4.1.4 Clinical Psychology & Mental Health

Process of synaptic transmission (comes up in 3.2.2 Biopsychology but is useful for this topic): 1)Action potential arrives at the presynaptic neuron 2) Vesicles release neurotransmitters into the synaptic gap 3) The neurotransmitters travel across the synaptic gap via diffusion 4) The neurotransmitters bind to receptors on the post-synaptic neuron 5) Either a new action potential starts in the post-synaptic neuron, or there is a reduced likelihood of an action potential (excitatory = increased likelihood, inhibitory = decreased likelihood) 6) Excess neurotransmitter is either reabsorbed into the presynaptic neuron through transport proteins or is broken down

What 4 ways can be used to define abnormality?

• Statistical infrequency

• Deviation from social norms

• Failure to function adequately

• Deviation from ideal mental health

Define statistical infrequency

Abnormality is defined by what falls outside of the statistical average

Evaluate statistical infrequency

Strengths:

• Objective

• Scientific (statistical)

Weaknesses:

• Some uncommon traits are desirable, therefore would not be considered ‘abnorma'l’ e.g. high IQ

• Not all disorders are uncommon e.g. lifetime prevalence of depression is 20%

Define deviation from social norms

Abnormality defined as behaviour which goes against the standards of behaviour set by a society

Evaluate deviation from social norms

Strengths:

• Flexible dependent on situation & age

Weaknesses:

• Subjective - how society views it

• Societies vary across time & cultures e.g. hearing voices is highly considered abnormal in western culture but is seen as normal by the Maori people of New Zealand

• Not all behaviour that deviates from social nroms are a sign of mental illness

Define failure to function adequately

Abnormality defined as a person that can no longer cope with the demands of everyday life

What are the signs that someone is failing to function adequately?

• Personal distress

• Maladaptive behaviour

• Irrationality

• Do not conform to standard impersonal rules e.g. personal space

• Becomes a threat to the safety of themselves & others

Evaluate failure to function adequately

Strengths:

• Recognises person's perspective

Weaknesses:

• The definition is too demanding

• Not all abnormality is harmful

Define deviation from ideal mental health

Mental ill health (abnormality) is the failure to achieve good mental health (normality)

What is Jahoda’s criteria for having ideal mental health?

• Positive self attitudes

• Self-actualisation (reaching our full potential)

• Self-esteem

• Ability to cope with stress

• Environmental mastery

• Sense of reality

Evaluation of deviation from ideal mental health

Strengths:

• Allows for clear goals to be set

• Allows for an individual that is struggling to have targeted intervention if their behaviour is not ‘normal’

• Positive

Weaknesses:

• The criteria makes ideal mental health seem almost impossible to achieve

• Subjective

Define phobias

An anxiety disorder characterised by excess fear and anxiety in response to an object or situation

What are the behavioural characteristics of phobias?

• Avoidance

• Panic

• Endurance

What are the emotional characteristics of phobias?

• Anxiety

• Fear

What are the cognitive characteristics of phobias?

• Selective attention

• Irrational beliefs

What are the behavioural characteristics for depression?

• Insomnia

• Changes in energy levels

• Changes to eating behaviour

• Suicidal behaviour/self-harm

What are the emotional characteristics of depression?

• Hopelessness

• Worthlessness

• Anger & irritability

• Loss of interest or pleasure in previously enjoyed activities (anhedonia)

What are the cognitive characteristics of depression?

• Impaired concentration

• Indecisiveness

• Negative self-concept

• Thoughts of death

• Suicidal ideation

• Lack of motivation

• Absolutist (black & white) thinking

What is the behaviourist approach to explaining phobias?

Phobias are gained from experience (trauma)

What is classical conditioning?

Learning through association

What is operant conditioning?

Learning through consequences

What is the two-process model?

• Phobias are aquired through classical conditioning

• Phobias are maintained through operant conditioning

Explain the process of classical conditioning

1. The neutral stimulus does not produce a response

2. The unconditioned stimulus produces the unconditioned response of fear

3. The neutral stimulus is paired with the UCS which produces the UCR of fear

4. The neutral stimulus has now become the conditioned stimulus; it can now produce the conditioned response of fear itself

How are phobias maintained through operant conditioning?

Negative reinforcement:

• Avoiding the phobic stimulus reduces anxiety, which acts as a reward so the behaviour will likely be repeated

What is positive reinforcement?

Adding something positive to increase/encourage behaviour

What is negative reinforcement?

Removing something negative to increase/encourage behaviour

What is positive punishment?

Adding something negative to decrease behaviour

What is negative punishment?

