Discuss issues of reliability and validity associa
There are issues surrounding the diagnosis of depression such as reliability and validity of methods used. Professionals use the DSM-IV (published in 1994) and in some cases the ICD as a manual to aid the diagnosis and classification of patients with depression. However there are risks of using such manuals as the professional runs the risk of using jargon from the manual that ordinary people may not fully understand.
Reliability is a measure of consistency within a set of scores or items and also over time so that it is possible to obtain the same results on subsequent occasions when the measure is used. Reliability contains sub-sections such as inter rater reliability and test-retest reliability.
Low levels of inter rater reliability related to any classification procedure suggests that it might lead to faulty diagnosis and inappropriate treatment. Lobbestael et al assessed the inter rater reliability of the Structured Clinical Interview for the assessment of major depressive disorder, in a mixed sample of patients and non-patient controls, with the results revealing moderate agreement with an inter-rater reliability. In addition Keller et al looked at reliability using the DSM and found that the inter rater reliability was “fair-good- and that the test-retest was only “fair”.
Keller et al suggested a number of possible reasons why the DSM diagnosis of depression might lack reliability. One of these is, in order to be classified as depressed a minimum of 5 out of 9 symptoms must be present, therefore if a patient is just at the diagnostic threshold a one item disagreement may result in wrong diagnosis. The consequences of this involves the chance of misdiagnosis which could lead to the wrong treatment or infact the patients depression progressing.
Field trials of the latest version of DSM have emphasised the importance of test-retest reliability and have this as a major goal of the new system. Current measurement scales such as the Best Depression Inventory (BDI) have been assessed for their test-retest reliability.
However there may be ways of simplifying the diagnosis process. Zimmerman et al claims that the DSM IV criteria for major depressive disorder are unnecessarily lengthy and that treatment doctors frequently have difficulty recalling all 9 symptoms that the patient has, therefore this could lead to misdiagnosis so by reducing the criteria for major depression may simplify diagnosis and make it more reliable.
The BDI is a 21-item self-report questionnaire designed to measure the severity of symptoms in individuals diagnosed with depression. It is thus able to distinguish between different types of depression, such as major depressive disorder and dysthymia. Beck et al (1996) went on to study the response of 26 outpatient tested at two therapy sessions one week apart, using the BDI. There was a correlation of .93 indicating a significant level of test-retest reliability. The consequences of this is that a food level of test-retest shows that the BDI is a reliable source to use in the diagnosis and classification of depression.
Validity refers to the legitimacy of a study and the extent to which the findings can be applied beyond the research setting as a consequence of the study’s internal and/or external validity. Validity is split into sub-sections including comorbidity, content validity and concurrent validity.
Comorbidity is an important issue for the validity of diagnosis of mental illness such as depression as it refers to the extent that two or more conditions co-occur. For example, research has shown that the presence of an anxiety disorder is the single biggest clinical risk for the development of depression. The experience of anxiety serves as a compounding stressor that leads (especially in patients with a genetic vulnerability) to major depression.
Content validity refers to whether the items in a test are representative of that which is being measured. The BDI is considered to be high in content validity because it was constructed as a result of a consequence among mental health clinicians concerning symptoms found among psychiatric patients.
Concurrent validity is a measure of the extent to which a test concurs with already existing standard ways of assessing the characteristics in question. Research by Beck et al has consistently in concurrent validity between the BDI and other measures of depression, such as the Hamilton Depression Scale.
There may be problems in the way in which GP’s diagnose patients as typically the diagnosis of depression is given by the local GP, however one study shows that diagnosis of depression made by GP’s are made against a background of previous patient knowledge and therefore could be biased. This has serious effect on the validity of the diagnosis of depression and a consequence of this is the incorrect treatment being administered to the patient.
In addition there may not be distinct types of depression as the diagnosis requires clinicians to differentiate among several distinct subtypes of the disorder; however one researcher, after comparing over 600 outpatients all with different types of depression found few differences on a range of clinical, psychosocial and treatment response variables. This suggests that distinctions between the different subtypes of depression may not be valid enough to diagnose people successfully and therefore consequently, a patient is not actually treated for depression.
There may be cultural differences in the diagnosis of depression as in the Western world typically, depression is seen as a disease that you need to seek professional help for in order to overcome it; however within some ethnic minorities depressive symptoms are viewed as social problems or emotional reactions to situations. This therefore suggests that people’s views on depression throughout the world varies and therefore what somebody may class as depression others may not, leading to problems with classification and diagnosis of depression, the consequence of which is people in non-Western cultures will not get treatment which will only make the problem worse.
