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Definition and Background to Psychopathology and Therapies

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Published: Mon, 5 Dec 2016

Psychopathology, as defined by Davison and Neale (1996) is “the field concerned with the nature and development of mental disorders”. As a specific aspect of medicine, it tries to understand and define the causes and effects of mental disorders as well as proposing treatments for such disorders. Amongst the most well-known and widely studied mental disorders are depression, eating disorders and schizophrenia. Each of these has been given a lot of attention not just in the medical context but in society in general, with the media devoting much time and space to discussing the various manifestations of these mental disorders. This can have the effect of causing panic or raising stigmas against sufferers, which in turn can affect sufferers own attitudes to their condition. One of the most significant developments in psychopathology has been to research mental disorders thoroughly and to try to explain causes not just identify symptoms and thereby remove some of the misconceptions. This in turn can help patients and doctors to better understand the disorders as well as make their treatment more effective.

Depression is now identified as being a very common mental disorder.

20% – 26% of women and 8% – 12% of men develop depression at some point in their lives. 78% will experience more than one episode over the next 10 years.

10% of those attending GPs have depression; 5% have Major Depression

Between 3000 and 7000 people each year take their lives whilst suffering from depression.

(Blacker, 2000)

The Diagnostic and Statistical Manual (Fourth Edition) – DSM – which lists the diagnostic criteria for mental disorders suggests that 80-90% of depressed patients have symptoms associated with anxiety disorders, such as poor concentration, insomnia, loss of energy, mood swings, worries about health or more specific panic attacks. Researchers have attempted to explain the causes of depression in relation to these symptoms. The most influential theoretical approach which attempts to explain depression is the cognitive model, as presented by Beck (1963) in the ‘cognitive triad of depression’ which shows types of negative thought:

The self (i.e., self is worthless)

The world/environment (i.e., world is unfair), and

The future (i.e., future is hopeless).

Each of these ways of thinking interact and reinforce each other which eventually leads to depression.

In discussing the causes of depression, researchers have identified two categories of factors. Firstly there are the Biological factors which are usually used within the ‘medical model’ of treatment. Of these, Genetic factors refer to inherited genes which might indicate a handing down of a condition. Biochemistry, on the other hand, looks at levels of brain chemicals and the association of different levels of chemicals with mental disorders.

The second set of factors are Psychological, which are used in ‘cognitive’ and ‘psychodynamic models’ of treatment. In this context, cultural (values and expectations of specific cultures), social (as with coming from a dysfunctional family) and experiential (interaction with the environment) factors are given attention.

To consider first the idea behind genetic factors, it is found to be the case that parents, siblings and children of depressed patients have a higher risk of suffering from depression themselves – 10-15% higher chance. Egeland et al. (1987) actually proposed that a specific gene could be identified for bipolar depression amongst some Amish families; however a similar study by Hodgkinson (1987) of extended families in Iceland did not find evidence of bipolar disorder in relation to a specific gene. Nevertheless, adoption studies such as that by Gelder et al. (1999) and Twin studies (for example McGuffin et al. 1996) confirm that genetic factors are indeed a significant factor. Monozygotic twins (identical) are consistently seen to have higher incidence of unipolar and bipolar disorder than dizygotic twins but in both cases, incidents of depression are higher in twins than in the general population.

In attempting to evaluate the genetic factor explanation for depression, it must be acknowledged that while twin studies do indeed show higher rates of depression, suggesting that genetic influences are indeed significant, this is more certain for bipolar disorder rather than unipolar disorder. Also, another potential problem with this biological explanation is that it does not take into account environmental influences such as stressful family environments, when considering the causes of depression.

