Psychopathology

Statistical Infrequency : 

Regards behaviours that are very rare as abnormal. Uses descriptive statistics which can be used to represent the typical value in any set - can be used to define what is common and thus what is not common.

Deviation from Social Norms:

Regards deviation from social rules as abnormal behaviours. In societies, there are standards of acceptable behaviour that are set by the social group and adhered to by that group. So, anyone who behaves differently is seen as abnormal.

Failure to Function Adequatley:

Regards not being able to cope with everyday living as abnormal behaviour e.g. eating regularly and going to a job. Not functioning adequately causes distress to the person and sometimes to others.

Deviation from Ideal Mental Health:

The absence of certain criteria which measure mental health indicates abnormality: self-attitudes, personal growth and self-actualisation, autonomy, having an accurate perception of reality and mastery of the environment.

Phobias: 

A group of mental disorders in which the person experiences high levels of anxiety and an irrational fear of a stimulus or a group of stimuli.

Depression:

A mood disorder in which the person feels sad and can lose interest in normal activities.

OCD: 

An anxiety disorder in which obsessions and compulsions cause anxiety. The individual believes that the compulsions will reduce the anxiety.

Emotional :

Marked and persistent fear which is likely to be excessive and unreasonable. Feelings of anxiety and panic as well. Emotions are cued by the presence or anticipation of a stimulus.

Behavioural:

Avoidance - when a person has a phobia and is faced with that stimulus, they try to avoid it. This interferes with the person’s normal routine and life. There is also the opposite response to freeze or faint.

Cognitive:

Irrational thinking and resistance to rational arguments. The person recognises their fear is excessive or unreasonable.

Emotional:

Sadness is very common, along with feeling empty - they may feel worthless and have a low self-esteem. There are feelings like despair and a lack of control which are linked to a lack of interest in usual activities. Also, there are feelings of anger.

Behavioural:

Shift in activity level - reduced or increased. They may want to sleep all the time but some become increasingly agitated and restless. Some sleep more whereas others find it difficult sleeping. Appetite may also be affected.

Cognitive:

People experience negative thoughts, like a negative self-concept. They have a negative view of the world and expect things to go wrong. These negative thoughts are irrational and do not reflect reality.

Emotional: 

Obsessions and compulsions cause anxiety and distress. People know that their behaviour is excessive - causes feelings of embarrassment and shame.

Behavioural:

Compulsive behaviours are repetitive and unconcealed. People feel they have to perform these acts otherwise something terrible might happen.

Cognitive:

Obsessions are repetitive, intrusive thoughts which are seen as inappropriate and may be embarrassing or frightening. These thoughts are seen as uncontrollable. They recognise that these thoughts come from their mind.

OCD seems to be a polygenic condition, where a number of genes are involved in its development. Family and twin studies suggest the involvement of genetic factors. The prevalence of OCD in the random population (about 2–3%) is the baseline against which the concordance rates can be compared.

The SERT gene (Serotonin Transporter) appears to be mutated in individuals with OCD. The mutation causes an increase in transporter proteins at a neuron’s membrane. This leads to an increase in the reuptake of serotonin into the neuron which decreases the level of serotonin in the synapse.

The COMT gene is a gene that regulates the function of dopamine. It appears that this gene is also mutated in individuals with OCD. However this mutation causes the opposite effect as the SERT mutation discussed above. The mutated variation of the COMT gene found in OCD individuals causes a decrease in the COMT activity and therefore a higher level of dopamine.

One region of the brain; the prefrontal cortex (PFC), is involved in decision making and the regulation of primitive aspects of our behavior. An over active PFC, causing an exaggerated control of primal impulses.

For example, after a visit to the bathroom, your primal instinct to survive by avoiding germs is brought to your attention. You may make the decision to wash your hands to remove any harmful germs you may have encountered.

Once you have performed the appropriate behavior, the PFC reduces in activation and you stop washing your hands and go about your day. It has been suggested that if you have OCD, your PFC is over activated. This means the obsessions and compulsions continue, leading you to wash your hands again and again.

Abnormalities, or an imbalance in the neurotransmitter serotonin, could also be related to OCD. Reduced serotonin and excessive dopamine may cause OCD.

Serotonin is the chemical thought to be involved in regulating mood. OCD patients have low levels of serotonin.

Additionally Dopamine is abnormally high in individuals with OCD. High levels of dopamine have been thought to influence concentration. This mayexplain why OCD individuals experience an inability to stop focussing on obsessive thoughts and repetitive behaviors.

