Emotion: can it be defined?

What is emotion? Try for a moment to remember an emotionally rich event in your life. Graduations are a useful example, where people typically feel intensely proud, experience a rush of pleasure and excitement, believe that the world is full of promise, and throw their mortar boards in the air, out of sheer joy. It is difficult to unpick this complex experience, but basically it comprises the following responses:

A physiological response to an emotionally intense life event at the other end of the spectrum could be a frightening situation, such as a house fire. This situation would involve the release of stress hormones (e.g. cortisol), activation of the sympathetic nervous system and a preparation of the musculoskeletal system for a fright, flight or fight reaction. A psychological response in such a scenario could be your belief that you’re in imminent danger, which in turn motivates you to flee, while a typical behavioural reaction would be to scream for help, adopt a defensive posture and run for safety.

Some psychologists have made attempts to define emotion. Here is an example by Smith (1993):

Although this is a very inclusive description, one could argue that its broadness jeopardises its specificity. It is probably more useful to have an understanding of different types of emotion, than to worry about comprehensively capturing this complex concept.

When we think of an emotion, we may be inclined to think that this is unique to each of us – specific to our own individual world of experience only. Although it is attractive to indulge in the notion of a strictly private world, ground-breaking work by Darwin in the 1850s confirmed that there are around six basic facial expressions, each conveying a distinct emotion, which are understood the world over (Darwin 1865, cited in Berthoz 2003). These universal facial expressions communicate:

Pioneering work by anthropologist Ekman in Papua New Guinea, where until that time no Westerner had set foot, confirmed these basic emotions; when told an emotionally charged story and asked to express what this felt like, local inhabitants showed facial expressions that could readily be understood by people from Western civilisations (Ekman 1984).

This universality in basic emotions makes sense from the perspective of survival: before the arrival of the communication technologies we use today, facial expressions were our primary means of communicating to our immediate social network how we felt. If there is danger, communicating fear is essential to warn others around us. Disgust may signal food that is inedible, while an angry face conveys a warning. This universality suggests that some of our emotional expressions are ‘hardwired’ in the brain – a topic we will come to later.

We will now turn to the topic of depression, one of the most common mental health problems in both the general population, and in people with long-term neurological conditions.

Classification of depression

Depression comes in different forms. It used to be thought that depression could be simply classified in two ways – reactive and endogenous. With reactive depression there is usually a very specific, clear psychological cause (e.g. a bereavement, the loss of a job, the break-up of a long-term relationship). This type of reactive change may occur following, for example, a stroke where the patient has had a significant loss of function and is no longer able to engage in certain activities and life roles that they were able to do pre-stroke. Unlike reactive depression, there appeared to be no clear cause for endogenous depression (hence the name). Patients suffering from endogenous depressions often express more severe symptoms (e.g. suicidal thoughts). It is important to correctly diagnose which form of depression an individual has, as evidence suggests that endogenous depression responds better to drug therapy (see later in this chapter).

An alternative way to consider depression is to classify the level of disability produced as being either a major depression or a dysthymia. A major depression will interfere quite markedly with the individual’s ability to work, study, sleep, eat or enjoy pleasurable activities. Such a level of dysfunction may only occur once, but it is quite common for such a disturbance to occur on multiple occasions throughout life. Chronic major depression of this nature may require an extensive period of appropriate treatment. Dysthymic disorder, or dysthymia, produces symptoms of a less severe nature; however, they can still be chronic and long-lasting. Dysthymia does not necessarily seriously disable the individual, but it can keep them from feeling and functioning well. It is also possible that a person with dysthymia may also experience a major depressive episode at some point in their life.

Causes of depression

The actual cause of depression is still unknown. In some families it can be apparent that depression occurs from generation to generation, however, it can also occur in a person with no family history of depressive illness. It is also widely accepted that depression is a combination of genetic, psychological, social and environmental factors.

Current biomedical views on the cause of depression centre round the monoamine hypothesis, which was first proposed in 1965 by Schildkraut. This hypothesis puts forward the idea that depression occurs as a consequence of abnormalities in the levels of the monoamine neurotransmitters (noradrenaline [NA], serotonin [5-HT]) in the limbic system. As mentioned in Chapter 2, the limbic system is the ‘emotional part’ of the brain and this system will be described more in detail below. Research points to particular evidence that reduced serotonergic neurotransmission is involved. It is hypothesised that depression is caused, in part, by a number of biochemical/pharmacological changes within the limbic system.

These changes include a lower level of monoamine transmitters (NA, 5-HT) and/or an upregulation of presynaptic autoreceptors (located on the presynaptic terminal) and somatodendritic autoreceptors (located on the dendrites of the presynaptic cell) that control monoamine release. This increase in the presynaptic receptors and those found on the dendrites result in an enhancement of the normal negative feedback mechanism, thereby causing a subsequent greater reduction in further monoamine release. Over time this mechanism would result in a significantly lower release of the transmitters.

There are a number of key pieces of evidence that both support and refute the monoamine theory.

Treatment of depression

The mechanisms of action of the antidepressants covered next can be seen in Figure 13.1. This diagram shows a single synapse containing both NA and 5-HT, although in reality there would be either a noradrenergic synapse or a serotonergic synapse.

Fig. 13.1 • The mechanism of action of some antidepressants.

(Based on Waller et al 2001, with permission)

Non-pharmacological management of depression

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