In this paper we will show how affect theory, introduced by Silvan S. Tomkins (1962, 1963, 1991), can influence our practice of psychopharmacology. Biology, psychology, and descriptive psychiatry are linked by their relation to the affect system; such an understanding allows greatly increased sophistication for our efforts to ameliorate certain unpleasant affective states.
Tomkins (1962) stressed that each affect functions as an amplifier
that calls attention to anything with which it becomes associated
or "coassembled." There are nine of these nonspecific
amplifiers, and therefore nine different ways that affect can,
by this amplification, increase the likelihood that the information
with which it has been assembled will be used by the organism.
Interest-excitement and enjoyment-joy, the two positive affects,
are counterbalanced by six decidedly negative affects (fear-terror,
distress-anguish, anger-rage, dissmell, disgust, and shame-humiliation),
all of which may be halted instantly by surprise-startle, an affect
that is too brief to have either a positive or a negative flavor.
By their effects on bodily structures that evolved for other reasons
(heart rate, voice, facial musculature, sweat, etc.) these nine
innate affects call attention to their triggering source in nine
quite different ways.
Important things feel important because they have been
amplified by affect. Amplification provides both the power to
cause awareness and the motivation to make us take action. Yet
these psychological qualities of the affect system are
completely dependent on the gestalt formed by the biological
effects triggered at what Nathanson (1988, 1992) has called the
sites of action for each mechanism. Although the circulatory system
did not evolve so that the heart might thump harder in excitement
or fear, the affect system evolved to act on or influence circulatory
function in highly specific ways. Similarly, the mechanisms for
the control of sweating, breathing, and a wide range of voluntary
muscles may be placed momentarily under the command of the affect
system.
All of these sites of action for innate affect are quite ordinary
biological mechanisms set off by well known groups of neurotransmitters.
Since these sites of action can be set off under the control of
affect programs, we infer that one of the properties of the affect
system is to direct the release of neurotransmitters. If some
aberration of neurotransmitter metabolism causes things to happen
at the sites of action normally associated with one or another
innate affect, we humans are likely to mistake the pattern of
actions so released as the gestalt normally associated with a
normal affect. In such situations, the psychopharmacologist looks
for medication that normalizes affect physiology.
As Nathanson (1992) has suggested by his computer analogy for
the division of affect-related information, affective disorders
may result from malfunctions of hardware, firmware, or software.
Psychopharmacological treatment may be indicated for defects occurring
at the hardware or firmware levels, or in those special circumstances
when problems in living push the software of affect management
into realms that overload cognition.
The first goal of psychopharmacologic evaluation is to ascertain
whether the patient's affects are serving as a source of information
for living or in some way interfering with effective living. Often
patients will assume that only illness brings negative affect,
or that negative affect has no value and should be eliminated.
By its nature, negative affect is unpleasant and motivates us
to "turn off" whatever has triggered it; it is only
logical to expect that some people might wish to get rid of the
affect mechanism itself rather than use it to locate whatever
potential danger it is amplifying.
Nevertheless, just as we would be at risk were we to lose our
ability to sense pain, our ability to live in the world is assisted
by the information given us through unpleasant emotional experience.
In many ways, the affects are analogous to the gauges on the dashboard
of a car. A temperature gauge that reads in the red provides information
that is neither pleasant nor welcome-yet it is of no use to ignore,
blame, rage at, or be ashamed of the gauge. Many people fail to
process the subtle data provided by the affect system; they seem
unable to learn how to make use of the information so amplified.
Recognition and acceptance of affect is central to competent human
performance.
Much of our work as psychotherapists requires a solid understanding
of innate affect. Yet the patients who are referred to a psychopharmacologist
often experience affect at levels of intensity and over durations
that cannot be explained by what we know to be the normal range
of physiological affect mechanisms. In such cases, affect provides
information that misleads, or that takes over consciousness to
an untoward degree.