Consequences - people in non-western will not get treatment and make problem worse.
Discuss two or more biological explanations of dep
Depression is one of the most common mental illnesses in the world with approximately 1 in 10 people in the UK suffering from it. Hammen suggests that there are 4 aspects of depression that suggest a biological link. These are: physical changes, family history and the use of drugs to treat it.
One biological explanation of depression is genetic factors. There have been family studies that suggest having a first-degree family member with depression is a risk factor. Researchers select families with a member suffering from depression and examine whether other members have been, or could be diagnosed with depression. If a genetic link is present, first-degree relatives of the participant will show higher rates of depression compared to the rest of the population. Harrington et al found that 20% of such relatives have depression compared to 10% of the public at large.
In addition twin studies are used to investigate the biological explanation of depression. Such studies are based on monozygotic twins sharing all of the same genes and dizygotic twin sharing half their genes. If it assumed that the environment shared by both are the same, therefore, any greater similarities in monozygotic pairs in comparison to dizygotic pairs show the action of genes. McGuffin et al found that the concordance rate for first-degree relatives was 46% for monozygotic and 20% for dizygotic twins, suggesting that depression has a substantial hereditary component. However the concordance rate is not 100% as would be expected of twins, therefore depression cannot solely be due to biology.
Adoption studies are also used in the investigation of biological factors and depression. Wender et al found that adopted children who developed depression were more likely to have a biological parent with depression, even though adopted children are raised in different environments, implying that biological factors are more important than the environment in which they are brought up.
The relatively low concordance rate of genetic factors may be due to comorbidity, this is when two or more mental illnesses occur together and perhaps have a common cause. This suggests that some disorders, such as depression, are a product of genes that underlie a number of different disorders with the actual symptoms and disorder that develope could be related to environmental triggers and (the diathesis-stress model).
A second biological explanation of depression is neurotransmitter dysfunction. It seems that depression comes from a deficiency of the neurotransmitter noradrenaline. Post mortem studies have revealed that the densities of noradrenaline receptors in depressed suicide victims increase in an attempt to pick up whatever signals are available, this is known as up-regulation.
There is a link between noradrenaline and depression as supported by Kraft et al who studied people with major depression who were treated with serotonin-noradrenaline reuptake inhibitor (SNRI). This showed a positive response, strengthening the link between low levels of neurotransmitters and depressive symptoms.
There is also a link between depression and serotonin levels, which is cerebral fluid in depressed patients. The introduction of SSRIs confirmed the association between low serotonin and depression.
However, the link between depression and serotonin is not straightforward as some studies use patients whose depression is, at the time, in remission. The patients are given an amino acid mixture that will decrease serotonin levels in the brain temporarily, experiencing a brief relapse of serotonin levels results in depression. However, individuals who had never been depressed nor had a family history of depression tended to not show any mood changes, therefore suggesting that low serotonin levels may not be a direct link to depression.
There is in addition support for the evolutionary theory to suggest that depression has a genetic bias. The fact that depression is so widespread among humans suggests that it may have some evolutionary significance and therefore may not be purely down to biological factors.
The diathesis stress model, as part of the genetic explanation of depression suggests that there is a link between genetic predisposition and an environmental stressor acting as a trigger. A diathesis-stress explanation may be better used to explain depression as although there this a biological explanation there needs to be environmental triggers to set the depression off.
Discuss two or more psychological explanations for
One psychological explanation of depression is the Psychodynamic explanation by Freud who says the explanation lies in the early relationship between parents. He noticed a similarity between depression and grief as depression is “excessive or irrational grief” as a reaction to loss. This loss can be either real or imagined loss of affection from the parent the person is most dependant upon. I is suggested that future, actual losses lead to the re-experiencing of parts of our childhood, meaning that we become dependant and clingy. Freud said that the greater the experience of loss the greater amount of regression as an adult, unresolved feelings of hostility towards parents can be directed inwards as guilt. With guilt leading to feelings of unworthiness or suicide.
There is research support for the role of early loss in later depression, as Barnes and Prosen found that men who had lost their fathers through death during childhood scored higher on a depression scale that those whose fathers had not died. Therefore suggesting that the psychodynamic approach is accurate and early loss does affect the likelihood of developing depression.
