In answer to this question there should be some indication of the difficulty in measuring emotion by questionnaire. For example, the response to questions such as "Are you an anxious person?" may not be interpreted in the same way by persons responding to the questionnaire. Also, the difficulty in interpreting psychophysiological signs of arousal e.g. increased sweating according to a GSR measure. Such signs of arousal may be associated with a number of emotions and thoughts, some of which may be unrelated to the cue or question supplied by the examiner. This is why the polygraph (lie detector) is not accepted in courts in many countries of the world.

Many of the difficulties of research in this area are shared with other areas of neuropsychology, for example, the generalisation of animal research to humans. The finding that different species behave differently with the stimulation of the same structure depending on whether they are carnivores or herbivores; the difficulty of interpreting the emotional behaviour of animals; the difficulty in finding humans with lesions isolated to an area that has been found to be theoretically interesting. Hopefully you will be able to supply other difficulties.

Historically there have been theories of personality and emotion that have ignored the view that our emotions are designed to help us in social situations and give us special impetus during periods of threat. Studies by Hess and others showed that emotions could be studied scientifically and that there were neurobiological mechanisms responsible for emotional behaviour that could be studied like other areas of science. A mention of Darwin's work in this area is also important.

It will probably be used for some time yet to describe the part of the brain that is devoted to emotion, but in the author's opinion it has changed sufficiently to be past its "use by date". Often when a non-specialised text uses this term it is difficult to know what is being referred to. The original concept included the hippocampus and some areas of the cingulate that clearly are not relevant to modern day conceptions of the emotional brain.

The behaviour of animals and later human subjects with this syndrome suggested that they were not able to perceive objects around them and that they were seeking further information by tasting and mouthing objects. The original lesions included areas of the posterior temporal lobe that when damaged would have produced agnosia being lesions to the visual what pathway (see chapter on Perception).

The AM has been attributed the role of interpretation of threatening and novel information. Such information may include facial expressions, body language, feared animate and non-animate objects and some sounds e.g. scary music. There is a tendency for patients with bilateral lesions to the AM to avoid looking at the eyes of a person when recognising emotional expression. This may be because they get less information from this area than controls. They do improve, however, if asked to look into the eyes as a source of emotional information. It is likely that we learn from an early age the look of a person that we regard as being untrustworthy and this information is no longer accessed by these patients. The failure to recognise threatening information means that they also show a reduction of feelings of being threatened or a need to escape. This failure which is related to the bilateral destruction of the AM is related to the robust pathways between the AM and structures such as the hypothalamus with its associated sympathetic autonomic system. Such neurophysiological visceral reactions are associated with feelings of anxiety and fear that with the perceptual recognition allow us to act appropriately to social threat.

Lesions to the amygdala do not interfere with the consolidation of new memories; they just reduce the emotional connotations and associations that may be stored with a memory. Following bilateral amygdalectomy patients cease to respond psychophysiologically to arousal e.g. GSR when exposed to stimuli that the patient has been trained to fear. However, they may still remember the training and so while not being aroused by the feared stimulus may nevertheless avoid the stimulus because they remember the consequences of dealing with the stimulus, whereas lesions to the hippocampus undermine the consolidation of new memories. The amydgala still influences the storage method in a process referred to in the Memory chapter as reconsolidation. Sometimes we look back on a terrifying event and become aroused all over again. In the author's teenage years he once climbed a mast to release a flag stuck in a block/pulley. It was just out of reach which required a brief moment in which there was a trust in the balance straddling a near horizontal pole. This was all done some 30 to 40 feet above the deck of a ship when a slight miscalculation would have resulted in death. Over the years a reflection on this incident has revived feelings of arousal and discomfort that remind me I should never do anything like this again. It is the amygdala with the consolidation system that is maintaining these feelings of fear as a protective mechanism.

This is not a straightforward hierarchical relationship, but the role of the OFC as an evaluator of rewards and its potential for an inhibiting influence on the AM and the hypothalamus. It is likely that while the AM is quick to respond to a threat and past memories of negative information contained faces and other visual and auditory memories (connections with the perirhinal cortex), the OFC may have a broader evaluative role that takes into account the negative and positive outcomes that relate to a more immediate response by the AM.

The AM has a role in classical conditioning that allows an immediate visceral warning of imminent threat. The AM also has connections with the pulvinar that allows immediate visual attention to an ambiguous or novel stimulus as a means of verifying the nature of a potentially threatening stimulus.

