There also appear to be significant gender differences in the serotonergic systems of both animals and humans. Mirko Diksic, Sadahiko Nishizawa and their colleagues at McGill University recently provided the most dramatic example: to measure serotonin synthesis in the human brain, they devised a new technique using PET neuroimaging and found that the average synthesis rate was 52 percent higher in men than in women. The investigators note that with the exception of estrogen binding sites, this gender difference in the brain is one of the largest ever reported. The lower rate of serotonin synthesis in women might increase their overall risk for depression - especially if serotonin stores are depleted during stress or winter darkness.
Meir Steiner and his co-workers at McMaster University suggest that if serotonin mediates between an organism and its environment and if the neurotransmitter is regulated differently in men and women, it might explain gender patterns not only in depression but also in a range of psychiatric illnesses. Specifically, whereas depression and anxiety are more common among women, alcoholism and severe aggression are more common among men. And just as low serotonin levels have been implicated in depression and anxiety disorders in women, they have also been found in the brains of men with severe forms of alcoholism and aggression.
Such gender differences in the serotonergic system might ensure that females respond to stress with psychiatric disturbances that involve behavioural inhibition, whereas men respond to stress with a loss of behavioural control. Steiner suggests that such gender differences in the serotonergic system evolved because child rearing is more successful (in the narrow sense of more children surviving to adulthood) in species in which aggressive impulses are cu
A researcher espousing either the sociological or psychological explanation of depression's gender bias might counter Steiner's theory by arguing that men are socialized to respond to stress with "acting out" behaviours, such as alcoholism or aggression. In contrast, society teaches women to respond to stress with "acting in" behaviours, such as depression. To support this idea, they might point to epidemiological studies done in Amish and Jewish populations. In these communities, alcoholism is less common than in the population at large, and, interestingly, the rates of depression are as high in men as in women.
These contradictory data leave no doubt that the explanations behind depression and other psychiatric diseases are not straightforward. Biological and social influences not only coexist but also probably reinforce one another. After all, we would expect gender socialization patterns to evolve so that they complement biological differences between the sexes. In other words, we would expect "nurture" to reinforce rather than oppose "nature." And because nurture involves learning - and learning occurs when certain neural connections in the brain are strengthened - it is clear that both nurture and nature involve biological processes.
Scientists have made tremendous strides in treating depression. With the advent of such antidepressants as Prozac (which acts on the serotonergic system), more than 80 percent of depressed patients now respond to medication or psychotherapy, or a combination of the two. But much more work remains to be done. Because depression is so common, its cost to society is high. The National Institute of Mental Health estimates that depression claims $30.4 billion in treatment and in lost productivity from the US economy every year.
And these costs are on the rise: depression is becoming more common in successive generations (the so-called cohort effect). No one knows what is causing the cohort effect - but it is moving much too quickly to have a genetic basis. Theories about what is causing the cohort effect range from increased drug abuse and familial disarray to the suggestion that perhaps older people are simply more likely to forget past depressive episodes when asked. The cohort effect and depression in general remain very much a mystery. And for the men and women who suffer from it, it is a mystery that cannot be solved soon enough.
When the electrical signal reaches the tip of an axon, it stimulates small presynaptic vesicles in the cell. These vesicles contain chemicals called neurotransmitters, which are released into the microscopic space between neurons (the synaptic cleft). The neurotransmitters attach to specialized receptors on the surface of the adjacent neuron. This stimulus causes the adjacent cell to depolarize and propagate an action potential of its own. The duration of a stimulus from a neurotransmitter is limited by the breakdown of the chemicals in the synaptic cleft and the reuptake by the neuron that produced them. Formerly, each neuron was thought to make only one transmitter, but recent studies have shown that some cells make two or more.
Serotonin neurotransmitter, or its valuing chemical that transmits messages across the synapses, or gaps, between adjacent cells. Among its many functions, serotonin is released from blood cells called platelets to activate blood vessel constriction and blood clotting. In the gastrointestinal tract, serotonin inhibits gastric acid production and stimulates muscle contraction in the intestinal wall. Its functions in the central nervous system and effects on human behaviour - including mood, memory, and appetite control have been the subject of a great deal of - research. This intensive study of serotonin has revealed important knowledge about the serotonin-related cause and treatment of many illnesses
Serotonin is produced in the brain from the amino acid tryptophan, which is derived from foods high in protein, such as meat and dairy products. Tryptophan is transported to the brain, where it is broken down by enzymes to produce serotonin. In the process of neurotransmission, serotonin is transferred from one nerve cell, or neuron, to another, triggering an electrical impulse that stimulates or inhibits cell activity as needed. Serotonin is then reabsorbed by the first neuron, in a process known as reuptake, where it is recycled and used again or converted into an inactive chemical form and excreted.
While the complete picture of serotonin’s function in the body is still being investigated, many disorders are known to be associated with an imbalance of serotonin in the brain. Drugs that manipulate serotonin levels have been used to alleviate the symptoms of serotonin imbalances. Some of these drugs, known as selective serotonin reuptake inhibitors (SSRIs), block or inhibit the reuptake of serotonin into neurons, enabling serotonin to remain active in the synapses for a longer period of time. These medications are used to treat such psychiatric disorders as depression; obsessive-compulsive disorder, in which repetitive and disturbing thoughts trigger bizarre, ritualistic behaviours; and impulsive aggressive behaviours. Fluoxetine (more commonly known by the brand name Prozac), is a widely prescribed SSRI used to treat depression, and more recently, obsessive-compulsive disorder.
Drugs that affect serotonin levels may prove beneficial in the treatment of nonpsychiatric disorders as well, including diabetic neuropathy (degeneration of nerves outside the central nervous system in diabetics) and premenstrual syndrome. Recently the serotonin-releasing agent dexfenfluramine has been approved for patients who are 30 percent or more over their ideal body weight. By preventing serotonin reuptake, dexfenfluramine promotes satiety, or fullness, after eating less food
Drugs known as antagonists bind with neurons to prevent serotonin neurotransmission. Some antagonists have been found effective in treating the nausea that typically accompanies radiation and chemotherapy in cancer treatment. Antagonists are also being tested to treat high blood pressure and other cardiovascular disorders by blocking serotonin’s ability to constrict blood vessels. Other antagonists may produce an effect on learning and memory in age-associated memory impairment.
Neurotransmitters are released into a microscopic gap, called a synapse, that separates the transmitting neuron from the cell receiving the chemical signal. The cell that generates the signal is called the presynaptic cell, while the receiving cell is termed the postsynaptic cell.
Neurotransmitter, chemical made by neurons, or nerve cells. Neurons send out neurotransmitters as chemical signals to activate or inhibit the function of neighbouring cells
Within the central nervous system, which consists of the brain and the spinal cord, neurotransmitters pass from neuron to neuron. In the peripheral nervous system, which is made up of the nerves that run from the central nervous system to the rest of the body, the chemical signals pass between a neuron and an adjacent muscle or gland cell.
Nine chemical compounds - belonging to three chemical families - are widely recognized as neurotransmitters. In addition, certain other body chemicals, including adenosine, histamine, enkephalins, endorphins, and epinephrine, have neurotransmitter like properties. Experts believe that there are many more neurotransmitters as yet undiscovered.
The first of the three families is composed of amines, a group of compounds containing molecules of carbon, hydrogen, and nitrogen. Among the amine neurotransmitters are acetylcholine, norepinephrine, dopamine, and serotonin. Acetylcholine is the most widely used neurotransmitter in the body, and neurons that leave the central nervous system (for example, those running to skeletal muscle) use acetylcholine as their neurotransmitter; neurons that run to the heart, blood vessels, and other organs may use acetylcholine or norepinephrine. Dopamine is involved in the movement of muscles, and it controls the secretion of the pituitary hormone prolactin, which triggers milk production in nursing mothers.
The second neurotransmitter family is composed of amino acids, organic compounds containing both an amino group (NH2) and a carboxylic acid group (COOH). Amino acids that serve as neurotransmitters include glycine, glutamic and aspartic acids, and gamma-amino butyric acid (GABA). Glutamic acid and GABA are the most abundant neurotransmitters within the central nervous system, and especially in the cerebral cortex, which is largely responsible for such higher brain functions as thought and interpreting sensations.
The third neurotransmitter family is composed of peptides, which are compounds that contain at least 2, and sometimes as many as 100 amino acids. Peptide neurotransmitters are poorly understood, but scientists know that the peptide neurotransmitter called substance P influences the sensation of pain.
Neurotransmitters are manufactured from precursor compounds like amino acids, glucose, and the dietary amine called choline. Neurons modify the structure of these precursor compounds in a series of reactions with enzymes. Neurotransmitters that come from amino acids include serotonin, which is derived from tryptophan; dopamine and norepinephrine, which are derived from tyrosine; and glycine, which is derived from threonine. Among the neurotransmitters made from glucose are glutamate, aspartate, and GABA. Choline serves as the precursor for acetylcholine
Neurotransmitters are released into a microscopic gap, called a synapse, that separates the transmitting neuron from the cell receiving the chemical signal. The cell that generates the signal is called the presynaptic cell, while the receiving cell is termed the postsynaptic cell.
After their release into the synapse, neurotransmitters combine chemically with highly specific protein molecules, termed receptors, that are embedded in the surface membranes of the postsynaptic cell. When this combination occurs, the voltage, or electrical force, of the postsynaptic cell is either increased (excited) or decreased (inhibited).
When a neuron is in its resting state, its voltage is about -70 millivolts. An excitatory neurotransmitter alters the membrane of the postsynaptic neuron, making it possible for ions (electrically charged molecules) to move back and forth across the neuron’s membranes. This flow of ions makes the neuron’s voltage rise toward zero. If enough excitatory receptors have been activated, the postsynaptic neuron responds by firing, generating a nerve impulse that causes its own neurotransmitter to be released into the next synapse. An inhibitory neurotransmitter causes different ions to pass back and forth across the postsynaptic neuron’s membrane, lowering the nerve cell’s voltage to -80 or -90 millivolts. The drop in voltage makes it less likely that the postsynaptic cell will fire.
If the postsynaptic cell is a muscle cell rather than a neuron, an excitatory neurotransmitter will cause the muscle to contract. If the postsynaptic cell is a gland cell, an excitatory neurotransmitter will cause the cell to secrete its contents.
While most neurotransmitters interact with their receptors to create new electrical nerve impulses that energize or inhibit the adjoining cell, some neurotransmitter interactions do not generate or suppress nerve impulses. Instead, they interact with a second type of receptor that changes the internal chemistry of the postsynaptic cell by either causing or blocking the formation of chemicals called second messenger molecules. These second messengers regulate the postsynaptic cell’s biochemical processes and enable it to conduct the maintenance necessary to continue synthesizing neurotransmitters and conducting nerve impulses. Examples of second messengers, which are formed and entirely contained within the postsynaptic cell, include cyclic adenosine monophosphate, diacylglycerol, and inositol phosphates.
Once neurotransmitters have been secreted into synapses and have passed on their chemical signals, the presynaptic neuron clears the synapse of neurotransmitter molecules. For example, acetylcholine is broken down by the enzyme acetylcholinesterase into choline and acetate. Neurotransmitters like dopamine, serotonin, and GABA are removed by a physical process called reuptake. In reuptake, a protein in the presynaptic membrane acts as a sort of sponge, causing the neurotransmitters to reenter the presynaptic neuron, where they can be broken down by enzymes or repackaged for reuse.