The second biological explanation, biochemical factors as a cause for depression, has seen researchers focus on levels of neurotransmitters (noradrenaline, dopamine and serotonin) in the body and their subsequent effect on mood. This is the monoamine hypothesis (MAOH). Teuten, Rosen and Hirschfeld (1981) were able to show that depressed patients had lower levels of neurotransmitters in their urine than non-depressed patients. So, biochemistry does indeed seem to be a relevant factor. The problem, however is that another study, (Thase et al., 2002) whilst identifying neurotransmitters as a definite ‘marker’ in differentiating depressed patients from non-depressed patients, found the opposite – that there were increased levels of neurotransmitters, not reduced levels in depressed patients. Another problem with how to interpret and respond to this evidence is the fact of whether the different levels of neurotransmitters in an individual are the cause or the consequence of depression.

Anti-depressants have long been prescribed for the treatment of depression but these again throw into some doubt the biochemical explanation for depression. There is some evidence to suggest that anti-depressants can work immediately on some patients, whilst on others it can take a much longer time. Also, experiments such as depletion studies which manipulate levels of neurotransmitters in the body have not been seen to bring about depression (Claridge and Davis, 2003)

An associated biochemical explanation for depression is the focus on hormones and the endocrine system in the body, particularly in women. Premenstrual syndrome and Postpartum depression after childbirth when hormone imbalances are common, are clearly identified conditions associated with depression and are offered as one reason why women suffer higher levels of depression than men. However, quite often women who suffer from Postpartum depression have previously suffered from depression which suggests psychological factors may also contribute, making the biochemical explanation for depression not comprehensive or adequate in itself.

Amongst the psychological explanations for depression, ‘attributional theory’ attempts to offer a cognitive explanation (Abraham, Seligman and Teasdale 1978) by focusing on the thoughts of people suffering from depression. When things go wrong, they attribute this either to an internal cause (themselves) or an external cause (other people, events, circumstances). The evidence was sought during an experiment involving college students who were given an Attributional Style Questionnaire (Seligman et al., 1979) and indeed, mildly depressed students more often attributed their failures to faults within themselves which they felt cannot be changed (hopelessness/ helplessness.) This suggests a predisposition towards depression. However, the students selected for these experiments were chosen using Beck’s Inventory of Depression (BDI) and this can only measure severity amongst those already diagnosed. Also, testing the students a few weeks later threw up quite different results. Research by Lewinsohn et al. (1981) looked into negative attitudes and thoughts in participants before any of them became depressed and found that “people who are vulnerable to depression are not characterised by stable patterns of negative cognitions. Negative thoughts can make people vulnerable to depression but most of the evidence suggests that negative thoughts and actions are caused by depression.

Another psychological explanation for depression is the behavioural theory which suggests that depression comes from reduced levels of reinforcement of reward (Lewinsohn 1974). This is linked to the psychodynamic view that depression can result from the loss of an important relationship, or, for example, losing one’s job – the relationship or working context being an important source of positive reinforcement for the individual. The problem with this explanation is that it is too simplistic. Dawson and Neale (1990) showed that there was no clear evidence to suggest that a depressed person who has suffered a loss feels somehow that they have been rejected or deserted. Also, not everyone who has suffered a loss becomes depressed. Finally, if a depressed person suffers more negative experiences, it is difficult to prove that this has caused the depression.

One other psychological explanation for depression considers social factors which impact on an individual. These can best be understood as ‘life events’ – death of a spouse, divorce or separation, children leaving home, sexual problems. Each of these can cause high levels of stress. Brown and Harris (1978) and subsequently reviewed by Brown (1989) showed that on average, 55% of patients had at least one severe life event in the months leading up to their diagnosis of depression. However, there were sufficient numbers involved in the research who did not suffer so once again, this kind of psychological explanation is limited. Also, in some cases the impact of major and stressful life events can be reduced if the person encounters other, positive social factors such as support from friends and family. Finally, the impact of life events can be very different on different people, depending on their personal and social circumstances.

To summarise then, it seems as if each of the various explanations for depression whilst contributing some useful evidence in support of a given theory, cannot be seen to satisfactorily define the whole context for depression. However, it is precisely for this reason that a multi-dimensional approach to identifying and then treating depression is very important.