Who is sent to the psychopharmacologist? Some people are sent
to us simply because the primary therapist has given up. Stubborn,
recalcitrant, difficult patients are referred for medication in
hope that something will shock their system into readiness
for change. Even though we may try one or another kind of medicine,
here the real need is for change in the paradigm on which treatment
has been based (Kluft, 1992). It is our responsibility to determine
whether the patient's emotionality comes from memory that has
been repressed, ignored, or forgotten, from obligatory interaction
with family members whose contribution to one's daily life has
been overlooked, or from a flawed or faulty system of cognitive
processing. A switch to family therapy, psychoanalysis, cognitive-behavioral
therapy, or hypnotic intervention involves the software of human
emotion, rather than its hardware.
Most of the time, however, patients come to us because they seem
locked in one emotion or another. All of us get stuck every once
in a while; the competent adult knows how to take a break, go
to a movie or sporting event, drink a modest amount of alcohol,
or find some other way of shifting our affect away from the subject
of the moment. On occasion, psychiatric medication will be needed
to modulate an affect that we cannot handle any other way: Low
dose phenothiazines and benzodiazepines are excellent medications
for the acute relief of uncontrollable, high density fear-terror
or distress-anguish. The best among us may get overloaded every
once in a while and need the kind of momentary relief available
by taking a milligram or so of trifluoperazine (Stelazine),
or a modest amount of alprazolam (Xanax).
On the other hand, the persistent distress-anguish of a weeping
dysthymic disorder, the rampant fear-terror of panic disorder,
the polarity of inappropriate interest-excitement and the counterbalancing
inability to trigger positive affect seen in bipolar affective
illness seem to represent true disorders of affect mechanisms.
We assume that some defect of neurotransmitter metabolism has
altered normal affect physiology, and we try to repair the hardware
defect with medication that returns this physiology toward normal.
Certainly it is easy enough to spot the patient whose complaints
fit into one of the classical symptom patterns mentioned above.
Bruce J. Berg (personal communication, 1993) has suggested that
each of the affect programs has evolved as patterns of effects
involving many neurotransmitters, while the best known affective
disorders are more likely experienced as the gestalt of the effects
of single neurotransmitter action. While the patient assembles
the data provided at the various sites of action as if it represented
an ordinary innate affect, we recognize instead the more limited
action of an aberrant neurotransmitter system. The psychopharmacologist
is faced with patients who complain about unpleasant symptoms
that fall into subtle patterns that both resemble innate affect
and differ from it. Our search for affective experience that is
of greater than normal intensity and/or duration is also aided
by a clear understanding of normal affect.
Innate affect is always associated with a triggering event. For
the affect shame-humiliation, this involves any impediment to
the continuation of the positive affects interest-excitement or
enjoyment-joy. But physiological shame affect is not what we have
been brought up to think of as the emotion shame. The model elaborated
by Nathanson (1992) as the compass of shame suggests that any
such impediment to positive affect may initiate one of four distinctly
different patterns of behavior-withdrawal, attack self,
avoidance, and attack other. Experienced by the
individual or witnessed by outsiders, the events associated with
shame affect may therefore include actual withdrawal, masochistic
submission to the will of others, narcissistic avoidance of shame,
or actual attack on the person of others. In the adult, shame
may be triggered when the interpersonal bridge is broken (Kaufman,
1985), when something has been revealed that we would have preferred
kept private, or when we fail.
Guilt seems to have developed as a subset of shame: Our studies
of the developmental pathways for guilt (Nathanson, 1987) suggest
that the mature emotion involves two affects-shame at the discovery
of one's action, and fear of reprisal. In brief, we are ashamed
when something hidden is exposed, and guilty when improper actions
have been revealed. The normal operation of the hardware, firmware,
and software of emotion would explain any moment of shame or guilt
brought on by such triggers.
