Social learning theory emphasises the importance of modelling others’ emotional reactions as a means of developing emotional patterns and responses. The behaviourists have developed a number of various classifications of behavioural theory, depending largely on the degree to which they refer to metaphysical or epistemological claims in their explanations of emotion. The two main categories of behaviour theory are psychological behaviourism and philosophical behaviourism. The psychological behaviourist approach to emotions can best be exemplified by the theories of James Watson and B. F. Skinner. Watson, in 1919, described emotion as ‘a hereditary pattern-reaction involving profound changes in bodily mechanisms as a whole, but particularly of the visceral and glandular systems’.

In Watson’s model of emotion, only three emotions can be distinguished: fear, rage, and love. He further states that these primary emotions can only by demonstrated in the newborn. Watson’s major contribution was his finding that emotional reactions could be learned through classic conditioning (Watson & Raynor 1920).

In 1967, Etzel and Gewirtz demonstrated that operant conditioning could have an impact on emotional development. Skinner refined Etzel and Gerwirtz’s work into a complex model where emotions evolve from an operant conditioning framework, where emotion is defined by the sets of operants and reinforcers that one optimises in any given setting (Skinner 1974). One of the major criticisms of Skinner’s theory is that some emotions exhibit little or no operant behaviour. For example, grief, especially when about a loss or death, does not result in any operant behaviour because no behaviour can bring about the desired results (Lyons 1992).

One of the most influential philosophical behaviourists was Gilbert Ryle. In 1949, his work The Concept of Mind outlined that emotion can be described in four different ways: inclination, moods, agitations, and feelings. Ryle viewed inclinations as the permanent disposition state of personality. Moods, agitations, and feelings were short-term displays overlying the main inclination theme. For example, if a person has the inclination to be kind, he may still experience short-term occurrences of irritability or cruelty, which would be attributed to his mood or feeling swings.

Further expansion of the social learning theory in recent years has been accomplished by Albert Bandura, who has added a cognitive component. According to Bandura, as a person’s representational ability improves, he/she can engage in emotional self-arousal by thinking about their own emotionally charged past experiences or even by recalling the experiences of others (Bandura 1986, 1989, 1991).

One of the main criticisms of social learning/behavioural theory is that it cannot explain the emergence of emotions that have not been acquired through modelling or conditioning, but seem to appear spontaneously.

The theory that emotions are nothing more than chemical reactions at synaptic connections has not been a popular theory among psychologists in the past. However, several recent findings and advancements in understanding of the neurochemical component of emotion have caused a wave of interest in the theories of biological emotion. Many neurochemical systems now appear necessary for the understanding and expression of emotions. Several areas of the brain have been implicated in the development, generation, and expression of emotions, particularly those regions known as the limbic system, which includes the hypothalamus, hypothalamus–pituitary axis, the anterior thalamus, the cingulated gyrus, the hippocampus, and amygdala (Rolls 1992; Halgren & LeDoux 1993). The importance of the amygdala in particular has emerged in its ability to determine the motivational significance of a stimulus (Gaffan et al. 1988), in the assignment of reward value to a stimuli (LeDoux 1990), and in the stimulation of behavioural and autonomic responses.

Instead of viewing emotions as central forces in the development of social interaction, cognitive psychologists view emotions as by-products of cognitive processes (Berk 1994). Several examples of cognitive theories follow, including Hebb’s discrepancy theory, Alder’s style of life theory, Epsteins cognitive-experiential self theory, and Apler’s reversal theory.

Donald Hebb (1947, 1949) explained in his discrepancy theory how distress reactions are elicited by novel stimuli. According to Hebb, when a person encounters a new stimulus, they compare it to a scheme or internal representation of a familiar object. The discrepancy between the stimulus and the internal representation determines the emotional response. Other researchers have modified Hebb’s theory, suggesting that a wide variety of emotional reactions could be explained by Hebb’s theory. For example, they argue that a positive emotion such as happiness could result from only moderate discrepancies between current stimuli and the internal scheme. Negative emotions, such as anxiety and fear, could result as the discrepancy between the present stimuli and the interval scheme widens (McCall & McGhee 1977; Kagan et al. 1978). This theory falls short when it is observed that people sometimes willingly seek out activities that are new and not in agreement with their internal scheme.