As with depression, schizophrenia has also been studied in the context of biological and psychological factors which might be seen to cause this mental disorder. Schizophrenia is a very serious as well as very difficult condition to treat. In its simplistic sense, schizophrenics lose contact with reality which seen through distortions in their thoughts, emotions and behaviours.

When Kraepelin originally diagnosed schizophrenia in 1896, as dementia praecox, (‘senility of youth’), he was convinced it was a physical disease and for a long time has been treated along the lines of the ‘medical model’. Several researchers have suggested brain abnormalities are the reason behind this mental disorder – this is the neurodevelopmental hypothesis. Brain lesions in the embryo caused by flu during pregnancy (Wright et al. 1999) or nutritional deficiency during famine in parts of Holland in World War II (Suser et al. 1996) was thought to contribute to the development of schizophrenia in late adolescence or early adulthood. The use of MRI scans to take pictures of the brain also saw specific differences in brain structure in schizophrenics, and interestingly, even twin studies showed how schizophrenia could be predicted in one of the twins by the size of a part of their brain (Suddath et al. 1990). Whilst this seems like a positive finding, it also remains limited as an explanation. This is because the fundamental question of why some people develop schizophrenia and others don’t is not clear. According to Harrison (1995), schizophrenia cannot be diagnosed from merely looking at a brain scan. Chua and McKenna (1995) also found that there was insufficient evidence to show that an abnormality in the structure or the brain characterises schizophrenia. More significantly, many schizophrenic patients do not show any abnormal enlargement in their brain structure (Davison and Neale, 2001). Such an abnormality could make a person vulnerable to schizophrenia, not causing it. More specifically, some brain abnormalities generate some schizophrenic symptoms and no clear, overall conclusion can therefore be drawn.

Biochemical explanations are also offered for the diagnosis of schizophrenia. As with depression, neurotransmitters are seen to give evidence of this mental disorder. However, as with depression, the dopamine hypothesis was challenged by conflicting sets of results. In the 1950s and 1960s, the use of anti-psychotic drugs to treat schizophrenia was widespread and worked by reducing dopamine activity. But this in turn generated the symptoms of Parkinson’s disease. The treatment to manage Parkinson’s disease furthermore, can as a consequence produce symptoms seen in certain types of schizophrenia. The biochemical explanation for schizophrenia is therefore problematic – not all forms of schizophrenia can be related to dopamine production or receptivity. (Jackson 1990). The problem seems to be with the idea that schizophrenia is one condition:

“…if schizophrenia is not a clearly identifiable syndrome but an umbrella term covering a range of symptoms with unclear onset, course, and outcome, then it is obvious that much of the work investigating a specific biological basis will inevitably be inconclusive.” (Lavender 2000)

Moreover, anti-psychotic drugs have been found to be effective in sudden onset of schizophrenia but not so if there is a gradual development of the condition.

The other biological factor, genetics, as a way to explain schizophrenia does indeed conclude that the closer a genetic relationship between an individual and a patient, the greater the risk of being diagnosed (Kendler et al., 1996). However, this too is a limiting perspective as there remains the unquantifiable factor of environmental influences. One of the main problems with this explanation is that already outlined above, that schizophrenia is not one, distinct syndrome but has many different symptoms and different studies in different countries have used different criteria for diagnosing schizophrenia. If schizophrenia was a condition determined entirely by genetics, there would have been absolute consistency and agreement in the results drawn from each study. This is not the case.