Neurotransmitters also play a role in Parkinson disease, which slowly attacks the nervous system, causing symptoms that worsen over time. Fatigue, mental confusion, a mastlike facial expression, stooping posture, shuffling gait, and problems with eating and speaking are among the difficulties suffered by Parkinson victims. These symptoms have been partly linked to the deterioration and eventual death of neurons that run from the base of the brain to the basal ganglia, a collection of nerve cells that manufacture the neurotransmitter dopamine. The reasons why such neurons die are yet to be understood, but the related symptoms can be alleviated. L-dopa, or levodopa, widely used to treat Parkinson disease, acts as a supplementary precursor for dopamine. It causes the surviving neurons in the basal ganglia to increase their production of dopamine, thereby compensating to some extent for the disabled neurons.
Dopamine, chemical known as a neurotransmitter essential to the functioning of the central nervous system. In the process of neurotransmission, dopamine is transferred from one nerve cell, or neuron, to another, playing a key role in brain function and human behaviour.
Dopamine forms from a precursor molecule called dopa, which is manufactured in the liver from the amino acid tyrosine. Dopa is then transported by the circulatory system to neurons in the brain, where the conversion to dopamine takes place.
Dopamine is a versatile neurotransmitter. Among its many functions, it plays a major role in two activities of the central nervous system: one that helps control movement, and a second that is strongly associated with emotion-based behaviours.
The pathway involved in movement control is called the nigrostriatal pathway. Dopamine is released by neurons that originate from an area of the brain called the substantia nigra and connect to the part of the brain known as the corpora striata, an area known to be important in controlling the musculoskeletal system.
The second brain pathway in which dopamine plays a major role is called the mesocorticolimbic pathway. Neurons in an area of the brain called the ventral tegmentalarea transmit dopamine to other neurons connected to various parts of the limbic system, which is responsible for regulating emotion, motivation, behaviour, the sense of smell, and various autonomic, or involuntary, functions like heartbeat and breathing.
A growing body of evidence suggests that dopamine is involved in several major brain disorders. Narcolepsy, a disorder characterized by brief, recurring episodes of sudden, deep sleep, is associated with abnormally high levels of both dopamine and a second neurotransmitter, acetylcholine. Huntington’s chorea, an inherited, fatal illness in which neurons in the base of the brain are progressively destroyed, is also linked to an excess of dopamine.
Commonly known as shaking palsy, Parkinson disease is another brain disorder in which dopamine is involved. Besides tremors of the limbs, Parkinson patients suffer from muscular rigidity, which leads to difficulties in walking, writing, and speaking. This disorder results from the degeneration and death of neurons in the nigrostriatal pathway, resulting in low levels of dopamine. The symptoms of Parkinson disease can be minimized by treatment with a drug called levodopa, or L-dopa, which converts to dopamine in the brain.
Schizophrenia is a psychiatric disorder characterized by loss of contact with reality and major changes in personality. Schizophrenics have normal levels of dopamine in the brain, but because they are highly sensitive to this neurotransmitter, these normal levels of dopamine trigger unusual behaviours. Drugs such as thorazine that block the action of dopamine have been found to decrease the symptoms of schizophrenia.
Studies indicate that people who are addicted to alcohol and other drugs like cocaine and nicotine have less dopamine in the mesocorticolimbic pathway. These drugs appear to increase dopamine levels, resulting in the pleasurable feelings associated with the drugs.
Another group of antidepressants, known as selective serotonin reuptake inhibitors (SSRI), became available in 1987. SSRIs block the reuptake of the neurotransmitter serotonin into presynaptic neurons, thereby prolonging its activity. There are currently four SSRIs available for use in the United States: fluoxetine, sertraline, paroxetine, and fluvoxamine. Of this group, the best known is fluoxetine, commonly known by its brand name, Prozac.
Another antidepressant is venlafaxine, which works like TCAs but does not share their chemical structure, and it also causes different side effects. The antidepressant nefazodone prevents serotonin from binding to neighbouring neurons at one specific binding site (serotonin can bind to neurons on many sites). It also weakly blocks the reuptake of serotonin.
All antidepressants decrease symptoms of depression in about 70 percent of depressed people who take them. Most antidepressants take about two to three weeks of treatment before beneficial effects occur. Because no antidepressant is more effective than the others, doctors determine which antidepressant to prescribe according to the type of side effects an individual can tolerate. For instance, a person who takes TCAs and MAO inhibitors may notice dizziness and fainting when standing up, mouth dryness, difficulty urinating, constipation, and drowsiness. If people who take MAO inhibitors eat certain foods, such as aged cheese or some aged meats, they can experience severe headaches and raised blood pressure. SSRIs can cause side effects such as restlessness, difficulty sleeping, and interference with sexual function.
The theory Edward Bibring presents in ‘The Mechanism of Depression’ (1953) is deliberately limited to the ego of psychology depression. He wrote: ‘ . . . the conception of depression presents are not invalidated for which of an accepted theory of the role which orality and aggression play in the various types of depression’. Yet his theory points up the inadequacy of the theory, Bibring stated his view as follows ‘ . . . the oral and aggressive strivings are not as universal in depression as is generally assumed and . . . consequently the theories built on them do not offer sufficient explanation, but require . . ., modification.’
The basic proposition of Bibring’s theory is akin to the proposition which Freud built as the structural theory of anxiety. Freud wrote: ‘ . . . the ego is the real seat of anxiety . . ., Anxiety is an affective state which can, of course, be experienced only by the ego’. Bibring wrote" ‘Depression is . . . primarily an ego phenomenon’ [it] represents an effective state. ‘[Anxiety and depression are] both . . . frequent . . . ego reactions . . . [and since] they cannot be reduced any further, it may be justified to call them basic ego reactions’.
Bibring thus set out to explore the structure of depression as an ego state. He used Freud’s theory of anxiety., Fenichel’s theory of boredom, and some general observations of depersonalization as his points of departure.
We have here a structural theory which treats depression as the reactivation of a structural state. The universal experiences of grief and sadness, ranging from passing sadness to profound depression, indicate differences in the relative ease of and intensity of the reactivation of this state are determined by: (1) Both the constitutional tolerance for continued frustration. (2) The severity and extent of the situation of helplessness in early life. (3) The developmental factors which increase or decrease the relative ease with which this state is reactivated and modulate its intensity. (4) The kind and severity of the precipitating condition. As for the dynamic aspect of this theory, the depressive ego state is reactivated by an intra-ego conflict. The factors involved in this conflict, however, are not yet precisely defined. As for the genetic aspect of the theory: The depressive ego state is reactivated by an intra-ego conflict. As for the genetic aspect of the theory. The origin of the depressive ego state is clear and so is the epigenesis of the ‘narcissistic aspirations’ involved.
The economic and adaptive aspects of the theory, however, are mot directly treated by Bibring, but Freud made several attempts to account for various aspects of the economics of depression.
For instance, he wrote: ‘. . . the ego’s inhibited condition and loss of interest was fully accounted for by the absorbing work of mourning’, or, for instance:
An important school of thought is based on the teachings of the British psychoanalyst Melanie Klein. Because most of Klein's followers worked with her in England, this has come to be known as the English school. Its influence, nevertheless, is very strong throughout the European continent and in South America. Its principal theories were derived from observations made in the psychoanalysis of children. Klein posited the existence of complex unconscious fantasies in children under the age of six months. The principal source of anxiety arises from the threat to existence posed by the death instinct. Depending on how concrete representations of the destructive forces are dealt with in the unconscious fantasy life of the child, two basic early mental attitudes result that Klein characterized as a ‘depressive position’ and a ‘paranoid position’. In the paranoid position, the ego's defence consists of projecting the dangerous internal object onto some external representative, which is treated as a genuine threat emanating from the external world. In the depressive position, the threatening object is introjected and treated in fantasy as concretely retained within the person. Depressive and hypochondriacal symptoms result. Although considerable doubt exists that such complex unconscious fantasies operate in the minds of infants, these observations have been of the utmost importance to the psychology of unconscious fantasies, paranoid delusions, and theory concerning early object relations.
Psychotherapy is an important form of treatment for many kinds of psychological problems. Two of the most common problems for which people seek help from a therapist are depression and persistent anxiety. People with depression may have low self-esteem, a sense of hopelessness about the future, and a lack of interest in people and activities once found pleasurable. People with anxiety disorders may feel anxious all the time or suffer from phobias, a fear of specific objects or situations. Psychotherapy, by itself or in combination with drug treatment, can often help people overcome or manage these problems.
People with depression often experience feelings of worthlessness, helplessness, guilt, and self-blame. They may interpret a minor failing on their part as a sign of incompetence or interpret minor criticism as condemnation. Some depressed people complain of being spiritually or morally dead. The mirror seems to reflect someone ugly and repulsive. Even a competent and decent person may feel deficient, cruel, stupid, phony, or guilty of having deceived others. People with major depression may experience such extreme emotional pain that they consider or attempt suicide. At least 15 percent of seriously depressed people commit suicide, and many more attempt it.
The pervasive and chronic nature of personality disorders makes them difficult to treat. People with these disorders often fail to recognize that their personality has contributed to their social, occupational, and personal problems. They may not think they have any real problems despite a history of drug abuse, failed relationships, and irregular employment. Thus, therapists must first focus on helping the person understand and become aware of the significance of their personality traits.
People with personality disorders sometimes feel that they can never change their dysfunctional behaviour because they have always acted the same way. Although personality change is exceedingly difficult, sometimes people can change the most dysfunctional aspects of their feelings and behaviour.
Therapists use a variety of methods to treat personality disorders, depending on the specific disorder. For example, cognitive and behavioural techniques, such as role playing and logical argument, may help alter a person’s irrational perceptions and assumptions about himself or herself. Certain psychoactive drugs may help control feelings of anxiety, depression, or severe distortions of thought. Psychotherapy may help people to understand the impact of experiences and relationships during childhood.
Psychotherapy is usually ineffective for people with antisocial personality disorder because these individuals tend to be manipulative, unreliable, and dishonest with the therapist. Therefore, most mental health professionals favour removing people with this disorder from their current living situation and placing them in a residential treatment centre. Such residential programs strictly supervise patients’ behaviour and impose rigid, consistent rules and responsibilities. These programs appear to help some people, but it is unclear how long their beneficial effects last.
Therapists treating people with borderline personality disorder sometimes use a technique called dialectical behaviour therapy. In this type of therapy, the therapist initially focuses on reducing suicidal tendencies and other behaviours that disrupt treatment. The therapist then helps the person develop skills to cope with anger and self-destructive impulses. In addition, the person learns to achieve personal strength through an acceptance of the many disappointments and interpersonal conflicts that are a natural part of life.
cognitive view of behaviour assigns primary importance to the self-evident fact that people think. It assumes that the hidden nature and characteristics of thinking and resultant conclusions determine what people feel and do and how they act and react. This view of behaviour and psychopathology has a long history that bridges the disciplines of clinical psychiatry, clinical and academic psychology, and philosophy. The increasing reemphasis on the role of cognition in behaviour has been termed the ‘cognitive revolution’.
