Psycophathology Flashcards
What is statistical infrequency? (AO1)
Behaviours that are seen as statistically rare are considered abnormal. It looks at the prevalence of different things, such as mental disorders, and then identifies anything that does not fall into the areas of statistical normality, as a statistical infrequency.
What is an example of statistical infrequency?
For example, someone with a low IQ, like 70, would be considered abnormal by this definition as the average is 85-115. Only 2% are below 70. This would make them liable for a diagnosis of a psychological disorder i.e intellectual disability disorder
What is a strength of statistical infrequency? (AO3)?
This is a measurable way to identify abnormality, as can quantify mental health within a population. This can help inform governments to allocate appropriate funding to provide assessment + support to those who are suffering with mental health issues, therefore beneficial for the economy.
What is a limitation of statistical infrequency? (A03)
Identification of statistical infrequent behaviours can lead to labelling, which can lead to stigma/ negative association with diagnosed label.
Fails to acknowledge the desirability of the particular behaviour. Abnormally low IQ would be seen as undesirable, whereas we wouldn’t say the same of unusually high intelligence, although both are as infrequent. This shows that being unusual at one end of a psychological spectrum doesn’t necessarily make someone abnormal. This means that, although statistical infrequency can form part of an assessment + diagnostic procedures, it isn’t sufficient as the sole basis for defining abnormalities.
What is deviation from social norms? (A01)
Society sets norms or unwritten rules for acceptable behaviour (wearing clothes, going to work etc.). These norms are learnt via socialisation, interaction with others and are dependent on social group + cultural norms/values. If behaviour deviates from this, it is considered abnormal. Abnormality is therefore behaviour that violates social norms. This takes into account the desirability of behaviour, for both society and the individual.
Evaluate Deviation from social norms (AO3)
Social norms vary within + across cultures, therefore we must look at behaviours in social context. In the west, social norms adopted often reflect the behaviour of the majority ‘white@ population. Suggested that deviation from these norms by ethnic groups means that ethnic minorities are more likely to be over represented in the mental illness statistic. For example, overdiagnosis of schizophrenia, as in some cultures the experience of hearing voices is the norm (as a message from ancestors). This means there is an ethnocentric bias in diagnosis, and that it is difficult to judge deviation from social norms across cultures.
What is failure to function adequately? (AO1)
Occurs when someone is unable to cope with ordinary demands of day to day living
What did Rosenhan + Seligman suggest?
Suggested the concept of dysfunction includes:
Personal distress, maladaptive behaviour, irrationality, unpredictable, observer discomfort, violation of ideal moral standards
The more of these indicators that are present, the more abnormal an individual is considered to be
Evaluate failure to function adequately (AO3)
Most important criteria
Recognises the impact the disorder has on the individual in acknowledging personal distress.
However PD is subjective, something that causes high personal distress to one person may not be very distressing to another, making it difficult to measure.
Similarly, their are people who experience inappropriate mania (unbounded joy for no reason). Their behaviour doesn’t cause them distress but would be classed as evidence of a psychological disorder. It would also be abnormal to not suffer personal distress at some points in ones life, such as bereavement, which is not considered by tis definition. Overall, failure to functions subjective nature reduces its crediblity.
What is deviation from ideal mental health?
Focuses on what ideal mental health state is + outlines the major criteria for optimal living, promoting psychological health and wellbeing, so can identify who deviates from this ideal
What is Jahoda’s critter?
Suggested that we are in good mental health if we meet the following critter:
Autonomy (independency)
+ve attitude towards self
Resistance to stress
Accurate perception of reality
Environmental mastery
The further people are from these ideals, the more abnormal they are considered to be
Evaluate deviation from ideal mental health (AO3)
Overdemanding criteria, most people don’t meet all these ideals (self actualisation achieved by few) therefore most people could be classified as abnormal. However having such a comprehensive set of criteria for mental health to work towards might be of particular value to someone wanting to understand and improve their mental health
What is a phobia?
An irrational fear of an object or situation. The extent of the fear is out of proportion to any real danger present by the phobic stimulus. The individual doesn’t need to be aware that the threat is disproportional.
What are the categories of phobia recognised by the DSM-5?
Specific phobia-object/situation
Social anxiety phobia- social situations
Agoraphobia-being outside/public space
What are the behavioural characteristics of phobias?
Panic- crying, screaming
Avoidance- prevent coming in contact
Endurance- chooses to remain in presences of phobic stimulus
What are the emotional characteristics of phobias?