Alfred Adler, in his 1954 work Understanding Human Nature, was probably the first to integrate emotions, motivations, and cognition into one theory (Epstein 1993). According to Adler, individuals construct a belief system and a way of relating to the world which he termed a ‘style of life’. At the centre of a person’s style of life is a fictional goal which guides the individual in his attempts to overcome inferiority to gain social approval, a goal to which all humans strive. Emotions enter into Adler’s theory in two ways. Firstly, the quest for overcoming the feelings of inferiority provides an incentive for developing a style of life. Secondly, once the style of life has been developed, the emotions corresponding to that style of life are encouraged to develop. In other words, the style of life that one develops is a major determinant of the emotions that a person experiences, much like Aristotle’s ‘state of mind’ (Epstein 1993).

In the cognitive-experiential self theory (CEST), emotions are considered to be both influencing and being influenced by a person’s implicit theory of reality. The theory considers the primary emotions to be anger, sadness, joy, and affection. Cognitive affective units are constructed around the nuclei of the primary emotions. These cognitive units direct the development of critical adaptive behaviour patterns such as fighting, withdrawing, exploring, and showing affection. The development of these behavioural patterns results in emotionally rewarding experiences when they are consistent with a beneficial outcome to the individual (Epstein et al. 1992).

Apter’s reversal theory is explained in some detail here because it is one of the few theories that has a theoretical construct for encompassing changes over time in the individual which are clinically relevant for the functional neurologist. The centrepiece of reversal theory is a typology of distinct psychological states of mind. When people are in one of these states they want to experience a particular kind of emotion. The states are meta-motivational because they determine what types of experiences people want. In different states, people may react to the same stimuli in different ways, and experience distinctly different emotions. This theory focuses on how a person differs over time rather than on differences between people. Reversal theory suggests that there are eight different meta-motivational states, four pairs of opposite states. The reversal from one state to its opposite is the key feature of the theory. The two states of a pair are mutually exclusive and exhaustive; for example, a person is always in one state or the other, never both at the same time or neither state. The eight states of the reversal theory are serious–playful, compliant–defiant, power-oriented–affection-oriented, and self-oriented–other-oriented (Apter 1988). The first pair of meta-motivational states is composed of the telic and paratelic states. When in the telic state the person is primarily goal-oriented. Conversely, when a person is in the paratelic state they are best described as being playful. In this state the person does not attach much significance to what they are doing; they could not care less. The lability of a person, how readily they reverse back and forth between opposite states, varies at different times. The actual reversal process is dependent on one of three reasons: contingency, satiation, and frustration. Contingency is any change in the environment that instigates or necessitates a reversal. Satiation occurs when, in the absence of an environmental change, a reversal will eventually occur. Frustration–motivated reversals occur when a person remains in a particular state too long without achieving satisfaction (Frey 1997).

Reversal theory takes the approach of starting with motivation and experience and then interpreting the behaviour generated in light of these. Reversal theory emphasises that people are inconsistent and self-contradictory and goes so far as to say that healthy people are characterised by instability, not stability (Murgatroyd 1987).

Campos et al. (1994) define emotion as those processes which establish, maintain, change, or determine the relation between the person and the environment on matters of significance to the person. A person’s mood may be determined by a complex interplay of the emotions that they are experiencing at any one time as per the reversal theory. ‘Mood’ therefore can be defined as the way that we feel, while ‘affect’ can be defined as how we behave as a result of our mood. Neurologically, mood and affect depend on the complex interplay among diffuse networks of the frontal lobes and subcortical circuits. They can be influenced by genetic and environmental factors, similar to any form of activity in the nervous system. Long-term changes in mood and behaviour may occur because of ‘plastic’ changes in these networks. This refers to the moulding of nerve excitability and interconnectivity referred to as neural plasticity that occurs following repeated or essential exposure to an environmental stimulus, and subsequent alteration of gene expression in the associated nerves.