‘Cognition’ is a broad term that refers to both the content of thought and the processes involved in thinking, the mechanisms and content of memory and recall, and problem-solving attitudes and strategies are all aspects of cognition. In short, cognition encompasses the processes of knowing, as well as the products of knowing. Many of the complex processes subsumed under the term ‘cognition’ are still poorly understood. In the absence of as comprehensive theory of memory that would help to explain the consistencies in individual behaviour over time, the existence of‘ or ‘schemata’ has been postulated.
Cognitive structures are relatively enduring characteristics of a person’s cognitive organization. They are organized representations of prior experiences; different aspects of experience are organized through different schemata. The concept of cognitive structures or schemata can be used to explain why people react differently to similar or identical situations, while a particular individual may show the same type of response to apparently dissimilar events.
A schema allow a person to screen, code, and assess the full range of internal or external stimuli and to decide on a subsequent course of action. When a person is confronted with a particular situation, it is assumed that a schema is activated that is relevant to that stimulus confrontation with a particular situation, it is assumed that a schema is activated that a relevant to that stimulus confrontation. The different schemata in the cognitive organization may vary in their specificity and detail and the range of stimuli or patterns to which they apply. For example, a person may have a complex, multifaceted, and well-developed cognitive schema to deal with problems in mathematics, but a simple, narrow schema to deal with sexual encounters, in our use of the term, schemata encompass systems fo classifying stimuli that range from simple perceptual configurations to complex stepwise reasoning processes.
The cognitive e approach to behaviour and psychopathology is different in may ways from previous psychological perspectives. Precious models have used motivational or adaptational concepts that are so elaborate and remote from clinically observable phenomena as to preclude empirical validation, such as derived from the cognitive approach to depression are readily testable, and many of them have been supported by empirical evidence.
Contrary to common belief among clinicians, the cognitive approach to depression and psychopathology does not assume that a well-adjusted individual is one who thinks logically and solves problems rationally. What is assumed is that to understand and correct maladaptive behaviour, the idiosyncratic meaning people ascribe to their experiences must be uncovered. within this framework, we do not try to alter or remove all idiosyncratic evaluations but only those that are dysfunctional or maladaptive. The evaluations or idiosyncratic views that are pathogenic of depression are generally associated with negative value judgements. For example, a woman’s belief that she is unattractive may not be consensual validated, and this it may reflect an idiosyncratic cognition. Nonetheless, if the cognition did not interfere with her emotional well-being and general functioning, It would not be considered maladaptive. On the other hand, if the woman attached a negative value too her opinion of her appearance and consider appearance to be an important aspect of her desirability as a person, she would be likely to progress to inaccurate functional conclusions, such as, ‘Nobody could love me because I am ugly’ or ‘I might as well give up in life since I don’ t have much going for me’.
The cognitive perspective holds that mental illness results from problems in cognition - that is, problems in how a person reasons, perceives events, and solves problems. American psychiatrist Aaron Beck proposed that some mental illnesses - such as depression, anxiety disorders, and personality disorders - result from a way of thinking learned in childhood that is not consistent with reality. For example, people with depression tend to see themselves in a negative light, exaggerate the importance of minor flaws or failures, and misinterpret the behaviour of others in negative ways. It remains unclear, however, whether these kinds of cognitive problems actually cause mental illness or merely represent symptoms of the illnesses themselves.
Beck has provided the most comprehensive exposition of the cognitive view of depression. In contradistinction to current emphases that mood alternation is central in depressive syndromes, the cognitive approach focusses on self-castigation, exaggeration of external problems, and hopelessness as the most salient symptoms.
According to Beck, the depressed person’s thinking and preoccupation represent erroneous and exaggerated ways of viewing oneself and events. The depressed person is overly sensitive to obstacles to goal-directed activity, interpreted trivial impediments as a substantial, reads disparagement into innocuous statements by others, and, at the same time, devalues himself for herself, the characteristic depressive preoccupations are stereotypical and are evident in self-report, fantasy and dream content. Moreover, the cognitions are frequently irrelevant and inappropriate to the reality of the situation and mirror a consistent negative bias against oneself.
Profuse negative cognitions inevitably lead to dysphoria, reduced desire to provide for one’s pleasure or welfare, passivity and ultimately to giving up. The specific cognitive content is ‘chained’ to a particular affect. Thus concern about an anticipated threat is connected with feelings of anxiety, thoughts about being unloved and abandoned are associate with depressive feelings. Depressive cognitive content generally relates to notions of loss or perceived subtraction from what Beck refers to as one’s ‘personal domain’. The personal domain includes the individual significant others, value objects and attributes, and deals, principles, and goals held to be important. Thus if professional accomplishment is a central and cherished goal, a temporary setback may be magnified out of proportion and seen as having devastating implications about one’s abilities and one’s prospects for future achievement. As a consequence of such an over generalized negative interpretation, the depressed person is likely to experience increased dysphoria,, dejection, and discouragement.
In the clinical depression, the patient’s perceptions, interpretations and evaluations are not consensual validated, and the pervasive, negative bias against oneself remains relatively immune to conventional corrective feedback. This negative view of oneself and the future also militates against the reality testing of one’s idea, active exploration of problem solving alternatives, and appropriate use of other people as resources.
Beck’s approach to depression and its derivative treatment, cognitive therap y, is targeted on selected aspects of the patient’s thinking and behaviour.
The content of depressive cognitions is predominantly negative in tone and self-referential in direction; the individual is preoccupied with self-derogatory and self-blaming thoughts. Moreover, the depressed patient projects into the future his notions of real or imagined loss. He becomes pessimistic and hopeless and believes that the current discomfort is unending and unalterable. Beck has referred to the thematic content of depressive cognitions, the ‘negative cognitive trait,’ a negative, demeaning view of onself, the world, and the future. A number of empirical investigations support the common clinical observation that depression is associated with negative self-referential cognitive content.
Much of our knowledge about ourselves and the world is meaningful only when considered in a time dimension. In addition, most of our actions implicitly reflect future goal-orientation. It has long been noted that a disturbance in time orientation, such as a constricted time perspective, is unindicated by psychopathology. In the clinical interview the depressed patient’s highly constricted time perspective is evident in statements that he or she has ‘no future’ or ‘nothing to look forward to’. In other words, in depression the future loses its meaning as a foreshadowing for prospective e solutions. In that the patient’s eye s the future becomes singular state of unending pain and despair than a multiplicity of experiences and opportunities.
A number of studies have documented the fact that distorted constructions of temporal experience is of one of the characteristics of depressed cognitions. Compared with both nondepressed ‘normal’ people and nondepressed psychiatric patients such as schizophrenic and manic individuals, depressed patient manifest specific distortions of temporal schemata.
An additional aspect of cognitive functioning, is also characteristically skewed in depression. Depressed individuals selectively of neural or positively toned material. In the clinical interview they usually paint the bleakest picture of their background: positive material can be elicited only by the most pointed and specific questioning. Lloyd and Lishman reported empirical data that depressive recall is biassed toward negatively toned material the extent of negative recall is related to the severity of the depression and to depression as a diagnosis. The characteristically biassed recall was also documented by the work of Nelson and Craighead, who showed that depressed subjects tend to remember more experimental punishment and less positive experimental reinforcement than nondepressed experimental reinforcement than nondepressed subjects do: Other studies have indicated that depressed subjects underestimate the amount of positive experimental reinforcement they receive.
The depressed patient is specially prone to quality prior positive experiences and to personalized experiences of failure. Is that, they often interpret as indications of his or her blameworthiness. For example, a patient was not pleased when a short story she had written was accepted for publication because she attributed the acceptance to sheer luck. However, she regarded a rejected article as proof of her incompetence and felt distraught. As similar phenomenon was reported by Stuart, who found that depressive tendencies correlate with evaluative rather than classificatory associations, i.e., associating the word ‘apple’ with ‘sweet’ (evaluation) rather that ‘fruit’ (classification). Empirical work has documented the fact that depressed subjects personalize failure, they ascribe in an experimental task to lack of ability, while they do not attribute success to internal factors.
The depressed patient’s characteristic stereotypical conclusions and assessments reflect a combination of negative cognitive themes and certain systematic errors of thinking. A characteristic error in degressive e thinking is drawing conclusion in the absence of or contrary to evidence. This process of arbitrary inference is illustrated by the following cognition" ‘John didn’t call tonight . . . He probably doesn’t want to see me anymore’. When depressed pastiest are comforted with a negative event o r attribute they typically magnify its importance, however, the implications of a pleasant event or positive attribute are minimized. For instance, a patient evaluated a slight increase in her dysphoria to mean that she was ‘deteriorating’, while she viewed a well-done task as quite insignificant. In clinical work we typically find the patient selectively abstracts isolated elements of a situation that are most consistent with his or her negative and pessimistic world view and ignore other salient cues. A depressed patient decided that, for example, her boss’s failure to say hello was ominous; she completely ignored the fact that he was under considerable pressure and preoccupied. As Beck and Shaw have noted, the depressed patient’s invariant method of information processing results in over generalization and the ignoring of fine discrimination.
Hammen, Krantz, and Weintraub and associates and Beck have reported empirical data that document the presence and preponderance of erroneous cognitive processes in depressed college students and depressed patients. The depressive tendency to magnify negative experiences is reflected in depressed subjects’ hypersensitivity to experimentally manipulated failure, compared with the reactions of nondepressed subjects. Loeb and associates and Hammen and Krantz have documented the fact that such manipulations lead to increase dysphoria and pessimism, decreased levels of aspiration, and less positive predictions of one’s performance on subsequent tasks.
However, developments in the interactional description of schizophrenia has been parallelled in the area of depression. As yet, concept such as pseudomutality, double-bind, schism and skew have found no counterparts. Kubler and Stotland (1964)have argued; ‘emotional disturbance, even the most severe, cannot be undershoot unless the field in which it develops and exists is examined. The manifestations of the difficultly in the disturbed individual have meaning depending on aspects of the field. The significant aspect of the field usually interpersonal’, yet the study of depression has focussed on the individual and his behaviour out of his interactional context. To a large degree, the depressed person’s monotonously reiterate complaints and self-accusations, and his provocative and often annoying behaviour have distracted investigators from considerations of his environment and the role it may play in the maintenance of his behaviour. the possibility that the characteristic pattern of depressed behaviour might be interwoven and concatenated with a corresponding pattern in the response of others has seldom been explored.
To address to that possibility, for the most part, it has been assumed that the depressed person is relatively impervious to the influence of others. Ruesch (1962) stated that to talk to the depressed person makes little sense; to listen, little more. Grinker (1964) conceptualized symptomalogy as communication to others, but argued that the depressed person is not responsive to communication from others: The depressed person . . . cannot use information for the purpose of action, he cannot perceive the cues of reality, he makes statements but does not care if he is understood.
In terms of system theory (von Bertalanffy, 1950; Allport, 1960 and Miller, 1971), the usual conceptualization of the depressed person is one of a relative ly closed system. Grinker (1964)was explicit in stating that the depressed person repeats his messages and behaviour without reception or acceptance of resulting feedback. Beck (1964) described the cognitive distortions that dominate the information processing of the depressed person so that experiences are rigidly interpreted to maintain existing schema of personal deficiency, self-blame and negative expectations.