Two classes of drug have proved effective in the treatment of obsessive compulsive disorder: serotonin reuptake inhibitors (SRIs) and selective serotonin reuptake inhibitors (SSRIs). Both classes of drug increase serotonin levels, and so support the neural explanation / biochemical hypothesis.

Drugs that mainly affect neurotransmitters other than serotonin are of little or no value in treating obsessive compulsive disorder.

The cognitive triad are three forms of negative (i.e. helpless and critical) thinking that are typical of individuals with depression: namely negative thoughts about the self, the world and the future. These thoughts tended to be automatic in depressed people as they occurred spontaneously.The negative triad interacts with negative schemas and cognitive biases to produce depressive thinking.

Cognitive biases are distortions of thought processes. Individuals with depression are prone to making logical errors in their thinking and they tend to focus selectively on certain negative aspects of a situation while ignoring equally relevant positive information.

In addition to cognitive biases, the negative triad is also influenced by schemas. In essence, schemas can be seen as deeply held beliefs that have their origins primarily in childhood. Beck believed that depression prone individuals develop a negative self-schema. They possess a set of beliefs and expectations about themselves that are essentially negative and pessimistic.

Beck claimed that negative schemas may be acquired in childhood as a result of a traumatic event (e.g. parental or peer rejection). Schemas influence how a person interprets events and experiences in their life. Beck predicted that in depression ‘latent’ (i.e. dormant) negative schemas that have been formed in childhood become activated by a life events or ongoing stressors. Negative schemas and cognitive biases maintain the negative triad, a pessimistic view of the self, the world (not being able to cope with the demands of the environment) and the future.

Cognitive Behavioural Therapy aims to change the way a client thinks, by challenging irrational and maladaptive thought processes and this will lead to a change in behavior as a responses to new thinking patterns. Specifically, our thoughts determine our feelings and our behavior.

Therefore, negative - and unrealistic - thoughts can cause us distress and result in problems. When a person suffers with psychological distress, the way in which they interpret situations becomes skewed, which in turn has a negative impact on the actions they take.

Cognitive therapists help clients to recognize the negative thoughts and errors in logic that cause them to be depressed. The therapist also guide clients to question and challenge their dysfunctional thoughts, try out new interpretations, and ultimately apply alternative ways of thinking in their daily lives.

The clients learn to discriminate between their own thoughts and reality. They learn the influence that cognition has on their feelings, and they are taught to recognize observe and monitor their own thoughts.

The behavior part of the therapy involves setting homework for the client to do (e.g. keeping a diary of thoughts). The therapist gives the client tasks that will help them challenge their own irrational beliefs.

The idea is that the client identifies their own unhelpful beliefs and them proves them wrong. As a result, their beliefs begin to change. For example, someone who is anxious in social situations may be set a homework assignment to meet a friend at the pub for a drink.

The behavioural approach explains the development and maintenance of phobia mainly using the theories of classical conditioning and operant conditioning. These were first combined as a single explanation for phobia by Mowrer, in the two-process model of phobia.

According to the behaviorists, phobias are the result of a classically conditioned association between an anxiety provoking unconditioned stimulus (UCS) and a previously neutral stimulus. For example, a child with no previous fear of dogs gets bitten by a dog and from this moment onwards associates the dog with fear and pain. Due to the process of generalisation the child is not just afraid of the dog who bit them, but shows a fear of all dogs.

Operant conditioning can help to explain how the phobia is maintained. The conditioned (i.e. learned) stimulus evokes fears, and avoidance of the feared object or situation lessens this feeling, which is rewarding. The reward (negative reinforcement) strengths the avoidance behaviour, and the phobia is maintained.

Systematic Desensitisation is a type of behavioural therapy based on the principle of classical conditioning. This therapy aims to remove the fear response of a phobia, and substitute a relaxation response to the conditional stimulus gradually using counter conditioning. This will lead to extinction of the fear response. There are three phases to the treatment:

First, the patient is taught a deep muscle relaxation technique and breathing exercises. E.g. control over breathing, muscle detensioning or meditation. This step is very important because of reciprocal inhibition, where once response is inhibited because it is incompatible with another. In the case of phobias, fears involves tension and tension is incompatible with relaxation.

Second, the patient creates a fear hierarchy starting at stimuli that create the least anxiety (fear) and building up in stages to the most fear provoking images. The list is crucial as it provides a structure for the therapy.

