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Sunday, December 12, 2010


Freud (1975a, 1975b) had two theories of neurotic anxiety, both suggesting that it is made up of an unpleasant feeling, a discharge process, and a perception of whatever is involved with this discharge. Freud believed that anxiety develops through the trauma of birth, the loss of the caregiver, early uncontrollable threats or impulses, and, more specifically, fears of castration. In contrast to Freud’s theoretical framework, subsequent work (e.g. Bowlby 1973) has stressed the importance of separation from early attachments. For learning theorists (e.g. Mowrer, 1953), anxiety is a form of learned fear, particularly when the source of the fear is vague or repressed. Anxiety becomes a conditioned response that can then participate in new learning. Taking this a stage further, H. Eysenck (e.g. 1957) suggests that we inherit proneness to neurotic anxiety through the ANS, or learn it as conditioned fear. In searching for the physiological mechanisms that might underlie these processes, Gray (1982, 1987) states that he septalhippocampal region of the brain mediates anxiety. This brain system functions to inhibit behaviour that is a threat to the organism. Some recent theories of anxiety stress cognition. For example, M. Eysenck (1988) shows that those who are high or low in anxiety also differ in their cognition. So someone with a high trait anxiety (anxiety as a personality characteristic) is likely to have more worries stored in long-term memory than someone with low trait anxiety, and these worries will be much more easily accessed. One of the most telling contributions in this area comes from Barlow (e.g. 1991), who places anxiety and depression at the centre of emotional disorder. He argues that it is difficult to distinguish between anxiety and depression. However, whilst most depressed patients are also anxious, not all anxious patients are depressed. Barlow suggests that emotional disorders occur when chronic states of dysthymia (i.e. lowered mood) interact with briefer episodes of panic and depression. This mig t lead a depressed patient to misinterpret a personal or environmental event as a sign of personal inadequacy, which simply makes matters worse. Barlow’s general argument is that stress, anxiety and dysthymia can interact with everyday emotions of excitement, anger, fear and sadness. When this happens, the result is one of four kinds of emotional disorder – mania, outburst of temper, panic or depression. For fully fledged emotional disorders to occur, these emotions have to be experienced unexpectedly or inappropriately, and to be seemingly out of control. Finally, it is worth repeating that emotions can never be abnormal. Their expression or recognition may be awry, they might become too extreme for comfort, or they might contribute to mental illness, but even in these unfortunate circumstances, emotions always provide us with useful information. In the case of abnormalities, this is information that something is wrong and needs fixing.

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