1. How can such a brilliant girl be
1. Easily! Her illogical thinking is
so illogical?
the cause of her depression. If
she didn't continually focus on
negatives and disqualify positives,
she wouldn't be depressed so
often. Its your job to train her in
how to get over this.
2. But I can't. She's determined to
2. She doesn't have to give you any
beat me down. She won't give
satisfaction. Only you can do
me an ounce of satisfaction.
this. Don't you recall that only
your thoughts affect your moods?
Why not credit yourself for what
you did? Don't wait around for
her. You just learned some ex-
citing things about how to guide
people in making decisions.
Doesn't that count?
3. But she should admit I helped
3. Why "should" she? That's a fairy herl She should be grateful!
tale. If she could she probably
would, but she can't yet. In time
she'll come around, but she'll
have to reverse an ingrained pat-
tern of illogical thinking that's
been dominating her mind for
over a decade. She may be afraid
to admit she's getting help so she won't end up disillusioned again.
Or she might be afraid you'll say,
"I told you so." Be like Sherlock
Holmes and gee if you can figure
out this puzzle. It's pointless to
demand that she be different
from the way she is.
367
David D. Burns, M.D.
tive, and that will feel good. But every now and then, someone will not respond the way I want. If the response is unreasonable, this is a reflection on that person, not me, so why get upset over it?" This attitude has made life much sweeter for me, and overall I have been blessed with as much gratitude from patients as I could desire. Incidentally, Susan gave me a call just the other day. She'd done well at college and was about to graduate. Her father had been depressed, and she wanted a referral to a good cognitive therapist!
Maybe that was her way of saying thank you!
Coping With Uncertainty and Helplessness:
The Woman Who Decided to Commit Suicide
On my way to the office on Monday, I always wonder what the week will hold in store. One Monday morning I was in for an abrupt shock. As I unlocked the office, I found some papers had been slipped under the door over the weekend—a twenty-page letter from a patient named Annie. Annie had been referred to me several months earlier on her twentieth birthday, after having received eight years of completely successful treatment from several therapists for a horrible, grotesque mood disorder. From age twelve on, Annie's life had deteriorated into a nightmarish pattern of depression and self-mutilation. She loved to slash her arms to shreds with sharp objects, one time requiring 200 stitches. She also made a number of nearly successful suicide attempts.
I tensed as I picked up her note. Annie had recently expressed a deep sense of despair. In addition to depression, she suffered from a severe eating disorder, and the previous week had engaged in a bizarre three-day spree of compulsive, uncontrollable binge-eating. Going from restaurant to restaurant, she would stuff herself for hours nonstop. Then she'd vomit it all up and eat some more. In her note she described herself as a "human garbage disposal," and explained that she was beyond hope. She indicated that she had decided to give up trying because she realized she was basically "a nothing."
Without reading further, I called her apartment. Her roommates told me that she had packed up and "left town" for three days without giving any indication of where or why.
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FEELING GOOD
Alarms sounded in my head! This is exactly what she had done on her last several suicide attempts prior to treatment—she'd drive to a motel, sign in under an assumed name, and overdose. I continued to read her letter. In it she stated, "I'm drained, I'm like a burnt-out light bulb. You can pipe electricity into it, but it just won't light up. I'm sorry but I guess it's just too late. I'm not going to feel false hope any longer . . . During the last few moments I do not feel particularly sad. Once every so often I try to grasp onto life, hoping to clench my hands around something, anything—but I keep grasping nothing, empty."
It sounded like a bona fide suicide note, although no ex-plicit intention was announced. I suddenly became submerged by a massive uncertainty and helplessness—she had disappeared and left no traces. I felt angry and anxious. Because I could do nothing for her, I decided to write down the automatic thoughts that flowed through my mind. I hoped some rational responses would help me cope with the intense uncertainty I was facing (see Figure 16-3, page 370).
After recording my thoughts, I decided to call my associate, Dr. Beck, for a consultation. He agreed that I should assume she was alive unless it was proved otherwise. He suggested that if she were found dead, I could then learn to cope with one of the professional hazards of working with depression. If she was alive, as we assumed, he emphasized the importance of persisting with treatment until her depression finally broke.
The effect of this conversation and the written exercise was magnificent. I realized I was under no obligation to assume "
the worst," and that it was my right to choose not to make myself miserable over her possible suicide attempt. I decided I couldn't take on responsibility for her actions, only for mine, and that I had done well with her and would stubbornly continue to do so until she and I had finally defeated her depression and tasted victory.
My anxiety and anger disappeared completely, and I felt relaxed and peaceful until I received the news by telephone on Wednesday morning. She had been found unconscious in a motel room fifty miles from Philadelphia. This was her eighth suicide attempt, but she was alive and complaining as usual in the Intensive Care Unit of an outlying hospital. She 369
David D. Burns, M.D.