Removing something positive to decrease behaviour

What are the behavioural treatments for phobias?

• Systematic Desensitisation (SD)

• Flooding

What is counterconditioning?

Behavioural therapies aim to change a previously learnt fear response to a new learnt relaxation response

How does systematic desensitisation work?

1. Client is taught relaxation techniques e.g. breathing techniques or meditation → reciprocal inhibition - you cannot feel both frightened & relaxed at the same time

2. Client & therapist work together to form an fear hierachy from most to least fearful situations

3. Gradual exposure - client works their way up their fear hierachy, starting with the least fearful & moves on once they can confront the situation without feeling anxious

How does flooding work?

1. Client is taught relaxation techniques e.g. breathing techniques or meditation → reciprocal inhibition

2. Immediate exposure to phobic stimulus

Why does flooding use immediate exposure?

Fear is a time-limited response, meaning that after enough time has passed, the client will eventually feel exhausted & feelings of fear will deplete.

The client will realise that the phobic stimulus is not harmful, so will no longer produce the conditioned fear response.

What is refusal rate?

The rate at which people refuse to start treatment

What is attrition rate?

The rate at which people drop out of treatment before it is completed

Evaluate systematic desensitisation

• (+) Gives client control → done at the client’s pace, so lower refusal & attrition rate

• (+) Research support e.g. Gilroy et al. (2003)

• (-) Doesn’t work for all phobias → less effective at treating complex phobias (e.g. social phobias - has cognitive elements → behavioural treatments don’t attempt to address the way a client thinks. Cognitive therapies are more suitable as they aim to challenge irrational thoughts)

• (-) Time consuming → usually takes 6-8 sessions to complete

Evaluate flooding

• (+) Research support e.g. Wolpe (1973)

• (+) Less time consuming → requires 1 intense treatment

• (-) Less effecting at treating complex phobias (e.g. social phobias)

What is the cognitive approach to explaining depression?

It suggests that depression may be the result of faulty thinking

What are the two cognitive models of depression?

• Beck’s Negative Triad

• Ellis’ ABC Model

What is Beck’s Negative Triad?

3 interconnected types of negative thinking which come to people automatically:

• Negative view of the self

• Negative view of the world

• Negative view of the future

What is the Negative Triad a result of?

Negative schema - negative packets of information which may have formed due to childhood trauma

At some point in adulthood, these schema may be triggered due to stress

What ways do those with depression engage in “faulty information processing”?

• Over-generalisation: making irrational & extreme generalisations

• Catastrophising: exaggerating how bad something is

• Negative attribution: person may attribute blame for negative outcomes to themselves, ignoring factors outside of their control

• Absolutist thinking: all-or-nothing

What is Ellis’ ABC Model?

A = Activating event

B = Beliefs

C = Consequences

Some people react differently to events, these reactions may lead to depression

Evaluate the cognitive explanations of depression

• (+) Research support e.g. Grazioli & Terry (2000)

• (+) Real world applications → CBT

• (-) Doesn’t explain all forms of depression e.g. Bipolar disorder → can explain the depressed mood but may struggle to explain manic episodes

• (-) Not all depression has an activating event

What is the cognitive treatment for depression and what is its aim?

Cognitive Behavioural Therapy (CBT)

→ Aims to challenge negative/irrational thoughts

How does CBT work?

1. Identify irrational thoughts → helps client gain insight into their own thought processes

2. Dispute irrational thoughts based on either a logical argument or empirical argument

3. Therapist sets homework for the client → client objectively assesses the validity of their irrational beliefs, ‘patient as a scientist’

4. Behavioural activation → client is encouraged to continue going out & doing things they usually enjoy

What is a logical argument?

Arguing based on whether the client’s thoughts actually make sense

What is an empirical argument?

Arguing based on actual evidence

Evaluate CBT as a cognitive treatment for depression

• (+) Research support e.g. March et al. (2007)

• (-) CBT may not work for more severe cases → CBT requires high levels of motivation & engagement from the client (attending sessions). This may be difficult, so CBT will be ineffective

• (-) Overemphasises the role of cognition (addressing the way the patient thinks) → may ignore the impact of genuine problems in the patient’s life. Changing the way they think is unlikely to help if their circumstances don’t change as well

What is a candidate gene?

A specific gene (section of DNA that codes for proteins) which is thought to be involved in the development of a trait e.g. OCD

• Taylor (2013) estimates that up to 230 different genes contribute to OCD → polygenic

What are the genetic explanations for OCD?

• High activity SERT gene

• Low activity COMT gene

What is a SERT gene?

Gene that codes for a transporter protein - Serotonin Transporter

How does high activity SERT gene lead to OCD?