Anxiety-an unpleasant state of high arousal
Fear-immediate and extremely unpleasant response (more intense, shorter then anxiety)
Emotional response is unreasonable- anxiety/fear is disproportionate to any threat posed
What are the cognitive characteristics of phobias?
Selective attention to the phobic stimulus
Irrational beliefs- thoughts don’t have any basis in reality
Cognitive distortions-their perceptions are inaccurate/unrealistic
What is the two-process model?
Proposed by Mowrer in 1960 based on the behavioural approach to phobias. This states that phobias are acquired by classical conditioning and then continue because of operant conditioning
Explain acquisition of phobias by classical conditioning
CC involves learning to associate something of which we originally have no fear (neutral stimulus) with something that already triggers a fear response (unconditioned stimulus)
This was illustrated by Watson +Raynor (1920) who created a fear in a 9 month old baby referred to as little albert. For babies, loud noise is an UCS that caused the UR of fear. They repeatedly paired the NS of a white rat with a loud noise, causing little Albert to develop a phobia of white rats (CS).
The process of generalisation then occurs, in which the conditioned response of fear is generalised to other stimuli similar to the CS of rat, so Albert feared other white fluffy things.
How are phobias maintained by operant conditioning?
Responses acquired by CC decline overtime, but phobias are less likely to decline. This is because OC reinforces the fear, so the fear actually increases. It does this through negative reinforcement. Avoiding the phobic stimulus gets rid of the anxiety that we would have experienced had we faced the phobic stimulus. This reduction in fear reinforces the avoidance behaviour and so the phobia is maintained.
What is a strength of the two-process model (AO3)?
There is supporting evidence. In the Little albert study, they were able to show the acquisition of his phobia in a scientific way via an observation in an experimental setting. They were able to isolate the exposure to the stimulus (rat + bar) and measure the learned fear response. Could see the behaviour change overtime, therefore proved the theory to be corrected as little albert developed the phobia after the CC processes. This means that the theory is high in validity as can be observed and measured.
Principles of OC applied to systematic desentatsion
What is a limitation of the two-process model? (AO3)
Not a complete explanation as there are alternative theories. Biological preparedness suggest that there is a biological predisposition for the phobic stimulus that posed a real threat in our evolutionary past, such as the dark, and exposure to the stimulus with fear/observation of a phobic response in someone else. It would therefore be a more holistic view if took into account conditioning triggering biology.
Can’t explain all phobias as doesn’t apply to abstract concepts such as a fear of death. Lots of people have had traumatic driving experiences however a fear of cars would be viewed as abnormal. These individual differences reduces its validity.
Describe systematic desensitisation (AO1)
A behavioural therapy designed to gradually reduce phobic anxiety through the principles of CC. A new response of relaxation is learnt in response to the phobia instead of anxiety-counterconditioning.
1. anxiety heiracy
2. Teaches relaxation techniques-breathing, mental imagery. It is impossible to be afraid and relaxed at the same time (para/sympathetic), know as reciprocal inhibition.
3. Exposure- exposed to the phobic stimulus whilst in a relaxed state. Done across several sessions, starting at the bottom of hierarchy.
Treatment is successful when client can stay relaxed in situations high on the anxiety scale.
Describe flooding as a treatment for phobias
Involves immediate exposure of the phobic stimulus to an individual with the phobia. Typically longer sessions then SD (2-3hours) but only one session may be needed to cure phobia.
Works by stopping phobic responses very quickly as without the option of avoidance behaviour the client quickly learns their is no threat. This process is know as extinction. A learned response is extinguish when the CS (phobia) is encounter without the UCS (pain), so phobia no longer produces conditioned response of fear
Evaluate treatment for phobias (AO3)
Only masks the symptoms and so doesn’t treat the underlaying cause of why the phobia developed in the first place. The only evidence for symptom substitution comes in the form of case study evidence, which may only be generalised to the phobias in the study
Requires high level of motivation, only treat those with depilating fears, not mild.
Can’t treat abstract conceptualised concepts (death), need CBT individual differences
Flooding is highly unpleasant experience as must confront phobic stimulus provoking tremendous anxiety-unethical?
What is depression?
A mental disorder characterised by low mood and energy levels
What type of depression are there?
Major-depressive disorder: serve but short term
Persistent depressive disorder-long term
Premenstrual dysphoric disorder
What are the behavioural characteristics of depression?
Activity levels-reduced energy–>withdraw from work/friends
Disruption to sleep + eating behaviour-reduced sleep/increased need for sleep. Wait gain/loss
Aggression and self harm- irritable
What is psychomotor agitation?