The implicit assumption of these and other writers has been that the support and information available to the depressed person are incongruent with his depression, and the persistence of his symptomatology is evidence of a failure to receive or accept this information. Withdrawal of depressive schema and affective-structures, produce a downward depressive spiral. Such that an alternative argument that the depressed person is lost and depressive information elicited. However, this in turn increases the level of depression and strengthens the pathogenic pattern of depressed behaviour and response of others. If a depressive spiral develops, it is mutually causative, deviation-amplifying process (Maruyama, 1963) in the interaction of the depressed person with his environment. Thus, what is customarily viewed as some internal process is, that such of what is customarily viewed as cognitive distortion or misperception is characteristic of information flow from the environment. It should be noted that while the depressed person’s different interpretation of his predication is traditionally attributed to his distortion or misperception, generally disorders of thought and perceptions are neither defining criteria nor common among depressed patients (McPartland and Hornstra, 1964). An observer who fails to take into account the intricacies of someone’s relationship to his environment frequently attributes to him characteristics that he does not posses, or leaves significant aspects of his experience unexplained (Watzlawick et al., 1967). Feedback introduces phenomena that cannot be adequately explained by reference to the isolated individual alone (Ashby, 1960, 1962). For the study of depression, identification of a pattern of depressive feedback from the environment demands a more complex conceptualization of the disorder than one explaining its phenomena with reference to the isolated depressed person.
Lemert (1962), in his study of the interpersonal dynamics of paranoia, argued that the net effect of the developing interaction pattern between the paranoid person and others is that (1) The flow of information to the person is stopped, (2) A real discrepancy between expressed ideas and affect among those with whom he interacts is created, and (3) The situation or group image becomes as ambiguous for him as he is for others. In this context of attenuated relationships, exclusion, and disrupted communication, the paranoid person cannot get the feedback on his behaviour that is essential in order for him to correct his interpretations, and at, least be delusional, but that it is also true that in a very real sense he is able to elicit covertly organized action and conspiratorial behaviour.
The concurrent manners of the interpersonal dynamics of depression, that includes the interaction and information flow pattern congruent with the established phenomena of depression, and at the same time, indications as to why this than alternative patterns. Persist in the apparent absence of external; constants. Existing descriptions of the interpersonal behaviour of the depressed person will be examined as the attempt to make to reconstruct the interactional context in which this behaviour has meaning.
It should be made clear that such perspective does not deny the existence of important intrapersonal factors in depression, as Chodoff, (1972) and McCranie (1971) have argued that there is a ‘depressive-core’ in the personality of the depression-prone person, consisting of a tendency to feel worthless and helpless and an over-sensitivity to stimuli that impinge on or upon these feelings. Together, these are aroused from dormancy by specific situations such as loss of self-esteem. However, the emphasis of this is shown to be on means by which the environment comes into congruence with these feelings. The depressive’s vague, generalized feeling that there is something wrong with him, and his search for this among his minor defects, imperfections, and personal attributes, may arise from a depressive core to his personality, but at the same timer, the confusing response from the environment serves to validate these feelings. Likewise, conflicts about the reception of support and approval from others may be deeply rooted in the depressive’s intrapersonal style, but these conflicts can only be aggravated by the mixed messages of approval and rejection received from significant others, and by their withdrawal from him despite reassurances to the contrary.
Furthermore, the present exposition does not deny the importance of possible biochemical or genetic factors in the etiology of depression. Price (1974) has argued that even in disorders in which the importance of such factors has been clearly established, there may be a large number of links in the causal chain between specific etiological factors and the symptoms displayed by an individual. Social and interpersonal variables may determine to a large degree whether a disorder occurs and the form its symptoms will take. It is assumed that to initiate the process as a person need only begin to display depressive behaviour.
Since Freud, real and imagined objects losses have been given prominence in the explanation of depression, and depressive process has often been seen as miscarried restitutive work. While most early formulations focussed on intrapsychic phenomena, there were implications for interpersonal behaviour. As early as Abraham (1911, 1916), the over-demanding aspects of the depressive’s orality were noted. Radô (1928) assigned major ethological importance to an accentuated need for dependency in the depressed person. Fenichel (1945) described the nourotically depressed person’s interpersonal manoeuvres - his demonstrations of his misery, his accusations that others have brought about the misery, and even his blackmailing of others for attention - as desperate attempts to force others to restore damaged self-esteem. Yet in seeking this gratification, he is at the same time afraid to receive it because of the revenge that he expects will accompany it. In the psychologically depressed person, the loss is more complete, the objects have fallen away, and the restitutive effort is aimed exclusively at the superego.
Bonime (1960, 1966) described how the depressed person can dominate his environment with his demands for emotionally comforting responses from others. He considered depression to be a practice, an active way of relating to people in order to achieve pathological satisfactions, and he dismissed any suffering the depressed person may incur as secondary to the satisfaction of manipulative needs.
Aggression played a central role in early psychoanalytic formulations of depression (Abraham, 1911; Freud 1917), but later writers have increasingly disputed its role. Bibring (1953) went so far as to declare that depression was an ego phenomenon, ‘essentially independent of the vicissitudes of aggression as well as oral drives.’
Fromm-Reichmann (1959) argued that aggression had been considered overstressed as a dynamic factor in depression, and that if hostile feelings were found in the depressed person,. They were the result of the frustration of his manipulative and exploitative needs. Cohen et al., (1954). On the other hand, Bonime found the hurting or defying of others to be essential to depressed behaviour.
Renewed interest in the relationship between hostility and depression - particularly in the psychoanalytic view that depressed persons turn hostility that had originally been directed at others (hostility-out-ward), against themselves (hostility-inward) - has generated a number of empirical studies. Wessmann et al., (1960) suggested that relatively normal persons became hostile outward when depressed, whereas persons tending to become severely depressed were more likely to internalise or suppress this hostility. The data of Zuckerman et al., (1967) supported this view, indicating that only in the relatively normal was hostility correlated with depression on mood questionnaires or as rated by interviewers. Friedman (1964) found depressives to have more ‘readily expressed resentment’ as shown by their endorsement of adjectives such as ‘bitter’, ‘frustrated’, and ‘sulky’, yet found no greater overt hostility. In a later study, Friedman (1970) showed that feelings of depression and worthlessness were consonant with hostile and resentful feelings, even though depressed persons were not more likely to directly express these feelings to persons in the environment. Schless et al, (1974) found equal numbers of depressed patients turning hostility inward and outward, with both types of hostility increasing as depression became more severe. However, because these patients also saw other people’s anger as more readily expressed and more potent, that feared retaliation, and therefore expressed hostility in the form of resentment. In recent studies have been interpreted so as to call into question classical psychoanalytic formulations of the relationship of depression, hostility-inward and hostility-outward. On the other hand, the view that hostility may serve a defensive function against depression has been supported. That depression is preceded by increases in hostility that is directed out but cannot be expressed directly to appropriates that is directed out but cannot be expressed directly to appropriated objects in the environment, is taken as a failure of this defensive function (Friedman, 1970; McCranie, 1971; Schless et al., 1974).
Most writers who comment on the complaints and self-accusations of the depressed person have rejected the idea that they should be taken literally. Lichtenberg (1957) found that attempts to answer them directly with assurance, granting of dependency, and even punishment all increase depression and feelings of personal defect. Freud (1917) suggested that the self-accusations are actually aimed at someone else, a lost love object, and further notes, ‘ . . . it must strike us that after all the melancholic does not behave in quite the same way as a person who is crushed by remorse and self-reproach, which would more than anything characterize this latter condition, are lacking in the melancholic, at least, they are not prominent in him. One might emphasize the presence in him of an almost opposite trait of insistent communicativeness which finds satisfaction in self-exposure.
In an attempt to modify depressive behaviour in a family situation (Liberman and Raskin, 1971) the baseline data indicated that other family members rejected opportunities to interact with the depressed person, and that all initiations of interaction between him and his family in the baseline period were undertaken by him.
Paykel and Weissman (1973) reported extensive social dysfunction in women during depressive episodes. Interpersonal friction, inhibited communication, and submissive dependency occurred in both the initial episodes and in subsequent relapses. Onset of social difficulties was related to symptoms, but these difficulties continued months after the symptoms remitted, a fact that Paykel and Weissman argue must be taken into account in any treatment plan.
The provocative and often annoying behaviour of the depressive has distracted investigators from considerations of the role of the responses of others. An exception, Jacobson (1954) noted that ‘however exaggerated the patients’ hurt, disappointment, and hostile derogation of their partners may be, their complaints are usually more justified that may appear to the surface’. According to her, the depressed person often makes his whole environment feel guilty and depressed, and this provokes defensive aggression and even cruelty precisely when he is most vulnerable. Depressives also have a tendency to develop an ‘oral interplay’ with those around them, so that mutual demands and expectations are built up to inevitable disappointment and depression for everyone concerned.
Cohen et al., (1954) found therapists generally uncomfortable working with depressed patients. They identified a tendency of therapists to react to depressive manipulations with unrealistic reassurance and ‘seductive promises too great to be fulfilled’, followed by hostility and rejection. Such that it became aware of a dramatic example of this when a student therapist showed up at a Florida suicide prevention centre with a recent client. The therapist had attempted to meet her client’s complaints of worthlessness and rejection with explicit reassurances that she more than understood her and cared for her, she loved her. After weeks of such reassurance and increasingly frequent sessions, the client finally confronted the therapist with the suggestion that if the therapist really cared for her as she said, they should spend the night together. The therapist panicked and terminated the case, suggesting that the client begin applying her newly acquired insights to her daily life. The client continued to appear for previously scheduled appointments and made vague suicidal gestures, at which time her therapist brought her to the suicide prevention centre. When it was suggested that the therapist should honestly confront her client with what had happened in the relationship, the therapist angrily refused to speak to her, stating that she truly loved her client and would do nothing to hurt her.
Lewinsohn and his associates (Lewinsohn and Shaw, 1969; Lewinsohn, 1969, Lewinsohn, 1970; Libet and Lewinsohn, 1973) have undertaken an ambitious clinical research program focussing on a social interaction of the depressed person from a behavioural point of view. In attempting to develop hypotheses about the reinforcement contingencies available to the depressed person, they have attempted a precise specification of the social behaviour of the depressed person. Libet and Lewinsohn found depressed persons in group therapy to be lower than controls on a number of measures of social skills: Activity level, interpersonal range, rate of positive reactions emitted and action latency. Their data are subject to alternative interpretations, however,, particularly since they also found that rate of positive reactions emitted was highly correlated with rate of positive reaction elicited. While depressed persons may well be deficient in social shills, some of the observed differences in group interaction situations may be due to the fact that fewer people are willing interact with depressed persons (which results in a narrower interpersonal rang e and less opportunity for activity), and in this interaction emitted fewer positive responses (thereby also reducing the positive responses elicit from the depressed). The most useful behavioural conceptualization of social interaction involving depressed persons would specify the lack of social skills of all participants, as evidenced by their inability to alter the contingencies offered or received. Behavioural interventions in the depressed person’s marital and family relationships would therefore involve training all participants in these social skills, and go beyond simply altering the contingencies available to the depressed person. Behavioural observations and self-reports of a couple in the Lewinsohn study (Lewinsohn and Shaw., 1969) seem to support such a view.