Adoption studies and twin studies do over some convergence of evidence for the genetic explanation. The ‘heritability’ of schizophrenia is similar to that of other major medical conditions which are known to have a genetic link, such as diabetes and heart disease. However, the most widely accepted view now is that a number of genes are involved which can make an individual vulnerable to the condition but that environmental factors are responsible for triggering the symptoms – the diathesis-stress model, suggesting ‘predisposition. In this respect the explanation is very similar to that discussed earlier in relation to depression. This is further supported by Zubin and Spring (1977) who believed that environmental stresses such as severe malnourishment or viral infections during pregnancy can raise levels of vulnerability. In conclusion, the genetic explanation, underlined by the diathesis-stress model, is restricted to the assertion that inherited factors can raise the likelihood of developing schizophrenia but do not guarantee that the condition will affect any individual with inherited genes.

The opposite view to that of schizophrenia being caused by a biological set of factors is that which focuses on social factors. The developments in psychiatry during the 1950s and 1960s saw influential exponents such as Laing, Cooper and Esterson challenging the ‘medical model’ with a radical idea: that society was itself the problem affecting an individual’s mental health; that the term and diagnosis of schizophrenia was a “metaphor for dealing with people whose behaviour and experience failed to conform to the dominant model of social reality” (The Psychology of Mind and Behaviour – Richard Gross). Three major books published by Laing, The Divided Self (1959), In Self and Others (1961) and The Politics of Experience (1967) advanced the explanation to propose that schizophrenia is “itself a natural way of healing our own appalling state of alienation called normality”, that it is a journey to an “inner space”, a “natural healing process” (Laing, quoted by Gross). Whilst these ideas will have influence in approaches to treating the condition, within the psychological explanations for schizophrenia, they sit alongside theories which suggest that families which have schizophrenic members are themselves often affected by abnormal or inadequate interpersonal communication – a wider social explanation. The research shows that poor communication can both generate symptoms of schizophrenia but can also be a consequence of the presence of schizophrenics in the family (Mischler and Waxler, 1968). Another social explanation is the ‘expressed emotion’ theory – families where criticism, hostility as well as over-protectiveness are at high levels can raise the symptoms of a schizophrenic patient (Kavanagh 1992). Much research finds that members of lower social classes are more likely to suffer from schizophrenia than those from middle- or upper-classes. However, as with depression, the social explanation remains challenged by the issue of whether belonging to a lower social class triggers schizophrenia or schizophrenia results in a lowering of social status. The same can be said for stress as a contributory factor.

Another and increasingly prevalent mental disorder is seen in the whole spectrum of eating disorders. The three main types of eating disorder are anorexia nervosa, bulimia nervosa and obesity. Each of these are characterised by physically or psychologically harmful eating patterns. Of these, obesity is not yet identified by the DSM but is increasingly presented as an eating disorder. The statistics are quite alarming. There are 3.5 million anorexics and bulimics in the U.K. An article in Cosmopolitan Magazine (1989) proposed that “at least 50% of British women have a distressed relationship with food.” 90% of suffers are female and 105 are male. The incidents of eating disorder suffers is increasing in those who are very young, children aged between 6 and 12 years are becoming very concerned about their body image. The extensive research into the explanations for eating disorders generally settles upon the idea that these form part of a western, ‘culture-bound’ syndrome. DiNicola (1990) suggests that the focus must be on social and cultural factors rather than on the individual. Nevertheless, as with Depression and schizophrenia above, eating disorders cannot be explained by one set of factors, that is culture is one of many factors”

“…cultural factors can only be understood as they interact with the psychology and biology of the vulnerable individual … a culture cannot cause a disorder.” (Fedoroff and McFarlane, 1998)

What is generally agreed upon is that eating disorders are definitely linked to the widely-held perception that being thin equates to being attractive. The media has been blamed for much of this presentation. The relation to ‘western’ society and its values is supported by research into other cultures. For example, in Pakistan, English-speaking girls from upper social classes which adopt western lifestyles how similar rates of some eating disorders to white schoolgirls in Britain (The Psychology of Mind and Behaviour – Richard Gross).

One of the most convincing explanations for eating disorders centres upon the developing role and identity of women:

“…because eating disorders affect mainly females and revolve around issues of identity and body image, it is not surprising that observers have linked the rise of eating disorders in the West with the crises of female identity and the forces impinging on women that followed the cultural upheavals of the 1960s…” (Gordon, 2001).