Both the AM and the OFC have connections to tertiary perceptual input, in other words, perceptual analysis that is largely at a completed level. Therefore both the AM and the OFC areas are able to respond according to what is known about the external world. The AM has the ability to control attention towards an ambiguous or threatening stimulus. There are also connections between the AM and the perirhinal cortex which the chapter on memory has informed us is an area important to the recognition memory for visual information including faces. OFC lacks these attentional skills and as part of the cortex may take too long to respond to an immediate threat. However, the OFC has a role in the evaluation of environmental stimuli that lead to positive reward or punishment and it is assumed that this is based on a more considered evaluation with a judgement of outcome of behaviour.

Sometimes, there may be a tendency to respond in an immediate way because we are classically conditioned to fear a stimulus. In cases where this is an irrational response it is likely that the OFC is able to process the actual future outcome and modulate the AM and the hypothalamus. This view is encouraged by the finding that the OFC has been found to be involved in inhibition of a classical conditioning and habituation process that reduces these rather reflexive responses. However as will be revealed later this important relationship needs further clarification. Therefore these structures work together to provide an appropriate emotional response: the AM supporting attention to a potential threat and eliciting an autonomic response from the hypothalamus while the OFC evaluating the necessity for such a response.

This is more likely to be an essay question, but it may be important to have a grasp of an overview of the main areas that may contribute to pseudopsychopathy.

Hopefully, there has been an attempt to answer this question, given the answer is quite subjective. Any answer must consider, the sometimes, unfortunate privatisation of prisons without governmental conditions. Such conditions would provide incentives that require levels of rehabilitation and conditions of reassimilation back into society with a goal of reduced offending.

On another but related clinical issue is the assessment of patients who are malingering. This is not always about unimpaired persons attempting to gain unwarranted compensation. Sometimes patients who are impaired following the accident also attempt to perform at a lower level. Such patients often fake badly because of their impairment and are easily detected. Should we penalise and condemn such behaviour or rather attempt to gauge such a patient's claim and seek to gauge the real level of impairment without a moral judgement?

This is a question that encourages a more holistic view of patients' emotional well-being. A start with a list of these factors within the text will show that emotional health of the patient may be determined by their situation, support and other factors such as their level of insight into their handicap. These factors interact with the vulnerability of the patient due to more organic factors e.g. brain damage to a brain area playing a role in emotion.

There is some differentiation between studies with healthy participants and those suffering phobias. Further differences may be found between persons suffering different phobias. However, there appears to be some consistency with the initial activation of the AM and there is then increased activation of either ventromedial (vmPFC) or ventrolateral PFC (vlPFC) with a subsidence of AM activation. Some reviews have found a relationship between the AM and the vm and vlPFC when successful regulation has taken place. Often in such studies when activation of AM is high vmPFC is low and vice versa. In these cases then there is a direct conditional relationship that has suggested to some that these areas have a controlling relationship with the AM. This proposal is further encouraged by the non-human studies, for example, the vmPFC is associated with a role in extinction and habituation of a learned response. Also there are psychopharmacological studies e.g. cortisol relationships and studies with spider and other phobics that support this role. It should be noted that the social phobics are not so associated with activation of the AM. The finding that AM activation may reduce during an anticipation of a threat suggests that the AM is most important in registering the presence of novel or unexpected visually threatening material and once this has been ascertained then other areas are more likely to be involved.

Other activations during the regulation of emotions that have been associated with an intensification of emotions are the dorsolateral PFC (DLPFC) and the dorsomedial PFC (DMPFC). The DLPFC is seen as being important to strategic control and working memory, while the DMPFC may be related to some self-introspection and conscious monitoring. It should be remembered that in the chapter on executive dysfunction inferior aspects of DLPFC is seen to have a role in arresting a response, and this was described with connections in a network with an inhibiting mechanism ascribed to areas within the basal ganglia. The insula especially the right insula may have a role in feelings of fearful anticipation and disgust. There is some support for this in other studies previously mentioned. Less explainable is the activation of the anterior hippocampal area but this area has close relationship with the perirhinal cortex, and the recognition memory for visual features is no doubt required in some of these studies.

While the vmPFC and vlPFC are seen as having an influential role in modulating the level of activation of the AM and perceived threat in regulation of emotion studies this is a large area of the brain and part of this area such as the OFC is seen to have a role in the evaluation of rewards. Also, there is a subgenual area that is either an area that is implicated in the attempt to control depression or is an area that is responsible for the feeling of depression. This is most likely related to the feelings of depression given that this area is closely associated with emotional self-introspection and emotional theory of mind. The subgenual area is smaller in patients with familial depression but it is more active. See a list of further support for this role in the text.