Studies of suicide attempts and their effects on interpersonal relationships also provide data relevance, while suicide attempts do not have an invariable relationship on depression, there is a definite association. McPartland and Hornstra (1964) examined the effects of suicide attempts on subsequent level of depression. They conceptualized depressive symptomatology as ‘a set of messages demanding action by others to alter or restore the social space’. And examined the relationships between suicide attempts and the ambiguity of the depressive message and the diffuseness of its intended audience. They were able to realizably place depressed patients at definite points along a dimension of interactive stalemate on the basis of the range of intended audience and the stridency of message in depressive communications. Patients who were farthest along this continuum, whose communication was most diffuse, nonspecific, strident and unanswerable. Were most likely to have long hospital stays and diagnoses of psychosis. Suicide attempts tended to reduce the level of depression, apparently by shifting the interactive burden onto others. Other studies (Rubenstein et al., 1958; Moss and Hamilton, 1956' Kubler and Stotland, 1964) have indicated that suicidal patients who improve following their attempt on their lives consistently have effected changes on social fields, and those who fail to improve generally have failed to change their situation fundamentally.
Depression is viewed as a response to the disruption of the social space in which the person obtains support and validation for his experience. This view, and a view of depressive symptomatololgy in terms that is similar to that of McPartland and Hornstra (1964). However, one of the implications of the approach taken, is that an understanding of the social context is vital to an understanding of depression, although traditionally it has been largely ignored.
Social stresses leading to depression includes loss of significant relationships, collapse of anticipated relationships, demotions (and in some cases, promotions), retirement, missed chances, or any of a variety of other changes in a person’s social structure. Depressive symptomatololgy is seen as a set of massages demanding reassurance of the person’s place in the interactions he is still able to maintain, and further, action by others to alter or restore his loss.
Initial communications - verbal expressions of helplessness and hopelessness - tend to engage others immediately and to shift the interactive burden to others. The receivers of these messages usually attempt to answer the depressed person’s request directly, however, as previously noted by Grinker (1964) and Lichtenberg (1957), their literal responses present him with a dilemma. Much of the depressive’s communication is aimed at ascertaining the nature of relationships or context in which the interaction is taking place. Grinker (1964) has compared this to the various ‘how’ and ‘why’ questions that young children direct to their parents, and has suggested that both children and depressive’s will be left feeling rejected, ignored, or brushed aside if provided with a literal response.
If communication took place at only one level, depression would probably be a less ubiquitous problem. However, the problem is that human beings not only communicate, but communications about this communicative communication, qualifying or labelling what they say by (1) The context or relationship in which the communication takes place, (2) other verbal messages, (3) vocal and linguistic patterns, and (4) bodily movement (Haley, 1963). A person may offer support and reassurance with a rejecting tone or he may offer criticism in a supportive and reassuring tone.
It is enough that vocal and linguistic patterns and body movement are ambiguous and subject to alternative interpretations. However, a further problem for the depressed person is that the context, the nature of the relationship between the depressed person and the persons communicating to him, may require time and further messages to be clearly defined.
The depressed person’s problem is to decide whether others are assuring him that he is worthy and acceptable because they do in fact maintain this attitude toward him, or rather only because he has attempted to elicit such responses, unwilling or unable to endure the time necessary to answer this question, the depressive uses his symptoms to seek repeated feedback in his testing of the nature of his acceptance and the security of his relationships.
While providing continual feedback, these efforts are at the same time profoundly and negatively affecting these relationships. The persistence and repetition of the symptoms is both incomprehensible and aversive to members of the social environment. However, the accompanying indication of distress and suffering is powerful in its ability to arouse quilt in others and to inhibit and direct expression of annoyance and hostility from them, as observed in both the family difficulties of depressed persons (Jacobson, 1954) and the problems therapists report in their efforts to relate to depressed patients (Cohn et al., 1954).
Irritated, yet inhibited and increasingly guilt-ridden, members of the social environment continue to give verbal assurance of support and acceptance. However, a growing discrepancy between the verbal content and the affective quality of these responses provides validation for the depressive’s suspicions that he is not really being accepted and that further interaction cannot be assured, to maintain his increasingly uncertain security, the depressive displays more symptoms.
Nonetheless, at this point the first of a number of interactive stalemates may be reached. Members of the depressed person’s environment who can find a suitable rationalization for their behaviour may leave the field or at least, reduce their interactions with him. Considerable effort may be involved in efforts to indicate that this is not in fact rejection, but given the context, these efforts do little more than reduce credibility and increase the depressive’s insecurity. With those members of the social environment who remain, a self-maintaining pattern of mutual manipulation is established. Persons in the environment find that they can reduce the aversive behaviour of the depressed person and alleviate the guilt that this depressed behaviour has an uncanny ability to elicit, if they manipulate him with reassurance, support, and denial of the process that is taking place. The depressed person, finds that by displaying symptoms he can manipulate his environment so that it will provide sympathy and reassurance, but he is aware by now that this response from others is not genuine and that they have become critical and rejecting. While this situation is attractive for neither the depressed person nor members of social environment, it provides a stabilization of what has been a deteriorating situation.
One alternative facing the depressed person is for him to accept the precipitating disruption of his social space and the resulting loss of support and validation. However, now that he has begun showing symptoms, he has invested portions of his remaining relationships in his recovery effort. That is, he was tested these relationships, made demands, and has been frustrated in ways that seriously call into question his conception of these relationships. If he abandons these efforts, he may have to relinquish the support and validation derived from these relationships while accepting the precipitating loss. At this point he may be too dependent upon the remaining relationships to give them up. Furthermore, as a result of the mixed messages he has been received from others, he now has an increasingly confused and deteriorate self-concept, which must be clarified. With new desperation more symptoms may be displayed.
Various possible efforts by the depressed person to discover what is wrong with him (i.e., why he is being rejected and manipulated) and to reestablish amore normal interactive pattern are in this context indistinguishable from the manipulation he has used to control the responses of others. Therefore they are met with the usual counter manipulation. Requesting information as to how people really view him is indistinguishable from symptomatic efforts. If the depressed person attempts to discuss the interpersonal process that is taking place, he touches on a sensitive issue, and is likely only to elicit denial by the others or an angry defensive response. Yet , efforts by others to assure the depressed person that he is really accepted and that they are not rejecting him are in this context also indistinguishable from previous manipulations that they have employed, and therefore serve to strengthen the developing system. Thus, interpersonal manoeuvres directed at changing the emerging pattern become system-maintaining and any genuine feedback to the depressed person is also indistinguishable from manipulations. Persons leaving the social field increase both the depressed person’s feelings of rejection and his impetus to continue his behaviour pattern. Persons just entering the social field can be quickly recruited into the existing roles, since their efforts to deal with the depressed person - even if genuine- are likely to be quite similar to those now being employed manipulatively. They therefore become subject to the compelling coantermanipulations of the depressed person, come to respond manipulatively themselves, and are inducted into the system.
Descriptions of the depressed person at this point in his career focus on the distortions and misperceptions that serve to maintain his depression. What is generally ignored is that these ‘distortions’ and ‘misperceptions’ are contingent with the social system in which the depressed person now finds himself. The specific content of the depressive’s complaints and accusations may not be accurate, but his comments are a recognition of the attenuated relationships, disrupted communication, and lack of genuineness that he faces. These conditions serve to prevent him from receiving the feedback necessary to correct any misperceptions or distortions. He has played a major role in the creation of this social system, but the emergence of the system has also required the cooperation of others, and once established, it tends to be largely beyond th control of its participants.
Depending on characteristics of both the depressed person and his environment, a number of punishing variations on the above patterns may develop. Members of the social environment who have been repeatedly provoked and made to feel guilty may retaliate by withholding the responses for which the depressed person depends on them. The depressed person may become aware of the inhibiting influence his symptoms have on the direct expression of negative feelings, and may use these symptoms aggressively, while limiting the forms that counter-aggression can take. He may also discover and exploit the interdependence of others and himself. While he is being made acutely aware of his dependence on others and the frustrations it entails, he may also become aware of the extent to which others are dependent on him. In that their own maintenance of mood and their ability to engage in varieties of activities required in some way his cooperation. Either because of outright hostility, or as a self-defeating effort to convince other of their need to renegotiate their relationship with him, the depressed person may become symptomatic in his withholding of these minimal cooperative behaviours. While hostility may not necessarily be a more etiological factor in depression, the frustrations, provocations, and manipulations occurring in interactions between depressed persons and others would seem to encourage it.
As efforts to end the interactive stalemate fail, there may be a shift in the depressive’s self-presentation to one indicating greater distress and implying that the environment has more responsibility for bringing about the necessary changes. McPartland and Hornstra (1964) found that they could unambiguously differentiate themes of hopelessness and helplessness from more disturbed themes and how energy and physical complaints in communications of depressed patients. The latter themes were associated with longer hospitalization when hospitalized depressed patients were sampled. McPartland and Hornstra give the examples of, ‘I can’t sleep and I can’t stand it any longer’. ‘I am too tired to move’: ‘My head and my stomach feel funny all the time’. Unable to restore his life space, the depressive now implicitly demands ‘a suspension of the rules; a moratorium on the web of obligations under which the person lives, such as admission to the sick role’ (McPartland and Hornstra, 1964). With immediate relationships deteriorating, the depressive addresses his plea to a more general audience, but in more confusing and unanswerable terms. Literal responses to his communications may involve medical intervention for his specific complaints, but this generally fails to alleviate the problem. Any efforts to move the interactional theme back to the depressive’s sense of hopelessness and helplessness threaten to reopen the earlier unfruitful and even punishing patterns of relations, and tend to be resisted. Unable to answer, or in many cases, even to comprehend the depressive’s pleas, members of the social environment may withdraw further from him, increasing his desperation, and quickening the depressive’s drift.
With a second interactive stalemate now reached, the depressed person may attempt to resolve it by increasing his level of symptomatology and shifting the theme of his self-presentation to one of the worthlessness and evil. ‘I am a failure; its all my fault; I am sinful and worthless’. Unable either to restore his social space or to reduce his obligations sufficiently for him to continue to cope, the depressive now communicates his bafflement and resignation. The intended audience is now more diffuse, relationships are even more attenuate, and the new message is more obscure and perplexing. The social environment and the depressive soon arrive at another stalemate. Otherwise helpless to alleviate the situation, remaining members of the environment may further withdraw or, alternatively, have the depressive withdrawn through hospitalization. In the absence on any relatedness to others, the depressive may drift into delusions and frankly psychotic behaviour.
Once an individual has suffered a disrupt ion of his social space, his ability to avoid depressive shift, or to abort the process once it has begun, depends on the structure of his social space and on his interpretational skills. With regard to the latter, it is generally ignored that the person facing this situation is dealing with a changing environment, and that the skills needed to deal with it are likely to be different from those required by a more stable, normal environment. Consequently, persons who previously have had adequate skills to deal with their life situation may lack the skills to cope with a disrupted social space. With regard to the structure of this social space, resistance to depression seems to depend on the availability of alternative sources of support and validation. Particularly of the type that cannot be threatened by depressive symptomatology, further, the availability of direct nonpunitive feedback should the person’s behaviour become annoying or incomprehensible, and the ability of the social space to generate new sources of support and meaning that are unambiguously independent of the presence or absence of symptoms. Earlier speculative writings (Abraham, 1911) and later behavioural studies (Lewinsohn, 1969) have suggested that depressive persons tend to be quite limited in their range of interactions, and that this may be a major source of their vulnerability.