These forces are not anymore confined to the West, as increasingly, the role and identity of women in non-western cultures become affected by the global trends of economic growth, prosperity, and the far-reaching effects of the mass-media. The fashion industry is one such global influence.

Although there seems to be an overwhelming body of evidence to support the sociocultural hypothesis to explain eating disorders, it remains the case that as with depression and schizophrenia, other individual factors in the patients physical and emotional make-up need to be taken into account. These could include pre-existing anxiety, depression, low self-esteem, obsessionality. The biochemical markers tend to be used to identify symptoms of eating disorders, as the body changes in its chemical balances to reflect the physical effects of eating disorders. These will inevitably influence approaches to treatment.

Amongst the best known approaches to treating mental disorders are the Psychodynamic, Behavioural and Cognitive models. All three of these approaches are based on the conclusion that thinking, behaviour and physiological processes are all highly interdependent and to treat mental disorders, producing changes in thinking and behaviour can directly impact on the patient’s condition. These therapies take a very different approach to biological therapies, which relate to the biological, medical model and mostly involve being treated with drugs, surgery or electroconvulsive therapy.

The Psychodynamic approach has as its most famous exponent, Sigmund Freud who argued that in order to treat patients with mental disorders such as depression, the Psychoanalyst needed to uncover ‘layers of conscious and subconscious memories which include repressed ideas and conflicts, like an archaeologist. This is the approach of ‘talking cures’.

The material during therapy is drawn on childhood experiences and unresolved conflict. The skill of the therapist is to encourage the expression of these deeper feelings and, without passing judgement to help the patient to interpret what they reveal and to gain a better understanding of it. The patient can also transfer these feelings on to the therapist and this cathartic or cleansing process bring a form of release. The process is known as ‘abreaction’.

This therapy has mainly been criticised for being difficult to prove scientifically. Also in terms of effectiveness, it is difficult to judge because it is very time-consuming and therefore can also be very costly. A significant ethical implication of this therapy is that two different therapists may bring two very contrasting sets of interpretation and response to the patient’s revelations which could mean that the therapy could go in quite different directions depending on the knowledge interests and experiences of individual therapists. The psychodynamic therapy with which Freud was most famous for was dream analysis. Freud believed that dreams were ‘the royal road to the unconscious’ (1902). What he was alluding to here was the fundamental belief he had about the importance of the unconscious and sub-conscious within which a patient’s repressed feelings and desires were held. He believed that the dreams contained images and symbols which needed to be interpreted by the skills of the analyst. Once again, dream analysis aims to give the patient an insight into their own feelings and to help them resolve any conflicts which exacerbate their mental disorder. As with the talking cures, this therapy is clearly dependent on the skills of the analyst and once again, is difficult to prove scientifically.

The final psychodynamic therapy promoted by Freud focuses on personality. He puts a great deal of emphasis on psycho-sexual development and believes that the stages of development from childhood to adulthood can significantly impact on an individual’s personality. Any trauma experienced at any of these stages and particularly in childhood can lead to serious mental disorder. For example, a child who has been sexually abused will present complex and unhealthy responses when dealing with others, often leading to anxiety and depression.

Of each of these psychodynamic therapies, this last one which exposes problems experienced in childhood is perhaps the most empirical of the three in that cause relates to effect and can be measured. The difficulty of this approach nevertheless remains that it is entirely dependent on the patient-therapist relationship. In fact one of the dangers is that the patient gives responses that he or she constructs for the purposes of the session and because of an expectation that they must reveal something to their therapist. Another problem with this approach is that it focuses far too much on the past rather than dealing with the immediate and current difficulties that the patient has.