Individuals struggle to relax-pace up/ down room
What are the emotional characteristics of depression?
Lowered mood
Anger- directed at self or others
Lowered self-esteem -extreme self-loathing
What are the cognitive characteristics of depression?
The way depressed people process information
Poor concentration-hard to stick to a task/poor decision making
Absolutist thinking- black and white thinking
Attending to and dwelling on the negative-bias towards recalling unhappy events
Explain the cognitive approach to explaining depression: Beck
American psychiatrists Aaron Beck (1967) took a cognitive approach to explaining why some people are more vulnerable to depression then others. In particular, he believed it is a persons cognitions that create this vulnerability, and there are three parts to this. The first is faulty information processing, in which Beck believed that people who are depressed make fundamental errors in logic. They tend to selectively attend to the negative aspect of a situation and ignore the positive aspect. There is a tendency to blow small problems out of proportion with thinking in terms of black and white + ignoring the middle ground.
Moreover, depressed people have a negative self-schemas, which are packages of info and ideas developed through experience about our self and the world. A depressed person with a negative self-schema may develop the schema from bad experiences + is likely to interpret all information about themselves in a -ve way.
Finally, a person develops a dysfunctional view of themselves due to 3 types of thinking that automatically occur regardless of the reality, know as the negative triad, which is composed of a -ve view of the world, future & self.
Describe Ellis ABC model to explaining depression
Another American psychiatrist Ellis (1962), suggested a different cognitive explanation of depression. He stated that good mental health is the result of rational thinking, whereas depression is the result of irrational thoughts (thoughts that interfere with being happy and free from pain). Those thoughts that are unrealistic, negative or put pressure on us to succeed predispose us to overact when something goes wrong. He proposed the ABC model to explain how irrational thoughts can lead to depression. A stands for activating events, these are circumstances that trigger irrational beliefs. B stands for beliefs. Mustubation- succed or acieve perfection. If these beliefs are subject to cognitive bias then they can cause irrational thinking which may produce undesirable behaviours. C-consequences. When an activating event triggers irrational beliefs there are emotional and behavioural consequences. For example, if a person believes they must always succeed and then fails at something this can trigger depression.
Evaluate the cognitive approach to explaining depression? (AO3)
One limitation of the cognitive explanation is that we can’t establish cause and effect when explaining depression. We can not falsify if faulty cognitions are the direct cause of depression or the symptoms, i.e we can’t be certain that the faulty cognitions are directly causing the cognitive errors or if depression is causing the cognitive errors. This is due to the fact that we cannot expose individuals to faulty cognitions to see if they develop depression in the same way we can with classical conditioning to cause the acquisition of phobias. This reduces the ability to test the theory objectively and thus lowers its validity.
However, Becks cognitive explanation forms the basis of cognitive-behavioural therapy. All cognitive aspects of depression can be challenged in CBT, and it is used effectively to treat depression by changing faulty cognitions. This provides validity for this explanation as if depression can be reduced by changing faulty cognitions it suggests that they are the root cause of the disorder + not merely a symptom. This means the cognitive approach has some evidence and high particular value in treating individuals and therefore aiding the economy.
This explanation is reductionists as there are alternate explanations for depression. The biological approach to understanding mental disorders suggests that genes + neurotransmitters may cause depression. The success of SSRIS in treating depression suggests that neurotransmitters do play an important role; the medication alters the levels of specific neurotransmitters and reduces the symptoms. Prehaps the cognitive explanation is only a proximal explanation used to explain the mental processes of suffers, but the true root cause may be the underpinning biology-the distal explanation. It may be more useful to look at the interaction of both explanations. For example, a more holistic explanation could suggests that overtime faulty cognitions may change the neuronal functioning of the brain and therefore serotonin levels and so an interactional approach is more appropriate. At the very least, a diathesis-stress model may be advisable, suggesting that individuals with a genetic vulnerability for depression are more prone to the effects of living in a negative environment, which then leads to negative irrational thinking. Overall, the cognitive approach to explaining depression is incomplete when looked at in isolation, a more holistic view should look at the role of both biology and cognition and how they interact.
What is CBT?
CBT is a commonly used psychological treatment for depression and involves both cognitive + behavioural elements. It begins with a collaborative assessment, in which patients and therapist identifies the patient problems + identifies where there might be -ve and irrational thoughts that will benefit from being challenged. CBT then aims to replace these thoughts with more effective behaviours. CBT uses both Becks = Ellis theories to understand why people may be depressed.