Third, the patient works their way up the fear hierarchy, starting at the least unpleasant stimuli and practising their relaxation technique as they go. When they feel comfortable with this (they are no longer afraid) they move on to the next stage in the hierarchy. If the client becomes upset they can return to an earlier stage and regain their relaxed state.

Flooding (also known as implosion therapy) works by exposing the patient directly to their worst fears. (S)he is thrown in at the deep end. For example a claustrophobic will be locked in a closet for 4 hours or an individual with a fear of flying will be sent up in a light aircraft.

What flooding aims to do is expose the sufferer to the phobic object or situation for an extended period of time in a safe and controlled environment. Unlike systematic desensitisation which might use in vitro or virtual exposure, flooding generally involves vivo exposure.

Fear is a time limited response. At first the person is in a state of extreme anxiety, perhaps even panic, but eventually exhaustion sets in and the anxiety level begins to go down. Of course normally the person would do everything they can to avoid such a situation. Now they have no choice but confront their fears and when the panic subsides and they find they have come to no harm. The fear (which to a large degree was anticipatory) is extinguished.

Prolonged intense exposure eventually creates a new association between the feared object and something positive (e.g. a sense of calm and lack of anxiety). It also prevents reinforcement of phobia through escape or avoidance behaviors.

The approach can also be criticised for ignoring environmental influences. For example, people are not born with OCD they might learn it from their environment through the process of classical and operant conditioning.

Strengths of this approach include its testability via neuroscience research, evidence for genetic and neurotransmitter involvement in conditions such as schizophrenia. For example, the dopamine hypothesis argues that elevated levels of dopamine are related to symptoms of schizophrenia.

Biological explanations are reductionist as they focus on only one factor and at present our understanding of biochemistry is oversimplified. This means other psychological factors, such as cognitions are ignored.

The biological explanations are also deterministic because they ignore the individual’s ability to control their own behavior, which in turn may affect their biochemistry levels.

Studies using drugs have shown a reduction in dopamine levels is positively correlated with a reduction in OCD symptoms.

Experiments which inject animals with drugs that increased levels of dopamine have caused the animals to demonstrate OCD type behaviors.

Drugs that increase serotonin (anti depressants such as SSRIs) have been shown to reduce OCD symptoms. Soomro et al found that SSRIs were significantly better than placebos in reducing symptoms in 17 different clinical trials

But research results relating to serotonin are varied – sometimes symptoms have been made worse. There is a great deal of contradictory research. - Drugs seem to show only partial alleviation of the symptoms so the process is not fully understood. The exact function of neurotransmitters in the development of OCD is far from understood.

Most SSRIs have side effects which can be unpleasant, e.g. dry mouth, a slight tremor, fast heartbeat, constipation, sleepiness, and weight gain.

The success of antidepressant drugs as a treatment does not necessarily mean the biochemicals are the cause of OCD in the first place. This is known as the treatment aetiology fallacy and, using headaches as an example, aspirin works well as a treatment but this doesn’t mean the headache was due to an absence of aspirin.

It may be that negative thinking generally is also an effect rather than a cause of depression. Perhaps individuals only start experiencing negative thoughts after having developed depression. However, evidence that negative thinking can be involved in the development of depression was obtained by Lewinsohn et al. (2001).

They measured negative thinking in non-depressed adolescents. One year later, the life events of participants over the previous 12 months were assessed, and also whether they were suffering from depression.

The results showed those who had experienced many negative life events had an increased likelihood of developing depression only if they were initially high in negative attitudes. This study supports the theory that negative beliefs are a risk factor for developing depression when exposed to stressful life events.

The cognitive approach to depression is limited in that genetic factors are ignored.

Little attention is paid to the role of social factors relating to life events and gender in the cognitive explanation of depression.

The precise role of cognitive processes is yet to be determined. It is not clear whether faulty cognitions are a cause of the psychopathology or a consequence of it.

Sometimes these negative cognitions are in fact a more accurate view of the world: depressive realism.

Cognitive theories lend themselves to testing. When experimental subjects are manipulated into adopting unpleasant assumptions or thought they became more anxious and depressed (Rimm & Litvak, 1969).

A strength of this therapy is that it has shown to be very effective in treating depression, in fact, it has shown to produce longer lasting recovery than antidepressants.