Other probably genetically determined neural systems seem primed to perform a variety of innate activities called ‘fundamental functions’ in the cortex. Fundamental functions comprise diffuse, overlapping, or parallel units that contribute to more complex interactions and multimodal processing in the nervous system. The more recent definition of fundamental functions applies to frontal-subcortical and limbic circuits, which are largely intact from birth. Executive/integrative functions apply to the prefrontal circuitry, which also comprise diffuse, overlapping, or parallel influences that contribute to more complex interactions and multimodal processing in the nervous system. Fundamental functions are generally less modularised than motor or sensory functions. In other words, they are less dependent on one single area within the brain, and instead receive their input from multiple sources and generate an output that can influence the entire state of the individual. These wide-ranging functionally connected areas are often receiving similar information at the same time and are often referred to as parallel distributed processing circuits. Dysfunction associated with these networks can therefore lead to so-called ‘circuit-related disorders’ affecting complex aspects of cognition or leading to mood and behavioural changes. Therefore, abnormalities associated with fundamental or executive regions of the brain may result in either ‘negative’ or ‘positive’ symptoms. Negative symptoms or deficits generally refer to decreased expression of a normal function, whereas positive symptoms refer to release of primitive functions or new behaviours. An example of a negative symptom is depression, where a patient may exhibit withdrawal from normal activities and social interaction and less expression in their face and body movements. An example of a positive symptom can be seen clinically in paranoid schizophrenia where environmental stimulus is amplified and taken out of context of reality. Positive symptoms may also be referred to as productive symptoms, release or escape phenomena. A classic example of ‘escape’ phenomena is the exaggerated autonomic reactivity that may be observed in patients with panic or anxiety disorders. Primitive areas of the brain and brainstem are allowed to summate or increase their firing more easily because of a loss of descending reticular inhibition from the more developed frontal areas of the brain. Obsessive–compulsive disorder (OCD) can also be viewed as an example of a release phenomena. The patient develops an irresistible urge to perform a specific action that will bring about relief of tension. While not purely seen as a ‘disinhibition’ syndrome, the patient often feels compelled to carry out an action that interferes with their daily lives. Cortical and subcortical areas implicated in mood and behavioural functions receive tonic influences from a large array of different neuronal circuits, some of which involve parallel distributed processing circuits that utilise a wide variety of neurotransmitters including dopamine, serotonin, noradrenalin, and acetylcholine. Thus the cumulative activity of these various circuits results in a temporal variation in the relative concentrations of the neurotransmitters utilised in each circuit.

The concept of parallel distributed processing is essential for healthcare practitioners to gain an understanding of the link between psychological and somatic or visceral health complaints. Not only may somatic health complaints affect the ability of an individual to exercise their normal daily routines, thus leading to altered mood and behaviour, but direct physiological connections exist that involve somatic and visceral afferents and the limbic system or ascending reticular activating systems of the brainstem and hypothalamus. One example of parallel distributed processes is outlined below, involving the rostral cingulate cortex as the limbic motor response area that responds to parallel afferent information also received by the sensory cortex. The rostral cingulate motor area (area 24) is responsible for primitive motor behaviours (fear, avoidance, etc.) mediated via the corticospinal and reticulospinal pathways. Activity in this region is also dependent on activation of the caudal cingulate motor area (area 25), which orientates the body in space. These cingulate motor areas and receptive regions of the cingulate and insular cortex that project to it are not only influenced presynaptically by subcortical and spinal neurons carrying sensory information, but they are also heavily modulated by monoaminergic neurons from the brainstem. The influence of dopamine, noradrenalin, and serotonin on sensory modulation, arousal, and orientation is complex in nature and discussed in further detail in Chapter 9.

Several classifications of depression have been developed. The following classification is based on the age or stage of development of the individual.

This disorder involves both manic and depressive episodes. Usually, bipolar disorders will appear in the manic phase followed by a normal period then a depressed phase, although many different patterns have been identified. In rare instances the mood may alternate between manic and depressive states with no periods of normal functioning; this is referred to as the cycling type of bipolar disorder. Another rare form of bipolar disorder involves the appearance of manic and depressive episodes simultaneously, which is referred to as a mixed type of bipolar disorder. For example, the person may show manic hyperactivity but weep and threaten suicide at the same time.

