person also takes
lithium (Keck & McElroy, 2007; Thase & Denko, 2008).
Lithium is often effective in preventing cycling
between manic and depressive episodes (although not nec-
essarily for patients with rapid cycling), and patients with
bipolar disorder frequently are maintained on lithium
therapy over long time periods, even when not manic or
depressed, simply to prevent new episodes. Unfortunately,
several large studies recently have found that only about
one-third of patients maintained on lithium remained free
of an episode over a 5-year follow-up period. Neverthe-
less, patients on lithium maintenance do have fewer epi-
sodes than patients who discontinue their medication
(Keck & McElroy, 2007).
Lithium therapy can have some unpleasant side eects
such as lethargy, cognitive slowing, weight gain, decreased
motor coordination, and gastrointestinal diculties. Long-
term use of lithium is occasionally associated with kidney
malfunction and sometimes permanent kidney damage,
although end-stage renal disease seems to be a very rare
consequence of long-term lithium treatment (Goodwin &
Jamison, 2007; Tredget et al., 2010). Not surprisingly, these
side eects, combined with the fact that many patients with
bipolar disorder seem to miss the highs and the abundance
of energy associated with their hypomanic and manic epi-
sodes, sometimes cause patients to refuse the drug.
In the past several decades, evidence has emerged for
the usefulness of another category of drugs known as the
anticonvulsants (e.g., carbamazepine, divalproex, and val-
proate) in the treatment of bipolar disorder. These drugs
are often eective in patients who do not respond well to
lithium or who develop unacceptable side eects from it,
and they may also be given in combination with lithium.
However, a number of studies have indicated that risk for
attempted and completed suicide was nearly two to three
times higher for patients on anticonvulsant medications
than for those on lithium (Goodwin et al., 2003; Thase &
Denko, 2008), suggesting one major advantage of giving
lithium to patients who can tolerate its side eects. Both
people with bipolar or unipolar depression who show
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Mood Disorders and Suicide 267
BRIGHT LIGHT THERAPY In the past decade an alterna-
tive nonpharmacological biological method has received
increasing attention: bright light therapy (see Pail et al.,
2011, for a review). This was originally used in the treat-
ment of seasonal aective disorder, but it has now been
shown to be eective in nonseasonal depressions as well
(Golden et al., 2005; Lieverse et al., 2011).
Psychotherapy
Several forms of specialized psychotherapy, developed
since the 1970s, have proved eective in the treatment of
unipolar depression, and the magnitude of improvement
of the best of these is approximately equivalent to that
observed with medications. Considerable evidence also
suggests that these same specialized forms of psychother-
apy for depression, alone or in combination with drugs,
significantly decrease the likelihood of relapse within a
2-year follow-up period (Hollon & Dimidjian, 2009; Hollon
et al., 2005). Other specialized treatments have been devel-
oped to address the problems of people (and their families)
with bipolar disorder.
COGNITIVE-BEHAVIORAL THERAPY One of the two
best-known psychotherapies for unipolar depression with
documented eectiveness is cognitive-behavioral therapy
(CBT) (also known as cognitive therapy), originally devel-
oped by Beck and colleagues (Beck et al., 1979; Clark, Beck,
& Alford, 1999). It is a relatively brief form of treatment
(usually 10 to 20 sessions) that focuses on here-and-now
problems rather than on the more remote causal issues that
psychodynamic psychotherapy often addresses. For exam-
ple, cognitive therapy consists of highly structured, sys-
tematic attempts to teach people with unipolar depression
to evaluate systematically their dysfunctional beliefs and
negative automatic thoughts. They are also taught to iden-
tify and correct their biases or distortions in information
processing and to uncover and challenge their underlying
depressogenic assumptions and beliefs. Cognitive therapy
relies heavily on an empirical approach in that patients are
taught to treat their beliefs as hypotheses that can be tested
through the use of behavioral experiments.
One example of challenging a negative automatic
thought through a behavioral experiment can be seen in
the following interchange between a cognitive therapist
and a patient with depression.
Therapy Session: “My Husband Doesn’t Love Me
Anymore”
PATIENT: My husband doesn’t love me anymore.
THERAPIST: That must be a very distressing thought. What makes you
think that he doesn’t love you?
PATIENT: Well, when he comes home in the evening, he never wants
to talk to me. He just wants to sit and watch TV. Then he goes
straight o to bed.
THERAPIST: OK. Now, is there any evidence, anything he does, that
goes against the idea that he doesn’t love you?
PATIENT: I can’t think of any. Well, no, wait a minute. Actually it was my
birthday a couple of weeks ago, and he gave me a watch which
is really lovely. I’d seen them advertised and mentioned I liked it,
and he took notice and went and got me one.
THERAPIST: Right. Now how does that fit with the idea that he doesn’t
love you?
PATIENT: Well, I suppose it doesn’t really, does it? But then why is he
like that in the evening?
THERAPIST: I suppose him not loving you any more is one possible
reason. Are there any other possible reasons?
painless, and thousands of stimulations are delivered in
each treatment session. Treatment usually occurs 5 days a
week for 2 to 6 weeks. Many studies have shown it to be
quite eective—indeed in some studies quite comparable
to unilateral ECT and antidepressant medications (George
& Post, 2011; Janicak et al., 2005; Schulze-Rauschenbach et
al., 2005). In particular, research suggests that TMS is a
promising approach for the treatment of unipolar depres-
sion in patients who are moderately resistant to other treat-
ments (George & Post, 2011). Moreover, TMS has
advantages over ECT in that cognitive performance and
memory are not aected adversely and sometimes even
improve, as opposed to ECT, where memory-recall deficits
are common (George et al., 2013). Finally, TMS appears
to be safe for use with children and adolescents, with
only low rates of mild and transient side eects such as
headaches (12 percent) and scalp discomfort (3 percent)
(Krishnan et al., 2015).