There are limitations to the psychodynamic approach as loss probably only explains a relatively small percentage of cases of depression, it is estimated that only 10% of those who experience early loss later become depressed. Which is therefore contrasting the psychodynamic approach.
Furthermore, another issue with the psychodynamic approach is that it is unfalsifiable. The problem with the psychodynamic approach is it cannot be proven correct or disproved as the basis of the approach is based within the unconscious, this theory therefore could be lacking in validity but it cannot be disproved.
Another psychological explanation of depression is the Cognitive explanation. Beck’s theory of depression says that people suffer from depression due to their negative views of the world that they have learnt through childhood. The causes of which may be parental or peer rejection, or criticisms by teacher for example. These negative views of the world (e.g. expecting to fail) are activated whenever they encounter a new situation, such as sitting an exam. This maintains the Cognitive Triad of depression (negative views of self lead to those of the world and then those of the future).
Another part of the Cognitive explanation is learned helplessness as suggested by Seligman. This occurs when a person tries, but fails to control unpleasant experiences, causing them to acquire a sense of being unable to control events in their life. So, even if an event can be controlled in the future they make no attempt to do so. This is a characteristic of depression, Seligman found that depressed people looked at unpleasant events in a more pessimistic manner than others. He went on to conclude that a depressed person will see events as due to internal, global and stable causes, which is known as the attributional style.
There has been studies into humans that suggest the accuracy of learned helplessness as although initial research was conducted on animals one experiment by Hiroto and Seligman on college students showed that when exposed to uncontrollable, aversive events they were more likely to fail on cognitive tests. This study shows that not having control may lead to helplessness thinking and therefore supporting the learning helplessness - depression model
Discuss two or more biological therapies for depre
One therapy for the treatment of depression is antidepressants which are drugs that relieve the symptoms of depression. There are many different types of antidepressants including tricyclics, SSRI’s and MAOIs which are used to treat moderate to severe depressive illness.
Tricyclics block the transporter mechanism that reabsorbs serotonin and noradrenaline into the presynaptic cell after it has fired, meaning that more of the neurotransmitters are left in the synapse, prolonging the activity making the transmission of the next impulse easier.
SSRIs block serotonin, increasing the quantity available to excite neighbouring brain cells which reduces the symptoms of depression.
MAOIs stop serotonin, noradrenaline and dopamine being broken down so levels of these neurotransmitters increase. An altered balance of serotonin and other neurotransmitters is thought to play a part in causing depression. This can take up to 3 weeks to build up and work effectively and are normally prescribed when other forms of antidepressants have n=been unsuccessful in treating the effects of depression. They can be used to treat patients with moderate to severe depression; however, they do not work for everyone.
A strength of antidepressant treatments is that they are easy to use compared to other treatments, antidepressant drugs are the best choice for most people suffering from depression as they don’t have to dedicate time to treatment, they simply have to take a tablet every day. Therefore for people who lead busy lives, it is the easiest option for treatment available to them.
The use of antidepressants for treating depression in children and adolescents may not work as well as they do for adults. Hamen conducted double blind studies that consistently failed to demonstrate the superiority of antidepressant medications over placebo conditions within younger people but Ryan suggested that this could be to do with developmental differences in the brain neurochemistry. This suggests that antidepressant treatments may not be effective for all ages.
There are methodological issues when it comes to research into antidepressants and their effectiveness. Depressed people chosen for clinical trials are normally only moderately depressed, not suicidal and free form other disorders making accurate evaluations of antidepressants difficult. This means that some of the research conducted into the validity of antidepressants as a treatment as a treatment for depression cannot be generalised amongst all depressives.
Another therapy for the treatment of depression is Electroconvulsive Therapy (ECT) which is usually used in severely depressed patients when psychotherapy and medication have been ineffective. It is used when there is a risk of suicide as it has much quicker results than antidepressant drugs. It has been suggested that it should only be used in cases where all other treatments have failed or when the condition is considered potentially lie threatening. An electrode is placed above the temple of the non dominant side of the brain and a second in the middle of the forehead (unilateral), or one electrode above each temple (bilateral). A short acting general anesthetic is injected and a nerve blocking agent is given which paralyzes the muscles to prevent contraction during treatment causing fractures. Oxygen is given to compensate for their inability to breath. A small amount of electric current is passed through the brain for about half a second producing a seizure lasting up to a minuet affecting the whole brain. This treatment is usually given 3 times a week with a patient requiring between 3 and 15 treatments. It is the seizure rather than the electrical stimulus that generate improvement in depressive symptoms as it restores the brains ability to regulate mood by enhancing the transmission of neurochemicals or improving blood flow in the brain.