What is Becks cognitive therapy?
Beck’s cognitive therapy is the application of Beck’s cognitive theory of depression. The idea behind cognitive therapy is for a therapists to help the patient identify the -ve thoughts theu have in relation to themselves, their world and future from the negative tried. Once identified these thoughts are challenged, and this is a central component of the therapy. As well as challenging these thoughts directly, cognitive therapy seeks to help clients test the reality of their negative beliefs by allowing them to take an active role in their treatment though investigative tasks such as being ask to record when people are nice to them. From this the therapists can produce evidence that the patients beliefs are false.
Describe Ellis’s Rational emotive behavioural therapy
Ellis’s rational emotive behavioural therapy extends the ABC model to an ABCDE model to include D for dispute and E for effect. The central technique of REBT is to identify and dispute irrational thoughts. For example, someone might say they have been unlucky and a REBT therapists would identify this as an example of utopianism and challenge this is an irrational belief. This would involve a viragos argument, of which there are two types: empirical + logical. The intended effect of this argument is to change the irrational belief and so break the link between negative life events and depression.
What is behavioural activation?
Therapists also encourage patients to engage in more enjoyable activities. This is called behavioural activation and provides more evidence for the irrational nature of beliefs
Evaluate the cognitive approach to treating depression (AO3)
One limitation of the CBT is that the central compent of the treatment is challenging faulty cognitions, however we can not falsify if faulty cognitions are the direct cause of depression or the symptoms, i.e we can’t be certain that the faulty cognitions are directly causing the cognitive errors or if depression is causing the cognitive errors. This is due to the fact that we cannot expose individuals to faulty cognitions to see if they develop depression in the same way we can with classical conditioning to cause the acquisition of phobias, and thus can’t determine cause and affective. This reduces the ability to test the theory objectively and thus lowers its validity.
This treatment is reductionists as there are alternate treatments for depression. The biological approach to understanding mental disorders suggests that genes + neurotransmitters may cause depression. The success of SSRIS in treating depression suggests that neurotransmitters do play an important role; the medication alters the levels of specific neurotransmitters and reduces the symptoms. Perhaps the cognitive explanation is only a proximal explanation used to explain the mental processes of suffers, but the true root cause may be the underpinning biology-the distal explanation. It may be more effective to treat CBT using an interaction of both CBT and antidepressants, which is supported by March et al. in finding the most improvement in a group that took both (86%) Overall, the cognitive approach to treating depression is incomplete when looked at in isolation, a more holistic view should look at the role of both biology and cognition and how they interact in the body
What is OCD?
A type of anxiety disordered characterised by obsessions +/or compulsions. It is mostly centred around types of behaviour that are brought about by anxiety/fear
obsessive thought—>anxiety—>compulsive behaviour—>temporary belief
What are the behavioural characteristics of OCD?
Compulsions are repetitive
Compulsions reduce anxiety
Avoidance
What are the emotional characteristics of OCD?
Anxiety + distress
Accompanying depression
Guilt/disgust
What are the cognitive characteristics of depression?
Insight into excessive anxiety
Obsessive thoughts
Cognitive coping strategies
Describe the genetic explanation of OCD
one form of the biological explanation to OCD is the genetic explanation, which assumes OCD is heritable. Aubrey Lewis observed that of his patients with OCD, 37% had parents with OCD and 21% had siblings with OCD, suggesting that the condition is generationally transmitted, although what is probably being passed on is the genetic vulnerability, not the certainty of OCD. According to the diathesis-stress model, certain genes leave some people more likely to develop OCD, but it is not certain. Some environmental stress is necessary to trigger the condition. Researches have identified candidate genes as genes that code for vulnerability to OCD. Some of these genes are involved in regulating the development of the serotonin system, for example the gene 5HT1-D beta is implicated in the transmission of serotonin across synapses. However, like many conditions, OCD seems to be polygenic, meaning it isn’t caused by one single gene but by a combination of genetic variations that together significantly increase vulnerability. Steven Taylor (2013) found that at least 230 different genes may be involved with OCD, some of these are associated with the action of dopamine as well as serotonin: both neurotransmitters believed to have a role in regulating mood. Furthermore, one group of genes may cause OCD in one person but a different group of genes may cause the disorder in another. This is know as aetiologically heterogenous. There is also some evidence that different types of OCD may be the result of particular genetic variations, such as hoarding disorder and religious obsession.