Figure 16-3. Coping with Uncertainty.
Automatic Thoughts
Rational Responses
1. She's probably made a suicidc at 1. There's no proof she's dead. Why t e m p t — a n d s u c c e e d e d . n o t a s s u m e s h e ' s a l i v e u n t i l proven otherwise? Thcn you
won't have to worry and obsess
in thc meantime.
2. If she's dead, it means I killed 2. No, you're not a killer. You're her.
trying to help.
3. If I'd donc something different 3. You're not a fortunc teller—you last week, 1 could have prevented
can't predict the futurc. You do
this. It's my fault.
thc best you can based on what
you know—draw the line there
and respect yourself on this basis.
4. This shouldn't have happened— 4. Whatever happened did happen.
I t r i e d s o h a r d . J u s t b e c a u s e y o u m a k e m a x i m a l efforts, there's no guarantee about
the results. You can't control
her, only your efforts.
5. This means my approach is sec 5. Your approach is one of the o n d - r a t e . f i n e s t e v e r d e v e l o p e d , a n d y o u apply yourself with great effort
and commitment, and get out-
standing results. You are not
second-rate.
6. Her parents will .be angry with 6. Thcy may and they may not.
me.
They know how you've knocked
yourself out for her.
7. Dr. Beck and my associates will 7. Extremely unlikely. Well all be be angry with me—they'll know
disappointed to lose a patient
Fm incompetent, and they'll look
we've gone to such extreme
down on me.
lengths to help
, but your peers
won't feel you've let them down.
If you're at all concerned, call
theml Practice what you preach,
Burns.
8. I'll feel miserable and guilty until 8. You'll only feel miserable if you I find out what happened. I'm ex-make a negative assumption.
pected to feel that way.
Odds are (a) she's alive and (b)
she'll get better. Assume this and
you'll feel goodl You have no
obligation to feel bad—you have
the right to refuse to get upset.
FEELING GOOD
would survive, but would require plastic surgery to replace the skin over her elbows and ankles because of sores which had developed during the long period of unconsciousness. I arranged for her transfer to the University of Pennsylvania, where she would be back in my relentless, cognitive clutches again!
When I spoke with her, she was enormously bitter and hopeless. The next couple of months of therapy were especially turbulent. But the depression finally began to lift in her eleventh month, and exactly one year to the day of her referral, her twenty-first birthday, the symptoms of depression disappeared.
The Payofl: My joy was enormous. Women must have this feeling when they first see their child after delivery—all the discomfort of pregnancy and the pain of delivery are forgot-ten. It's the celebration of life—quite a heady experience. I find that the more chronic and severe the depression, the more intense the therapeutic struggle becomes. But when the patient and I at last discover the combination that unlocks the door to their inner peace, the riches inside far exceed any effort or frustration that occurred along the way.
371
PART VII
The Chemistry
of Mood
CHAPTER 17
The Consumer's Guide
to Antidepressant Drug Therapy
The Search for "Black Bile"
Throughout the ages, men have searched for the causes of depression. Even in ancient times there was some suspicion that blue moods were due, at least in part, to an imbalance in body chemistry. Hippocrates (460-355 B.c.) thought that "
black bile" was the culprit. In recent years scientists have spearheaded an intensive search for the elusive black bile.
They are frying to pinpoint the abnormalities in brain chemistry that cause depression. There are hints about the answer, but in spite of increasingly sophisticated research tools, the definitive solution is still just beyond our grasp. Sooner or later, neurochemists may provide us with frightening technology that will allow us to regulate our moods at will. This will represent one of the most extraordinary and philosophically confusing developments in human history. For the immediate future the goals are much more modest. We are aiming for increased precision in diagnosing depressive illnesses and the development of more humane and effective treatment methods.
What is the basis for believing that there may be a chemical component in depression? First, the physical (somatic) symptoms of depression support the notion that organic change is involved in at least some depressions. These changes in body function include, among others, agitation (
increased nervous activity such as pacing or hand-wringing), or retardation (motionless apathy—you feel like a ton of bricks and do nothing). You also may experience a "diurnal"
variation in mood (this refers to the worsening of symptoms 375
David D. Burns, M.D.
in the morning in some depressions), changed sleep patterns (
insomnia is the most common), constipation, abnormalities in appetite (usually decreased, sometimes increased), an impaired concentration ability, and a decreased interest in sex.
A second argument for a physiologic cause for depression is that at least some forms of mood disorders run in families, suggesting a role for genetic factors. If there is an inherited abnormality that predisposes some individuals to depression, it is likely to be in the form of a disturbance in body chemistry, as is the case with so many genetic diseases.