Bipolar disorder is much less common than major depression, occurring in about 0.4–1.2% of the population (Hirschfeld & Cross 1982). Bipolar disorder occurs in both sexes with equal frequency but in contrast to major depression is more prevalent in the upper classes (Bootzin & Acocella 1984). The premorbid history in bipolar disorder is usually normal with no warning symptoms and usually has its onset before age 30. The episodes of bipolar disorder are usually briefer and more frequent than major depression. Bipolar disorder is also more likely than major depression to have a familial connection.

Depression has been shown to be related to schizophrenia (Crow 1984), herpes simplex virus (Halonen et al. 1974), Ebstein–Barr virus (Amsterdam et al. 1986), human immunodeficiency virus (HIV) type I (Levy & Bredesen 1989), several autoimmune diseases (Johnstone & Whaley 1975), leukaemia (Greene 1954), and a variety of cancers (Persky et al. 1987). These relationships suggest disorders of the neuroimmune system in some fashion or other.

The role of neuroimmune function in depression has attracted attention for many years (Calabrese et al. 1987). Depressive illness poses a major public health problem with 2% to 3% of the population hospitalised or seriously afflicted at any one time; in this light, many investigators have approached depression from a neuroimmunological prospective (Stein et al. 1991). Many studies document that patients with depression show reduced immune function throughout a wide variety of immune function measures. Stein et al. (1985) found that in-patients with depression have poorer blastogenic responses than non-depressed controls. Depressed patients have also been shown to have a lower percentage of helper T-lymphocytes than non-depressed controls (Krueger et al. 1984). Irwin et al. (1990) showed that when compared to normal controls, men with major depressive disorder were associated with a 50% reduction in T-cell cytotoxicity. Not all research supports the above findings. Stein et al. (1991) reported in a comprehensive review that out of eight studies that they looked at only one found lymphopenia to be significant in depressive patients studied. Out of five additional studies examined by the same authors, again only one showed an alteration in neutrophil counts in depressed patients. Immune function studies in patients with depression have also been explored. Irwin et al. (1987b) found a decrease in cytotoxicity of natural killer cells in depressed patients as compared to controls. Other studies relating to natural killer cell cytotoxicity did not find any significant difference between controls and depressed patients (Mohl et al. 1987; Schleifer et al. 1989). It is important to consider that depression is a diagnosis derived from diagnostic criteria composed of many variables (DSM IV). It is also necessary to realise that a diagnosis of clinical depression does not preclude the coexistence of other dysphoric mood states including anxiety and/or hostility. Depressed patients may have different combinations of symptoms and still be diagnosed with depression. For example, a patient may have predominately psychological symptoms such as self-reproach, difficulty concentrating, loss of interest, and recurrent thoughts of death or suicide. In contrast, another patient may have predominately vegetative symptoms including poor appetite and weight loss, sleep disturbance, loss of energy, or psychomotor agitation. These two types of patients may have vastly different neuroimmunological alterations as a result of the same diagnosis. This heterogeneous population may in some way explain the inconsistent results obtained when populations are not controlled for variables such as those described.

The degree of immunosuppression may also be related to the severity of the depression studied (Stein et al. 1985). Kemeny (1994) found that higher levels of a depressed mood were associated with lower numbers of cytotoxic T cells. In both types of studies, functional and enumerative, no consistent results have been reported for any cell types or subtypes studied. This inconsistency, as described above, may be a result of both conceptual and methodological concerns that limit the interpretation and generalisation of these study results. Few of the studies distinguished between any of the many recognised types of depression. As previously stated, the severity of depression may play a role in the cytological response and distinguishing between types may be necessary for more consistency in results. Small sample size and no controls for age, ethnic backgrounds, gender, and medication status may also have led to the inconsistent results reported in the above-mentioned studies.

Loneliness is a paradigm closely related to depression and several studies have found similar results of decreased immune response and function in lonely subject populations studied. A team led by Kiecolt-Glaser in 1984 found in separate studies that both medical students (Kiecolt-Glasser et al. 1984a) and psychiatric patients (Kiecolt-Glasser et al. 1984b) suffering from loneliness had lower cytotoxic killer cell activity and lymphocyte responses to mitogen stimulation. It is clear that more research into this area is necessary to determine the true effects and modulating variables of depression and loneliness on neuroimmune system function, especially studies controlling for degree of severity and types of symptoms expressed in study populations.