DEEP BRAIN STIMULATION In recent years, deep brain
stimulation has been explored as a treatment approach for
individuals with refractory depression who have not
responded to other treatment approaches, such as medica-
tion, psychotherapy, and ECT. Deep brain stimulation
involves implanting an electrode in the brain and then stimu-
lating that area with an electric current (Mayberg et al., 2005).
Although more research on deep brain stimulation is needed,
initial results suggest that it may have potential for treatment
of unrelenting depression (see Chapter 16 for more details).
Neuroimaging has played a pivotal role in identifying some deep brain
stimulation targets.
Triff/Shutterstock
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268 Chapter 7
Teasdale, 2004). The logic of this treatment is based on find-
ings that people with recurrent depression are likely to
have negative thinking patterns activated when they are
simply in a depressed mood. Perhaps rather than trying to
alter the content of their negative thinking as in traditional
cognitive therapy, it might be more useful to change the
way in which these people relate to their thoughts, feelings,
and bodily sensations. This group treatment involves train-
ing in mindfulness meditation techniques aimed at devel-
oping patients’ awareness of their unwanted thoughts,
feelings, and sensations so that they no longer automati-
cally try to avoid them but rather learn to accept them for
what they are—simply thoughts occurring in the moment
rather than a reflection of reality. A recent meta-analysis of
findings from six randomized controlled trials of individu-
als in remission from depression suggests that mindful-
ness-based cognitive therapy is an eective treatment for
reducing risk of relapse in those with a history of three or
more prior depressive episodes who have been treated
with antidepressant medication (Piet & Hougaard, 2011).
Although the vast majority of research on CBT has
focused on unipolar depression, recently there have been
indications that a modified form of CBT may be quite useful,
in combination with medication, in the treatment of bipolar
disorder as well (Lam et al., 2003, 2005; Miklowitz, 2009).
There is also preliminary evidence that mindfulness-based
PATIENT: Well, he has been working very hard lately. I mean, he’s late
home most nights, and he had to go in to the oce at the
weekend. So I suppose it could be that.
THERAPIST: It could, couldn’t it? How could you find out if that’s it?
PATIENT: Well, I could say I’ve noticed how tired he looks and ask him
how he’s feeling and how the work’s going. I haven’t done that.
I’ve just been getting annoyed because he doesn’t pay any
attention to me.
THERAPIST: That sounds like an excellent idea. How would you like to
make that a homework task for this week?
(From Fennell, M. J. V. (1989). Depression. In K. Hawton, P. M. Salkovskis, J. Kirk,
& D. M. Clark (Eds.), Cognitive behaviour therapy for psychiatric problems: A
practical guide. Oxford University Press.)
The usefulness of cognitive therapy has been amply
documented in dozens of studies, including several stud-
ies on hospital patients with unipolar depression and on
patients diagnosed with depression with melancholic fea-
tures (Craighead et al., 2007; Hollon, Haman, & Brown,
2002; Hollon et al., 2006). When compared with pharmaco-
therapy, it is at least as eective when delivered by well-
trained cognitive therapists. It also seems to have a special
advantage in preventing relapse, similar to that obtained
by staying on medication (Hollon, 2011; Hollon & Ponniah,
2010). Moreover, evidence is beginning to accumulate that
it can prevent recurrence several years following the epi-
sode when the treatment occurred (Craighead et al., 2007;
Hollon & Dimidjian, 2009). Perhaps not surprisingly, some
recent interesting brain-imaging studies have
shown that the biological changes in certain brain
areas that occur following effective treatment
with cognitive therapy versus medications are
somewhat dierent, suggesting that the mecha-
nisms through which they work are also dierent
(Clark & Beck, 2010; Hollon & Dimidjian, 2009).
One possibility is that medications may target the
limbic system, whereas cognitive therapy may
have greater eects on cortical functions.
CBT and medications have been found to be
equally eective in the treatment of severe depres-
sion (DeRubeis et al., 1999; Hollon et al., 2006). For
example, one important two-site study of moderate
to severe depression found that 58 percent
responded to either cognitive therapy or medica-
tion (DeRubeis et al., 2005). However, by the end of
the 2-year follow-up, when all cognitive therapy
and medications had been discontinued for 1 year,
only 25 percent of patients treated with cognitive
therapy had had a relapse versus 50 percent in the
medication group (Hollon & Dimidjian, 2009;
Hollon et al., 2005). This is illustrated in Figure 7.10.
Another variant on cognitive therapy, called
mindfulness-based cognitive therapy, has been devel-
oped in recent years to be used with people with
highly recurrent depression (Segal et al., 2002,;
Prior CT Group (n = 20)
Prior ADM Group (n = 14)
161412 2018 22 24
Percentage of patients with no recurrence
Time following the end of continuation (months)
0
120
100
80
60
40
20
Figure 7.10
Survival curve illustrating how many months following the end of treatment it
took patients from the two groups before they had another episode of depres-
sion (recurrence). One group had previously received cognitive therapy (CT) and
the other group had received antidepressant medication (ADM).
(Based on Hollon, et al. (2005, April). Prevention of relapse following cognitive therapy
vs. medications in moderate to severe depression. Arch. Gen. Psychiat., 62(4), 417–26.
American Medical Association.)
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