• High activity SERT gene → more SERT proteins

• More SERT proteins → more serotonin reabsorbed

• More serotonin reabsorbed → less serotonin in the synaptic gap

• Less serotonin in synaptic gap → OCD (less regulation of anxiety caused by obsessions)

What is the COMT gene?

COMT is an enzyme used to break down dopamine in the synaptic gap

How does low activity COMT gene lead to OCD?

• Less active COMT gene → less COMT enzymes

• Less COMT enzymes → less dopamine broken down

• Less dopamine broken down → more dopamine left in synaptic gap

• More dopamine → OCD (more anticipation for rewards - compulsions become ritualistic to reduce anxiety from obsessions)

Evaluate the genetic explanation for OCD

• (+) Support from twin studies e.g. Nestadt et al. (2010)

• (-) Nestadt et al. (2010) findings → concordance rate for MZ twins (100% shared DNA) wasn’t 100%, so other factors play a role e.g. environments

• (+) The Diathesis-Stress Model → genetics give someone a vulnerability to developing a disorder, stressors in life then trigger the disorder - Cromer et al. (2007)

What are the neural explanations for OCD?

• Abnormalities in neurotransmitters

• Abnormalities in neuroanatomy

What are the abnormalities in neurotransmitters associated with OCD?

• Deficient serotonin

• Excessive dopamine

How does deficient serotonin lead to OCD?

Serotonin - inhibitory neurotransmitter involved in mood regulation

• Low serotonin = less able to regulate anxiety related to obsessions

• OCD patients rely on compulsions to reduce their anxiety

How does excessive dopamine lead to OCD?

Dopamine - excitatory neurotransmitter associated with rewards & anticipation of rewards

• OCD patients carry out compulsions to reduce anxiety - rewarding

• Excessive dopamin may lead to excessive reward anticipation → anticipate rewards from compulsions, which become ritualistic

Evaluate the abnormalities in neurotransmitters as a neural explanation for OCD

• (+) Support from drug treatments → SSRIs increase the effects of serotonin. If increasing serotonin alleviates OCD symptoms, it implies low serotonin was causing OCD

• (-) The Treatment-Aetiology Fallacy → just because increasing serotonin relieves OCD symptoms, doesn’t mean that OCD is caused by a lack of it. Some people don’t respond to SSRIs at all - Tukel et al. (2006) only 58% of patients respond to SSRIs. If low serotonin causes OCD, why doesn’t everyone respond?

What are the abnormalities in neuroanatomy associated with OCD?

• The worry circuit

How is The Worry Circuit supposed to operate?

1. Orbito-frontal cortex (OFC) sends worry signals to the thalamus

2. Thalamus sends signals around the body so the worry can be dealt with

3. Caudate nucleus supresses the signal from the OFC so that the worry can be dealt with

How does The Worry Circuit operate in OCD?

1. Orbito-frontal cortex (OFC) sends worry signals to the thalamus

2. Thalamus sends signals around the body so the worry can be dealt with

3. Caudate nucleus fails to suppress the signal from the OFC

4. As a result, the individual worries excessively (obsessions)

5. Individual may continue to try & deal with the worry (compulsions)

Evaluate the abnormalities in neuroanatomy as a neural explanation for OCD

• (+) Evidence from cognitive neuroscience → functioning neuroimaging shows that individuals with OCD have heightened activity in the OFC - its responsible for obsessions

• (-) Correlation does not mean causation → neurological changes may just be a symptom of the disorder, not the cause

What are the biological treatments for OCD?

Drug therapy:

• Selective Serotonin Reuptake Inhibitors (SSRIs)

• Serotonin-Noradrenaline Reuptake Inhibitors (SNRIs)

• Dopaminergic medication

How do SSRIs work?

• Blocks SERT protein so that serotonin cannot be reabsorbed into the presynaptic neuron

• More serotonin available in synaptic gap for longer

• More serotonin binds to receptors on post-synaptic neuron

→ helps with regulation of anxiety

How do SNRIs work?

Functions the same way as an SSRI - but blocks reuptake of serotonin & noradrenaline/norepinephrine.

Has more side effects than SSRIs, but may be more effective

Evaluate the biological treatments for OCD

• (+) SSRIs effective → support from Soomro et al. (2009)

• (-) SSRIs don’t work for everyone → some patients don’t respond to SSRIs at all - Tukel et al. (2006)

What are alternative treatments for OCD?

Exposure and Response Prevention (ERP):

Works similarly to SD (phobias)

• Client is encouraged to engage with their fears/triggers & have obsessive thoughts without acting on their compulsions

• They start with low level anxiety & build up