The modern era of research on the chemistry of mood disorders began several decades ago, when it was hypothesized that depression might result from decreased levels of certain brain substances known technically as "amines."*
What are amines? They are chemical transmitters which nerves use to send messages to each other. Amines are the brain's biochemical "mailmen," particularly concentrated in the limbic system, a primitive brain region which appears to be involved in mood regulation.
Discoveries resulting from several types of research have been consistent with this amine theory. The findings can be simplified as follows:
I. Some (but not all) drugs used in the treatment of high blood pressure appear to bring on attacks of depression in individuals predisposed to mood disorders. These drugs have a tendency to deplete the brain of the amine chemical messengers. The lowered amine levels may trigger the depressed mood.
2. Drugs which raise the brain levels of these amines cause increased activity and alertness in laboratory animals.
Conversely, drugs which block or reduce the activity of the brain amines cause sedation and lethargy in these animals While such increased or decreased activity In animals obviously does not constitute an adequate model for the possible physiologic cause of human elation or depression, it is true that changed activity and alertness levels are seen in human mood disorders. Thus, these laboratory observations are consistent with the amine theory.
* The amines currently implicated in mood disorders include nore-pinephrine, dopamine, and serotonin.
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FEELING GOOD
3. Most drugs used in the treatment of depression do po-tentiate the activity or raise the levels of the messenger amines in the brain. For example, in a remarkable series of recent experiments in New York, a group of depressed patients received a drug that causes a buildup in brain-amine concentrations. After several weeks of treatment, the patients were clinically improved. Then they were given a second drug that depletes the brain amines. The patients all relapsed into depression within a couple of days. When the second drug was withdrawn so that the brain-amine levels were allowed to rise, the patients again recovered. These findings raise suspicions that the brain amines may indeed be the chemical "culprits" in at least some depressions, since these patients' moods seemed to cycle up and down in response to changes in brain-amine levels.
4. Studies of these amine levels and their breakdown products in the blood, urine, and spinal fluid of depressed individuals have documented the predicted deficiencies in some (
but not all) depressed patients.
As you can see, some of the data looks promising. Does this mean we have pinpointed the precise cause of depression? Not by a long shot. Our understanding of how the brain functions is highly primitive. We're still in the Model-T
era waiting for the jet age. But an important research effort has been launched and is moving forward rapidly.
Eventually it probably will lead us to the final identification of the mysterious "black bile."
How Antidepressants Affect the Brain
In this section I have reduced to simple basics our current understanding of how antidepressant drugs influence the nerves in your brain. However, if the very word "chemical"
sends your mind reeling, just skip this section and go on to the practical details of drug administration in the next section.
The brain is essentially an electrical system. The nerves, or "wires," communicate their electrical signals to each other by way of chemical messengers (see Figure 17-1, page 378).
If the nerves become depleted of these chemical messengers, 377
David D. Burns, M.D.
These are the chemical messen-
gers, which have been released
into the "synapse," or junction
region.
Electrical
Electrical
impulse
" :;1410. n
impulse
/> Nerve 1
-1410. •
Nerve 2
91:1410.*
The "synapse": This is the fluid-
filled junction between the two
nerves. The chemical messenger
migrates across the synapse and
attaches to the membrane of
nerve 2.
These are packets at the end of
nerve 1 which contain the
chemical messengers.
Figure 17-1. How Nerves Send Messages to Each Other. An electrical impulse travels along nerve 1 until it reaches the terminal region. Here tiny packets containing chemical messengers rupture, and the messengers spill into the synaptic region. They then migrate across the fluid-filled synapse and become attached to the membrane of nerve 2. This triggers an electrical impulse in nerve 2. The chemical messengers are then destroyed, and the waste products are excreted from the brain and ultimately appear in the urine.
Nerve 1 must constantly manufacture fresh chemical messengers to replace those that are lost. A deficiency of messengers is thought to lead to depression. Antidepressants compensate for the postulated deficiency by raising the levels of chemical messengers, or by increasing the potency of the chemical messengers in the synaptic region.
378
Table 17-1. Tricyclic Antidepressants
Agents
Other Side Effects
Sedative
(Dry mouth, constipation,
Normally Effective
Time of Day to
Effects 2
blurred vision)a
Total Daily Dose 4
Take the Medicine a
Imiprtunine
moderate
moderate
150-300 mg
pattern 1
(Tofranil, Imanate,
Presamine, Slt-Pramine,
Janbufne)
Desipramine
moderate
moderate
150-250 mg
pattern 1
(Pertofrane, Norpramln)
Amitriptyline
substantial
moderate
75-300 mg
pattern 1
th
(Mull, Endep)
Nortiiptyline (
substantial
The Feeling Good Handbook Page 41