Emotions are mental states, sometimes described as ‘disturbances of mind’ that may be associated with certain subjective feelings and characteristic behavioural responses. In experimental psychology, emotions are generally described in terms of three dimensions: the visceral or physiological (including, for instance, AUTONOMIC NERVOUS SYSTEM activity), behavioural (facial expressions, angry postures for example) and the subjective (such things as emotional feelings). Understanding how these three dimensions interact and how they are coordinated is a major aim of research in this area. Related terms to emotion are AFFECT from the older psychological literature and MOOD, terms still commonly used in psychiatry. The distinction between emotions and mood is probably their chronicity: emotions are generally brief experiences of a matter of seconds, whereas moods are much longer lasting.
One of the most enduring questions about the emotions is how many basic forms exist. Charles Darwin (1809–1882) attempted to classify the basic facial expressions of human emotion as deriving from animal forms. Later, on the basis of cross-cultural studies, Ekman proposed that facial expressions of happiness, surprise, sadness, fear, disgust and contempt are human universals that correspond to the basic emotions. Furthermore, these facial expressions were associated with different patterning of responding in the autonomic system in terms of responses such as blood pressure and skin temperature. However, there is some evidence for rather general or overlapping changes in autonomic reactivity in contrasting emotions if these nevertheless both require behavioural action. There is considerable controversy about when infants develop the capacity to perceive a range of discrete emotions, as distinct from general feelings of contentment and distress. As shown by Bowlby and others, the latter is caused by separation from an attachment figure in unfamiliar circumstances and peaks at about 18 months of age, declining by about 3 years.
The psychological characterization of distinct and shared patterns of emotional response is paralleled by both differentiation and commonality in the neural mechanisms of the emotions. Thus, there is some evidence for discrete regions in control of basic motivational and emotional processes such as particular forms of FEAR or AGGRESSION, together with precise patterns of ENDOCRINE regulation, which may include NEUROPEPTIDES as neuromodulators of specific behavioural responses. The basic behavioural output systems are controlled to some extent by a network of structures termed the LIMBIC SYSTEM, which includes the AMYGDALA, SEPTAL NUCLEI and CINGULATE CORTEX, as well as their interconnecting structures. Theorists such as Jeffrey Gray have attempted to collapse the main emotions into a smaller set of those that are mediated by defined brain systems. For example, according to this scheme, ‘frustration’ is conceptually related to ANXIETY and is mediated by a brain BEHAVIOURAL INHIBITION SYSTEM that includes the septum and HIPPOCAMPUS.
Positive emotions or approach behaviour, by contrast, can be linked to the operation of a general incentive-motivational (see INCENTIVE MOTIVATION) or REWARD system which depends on the functioning of the MESOLIMBIC structures such as the amygdala and NUCLEUS ACCUMBENS. Our understanding of neural mechanisms of the emotions has been enhanced by study of the subjective effects of drugs in human subjects. Many ANTIDEPRESSANTS and ANXIOLYTIC drugs work either directly or indirectly on the ascending monoaminergic neurotransmitter systems (including NORADRENALINE and SEROTONIN, as Well as DOPAMINE). Drugs of abuse such as AMPHETAMINE may cause EUPHORIA, presumably by releasing brain dopamine, whereas compounds such as CHOLECYSTOKININ elicit PANIC-like reactions in volunteers. Nevertheless, the subjective effects of these drugs have been shown to depend considerably on the cognitive context in which they are experienced, as postulated in early theories of emotion such as that of Schachter (see JAMES-LANGE THEORY OF THE EMOTIONS).
There have been diverse theories about the causation and functions of emotions, beginning with the James-Lange theory, and its various manifestations, and culminating in more cognitive models emphasizing such factors as appraisal and attribution, and the use of emotions for setting priorities among various goals or as cues to alter goal-directed plans and actions, including social communication (see Oatley & Jenkins 1996 for a review). However, little is known about the cognitive nature and neural basis of these complex mental processes. A key issue is the role of conscious and unconscious emotions. The latter may play an important role in informing conscious DECISION-MAKING. Damasio has recently described how unconscious ‘gut feelings’ may provide somatic markers for decision-making in normal people that precede a conscious appraisal for making particular choices in a risky situation (see SOMATIC MARKER HYPOTHESIS). However, patients with damage to the ventromedial PREFRONTAL CORTEX apparently lose this capacity and hence continue to make highly risky decisions. It remains possible that the neurochemical basis of the somatic markers corresponds to activity in the central monoamine neurotransmitter systems which innervate the FRONTAL CORTEX. In this way, a central correlate of William James’s postulated visceral reactions underlying emotion may inform complex decision-making at the highest cortical level.
References
Damasio A.R. (1994) Descartes’ Error. Emotion, Reason and the Human Brain, Putnam Press: New York.
Ekman P. (1981) Face of Man, Garland: New York.
Oatley K. & Jenkins J. (1996) Understanding Emotions, Blackwell Scientific Publications: Oxford.
TREVOR W.ROBBINS
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