Behaviourist therapies drawn their approaches and practices from the fundamental assumption that we are conditioned by the world we live in and the environment to which we are exposed. Watson and Raynor (1920) took forwards Pavlov’s research in showing how, for example, fear can become a conditioned response if associated with a specific stimulus. This way of controlling responses can clearly be an advantage when dealing with mental disorders. The idea is that negative experiences can be disassociated from the original stimuli and so abnormal behaviour can be ‘unlearned’, managed and therefore controlled.

The process itself is known as Systemic Desensitisation. It has its basis on solid theoretical grounds. Wolpe (1958) invented this form of treatment and had a good deal of success with phobias and anxieties. Wilson and Davis (1971) developed the approach further to one of ‘extinction’ where deep relaxation was found to help patients very effectively in dealing with fear and anxiety. Systemic Desensitisation was proven to be more effective in treating mental disorders as it was possible to compare the effects on patients who had been offered this therapy as opposed to patient who had not (Choy et al 2007).

One of the problems with exposing patients to the source of their fears and anxieties is however that prolonged exposure can actually raise levels of anxiety initially to such an extent that they drop out of therapy rather than progress on to the other side. Another problem with this therapy is that it depends entirely on the successful identification of the specific source of the problem. Therefore more generalised anxiety disorders cannot be treated successfully with this approach. Moreover phobias are relatively insignificant when compared with the devastating effects of schizophrenia, depression or eating disorders, on patients’ everyday lives.

Cognitive Behavioural Therapy (CBT) is the more recent and more widely used approach to treatment. It developed out of the behaviourist approach which focuses on the here and now, as well as the psychodynamic approach, which focuses on past experiences. Cognitive psychology has been influenced by developments in computer technologies in that comparisons are made between how a computer processes information and how the human brain processes information. A strength of the approach is that it can be directed at a specific problem rather than a general problem. It works on the basis that disordered thinking leads directly to disordered behaviour, as an automatic consequence of the former, without the patient being fully aware that this is happening. For this reason, cognitive therapies can be very successful when treating depression. The theory is that negative behaviours can be unlearned, and that the patient’s thought processes can be observed, reflected upon, and brought into control. A strength of this approach is that the patient can be shown how to take control of their condition and deal with it in the present without being over-concerned with the past. The biggest issue with drawing on the past, is that it may well be misremembered. Nevertheless a patient’s past medical history including any biological explanations for their condition, are taken seriously. The role of the therapist is to help a patient clarify, and then change, the way they see themselves and the world around them. Both the cognitive process and the behaviour need to change in order to be successful. Butler at al (2006) undertook a major study on the therapeutic value of cognitive therapy, involving almost 10,000 patients. This therapy was found to be most successful when dealing with depression, general anxieties, post-traumatic stress and phobias. It was also found to be useful in the treatment of schizophrenia and produced longer-lasting positive effects that drug treatments.

The problem with CBT is that it does not give much status to other recognised and successful therapies such as those which reflect physiological or biological processes. Perhaps too little emphasis is placed on traumatic childhood experiences, as the focus remains on current and apparent symptoms. The therapy itself combines both cognitive and behavioural approaches, and so it is difficult to know which elements of each approach are more or less successful in contributing to a patient’s recovery. Not being able to measure this can mean that the programme of treatment may be less certain in its stages.

In conclusion there has been extensive research into causes of and treatments for mental disorders. The fact that the research is so extensive allows therapists to approach treatment strategies with more confidence, but it would seem that the most successful approaches to dealing with mental disorders, are those which integrate biological and psychological processes. The patient who is both involved in his or her own treatment as well as receiving treatment from a specialist in this more ‘holistic’ model has a higher chance of recovering good health.

Bibliogaphy

Northampton College Intranet resources

The Psychology of Mind and Behaviour (5th Edition 2005) – Richard Gross

AS Psychology (4th Edition 2008) – Michael W. Eysenck

A2 Psychology: Key Topics (2006) – Michael W. Eysenck

Wikipedia

www.ngfl-cymru.org.uk/vtc/ngfl/psychology


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