While the research on Vietnam veterans predictably finds fewer phobias in patients with damage to the amygdala, Tthe finding by Koenigs and others that patients with vmPFC damage also show less post traumatic stress disorder (PTSD) does not square with the idea that the vmPFC is a controller of emotion. However, Myers-Schulz and Koenigs' proposal is that this area, especially the subgenual area, is associated with the expression of negative effect. In this way the patients will not report the anxiety and negative effect that would normally be one of the cornerstone features of PTSD. In other words this does suggest that the vmPFC has a number of roles and this is also shown in studies of patients with lesions in this area who may suffer emotional blunting, poor perception of emotional stimuli and poor reversal learning which requires behaviour based on the judgement and evaluation of reward. The vmPFC area has therefore a number of roles that are not differentiated given a natural lesion such as brain tumour or damage following removal of a meningioma.

This is a question concerning the freezing or waiting prior to a decision to move versus fleeing stages versus imminent capture that were demarcated both by bio measures and brain area activation.

According to a human study the vmPFC was activated in the first stage which is seen as judging when or where to escape. This was accompanied by activity in the AM and bed of the stria terminalis and the three areas allowed the registration of the degree of threat. vmPFC became less active and the brain stem area including periaqueductal gray (PAG) became more active with peaks during imminent capture in the dorsal raphe nuclei. The PAG was most obviously the focus of stimulation during defensive action or escaping.

It is likely that the subgenual areas and insula serve a role in the production of negative feelings, but that these are further developed into conscious feelings within the dorsal anterior medial area e.g. dorsal anterior cingulate and neighbouring PFC areas that provide a level of introspective thought that may play a role in ruminations. More positive feelings involve a different area within the subgenual area. With positive conscious states the role of the dorsal anterior medial area remains the same but there appears to be a role for a structure called the nucleus of accumbens that is associated with feelings of elation commonly active during recreational drug taking. Feelings associated with emotional empathy and affiliative behaviour are likely to be related to ventromedial cortical activity. For example, patients with fronto-temporal-dementia who have atrophy in this area show reduced empathy and increased coldness to loved ones.

Also involved is a network which shows the highest activity in the septal and hypothalamic areas which is associated with oxytocin. Nasal sprays with oxytocin have been shown to increase feelings of affiliation and empathy. Also, as previously mentioned in this chapter, the septal area has a role in reducing anxiety. The corticotrophine hormone suppresses the role of the septum and prompts the release of adrenocortitrophine by the pituitary which in turn produces cortisol which when measured in the bloodstream is commonly used as an indicator of stress in research.

The role of the subgenual area, with its influence on depression, is smaller and more active in familial depression. As an indication of the importance of this area to the feelings of depression, deep brain stimulation in this area may be followed by an immediate recovery from the feelings of depression.

Mayberg and others note that CBT therapy may result in an increase in size of this subgenual area also with improvement in their depressed condition. Mayberg proposes that successful CBT treatment of depression is accompanied by a normalisation and a balance between subgenual and dorsomedial activation. There is also an interaction of these areas with the AM. Patients with smaller than normal subgenual areas might in the future be seen as candidates for deep brain stimulation in this field. However, long-term effects of this treatment are uncertain and the subgenual may also increase in size with CBT treatment.

Reduction in size of the subgenual area and the over-reaction of this area in patients with familial depression suggest that this is a key area that contributes in some way to depression. The argument is made that this area may be important for the expression of negative feelings but there are other areas that might lead to a more positive outlook. A lesion to both areas may be associated with emotional blunting. A lesion or deep brain stimulation to the subgenual area may lead to short-term alleviation of depression.

There is an assumption with simple phobias that there is over-active AM and a ventromedial PFC (VMPFC) that fails to inhibit the AM. In such studies the VMPFC is seen to have an inhibiting influence or an influence encouraging habituation of the classically-conditioned fear response, that may often be taken on prior to puberty.

However, PTSD appears to be different from these disorders in that some studies show a reduced AM activation. It is possible that this is related to an avoidance of the feared event. Features of PTSD include depersonalisation and avoidance that are thought to counter therapeutic intervention. The theory of therapy in this area provides that in order to deal with the past experience there must be some psychological attempt to come to terms with the past experience and the need to find cognitive strategies that deal with the discomfort.

With PTSD it has been found that there are often smaller areas that relate to the neuropsychology of emotion more generally, for example, the anterior cingulate cortex, vmPFC, left temporal pole/middle temporal gyrus, and left hippocampus. These areas have been found to be reduced in size in PTSD patients compared with individuals exposed to trauma but without PTSD. The difficulty in treating these persons may in part be related in that there is a difficulty not only in unlearning the phobic reactions but also a difficulty in learning that the stimuli associated with the PTSD are no longer harmful.