Yet there are many clinical situations characterized by shame
and guilt of far longer duration and far greater intensity than
would make sense in this model. Few of us would be puzzled by
a patient who complains ceaselessly about guilt for which no reasonable
cause may be ascertained. We understand unremitting guilt as part
of the pattern of symptoms associated with classical depression;
treatment with tricyclic antidepressants (TCAs) is usually quite
effective. Klein (ref) described patients with one subtype of
depression that included atypical vegetative signs such as hypersomnia
and appetite increase, a great deal of anxiety, and the triad
of chocolate craving, rejection sensitivity, and applause hunger;
all of which symptoms tended to respond poorly or incompletely
to the TCAs but rather well to the monoamine oxidase inhibitor
antidepressants (MAOIs). These "atypical" depressions,
which we now also treat with the selective serotonin reuptake
inhibitor antidepressants (SSRIs), have been described by Nathanson
(1987) as characterized by unremitting shame affect. Social Phobia
and the Avoidant Personality Disorder, both surely less about
fear than shame, may also be understood and treated as highly
patterned conditions associated with shame experience that has
been triggered by abnormalities of neurotransmitter function,
and that also respond well to SSRI or MAOI treatment.
The psychopharmacologist looks for averted gaze, downcast eyes,
and the stammer or moment of acute discomfort that so often accompanies
shame affect. We learn sensitivity to the brittle anger associated
with the attack other form of shame response, as well as
flashes of defensive narcissism and masochism. Much of the symptomatology
seen in the Borderline Syndrome involves shame affect displayed
as bursts of anger, "narcissism," and the well-known
oscillation between overvaluation and devaluation of the significant
other; it is these features of the borderline spectrum that respond
to treatment with the SSRIs fluoxetine, sertraline,
and paroxetine. Even when the borderline patient's unusual
sensitivity to shame has been ameliorated by such pharmacologic
intervention, much psychotherapy is needed to help normalize the
patient's relation to affect.
Because each affect appears as a specific pattern of bodily responses,
we outsiders may suspect the presence of an affect even when the
patient doesn't know one has been triggered. Among the motor movements
we study are facial expressions, as well as the pace, tone, and
volume of speech. The crying patient may display anger in the
motor pattern of reaching for tissues or the steady whining tone
of voice. In addition to these physiological patterns we also
note the associated cognitions-the paranoid patient who says he
feels people are watching him and laughing at him for being overweight
is dealing with shame, while the apparently equally paranoid patient
who claims the CIA is plotting against him because he is a threat
to world security is dealing with fear and anger. One might treat
the former patient with drugs like the SSRIs, which reduce or
detoxify shame experience, and the latter with phenothiazines
(which decrease fear).
Each class of medication deals with different neurotransmitter
systems and may be associated with different innate affects. We
think of the benzodiazepine tranquilizers as anti-anxiety agents
that are involved with the neurotransmitter gamma amino butyric
acid (GABA); now we must begin to wonder whether GABA is what
Nathanson (1988, 1992) calls a biochemical mediator of the affect
fear-terror. Just above we noted a group of clinical conditions
characterized by what appears to be an abnormal relation to shame
affect and a certain responsiveness to medications that increase
the amount of serotonin available in the central nervous system.
This neurotransmitter, then, may be involved in the mediation
of physiological shame affect. Though we must be cautious and
not conclude that serotonin neurotransmission abnormalities are
causal for this shame hyper-sensitivity. Snyder (19xx) suggests
that bipolar affective illness involves the messenger molecule
phosphoinositide; the affect theorist wonders whether the normal
expression of interest-excitement might be related to this second
messenger which has been linked to fifteen neuroreceptors (including
muscarinic cholinergic, alpha adrenergic, and 5-HT2) by Snider
et al (1987). It is generally assumed that abnormalities in the
manufacture, transport, or metabolism of specific neurotransmitters
may be responsible for specific classes of psychiatric illness.
Affect theory may explain the clinical presentation of these biochemical
defects and offer new ways to understand the biology of normal
emotion.
Take, for instance, the mildly hypomanic patient whose interest-excitement
is triggered not by the sort of data influx gradient normally
called novelty, but by the biochemical illness itself. Our life
experience of normal sequences of source and affect leads us to
believe that any particular moment of affect has been triggered
by its normal source. All our lives we have been excited only
when some triggering event has fulfilled Tomkins's criteria for
the release of the preprogrammed innate affect mechanism. Yet
when hypomanic, something else has released the neurotransmitters
(and therefore stimulated certain sites of action) normally associated
with excitement. We experience interest or excitement in the absence
of this normal sequence because we have deduced erroneously the
presence of the normal sequence of source and affect.