Describe the neural explanation of OCD
The genes associated with OCD are likely to affect the levels of key neurotransmitters as well as the structures of the brain, and these are known as neural explanations. Neurotransmitters are responsible for relaying information from one neuron to another, and one example of this is serotonin. If levels of serotonin are low, then normal transmission of info doesn’t take place + mood is affected. Some cases of OCD may be explained by a reduction in function of serotonin. This may be needed to stop the obsessive thoughts from returning after the compulsive behaviour has been displayed, this means the cycle had started again.
Some cases of OCD, especially hoarding, may be associated with poor decision making. This in turn may be associated with abnormal functioning of the lateral parts of the frontal lobe, which is responsible for logical thinking + decision making. There is also evidence suggesting that the left parahippocampal gyrus, associated with processing unpleasant emotions, functions abnormally in OCD suffers.
Evaluate the biological explanation to explaining OCD (A03)
One strength of the genetic explanation for OCD is the strong evidence base. Nestadt et al. (2010) reviewed twin studies and found that 68% of MZ twins both had OCD as oppose to 31% of DZ twins. This provides support that there is a genetic biological predisposition linking to OCD. The disorder can be passed on in the humane genome and the higher % of genes that someone shares with a suffer the more likely they are to develop the disorder. The evidence for this comes from the twin study, as a higher concordance rate was found between MZ twins then DZ twins (68%>31%), OCD must be to do with biology as MZ twins share 50% more of their genes then DZ, therefore a higher concordance rate would be expected if OCD is 100% down to genes, suggesting that genes are at least partially responsible for developing OCD. A concordance rate of 100% however as never been found in any psychological research into mental disorders, suggesting OCD cannot be purely down to genetics, meaning there must be another explanation as to why some twins develop OCD and some do not. There must be a reason why OCD is only seen in one twin 32% of the time, and this can be explained by the diathesis stress model. Perhaps the 68% CCR is due to the same shared experience needed to trigger OCD (such as trauma), and 32% of the twins did not have the same experiences trigger OCD in both twins. However, MZ twins also often share the same environment, both pre + post birth, and are treated more similarly by others. This shared environment may contribute to the increase concordance rate when it comes to DZ, so perhaps OCD is due to the environment and biology. A shared environment may inflate the concordance rate for MZ and therefore it is both nature and nurture that contribute to developing OCD. In reality it is impossible to separate the effects of both biology and the environment and so it is more holistic to consider the effects of both.
This highlights the reductionist nature of the biological approach as it attempts to explains OCD, which is very complex, in relation to cellular functioning- the lowest level of explanation. This is not very helpful as it ignores the experience of the individual and is therefore an incomplete explanation. Although, in being able to isolate low levels of serotonin at the core of OCD, it has led to the development of SSRI’s used to target serotonin levels in the brain specifically. This treatment has been successful and so providences evidence support and thus validity for the genetic explanation. This actively demonstrates the high particular value of the biologically approach in improving sufferers lives and thus aiding the economy.
Describe the biological approach to treating OCD
Drug therapy for mental disorders aims to increase or decrease levels of neurotransmitters in the brain or to increase/decrease their activity. The biological approach suggests that low levels of serotonin are associated with ocd. Therefore drugs to treat OCD work in various ways to increase the level of serotonin in the brain.
The standard medical treatment used to tackle the symptoms of OCD invloves a type of antidepressent called selective serotonin reuptake inhibitor. SSRIs prevent the reuptake from the pre-synaptic neuron by blocking the reuptake transporters from re-absorbing serotonin. This means that serotin remains in the synapse for longer, after it has passed te message onto the post synaptic neuron. This leads to a build up of serotonin in the synapse, which helps regulate mood. The typical dosage of SSRIs is 20mg to be taken daily, although this can be increased if its not benefiting the person. The drug is available as a capsule or liquid. It takes roughly 3-4 months of daily use for symptoms to improve, although this can vary from person to person.
There are several alternative to SSRIs. Tricyclics work by prolonging the action of noradrenaline + serotonin in the brain and block the action of acetylcholine. These tend to have more serious side effects so are usually only given if SSRIs don’t work. SNRIs can also be used, which are similar to SSRIs but act on nornadreline as well as serotonin. They have more selective action then tricyclics, so are sometimes preferred for treating more sever cases.
Evaluate the biological approach to treating OCD (AO3)
Treatment aetiology fallacy-just bc symptoms disappeared doesn’t mean been treated
Drugs have side effects-blurred vision/loss sex drive
Evidence linking the effectiveness of drugs may be subject to a publication bias, as drug companies have a vested interest in showing that they work
Cost effective, little effort