Several studies have demonstrated increased prevalence of depressed mood in patients who have suffered damage to the left frontal region of the brain compared to patients with lesions on the right. In addition, it was noted that the more anterior the location of the lesion, the more likely the patient would experience depression (Davidson 1992). The left brain is thought to be responsible for brain functions assigned to the will to perform or act. Right-handed reaching and positive affect are taken to be the collective manifestation of an approach system centred in the left frontal region. Damage to the left frontal region results in behaviour and experience which might best be characterised as a deficit in approach. Therefore, patients with damage or dysfunction involving the left hemisphere may lose pleasure and interest in people or objects and have difficulty initiating voluntary action. During withdrawal-related emotional states such as fear and disgust, the right anterior regions of the brain are activated. PET brain imaging has identified hyper-responsive regions of the right hemisphere that project to the amygdala in panic-prone patients. In order for depression to manifest clinically, more than just an injury to the left cortex is necessary. The person must also be exposed to the right set of environmental stimuli for the depression to be initiated. In a patient with left anterior cortical damage, depressive symptomatology would be expected only if that patient were exposed to the requisite environmental stresses. Left anterior damage is not in itself sufficient for the production of depressive symptomatology. We would therefore not expect all patients with left frontal damage to show depressive symptomatology. Only those exposed to an appropriate set of environmental stresses would be expected to show the hypothesised final state (Davidson 1992). Quantitative EEG studies have also proven to be effective in measuring changes in cortical activity associated with depression. Increases in left frontal alpha power are consistent with decreased activation of this area of the brain, along with frontal hypocoherence or decreased synchrony between the hemispheres.

In any discussion on depressive disorders, some discussion on suicide must be included because of the strong association between suicide and affective disorders. In his work The Savage God, Alvarez states, ‘The processes which lead a man to take his own life are at least as complex and difficult as those by which he continues to live.’ Yet we know that a major factor in deciding whether to take one’s own life is the feeling of hopelessness that occurs in depression. In a study of successful suicides, experimenters found that 94% of them had gone through episodes of serious depression (Robins et al. 1959).

The statistics on suicide are difficult to obtain because some who commit suicide want it to look accidental for a variety of reasons, some of which include insurance claims, or to spare families the shame that suicide usually brings. Some researchers have estimated that as many as 15% of all traffic deaths in the USA were suicides (Finch et al. 1970). Suicide is one of the top ten causes of death in the United States. About 1% of the population has attempted suicide at least once (Epstein 1974).

Among young people in New Zealand, between 15 and 24 years of age, it is considered the second leading cause of death. Three times as many women attempt suicide as men, but three times as many men than women actually succeed in killing themselves. Two times as many single people kill themselves as married people do. The most common profile to commit suicide is a native-born male, in his forties or older, who is depressed or ill and kills himself by hanging, shooting, or poisoning by CO (Shneidman & Farberow 1970).

Is there a certain personality type more likely to kill themselves than another? Apparently not! Freud even had suicidal thoughts throughout his life (Jones 1963). There are, however, certain types of reasoning that can lead people to kill themselves (Shneidman & Mandelkorn 1970).

The psychoses are usually divided into two broad categories:

The functional psychoses are divided into three classes:

Originally, this was thought to be an organic disorder involving a general affliction of the nervous system that produced various forms of bizarre nervous behaviour. Throughout the nineteenth century, those people who were demonstrably sane but nevertheless engaged in rigid and self-defeating behaviours were labelled neurotic and thought to be victims of some identified neurological dysfunction. Around the turn of the century, this biogenic view of neurosis was gradually replaced by Freud’s psychogenic view (Freud 1894). To Freud, neurosis was not due to organic causes, but rather to anxiety. As repressed memories and desires threatened to break through from the unconscious to the conscious mind, anxiety occurred as a danger signal to the ego. The neurotic behaviour that developed was either the expression of that anxiety or defence against it. This view has held until the past few decades where there has been a growing opposition to using the term neurosis to describe all of the anxiety disorders due to the fact that not all of the neuroses express anxiety directly.

The primary feature of this condition is a continuous, inescapable fear of disease. The fear is maintained by constant misinterpretation of physical signs and sensations as abnormal and representing clinical signs or symptoms of a disease process. Hypochondriacs have no real physical disability or disease process that can be clinically proven to exist.