Were the sites of action stimulated too few, or in no pattern
recognized by us as part of an innate affect, we might fail to
register or "think about" the effect of this neurotransmitter.
The sweat gland is a minor site of action for the affect fear-terror;
drugs that cause sweating are unlikely to make us think we are
afraid. But when enough of the pattern associated with an innate
affect has been triggered, we act as if an affect had been triggered
by its normal sequence of events, and scroll through our experience
in an attempt to explain this apparent affect. This is the reason
hypomanic patients seem interested in or excited by nearly anything.
The affect precedes its "assigned" trigger.
This is our model for classical depression. Whatever neurotransmitter
dysfunction is responsible for the persistent distress-anguish
associated with that syndrome, it makes the patient think about
life events that are steady-state and of higher than optimal intensity.
Whatever pattern of neurotransmitter malfunction is responsible
for classical depression may also trigger something that the patient
can only interpret as guilt, which must then be explained in terms
of our life experience of improper actions. One whose guilt is
completely and permanently relieved by confession and/or penance
has suffered this emotion for reasons associated with normal neurochemistry.
One who in therapy confesses and "works through" crime
after crime with scant relief of the underlying guilt is more
likely dealing with some pattern of affective experience brought
into consciousness by something wrong with neurotransmitter biology.
All emotional experience is a matter of the biology of affect
and the psychology associated with our life history. It is the
job of the psychopharmacologist to recognize the patterns into
which symptoms may be grouped, and to use these patterns to diagnose
and treat any persistent affective state that is due to aberrations
in the biology of affect.
Nevertheless, even a patient with a known disturbance of neurotransmitter
physiology (a biological defect responsible for a persistent affect
state), is capable of experiencing a normal affect when the trigger
for that affect is actuated. A hypomanic patient may still experience
profound excitement when exposed to something truly novel, just
as a borderline or social "phobic" patient may be embarrassed
in ways indistinguishable from normal. It is essential that we
instruct patients in the language and range of normal affective
experience in order that they learn to distinguish the normal
from what is part of their illness. A clear understanding of affect
theory will allow the clinician to answer the question so often
asked by patients: "Is my illness psychological or biological?"
A 40-year old lawyer had spent 12 years in psychotherapy for difficulty
making, forming, and maintaining intimate relationships, and the
sense that he rarely if ever "had a good time" anywhere.
The apparent normality of his self-image, thoughts and feelings
about the future, ability to work effectively, and involvement
in recreational activities had always convinced both him and the
treating therapist that he was not "depressed." On the
premise that his symptoms were caused by a relatively constant
shame state unassociated with triggers that could be found in
his present or past life, pharmacologic treatment was initiated
with sertraline in doses ranging from 25-50mg/d. Within
a few days of starting this regimen he reported significant improvement
in his general state of well-being and began to laugh with pleasure
at ideas and comments that earlier he would have ignored. Much
as if he were in the caboose of a train, viewing his life prior
to the institution of this medication, he now began to describe
a history of shame experiences of such constancy that he called
them the "atmosphere" of his life. Over a period of
two months he began to learn how to live without this painful
affective state, how to enter a new situation without his (previously
denied) expectation of inadequacy, incompetence, failure, "stupidity,"
or ungainliness. Of particular interest during his subsequent
psychotherapy were the moments when he was embarrassed for reasons
that might have caused shame for anyone, and that responded to
previously ineffective psychotherapeutic techniques. "I still
get embarrassed," he said, "but the 'hang time' of the
feeling is much shorter."
This case demonstrates how a subtle disorder of mood can become
so thoroughly integrated with the development of an individual's
personality that the relief of such a disorder requires or makes
possible massive revision of one's concept of self.
A 38-year old salesman had smoked marijuana at least twice each
day since his 12th birthday. Adolescence requires us to develop
scripts for the management of sexuality, increased body strength,
and a host of interpersonal tasks. For this patient, all of these
developmental milestones had been achieved through a haze of drug-induced
dissociation. Unless so protected, he tended to handle the experiences
of intense excitement, anger, distress, and fear by exploding
in rage. Each of his previous attempts to stop using marijuana
had been terminated by a rising tide of negative affect for which
he had no skills of modulation. Treatment aimed at the identification
of each innate affect and the development of techniques of affect
modulation allowed him to become who he might have been had these
life tasks not been influenced by his drug history.
