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 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.

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" 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.

Medication Response

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.

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????

CME Quiz

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

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