Stable relationships may generally provide a buffer against depression, but when they are stable yet low in support and validation, they may encourage a chronic depressive cycle. If, for instance, in a marriage of this type, the depressed person recognize that his spouse is tolerating more than is reasonable from him without protest, he may begin to assume that she is staying with him out of some obligations, rather than because she accepts him and wants a relationship (Haley, 1963). The depressed person may then test whether he is really accepted by driving the other person to the point of separation with his symptoms. Yet if the spouse passes the test by continuing to tolerate the annoying behaviour., the depressed person may not necessarily be reassured about his acceptance. rather he may only be convinced that his spouse remains because she is unable to leave. However, if she makes an effort to leave the situation, she may be indicating that their relationship has been voluntary and that he had been accepted. With reconciliation the spouse may again, seem too tolerant and a new series of doubts, testing, and strife may be enacted. While such a cycle may produce chronic difficulties, it may also be an alternative to a downward depressive spiral. Essentially the depressed person finds himself in the awkward situation of wanting to avoid rejection, yet at the same time fearing acceptance.
The constraints operating on the person who suffered a disruption in his social space are his need for support and validation, and the investment of his remaining relationships in his efforts to receive such support. the symptoms of the depressed person offer a powerful constraint on the ability of members of the social environment to offer adjustive feedback, and while eliciting verbal messages of sympathy, support, and reassurance, these symptoms disrupt the relationships and cultivate hostility and rejection.
Those who resist induction into the system without rejecting the depressed person do so because they are able to resist the pressure to convey discrepant messages. A successful therapist in Cohen et al., study stated, ‘I keep in mind that I am talking to the patients not so much verbally as preverbally. I use the verbal communication as a means of carrying inflection and an accompaniment of facial expression and postural components’.
Several writers have suggested that the emerging communication context can be disrupted by strong affective expressions such as anger, excitement, and amusement (Lazarus, 1968), which are incompatible with the pattern of mutual manipulation that maintains the context. Although many writers have indicated that a depressive reaction lifts when a patient regains his ability to express anger toward others (Friedman, 1970), some research indicates that the mobilization of anger is not necessary for symptomatic improvement (Weissman, et al., 1971; Klerman and Gershon. 1970). Interpersonally, hostility may be one of a number of means of disrupting or blocking the operation of a depressive interpersonal system. Involvement in this system is difficult to avoid once it has begun. The symptoms of depression have an ability to perpetuate themselves through the involvements of others in a system of manipulation and coantermanipulations that soon gets beyond the control of its participants.
Within the presently engaged research that examines the responses of others to depression and the quality of the communications context that emerges. Preliminary results from a study involving an interpersonal behaviour questionnaire suggest that a person is less likely to respond in an overtly hostile manner to the behaviour of another person when the second person is depressed. This inhibition persists even when it is indicate that the second person is responding hostility. The inhibition of appropriate hostile behaviour may be a characteristic of interactions involving the depressed person, and not just of the depressed person. Another study involves twenty-minute phone conversation between naive subjects and target individuals from three groups: Depressed outpatients, nondepressed outpatients, and normals. Preliminary results suggest that subjects respond with unrealistic reassurance and useless advice to the depressed outpatient. They are more likely to be depressed, anxious, and hostile themselves after conversations with depressed patients, and are more likely to reject opportunities for future interaction. For the most part, changes in the subjects’ mood remain concealed during the conversation, and the depressed patients are given little indication of their impact on occasional statements, such as ‘You certainty seem to have had a lot a problems, but problems are what allow us to grow, and so you’ll have lots of opportunity to grow in the future’;. Further research is needed to examine the nature of the depressive’s social field so that the specific relationships that resist or perpetuate the depressive interpersonal system can be identified and describe.
We use the term ‘depression’ to refer to the syndrome of behaviour that have been identified in descriptive studies of depressed individuals (e.g., Grinker, et al., 1961). It includes verbal statements of dysphoria, self-depreciating.,guilt, material burden, social insolation, somatic complaints, and a reduced rate of much behaviours. we assume depression to be a continuous variable which can be conceptualized as a ‘state ‘ which fluctuates over time as well as a ’trait’ (some people are mo e pone to becoming depressed than others). Being depressed does not exclude other psychopathological conditions such as schizophrenia, psychosis, sexual deviation, or alcoholism. For research purposes a patient (subject) is defined as ‘depressed’ if he meets certain experiential criteria (e.g., Lewinsohn & Libet 1972) based on selected MMPI scales and on the interview factor’s identified by Grinker (1961).
It would seem important that any study relying on differences between depressed and nondepressed groups for its conclusions have a ‘normal control’ as well as a ‘psychiatric control’ group (i.e., patients for whom anxiety or other neurotic symptoms but not depression constitute the major psychopathology (if any obersderd group differences are to be attributed to depression (depressed, psychiatric control normal control).
We accumulatively gather of three assumptions regarding the behavioural theory of depression: A schematic representation of the theory is shown by (I) A low rate of response-contingent positive reenforcement (resconposre) acts as an eliciting (unconditioned) stimulus for some depressive behaviours, such as feeling of dysphoria, fatigue, and other somatic symptoms (2) A low rate of resconposre constitutes a sufficient explanation for other part of the depressive syndrome such as the low rate of behaviour. For the latter the depressed person is considered to be on a prolonged extinction schedule. (3) The total amount of reconposre received by an individual is presumed to be a function of three sets of variables: (I) The number of events (including activities) that are potentially reinforced (PotRe) for the individual. PotRe is assumed to be a variable subject of individual differences, uninfluenced by biological (e.g., sex and age) and experiential variables, and (ii) The number off potentially reinforcing events that can be provided by the environment, i.e., the availability of reinforcement in the environment (AvaiRe). (iii) The instrumental behaviour of the individual, i.e., the extent to which he possesses the skill and emits those behaviours that will elicit reinforcement for him from his environment.
The behavioural theory requires that (1) the total amount of resconposre received by depressed persons be less than that received by nondepressed persons, and similarly, it will be less when the individual is repressed than when he is not depressed; (2) The onset of depression be accompanied by a reduction ion resconposre, (3) intensity of depression convary with rate of reconposre, and (4) Improvement be accompanied by an increase in reconposre. Even so, the following examinations of relevant empirical studies are several additional clarifications and hypotheses.
First, even were such predictions affirmed, further data would be needed to ascertain whether the differences between depressed and non-depressed individuals in regard to resconposre are due to: (x) differences in the number and kinds of activities and events which are potentially reinforcing ({PotRe); (y) and/or the possibility the depressed individuals ma y be more likely to be in situations which lack reinforcement for them (AvaiRe), (z) and/or differences between depressed and non-depressed individuals in those skills which are necessary to obtain reenforcement from one’s environment.
Second, the degree to which the individual’s behaviour is maintained (followed) by reinforcement is assumed to be the critical antecedent condition for the occurrence of depression, rather than the total amount of reinforcement received. It is a well-known clinical fact that ‘giving’ (i.e., noncontingently) to depressed individuals does not decrease their depression. We assume that the occurrence of behaviour followed by positive reinforcement is vital if depression is to be avoided. Such that depression when the probability is low that the individual’s behaviour will be followed by reinforcement, and also, when the probability is high that the individual will be ‘reinforced’ when he does not emit the behaviour (e.g., the retired person receiving his paycheck regardless of what he does). Under both conditions the probability of the individual emitting behaviour reduced.
The behavioural view of other aspects of depression may include :
1. Low self-esteem, pessimism, feelings of guilt, and other elated phenomena are cognitive changes which are commonly observed in depressed individuals, even though the specific manifestations vary considerably from individual to individual. Thus, there are depressed patient who do not have low self-esteem and there are many who lack feelings of guilt. theorists such as Aaron T. Beck (1967) assign primary causal significance to these cognitive changes. A behavioural theory assumes these qualify as secondary elaborations of the feeling of dysphoria, which in turn is presumed to be the consequence of a low-rate of reconposre. The first thing that happens when an individual becomes depressed is that he is experiencing an unpleasant feeling state (dysphoria). He is feeling bad. This feeling state is difficult for the individual to label; and a number of alternative ‘explanations’ are available to him including. ‘I am sick’ (somatic symptoms). ‘I am weak or otherwise inadequate’ (low self-esteem), ‘I am bad’ (feeling of guilt),. O r ‘I am not likeable’ (feelings of social isolation). The research of Stanley Schachter (Schachter & Singer 1962) may contain important implications for this aspect of the behaviour of depressed individuals and for treatment as well (cognitive relabelling). If the depressed individual can be helped to relabel his emotion (e.g., ‘I am worthless’ into ‘I am feeling bad because I am lacking something that is important to my welfare’), he may be in a much better position to do something about his predicament.
2. Relationship between hostility and depression, in which the role of hostility is central to psycho dynamically-oriented theories of depression (i.e., depression is caused by internalized hostility) is hypothesized to be secondary to the low rate of reconposre. In a manner analogous to the way in which aggressive behaviour is elicited by an aversive stimulus, in Azrin’s (1966) studies, aggressive behaviour may be assumed to be elicited by a low rate of resconposre in the depressed individual. When these aggressive responses are expressed, they serve to alienate other people and therefore contribute even further to the social isolation of the depressed individual. He therefore learns to avoid expressing hostile tendencies by suppressing (or repressing) them.
3. Role or precipitating factors in occurrence of depression, that in a substantial number of depressed patients, the depression can be shown to have begun after certain environmental events (e.g., Paykel. et al., 1969). Many of these events involve a serious reduction of positive reenforcement in that the event deprives the individual of an important source of reinforcement (e.g., death of spouse) or of an important set of skills (e.g., spinal cord injuries or brain disease). The relationship between the occurrence of such events and depression is considered with the behavioural theory of depression. There are, however, also instances of depression following ‘success’ experiences (e.g., promotions or professional success). It is also not at all uncommon for an individual to become depressed following the attainment of some important and long-sought goal (e.g., award of PhD degree). The existence of such precipitating factors would seem at first glance to contradict the notion of a relation between a reduction in positive reinforcement and depression. Two considerations would seem relevant (a) That the individual is judged to be a ‘success’ by external criteria (e.g., is promoted) events not necessarily mean that the number of potentially reinforcing events available to him has increased. Thus, for example, a promotion may actually involve a serious reduction in the amount of social reinforcements obtained by the individual. The behavioural theory would predict depression for an individual who attain a goal for which he has worked long and hard if the reward (e.g., aware of degree) turns out to be a weak reinforcement for him. In that case he has worked hard for too little, i.e., his rate of resconposre is low.