Just as a biological illness may produce the equivalent of an
innate affect that must be explained and handled like affect triggered
in the normal ways, an exogenous substance can influence affective
development. The chronic use of adrenergic substances taken for
the treatment of allergic rhinitis or asthma can have as much
influence on our ability to understand our emotional environment
as the presence in the bloodstream of too much or too little thyroxin.
Sophisticated treatment must take into account the relation of
such substances to the affect system. Although subtle neurotransmitter
defects may be responsible for some cases of substance abuse,
it is of perhaps equal importance to recognize that those whose
use of marijuana and alcohol has begun in early adolescence are
the most likely to have been reared in families that provide inadequate
psychosocial systems for the modulation of innate affect. Successful
pharmacologic intervention will often necessitate a prolonged
period of psychotherapy that fosters the integration of this new
affective climate.
It would be misleading and inaccurate to explain real life as
characterized by long periods of calm (during which no affect
is triggered) punctuated by bursts of stimuli that trigger discrete
episodes of innate affect that blend gracefully into the preexisting
calm. So much is going on at any moment that there are lots of
stimuli capable of triggering affect and therefore gaining amplification
and consequent entry into consciousness. Sources of affect give
way to one another constantly, producing the ebb and flow of feeling
that colors waking experience. Tomkins (1962) has codified all
19 of the possible interrelations and sequences of innate affect
in his chapter "Affect Dynamics," work that holds up
well even in this era of attention to affect analogues produced
by the disorders of biology that require pharmacotherapy.
The therapist skilled in the recognition of innate affect and
affect dynamics often finds our diagnostic nomenclature cumbersome
and inadequate. It would be so much easier were illnesses classified
by the affects responsible for the symptoms expressed and experienced.
The pleomorphic group of "depressions" is characterized
by varying mixtures of all the negative affects-only the chronicity
of the resultant assemblage validates the umbrella term "depression."
Let us examine very briefly some of the otherwise puzzling reactions
to medication seen in this group.
By the time they are referred for medication, many depressed patients
seem so frozen that they are nearly unable to express any emotion.
Some of these patients exhibit swings of affect that have puzzled
many writers. The anergic, nearly immobile patient who begins
to cry some weeks after starting an antidepressant is not getting
worse, despite the fears of family and friends. In these cases,
whatever has blocked the expression of affect has been released
enough that distress-anguish may peep through. Often this is a
sign that the drug really is working!
The affect interest-excitement can be inhibited by social rules
that prohibit its expression; people who are forbidden to look
or act excited will be seen as depressed. Anything that encourages
a broader range of affective expression will produce a release
of previously restricted positive affect. The phenomenology of
the cocktail party is dependent on the common observation that
modest doses of alcohol encourage the appearance of conviviality
and boisterous sociality when positive affect has been held in
check by work-related (shame-based) rules for affect modulation.
Klein (1980) has suggested that it is useful to segregate dysphoric
patients on the basis of their ability to respond with pleasure
to normal stimuli. In the language of this present paper, anhedonic
patients seem to have either primary dysfunction or massive suppression
of the affect interest-excitement, whereas mood-reactive patients
make and maintain enough of this positive affect that its acute
reduction can trigger enjoyment-joy. To the degree that one cannot
generate interest, a major substrate for the other positive affect
is lost; it is this combination of affective inhibitions that
we describe as anhedonia.
Early in the development of an intimate relationship, a lonely
and lovelorn individual may feel wonderful to the point of mild
grandiosity, require less sleep than usual, and greet the world
with far more "energy" than before. Love gives permission
for exuberant positive affect that is quenched and daunted when
the relationship fails. The therapist who has counseled a patient
through several sequences of apathy, excitement, loss, and a return
to apathy may well wonder whether these mood swings should be
treated with Lithium salts as a variant of Bipolar Affective Illness.
