Affect Theory and Psychopharmacology
Donald L. Nathanson and James M. Pfrommer
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.
The Function of Affect
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.
Disorders involving affect
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
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
Pattern Recognition and Affect Dynamics
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"
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
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
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
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.
The Shame of Psychopharmacology
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.
Summary and Conclusions
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.
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.
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.
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.
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.
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