The precise role of cognitive processes is yet to be determined. It is not clear whether faulty cognitions are a cause of the psychopathology or a consequence of it.

Sometimes these negative cognitions are in fact a more accurate view of the world: depressive realism.

Cognitive theories lend themselves to testing. When experimental subjects are manipulated into adopting unpleasant assumptions or thought they became more anxious and depressed (Rimm & Litvak, 1969).

An important advantage of CBT is that it tends to be short (compared to psychoanalysis), taking three to six months for most emotional problems. Patients attend a session a week, each session lasting either 50 minutes or an hour.

Another strength is that it can reduce ethical issues – the way this therapy works is that the client is actively involved and in control. They feel empowered as they are helping themselves.

There is empirical support to show how classical conditioning leads to the development of phobias. Watson and Rayner (1920) used classical conditioning to create a phobia in an infant called Little Albert. Albert developed a phobia of a white rat when he learned to associate the rat with a loud noise.

The behaviourist approach adopts a limited in the origins of a phobia, as it overlooks the role of cognition. Ignoring the role of cognition is problematic, as irrational thinking appears to be a key feature of phobias. Tomarken et al. (1989) presented a series of slides of snake and neutral images (e.g. trees) to phobic and non-phobic participants. The phobics tended to overestimate the number of snake images presented.

In theory anyone could develop a phobia to a potentially harmful object, although this does not always happen. Despite the fact the most adults have either experienced, witnessed or heard about car accidents were another person is injured, phobia of cars is virtually non-existent.

Seligman (1970) suggests that humans have a biological preparedness to develop certain phobias rather than others, because they were adaptive (i.e. helpful) in our evolutionary past. For example, individuals that avoided snakes and high places would be more likely to survive long enough and pass on their genes than those who did not.

The idea of biological preparedness is further supported by Ost and Hugdahl (1981) who claim that nearly half of all people with phobias have never had an anxious experience with the object of their fear, and some have had no experience at all. For example, some snake phobics have never encountered a snake. The cognitive approach criticise the behavioral model as it does not take mental processes into account. They argue that the thinking processes that occur between a stimulus and a response are responsible for the feeling component of the response.

Practical Issues...One weakness of in vitro systematic desensitization is that it relies on the client’s ability to be able to imagine the fearful situation. Some people cannot create a vivid image and thus systematic desensitization is not always effective (there are individual differences).

Systematic desensitization is a slow process, taking on average 6-8 sessions. Although, research suggests that the longer the technique takes the more effective it is.

Theoretical Issues...Systematic desensitization is highly effective where the problem is a learned anxiety of specific objects/situations (e.g. phobias). However, SD is not effective in treating serious mental disorders like depression and schizophrenia.

Studies have shown that neither relaxation nor hierarchies are necessary, and that the important factor is just exposure to the feared object or situation. Therefore, therapies like flooding may be more effective.

Social phobias and agoraphobia do not seem to show as much improvement. Could it be that there are other causes for phobias than classical conditioning? For example, if a fear of public speaking originates with poor social skills then phobic reduction is more likely to occur in a treatment which includes learning effective social skills than systematic desensitization alone.

Empirical Evidence...Rothbaum used SD with participants who were afraid of flying. Following treatment 93% agreed to take a trial flight. It was found that anxiety levels were lower than those of a control group who had not received SD and this improvement was maintained when they were followed up 6 months later.

Flooding is rarely used and if you are not careful it can be dangerous. It is not an appropriate treatment for every phobia. It should be used with caution as some people can actually increase their fear after therapy, and it is not possible to predict when this will occur. Wolpe (1969) reported the case of a client whose anxiety intensified to such as degree that flooding therapy resulted in her being hospitalized.

Also, some people will not be able to tolerate the high levels of anxiety induced by the therapy, and are therefore at risk of exiting the therapy before they are calm and relaxed. This is a problem, as existing treatment before completion is likely to strengthen rather than weaken the phobia.

However one application is with people who have a fear of water (they are forced to swim out of their depth). It is also sometimes used with agoraphobia. In general flooding produces results as effective (sometimes even more so) as systematic desensitisation. The success of the method confirms the hypothesis that phobias are so persistent because the object is avoided in real life and is therefore not extinguished by the discovery that it is harmless.

For example, Wolpe (1960) forced an adolescent girl with a fear of cars into the back of a car and drove her around continuously for four hours: her fear reached hysterical heights but then receded and, by the end of the journey, had completely disappeared.