These patients turn out to be exquisitely vulnerable to shame;
success in love provides external validation of their personal
adequacy and produces temporary lysis of their chronic shame state.
Affect theory provides a novel explanation of what is often called
"extreme mood reactivity." Tomkins (1962) has stated
that complete resolution of chronic and enduring shame will produce
intense enjoyment-joy, while incomplete resolution will produce
excitement. An understanding of the complex equilibrium between
shame and the positive affects fosters radical alterations in
psychotherapy. Many of these patients, long suspected to harbor
a mild form of Bipolar Affective Illness that may some day require
treatment with Lithium salts, are actually responding to the lysis
of chronic shame. Similarly, patients who seem literally to burst
into excitement when released by TCAs from chronic depression
may be expressing the normal dynamics of affect rather than a
subtle form of bipolar illness.
Describing this group of patients in a different frame of reference,
Klein (1980) has stated that the MAOIs damp the swings of such
moods; the SSRIs may be even more effective in such situations.
It is important to realize that directly proportional to the suddenness
of one's release from any chronic inhibition of positive affect
will be the magnitude and intensity of the positive affect released.
Both the released positive affect and the preexisting mood achieve
explanations based on the individual's life history, rather than
the more important dynamics of innate affect.
Whereas Freud saw all excitement as intrinsically connected to
the sexual drive, Tomkins maintains that the two mechanisms are
entirely separate despite the avidity with which they coassemble.
Nathanson (1992) suggests that the stimulus gradient provided
by the rising tide of sexual arousal is a perfect trigger for
interest-excitement, the drive and its amplifying affect then
forming a mutually reinforcing, apparently unitary pair that all
of us know as "sexual excitement." The loss of libido
so frequently associated with depressive anhedonia, as well as
the loss of appetite for food may be understood as failure of
the affective amplification necessary for normal function.
No matter what the cause, any difficulty in the generation or
maintenance of interest-excitement will be experienced as problems
with the functions normally amplified by that affect-memory,
concentration, motivation, or decision-making. Patients do not
complain about any specific problem with affect. Instead, they
describe their situation as the loss of the entire gestalt of
triggering stimulus and its analogic amplification: "There
isn't anything interesting in my life any more"; "I
haven't seen a good movie in months"; "He just isn't
as sexy as he used to be." It is the clinician who must determine
that affective amplification is lacking (as in the case of anhedonic
depression), or overmuch as in the case of shame affect in "atypical
depression" and interest-excitement in hypomania.
A 45-year old woman was referred for evaluation, saying that she
could not get over the feeling that she had failed to produce
a son for her husband. No longer able to enjoy her daughters,
she had lost interest in work, marriage, and all other aspects
of life. This Major Depression responded rapidly and completely
to a course of treatment with a tricyclic antidepressant. With
the return of her normal range of positive affect, she found it
hard to believe how she could ever have felt guilty about something
as removed from her personal control as the gender of her children.
Many of the older debates in clinical psychiatry can be resolved
by an understanding of the biological nature of the affect system.
No one would quibble with the psychoanalyst who prefers that the
analysand experience "anxiety" adequate to pry significant
memories loose from storage in the unconscious. Yet as Nathanson
(1992) has explained in his chapter "Overload: Affect Beyond
The Level Of Tolerance," both psychosocial interaction and
biological illness are capable of magnifying affect to levels
of intensity that can only be handled by methods inimicable to
uncovering therapy. In such situations, judicious use of medication
can normalize the biology of affect and augment the efficacy of
previously ineffective therapeutic techniques.
Although some systems of psychotherapy were always based on the
relationship between patient and therapist, psychopharmacology
began within a medical model characterized by gross asymmetry
of the therapeutic relationship. The laboratory-based physician
often comes to see the patient as little more than the vehicle
within which are stored certain mechanisms in need of repair,
and expresses displeasure when therapeutic recommendations are
seemingly ignored. Often a case seems to be "in trouble"
not because the medication chosen has turned out to be incorrect,
but because the patient feels defective or inadequate when offered
a diagnosis that refers to a biological defect. Such confusion
between the shame associated with an attribute of the person and
shame of the entire self is easy to understand. Of even more significance
is the possibility that biological illnesses characterized by
aberration of the physiology of the innate affect shame-humiliation
may magnify to literally toxic proportions the patient's affective
reaction to our offer of treatment. Central to good psychopharmacologic
practice is this understanding that anybody who is asked to take
chronic psychiatric medication will experience the therapeutic
interaction as intensely shaming. We must remain in good empathic
contact with the patient to whom we offer medication.