Developments in the interactional description of schizophrenia have not been parallelled in the area of depression. As yet, concepts such as pseudomutality, double-bind, schism, and skew found no counterparts. Kubler and Stotland (1964)have argued, ‘emotional disturbance’, even the most severe, cannot be understood unless the field in which it develops and exists is examined. The manifestations of the difficulty in the disturbed individual have meaning depending on aspects of the field. The significant aspects of the field are usually interpersonal. Yet, the study of depression has focussed on the individual and his behaviour out of his interactional context. to a larger extent, the depressed person’s monotonously reiterated complaints and self-accusations, and his provocative and often annoying behaviour have distracted investigators from considerations of his environment and the role it may play in the maintenance of his behaviour. The possibility that the characteristic pattern of depressed behaviour might be interwoven and concatenated with a corresponding pattern in the response of others has seldom been explored.
For the most part, it has been assumed that the depressed person is relatively impervious to the influence of others. Ruersch (1962) stated that to talk to the depressed person makes little sense, to listen, little more. Grinker (1964) conceptualized depressive symptomatology as communication tom others, but argued that the depressed person is not responsive to communication from others: ‘The depressed person . . . cannot use information for the purpose of action, he cannot perceive the cues of reality, he makes statements but does not care if he is understood.
Its difficulty of communication is the primary problem in therapy of establishing a communication relationship, which is, of course, a reflection on the patient’s basic life difficulties. The most characteristic aspect of the manic depressive’s defence in his ability to avoid anxiety by erecting conventional barriers to emotional interchange, we have learned to interpret this as a defence rather than a defect in the patient ‘s experience, and we have found that when it is interpreted as a defence, he responds by developing a greater ability to communicate his feeling and to establish empathic relationships.
Initial communications - verbal expressions of helplessness and hopelessness, withdrawal from interaction, slowing, irritability and agitation tend to engage others immediately and to shift the interactive situation to others, the receivers of these messages usually attempt to answer the depressive person’s requires directly. However, as previously noted by Grinker (1964) and Lichtenberg (1957), theory literal responses present him with a dilemma, much of the depressive’s communication is aimed at ascertaining the nature of relationship or context in which the interaction is taking place. Grinker (1964) has compared this to the various ‘how’ and ‘why’ questions that young children direct to their parents, and has suggested that children and progressives will be left feeling rejected, ignored or brushed aside if provided with a literal response.
Depression has been conceptualized as a self-perpetuating interpersonal system. Depressive symptomatology is congruent with th e developing interpersonal situation of the depressed person, and the symptoms have a mutually maintaining relationship with the response of th e social environment, essentially, the depressed person and others within his social space collude to create a system in which feedback cannot be received, and various efforts to change become system-maintaining.
Depressed persons tend to withdraw from social activities, and their close relationships tend to be strained and conflictual. Depressed women have more intensely studied than depressed men, in part because women are approximately twice as likely to be depressed (Radloff). Depressed women are dependent, acquiescent, and inhibited their communication in close relationships, and prone to interpersonal tension, friction and open conflict (Weissman & Paykel, 1974). Interestingly, the interpersonal difficulties of depressed persons are less pronounced when they are interacting with strangers than with intimates (Hinchcliffe, Hooper, & Roberrtys, 1975).
About half of all depressed persons report marital turmoil (Rousanville, Weissman, Prusdoff, & Heraey-Baron, 1979) there is considerable hostility between depressed persons and their spouses, but often there is more between depressed persons and their children. Being depressed makes it more difficult to be a warm, affectionate, consistent parent (McLean, 1976). The children of depressed parents are more likely to have a full range of psychological and social difficulties than the children of normal or even schizophrenic parents (Emery, Weintraub, & Neale, 1982), yet one must be cautious in making causal inferences. There is evidence that the child problems are more related to a conflictual marital relationship and stressful home life than depression of the parent per se (Sameroff,. Barocass, Siefer).
Depression thus tends to be indicative of an interpersonal situation fraught with difficulties, and this needs to be given more attention in both theorizing and planning treatment. Although depression is associated with interpersonal problems, within a sample of depressed persons the correlation between severity of depression and the extent of interpersonal problems tend to be modest. this may suggest that these problems are a matter no only of how depressed persons are functioning, but of the response of key people around them as well (Coyne, Kahn, & Gotlib, 1985).
One can make a list of the symptoms of depression, and assign any person a depression score on the basis of the number symptoms present. Even if one assumes a continuity between normal depressed mood and clinical depression, it may still prove useful to make a distinction between the presence or absence of significant depression. One may wish to insure that a research study does not include a preponderance of persons whose depression is only mild or transient. Virtually no signs or symptoms are specified to depression, and yet in many context, one may need to distinguish depression from other descriptors or explanations for a person’s distress and behaviour. In working with the elderly, for instance, it is important to distinguish between depression and dementia. In medical patients in general, there is a high prevalence of symptoms associated with depression, both because of physical illness and the stress of hospitalization (Cavanaugh, 1984), and, whether for research or practical purposes, one ,may wish to establish criteria for who is to be considered depressed and who is not. Finally, persons who are labelled schizophrenic or alcoholic for many purposes to lump them with those persons whose primary problem is depression. Thus, for the purpose of research, treatment, and professional communication, it proves useful to have some means of specifying some boundary conditions for the term ‘depression’, in terms of some minimal level of severity as well as some coherence and specificity to what is included in the concept - even if one rejects the notion that it is a discrete entity, discontinuous with normal mood.
The problem of diagnosis is most critical in biomedical approaches to depression. The assumption is generally made that depression is a matter of one or more disease entities with specific etiologies and treatment. The statement, ‘Nosology precedes etiology’ conveys the idea that th e ability to identify the causes of depression depends upon the existence of an adequate diagnostic and classification system. For instance, to take a simplified hypothetical example, suppose that a particular biological abnormality occurs in 60 percent of all depressed persons and is specified to depression. Suppose also that, with the accepted diagnosis criteria, only 60 percent of the persons identified as such are ‘actually depressed’. If these conditions occurred, then research might indicate that only 36 precent of depressed persons possess the abnormality.
An effective treatment for depression may also be misjudged or misapplied in the absence of an adequate diagnostic system. This was made apparent recently after a drug company had undertaken a large study to compare the effectiveness of a new drug to that of both an established drug treatment for depression and a placebo (Carroll, 1984). At five of the six research sites, the new drug proved to be no more effective than a placebo, but interpretation of this was limited by the additional finding that the established treatment proved no better. Patient s identified as depressed by current criteria did not respond to drug treatment that had proven efficacious in a large body of past research. Either the past research was misleading, the current diagnosis criteria invalid, or, most likely, they were misapplied by reputable investigators.
Contemporary diagnosis systems owe much to the work of Kraepelin at the turn of the century. He divided major psychopathology into two broad syndromes: Dementia praecox (schizophrenia) and manic-depressive illness. The latter category included almost all serious mood disturbance, including depression in the absence of an episode of mania. As retained today, the term generally is a synonym for bipolar disorder. Of all the distinctions that have been proposed, the most widely accepted and least controversial is that between unipolar and bipolar depressive. Classifying depressed patients into bipolar and unipolar subtypes was first proposed in 1962 by Leonhard et al., based on the clinical differentiation of depressed patients with and without mania, family history studies noted that patients with bipolar illness had more psychosis and suicide among their relatives than patients with unipolar illness. Since 1962 several studies in Europe and the United States have refined and extended this original observation. More importantly, a model for investigation in psychiatry has been developed to the point that genetic data are important for validating clinical diagnosis in psychiatry, particularly among the affective disorders.
Several lines of evidence suggest that some forms of depression may have an etiology on a genetic basis. In order for a genetic etiology to be proven, several factors should be evident. First of all, the disorder should cluster within families; patients with the illness should have relatives who also demonstrate studies of twins should show that the illness is more prevalent among monozygotic than dizygotic twins. A third line of evidence would come from adoption studies. Adoption studies are designed to differentiate environmental from genetic factors. Data from such studies should reveal that subjects who have a biological parent with illness but who were raised in foster home develop the illness nevertheless, whereas subjects whose biological parents do not have the illness but who were raised in a home. Where there is affective disorder, do not develop affective disorder in excess of controls. Fourth, the illness could be shown to be linked to a gene known of Mendelian transmission.
Affective disorders, particularly manic-depressive illness, are familiar. the evidence that bipolar illness clusters in families was reported by Leonhard et al., Perris and Angst both suggested that effectively ill relatives of bipolar patients tended to have bipolar and not unipolar disorders, whereas affectively ill relatives of unipolar patients tended to have unipolar illness and not bipolar illness. In the 1960s the Washington University group published a series of familiar studies in manic-depressive illness, particularly bipolar disorders. These studies showed a high familiarity risk for affective disorder in relatives of manic patients. Second, a very comprehensive family study of affective disorder suggested that manic-depressive illness may be linked to a gene transmitted on the X-chromosome. Subsequent studies in the late 1960s from th e National Institute of Mental Health (NIMH) also shows a differential familial loading for relatives of patients with bipolar compared with unipolar disorders. Relatives of bipolar patients had elevated morbid risks for bipolar illness, unipolar illness, and suicide, compared to relatives with unipolar patients.
Few twin studies of affective disorder appear in the literature of the last 10 years or so. Kallmasnn’s study is still considered the definite work, showing very high concordance rates for bipolar illness in monozygotic compared to dizygotic twins.
The adoption technique, utilized in the Danish studies of schizophrenia, has been tried in studies of bipolar illness. Data from adoptees in Iowo indicated that primary affective illness may have a familial factor. Another study of adoptees from manic-depressives also supports the concept of a genetic factor in the etiology of affective disorders.
In the search fo r genetic linkage of affective disorder, the studies of Winokur et al., pointed toward a genetic factor on the X-chromosome, colour blindness and XG blood type. Gershon et al., were unable to replicate these findings and subsequently criticized the data from the Mendlewocz studies on methodological grounds.
Clearly, unipolar illness as presently defined is a much more heterogeneous collection of disorders than bipolar disorder. Attempts to find subtypes of unipolar disorder using a genetic classification have not been particularly successful. However, Winokur’s group separated unipolar patients into women with an early age of onset (depressive spectrum disease) whose relatives showed depression and alcoholism, and depressed men with a late age of onset (pure depressive disease) whose relatives showed depression only.
The renewed interest in the genetics of bipolar and unipolar depression in the late 1900s and the interest in defining these disorders led to several family studies in the 1970s. The simplest method, the so-called family history method, was to ask patients about illness in their relatives. This tends to underestimate illness in relatives. An interview (Schedule for Affective Disorder and Schizophrenia-SADS) developed early in the 1970s was used to document illness in relatives. Interviewing relatives directly (the ‘family study) led to greater precision regarding the diagnosis of illness in relatives. In a refinement of this technique relatives are interviewed blind to the profound diagnosis in order to decease investigator bias. Most of the recent genetic studies conducted in the United States employed a blind gamily study method; wherein relatives were interviewed with a standardized instrument with the interviewer unaware whether the person being interviewed was the patient, relative , or a control.
Nonetheless, it seems that some observers have stated that in the intervals between attacks, the manic depressives has a character structure similar to that of th e obsessional neurotic. It has also been asserted that in the psychotic phase the manic-depressive illness is essentially schizophrenic. This latter statement is supported by the fact that many manic-depressives do, in the course of time, evolve into chronic schizophrenic psychoses, usually paranoid in character, and that there are many prosecutory ideas presented both in manic attack and in the depression. In general, there has always been much uncertainty as to who should be diagnosed manic depressive - an uncertainty which is reflected in the widely differing propositions of manic depressives and schizophrenic diagnosed in different mental hospitals.