There is research support for the effectiveness of ECT as Gregory compared ECT with sham ECT finding a significant difference in the outcome with real ECT being more effective. This suggests that it is the electric current and the following seizure that help treat depression.
In addition the effectiveness of ECT has been compared with drug therapy. Scott reviewed 18 studies with 1144 patients finding that ECT was more effective than drug therapy in the short term treatment of depression however, none of these trials compared ECT with newer antidepressant medications such as SSRIs.
There are ethical issues in biological therapies. The Department of Health report found that out of 700 patients who received ECT when sectioned under the mental health act, 59% had not consented to treatment, this means that there was a lack of informed consent and not all patients who volunteered were not fully informed about the possible side effects
Discuss two psychological therapies for depression
Cognitive Behavioural Therapy (CBT) emphasises the role of maladaptive thoughts and beliefs in the origins and maintenance of depression. The aim is to identify and alter these maladaptive cognitions as well as any dysfunctional thoughts that might be contributing to depression. It is intended to be relatively brief and is focused on current problems and dysfunctional thinking. The 2 main types of CBT are thought catching and behavioral activation.
Thought catching is where individuals are taught how to see the link between their thought and the way they feel. They may be asked to record any emotion arousing events, automatic negative thoughts associated with these events and their realistic thoughts that might challenge these negative ones. During their treatment, they are taught to challenge this association by asking themself questions that help to replace the dysfunctional thoughts with more constructive ones.
Behavioral activation is based on the common sense ideal that being active leads to rewards that act as an antidote to depression. Therapist and client identify potentially pleasurable activities and anticipate and deal with any cognitive obstacles.
There is research support for the effectiveness of CBT. Robinson et al conducted a meta analysis that found that CBT was superior than non treatment control groups however, when these control groups was subdivided into non treatment and the placebo groups, CBT wasn’t significantly more effective than the placebo condition at reducing depressive symptoms.
Therapist competence has been found to explain a significant amount of variation in the outcomes of CBT. Kuygen and Tsivrikos support this claim as the concluded that as much as 15% of the variants in outcome was due to therapist competence. The implications of this are that the success of CBT relies partly on therapist skill and therefore, if a good relationship is not present the likelihood of success decreases.
Due to the fear that some antidepressant drugs might increase the risk of suicide, researchers are considering the possibility that combining antidepressants with CBT might reduce the risk. The treatments for adolescents with depression study enrolled 327 adolescents aged between 12 and 17 diagnosed with major depression. They were randomly assigned to an SSRI alone, CBT alone or a combination. After 12 weeks 62% had responded positively to the drug treatment alone, 48% to CBT and 73% for the combination, all of which increased after 36 weeks. However, further analysis found that CBT significantly reduced suicidal thoughts and behaviour as at the end of the study only 15% of those on drug treatments expressed suicidal thoughts compared to 6% for those who had CBT.
Another psychological therapy for the treatment of depression is Psychodynamic Interpersonal Therapy (PIT) which emphasizes the conversation between the therapist and a client about their problems that are not only talked about as past events but actively re-lived and resolved in the present. It way believed that symptoms of depression occur due to disturbances and interpersonal relationships which can only be explored and modified effectively through a therapeutic relationship, meaning that the quality of relationship is crucial.
There are 7 components: 1) exploratory rational, 2) shared understanding, 3) staying with feelings, 4) focus on difficult feelings, 5) gaining insight, 6) sequencing of interventions and 7) change.
There is research support for PIT. Paley et al showed that outcomes for PIT are equal to those achieved by CBT. However, changes in life events were not monitored during the study therefore any observed clinical progression (or lack of) cannot be attributed solely to therapeutic intervention.
PIT emphasisies importance of interpersonal relationships in the treatment of depression. Guthrie argues that explanations concentrate solely on cognitive processes in the development of depression, neglect the important role of interpersonal relationships making PIT important in the treatment of cases of depression that result from dysfunctional relationships. As a result research consistently shows that the quality of the relationship between therapist and client determines the outcome of the therapy.
The effectiveness of PIT has been demonstrated through the collaborative psychotherapy project. Barkham et al found that PIT and CBT were equally effective in reducing severity of depression which supports findings from Paley et al. However, after 12 months those treated with PIT or CBT showed tendencies for the reoccurrence of symptoms limiting long term effectiveness.