Most of our current diagnostic categories and therapeutic concepts
must be revised in terms of this new understanding of human emotion.
Nowhere is this more critical than in the realm of psychopharmacology,
which seeks to normalize neurobiology to the extent that an individual
can experience innate affect at an intensity that allows optimal
information processing, and only when triggered by the innate
triggers for which it has evolved.
Tomkins, Silvan S. (1962, 1963, 1991, 1992) Affect, Imagery,
Consciousness Volumes I-IV. New York: Springer.
Nathanson, Donald L. (1987) A timetable for shame. in: D. L. Nathanson,
ed. The Many Faces of Shame. New York: Guilford.
_______________ (1988) Affect, affective resonance, and a new
theory for hypnosis. Psychopathology 21:2-3; pp.126-137.
_______________ (1992) Shame and Pride: Affect, Sex, and the
Birth of the Self. New York: W. W. Norton.
Klein, Donald F.; Gittleman, Rachel; Quitkin, Frederick; and Rifkin,
A. (1980) Diagnosis and Drug Treatment of Psychiatric Disorders:
Adults and Children. Baltimore: Williams & Wilkins.
Kluft, Richard P. (1992) Paradigm exhaustion and paradigm shift:
Thinking through the therapeutic impasse. Psychiatric Annals
22:10 pp.502-508.
Kaufman, Gershen (1985) Shame: The Power of Caring. Cambridge,
Massachusetts: Schenkman.
Snider, Michael R.; Fisher, Stephen K.; Agranoff, Bernard W. (1987)
Inositide-Linked Second Messengers in the Central Nervous System
In Meltzer, Herbert Y., ed. Psychopharmacology The Third Generation
of Progress Raven Press
Snyder, Solomon (date) second messenger system????
All of the following statements about affects are true except:
A. They are dependent upon and directly influenced by neurotransmitters
and receptors.
B. They may be influenced by drugs and medications.
C. They are non-specific amplifiers and analogues of their triggers.
D. They are the result of early learning which research now show
occurs before the age of 6 months.
Answer: D
All of the following represent examples of syndromes where the
affect Shame/Humiliation appears to play a primary role except:
A. Social Phobia
B. Narcissistic Personality Disorder
C. Obsessive Compulsive Disorder
D. Atypical Depression as described by Klein et al.
Answer: C
Which of the following differentiate between a patient with Bipolar
Affective Disorder and one with extreme mood reactivity:
A. The presence of increased energy, talking, self-esteem, and
a decreased need for sleep.
B. A mood inconsistent with the quality of the patient's current
life circumstances or recent triggering events.
C. The appearance of a hypomanic state in response to antidepressant
medication.
D. A depression appearing to have been triggered by a major loss
in the patient's life.
Answer: B
Emotions may be influenced by:
1. Learning and prior experience.
2. Acquired or inherited biological abnormalities.
3. The view a person holds and his thoughts about a subject.
4. Ingestion of drugs or medications.
Answer: E
Major Depression as defined by DSM III R criteria:
1. Represents the results of one specific pattern of receptor/neurotransmitter
abnormality.
2. Is divisible into distinct subtypes having differential responsiveness
to our currently available antidepressant agents.
3. Is endogenous rather than exogenous or reactive.
4. May be the result of abnormalities at what Nathanson defines
as the Hardware, Firmware, or Software levels.
Answer: C
In which of the following syndromes do symptoms of the primary
illness often trigger a significant secondary shame reaction:
1. Panic Disorder
2. Obsessive Compulsive Disorder
3. Post-Traumatic Stress Disorder
4. Attention Deficit Disorder
Answer: E
Get your own Free Home Page