What, then, is the point of singling out a diagnosis category called manic depressive? In our opinion, the manic-depressive syndrome does represent a fairly clear-cut system of defences which are sufficiently unique and of sufficient theoretical interest to deserve special study. We feel that equating the manic-depressive character with the observational character overlooks the distinguishing difference to the manic depressive, uses substitutive processes as his chief defence. The manic, uses the previously mentioned lack of interpersonal awareness as his chief defence, together with the defensive processes themselves. The object relations of the obsessional are more stable and well-developed than those of the manic depressive. While th e obsessional’s relations are usually integrations in which there is an intense defence of hostility, control and envy, they do take into consideration the other person as a person. The manic depressive develops an intensely dependent, demanding, oral type of relationship which overlooks the particular characteristic and qualities of the other.
According to Sullivan’s conceptualization of th e schizophrenic process, the psychosis is introduced typically by a state of panic, in which there is an acute break with reality resulting from the upsurge of dissociated drives and motivations which are absolutely unacceptable and invest with unbearable anxiety. Following this acute break, a variety of unsuccessful recovery or defensive processes ensue, which we call paranoid, catatonic, or hebephrenic. These represent attempts of the personality to deal with the conflicts which brought about the panic: The paranoid by projection, th e catatonic by rigid control; the hebephrenic by focussing on th e bodily impulses. According to this conception, the manioc depressive can be differentiated from the schizophrenic by the fact that he does not exhibit the acute break with reality which is seen in the schizophrenic panic. His psychotic processes of depression or, of manic, he can be thought of asserting a depressive function against the still breaker personality disintegration which is represented by the schizophrenic state. This, in persons whose conflicts and anxiety are too severe to be handled by depressive or manic defences, a schizophrenic breakdown may be the end result.
Contrasting the schizophrenic and the manic depressive from the point of view of their early relationships, we see that the schizophrenic has accepted the bad mother as his fate, and his relations. He therefore attenuated. He is inclined to withdraw into detachment. He is hypercritical of family and cultural values. he is sensitive and subtle in his criticisms, original but disillusioned. He is disinclined to rely on others and is capable of enduring considerable degrees of loneliness. His reluctance to make demands on the therapist makes the therapist more feel and more sympathetic, and therefore the therapist is frequently in his aggression, he can take the risk of attacking, for he is less afraid of loneliness. He is more sensitively aware of the emotions of the therapist, since the boundaries between ego and environment are more fluid. The schizophrenic is not inclined to pretend, and is not easily fooled by other people’s pretenses, Dream and fantasies are nearer to awareness and guilt feelings are also more conscious than unconscious.
The typical manic depressive has not accepted the ‘bad mother’ as his fear. He vacillates between phases in which he fights with the bad mother, and phases in which he feels reunited with the good mother. In there manic phase, his, relationships with reality is more tenuous; he shows a lack of respect for other people, and reality considerations are dismissed for the dark of magic manipulation to make the bad mother over into a good mother. The manic depressive is therefore, mostly a good manipulator, a salesman, a bargaining personality. He is under-critical instead of being hypocritical. He easily sells out his convictions and his originality in esteem. In the depressive phase, he sacrifices himself to gain a good mother or to transform the bad mother into a good mother. In order to do this, he calls himself bad, and suffers to expiate his sins, but these guilt feelings are, in a sense, artificial or expedient, utilized in order to manipulate the bad mother into becoming a good mother. The depressive does not come to terms with realistic guilt feelings. Instead, he uses self-accusations, which frequently sound hypocritical, to convince the mother or a substitute that his need to beloved has absolute urgency. He denies his originality because he is terribly a afraid of aloneness, he is more of a follower than a leader. He is dependent on prestige, and is quite unable to see through the pretense of his own or other people’s conventionalities. He shows a high degree of anxiety when his manipulations fail. His lack of subtlety in interpersonal relationships is due to his overruling preoccupation with exploiting the other person in order to fill his emptiness. This operate s as a vicious circle as he has maintained his claims for as good fulfilling mother, but his search for fullness manipulation of another makes him feel helpless and empty. This incorporates of another person fo r the purpose of filling an inward emptiness, of acquiring a borrow self-esteem, is very different from the lack of ego boundaries in the schizophrenic. The schizophrenic is in danger of losing his ego., and he expresses his danger in fantasies of world catastrophe. the manic depressive is threatened by object loss, since h e habitually uses the object to patch up his ego weakness. Object relations in the manic depressive are, therefore clouded by illusions, but even when he waits, demands, and blames the frustrating object, he is - by this very agitated activity in behalf of his own salvation, ineffective as it may be - defended against the loss of the ego. When the manic depressive becomes schizophrenic, this defence breaks down.
It should be noted that the infantile dependency and manipulative exploitativeness seen in the manic depressive are not unique to this type of disorder. They occur, in fact, in many forms of severe mental illness. The hysteric, for instance, exemplifies infantile dependency and exploitativeness as dramatically as the manic depressive, and in ‘la belle difference’ one may see a resemblance to the euphoria of the manic or hypomanic. However, the combination of the dependent and exploitative traits with the other outstanding characteristics of the cyclothymic personality - particularly the communicative defect and the accompanying inability to recognize other persons as anything but good-bad stereotypes and the conventional but hypermoralistic values - does become sufficiently distinct and unique to distinguish these patients characterologically from other types.
The diagnosis of manic-depressive character has, in the past, been made largely on the basis of the patient’s exhibiting the classic manic and depressive symptomatology. It can, however, be as validly made on th e basis of the transference-countertransference pattern, which is set up between the patient and the therapist. The transference pattern is particularly characteristic; the countertransference pattern would, of course, vary considerably according to the personality of the therapist, although it, too, shows a number of quite typical features.
The transference pattern shows two outstanding characteristics which could be labelled (1) the exploitative clinging decency, and (2) the stereotyped approach other persons, who are not seen aa personalities in their own right.
1.The dependency as with other workers in the field of the study of manic depressive illness have apply documented the deep-seated dependency of this type of person (Abraham, Freud, Rado, Klein). The dependency attitudes toward the object are highly ambient. Gratification is demonstrated, but not accepted or experienced as such, and the patient feels that attention, car e, and tenderness must be forced from the other person. The force applied is that of demonstrating to the other person how miserable he is making one, how much the depressed one need the other, and how responsible and culpable the other is if he fails to meet the depressive’s needs. The demands are not directly verbalized but rather consist of a wordless exploitation: The reactive hostility is not experienced as such, but instead is experienced as depression.
In the depths of the depression, It seems impossible to satisfy the patient’s dependency needs. As one therapist mentions, th e patient seems to be saying, ’I am starving, and I won’ t get what I need.’ The amount of time and attention the patient receives, crying out for more. We sense if satisfaction. He remains depressed, We have not tried the experiment of spending the major portion of each day with a depressive person. Certainly 24-hour-a-day nursing does not suffice to give th e patient a sense of gratification. Whether unlimited time from a therapist would have more effect is debatable, in the light of our experience with Mr. Richard, such that when the patient is in a period of relative mental health, these needs are less apparent, this raises the question of what becomes of these needs during such periods: Ar e the y not present and only stirred up again when some unusual deprivation nor treat to security occurs, or are they successfully kept t in repression during the healthy phase?
In the manic phase, the demandinngness is much more open but seen by the patient as demanding his rights rather than as asking for favours. Rejection of th e demand is met with t hostility rather than with a depressive response. The manic, of course, shows, in addition to the demandingness, the tendency to take what he needs by force, if necessary and he will use direct aggression - in contrast to the depressive, who uses reproaches against the other person as a forcing manouevre.
2. The stereotyped response of the manic-depressive personality shows a highly characteristic tendency to look upon others as stereotyped repetitions of parental figures. This has been described elsewhere in reporting as ‘a lack of interpersonal sensitivity’. The therapist is regarded, (x) as an object to be manipulated for purposes of getting sympathy and reassurance, (y) as a moral authority who can be manipulated into giving approval, and (z) as, in actuality, a critical and rejecting authority figure who will not give real approval but can be counted on only for token approval which can be achieved by proper behaviour manipulation. This uncritical categorization of the therapist results in the patient’s inability to use the therapist to provide himself with a fresh point of view. Everything that the therapist says is reworked into the old pattern of concealed disapproval covered over with the sugar of artificial reassurance. this impenetrability to the reception of new ideas from the therapist represents one of the great obstacles in therapy with this type of patient, who will give lip service to the role of the therapists a noncritical authority without a feeling of conviction that this is do. However, the lip service itself then becomes incorporated into the set of manipulative acts which will receive approval and adds another wall to their defence.
Early in the study of these patients, it was felt that the lack of ability to appraise the therapist as a person represented a real learning defect in the patient and that one of the therapeutic tasks therefore was a somewhat educational one of showing the patient how one person could be different from another. On further study we have come to the conclusion that the defect is not an educational one, as evidence for this being that as the anxiety diminishes in an interpretational relation, the sensitivity increases. Mr. Richard is an excellent illustration of this point. his therapist spoke if him as follows:
Whereas states of morbid anxiety have been dealt with in detail in the literature of psychoanalysis, depressive states have hitherto received less attention. Nevertheless the affect of depression is as widely spreading all forms of neurosis and psychopsis is that of anxiety. The two affects often present together or successively in one individual; so that a patient suffering from an anxiety-neurosis will be subject to states of mental depression, and a melancholic will complain of having anxiety.
One of the earliest results of Freud’s investigations of the neurosis was the discovery that neurotic anxiety originated from sexual repression, and this origin served to differentiate it from ordinary fear. In the same was we can distinguish between the affect of sadness or grief and neurotic depression, the latter being unconsciously motivated and a consequence of repression.
Anxiety and depression are related to each other in the same way as are fear and grief. We fear a coming evil; we grieve over one that has occurred. A neurotic will be attacked with anxiety when his instinct strives for a gratification which repression prevents him from attaining; depression sets in when he has to give up his sexual aim without having obtained gratification. He feels himself unloved and incapable of loving, and therefore he despairs of his life and the future. This affect lasts until the cause of it ceases to operate either through an actual change in his situation or through a psychological modification of the displeasurable ideas with which he is faced. Every neurotic state of depression, just like every anxiety-state, to which it is closely related, contains a tendency to deny life.
Meaning is not embedded in some obscure ‘inner human nature’, nor something that is desired to be destined to be developed by successively ‘higher forms of life’. There is, in short, nothing vitalistic or mysteriously emergent implied in the idea of meaning. Meaning is the elaboration of an increasingly intricate ground plan of broad relationships and ramifications. It is the establishment of dependable cause-and-effect sequences which permit ego-mastery and action. Meaning is at the heart of life because it is inseparable from action sequence with an intricate symbolism, the dependable becoming the indispensable the satisfying becomes the necessary as Man’s symbolic life is an imbibing of meaning and a relentless creation of it. This symbolic elaboration of meaning is Homo sapients sapient - home, so to speak - brought by him onto the evolutionary scene and manufactured solely for his use and delight, by means of it, man intoxicate’s himself into the illusion that his particular meaning-fabric, his culture’s concoction of symbols and action, is god-given and timeless. In his imagination, man fuses symbols and action into a cohesion that has atomic tenacity.