Often when hypochondriacs present at a health professional’s office, they have already diagnosed their condition, for they are usually avid readers of medical textbooks, and have spent countless hours on the Internet searching their symptoms for the diseases that cause similar symptoms. When the healthcare professional tells them that they can find no physical cause for their symptoms and there is actually nothing wrong with them they are disappointed and will often change healthcare professionals until they find someone who at least agrees to perform more tests to prove that they do, in fact have, a disease or condition. Often these people go through several healthcare professionals per year.

It should be noted that hypochondriacs do not fake their symptoms. They truly feel the pains they report. They cannot be reassured by the medical evidence presented to them that their fears are irrational (Bootzin & Acocella 1984). However, these fears do not have the bizarre quality of the disease delusions experienced by psychotics, who will report that their feet are about to fall off or their brains are shrivelling. Instead, hypochondriacs tend to confine their anxieties to more ordinary syndromes, such as heart disease or cancer. Eventually, they generally focus on a single disorder.

This disorder is also known as Briquet’s syndrome (Bootzin & Acocella 1984). This condition is characterised by numerous and recurrent physical complaints which have persisted for several years and have caused the person to seek medical help, but for which no medical or scientific explanation can be given. This condition resembles hypochondriasis in that it involves symptoms with no demonstrable physical cause. Yet the two disorders differ in the focus of the patient’s distress. What motivates the hypochondriac is the fear of disease, usually a specific disease. The symptoms are troubling only because they indicate the presence of that disease. In contrast, it is actually the symptoms themselves that concern the patient with somatisation disorder.

The diagnosis of this condition can be extremely complicated and frustrating for a number of reasons. Firstly, the patient usually describes dramatic and exaggerated symptoms. Secondly, in the case of hypochondriac’s, they often fear one particular disease, and therefore their complaints tend to be fairly limited. In someone with somatisation disorder, on the other hand, the complaints are many and varied. In fact, this condition requires 12 to 14 different kinds of complaints for this diagnosis to be given. The occurrence is more common in females than males and 1% of women may develop some form of this disorder throughout their lives (Bootzin & Acocella 1984).

In hypochondriasis and somatisation disorder, there is no real physical disability, only a fear of, or complaints about, an illness or disability. In conversion disorder, there is an actual disability. The disability usually includes the loss or impairment of some motor or sensory function (Bootzin & Acocella 1984). Formerly known as hysteria, conversion disorder has played a central role in the history of psychology (see Quick Facts 16.4).

Like the symptoms in hypochondriasis and somatisation disorder, conversion symptoms are not supported by medical evidence. But neither are they faked. The symptoms are involuntary responses, which are not under the person’s conscious control. At the same time, they contradict the physiological facts; for instance, upon examination, the eyes will be found to be perfectly free from defect or damage and yet the person will not be able to see. Thus, conversion disorders differ from psychosomatic disorders such as ulcers in that in psychosomatic disorders there is an observable medical dysfunction.

Conversion symptoms vary considerably. Among the most common are:

Many patients with conversion disorder seem completely unperturbed by their symptoms. Whereas most people would react with horror to the discovery that they were suddenly blind or could no longer walk, the conversion patient is relatively unconcerned. This phenomenon is referred to as ‘La belle indifference’. In fact, they are typically eager to discuss their symptoms and will describe them in the most full and vivid terms to anyone who will listen. They also do not seem particularly eager to part with their symptoms.

In conversion disorder patients the patient’s body appears to be in good health. Biologically and physiologically, conversion patients can do whatever it is they say they cannot do. However, either by trickery or under hypnosis or the influence of drugs they can perform the task that they deny the ability to perform. Further evidence for their lack of organic pathology is that the symptoms are often selective. For example, conversion epileptics seldom injure themselves or lose bladder control during a seizure as do true epileptics. Likewise, in conversion blindness, patients rarely bump into things. It must be reinforced at this time that conversion patients by definition are not consciously refusing to use parts of their body. Their response is involuntary.

Diagnosis of this disorder is difficult. First, malingering, the conscious faking of a symptom in order to avoid some responsibility, must be ruled out. The second and much more difficult task is ruling out an actual organic disorder. Certain signs may suggest conversion disorder. These include: