Psychopathology - The Biological Approach to explaining and treating OCD Flashcards
What are the emotional characteristics of OCD?
- Depression
- Guilt
- Anxiety
- Disgust
What are the behavioural characteristics of OCD?
- These characteristics focus on the compulsive behaviours experienced by sufferers - these compulsions have two properties; compulsions both reduce anxiety and are repetitive
- Avoidance
What are the cognitive characteristics of OCD?
- Hypervigilance - fear of contamination
- Catastrophic thinking
- Cognitive strategies to deal with compulsions and insight into anxiety
- Obsessive thoughts
- Repetitive thoughts
- Selective attention
What is OCD?
- Obsessive compulsive disorder is classed as an anxiety disorder, characterised by obsessive thinking and repetitive behaviours.
- Obsessions = internal components because they are intrusive thoughts (something you think).
- Compulsions = external components because they are repetitive behaviours (something you do). These reduce anxiety.
Biological explanations for OCD
- The biological approach sees abnormal conditions, such as OCD, as being similar to physical illnesses caused by abnormal biological processes.
There are two main biological explanations for OCD:
1) Neural explanations – the occurrence of OCD through abnormal functioning of neural (brain) mechanisms and neurotransmitters.
2) Genetic explanations – hereditary influences through genetic transmission from parent to offspring (i.e. inheritance).
Biological Approach - The Neural Explanation; Synaptic transmission
- Action potential reaches the pre-synaptic terminal
- This triggers the synaptic vesicles to release neurotransmitters into the synaptic gap
- These neurotransmitters are either inhibitory or excitatory
- The neurotransmitters diffuse across the synaptic gap between the pre and post-synaptic cells
- The neurotransmitters bind to the post-synaptic receptor sites on the membrane of the post-synaptic neuron’s dendrite
- this stimulation of the post-synaptic receptors converts the chemical message back to the electrical impulse
- The process of transmission begins again in the post-synaptic neuron
- If the neurotransmitter is excitatory, this causes excitation of the post-synaptic membrane, and so the post-synaptic membrane is more likely to fire the action potential
- If the neurotransmitter is inhibitory, this inhibits the post-synaptic membrane and so the post-synaptic neuron is less likely to fire an action potential
- The excitatory and inhibitory influences are summed (summation) - if the net effect is excitatory, the action potential is fired, if it is inhibitory, it is not (stops overreaction)
- The effects are terminated by a process called re-uptake - neurotransmitters are taken up by the pre-synaptic neuron where they are again stored in a synaptic vesicles ready for later release.
Neural explanation cont; neurotransmission
Abnormal levels of neurotransmitters (chemical messengers) –
- Dopamine levels are thought to be abnormally high in people with OCD.
- Lower levels of serotonin activity (an inhibitory neurotransmitter) in the brain are also associated with OCD.
Neural explanation - Abnormal circuitry
Several areas of the frontal lobes are thought to be abnormal in people with OCD:
- OCD is associated with high levels of activity in the orbital frontal cortex (OFC), a brain area associated with higher-level thought processes and the conversion of sensory information into thoughts
- The OFC sends signals to the thalamus about things that are worrying, such as a potential germ hazard; upon receiving the signal, this leads to an impulse to act; for example, a non-sufferers’ OFC may send a signal to the thalamus when their hands are dirty which leads to an impulse to wash their hands - once this is done, the impulse to perform the activity stops and thus so does the behaviour, with the caudate nucleus suppressing signals from the OFC
- It may be that those with OCD have difficulty in switching off or ignoring impulses because of damage to the caudate nucleus, and so the impulses turn into obsessions that become compulsive behaviours
- When the caudate nucleus is damaged, it fails to suppress minor ‘worry’ signals from the OFC and the thalamus is alerted which in turn sends signals back to the OFC, acting as a worry circuit
Abnormal circuitry - definitions
- OFC – sends signal to the thalamus about things that are worrying.
- Thalamus – leads to impulse to act and then to stop activity when the impulse lessens.
- Caudate nucleus - normally suppresses signals from the OFC. If damaged, it fails to do this and so the thalamus is alerted about minor ‘worry’ signals. It sends signals back to the OFC acting as a worry circuit.
Evidence for abnormal circuitry
- This is supported by PET scans of patients with OCD, taken while their symptoms are active, which show heightened activity of the OFC when for example, a person with a germ obsession holds a dirty cloth
- Serotonin and dopamine are linked to regions of the frontal lobes, with Comer (1998) reporting that serotonin plays a key role in the operation of the OFC and caudate nuclei, and it would therefore appear that abnormal levels of serotonin could cause these areas to malfunction
- Dopamine is also linked to this system, as it is the main neurotransmitter of the basal ganglia (remember the caudate nucleus is located in the basal ganglia) High levels of dopamine lead to over activity of this region
Genetic explanation for OCD
There are genes that are thought to contribute to OCD as they impact these neurotransmitter levels.
- COMT -> May contribute to OCD, and gains its name is it is involved in the production of catechol-O-methyltransferase, and this gene regulates the production of the neurotransmitter dopamine; if it is not sufficient, dopamine levels will be abnormally high. All genes come in different forms (alleles) and the form of the COMT gene that has been found to be more common in OCD patients than people without this disorder; this variation produces lower activity of the COMT gene and higher levels of dopamine (Tukel et al, 2013)
- SERT (5-HTT) -> Affects the transport of serotonin, creating lower levels of the neurotransmitter, and these lower levels are implicated in OCD; Ozaki et al (2003) found a mutation of this gene in two unrelated families where 6 of 7 family members had OCD -> SERT gene associated with OCD as a result
To treat the genetic deficiency -
- COMT -> give a drug that causes reuptake to happen in order to lower dopamine levels in synaptic transmission
- SERT -> give a drug that inhibits serotonin uptake in the synapse in order to heighten levels
Evaluation of the biological approach to explaining OCD - strengths and weaknesses of the genetic explanation
Strength 1) There is evidence that people are vulnerable to OCD because of their genetic make-up; for example, a review of twin studies found that 68% of identical twins shared OCD compared to 31% of non-identical twins
- This supports the explanation that genes cause OCD, as the more identical the gene pool the more likely the twins were to share OCD regardless of their nurture - it provides external validity to the biological approach; not 100% genetic but has some genetic component
Weakness 1) Twin studies make the assumption that identical twins are only more similar than non-identical twins in terms of their genes, overlooking that they may also be more similar in terms of shared environments
- This suggests that the studies lack internal validity due to confounding / extraneous variables in the home, limiting the support they are able to provide for the genetic explanation
Evaluation of the biological approach to explaining OCD - Weaknesses of the genetic explanation
Weakness 2) Psychologists have not been very successful at determining which genes are involved in OCD; one reason for this is that it seems that several genes are involved and that each genetic variation only increases OCD risk by a fraction
- This suggests that the explanation is too narrow as it does not accommodate for the interaction of a range of genes that may all cause OCD; little success pinpointing genes
Weakness 3) Environmental factors can also trigger or increase the risk of developing OCD, as it has been found that over half of OCD patients in one study had a traumatic experience in their past, and that OCD was more severe in participants with more than one trauma
- Low internal validity as it ignores extraneous variables such as trauma that could contribute to the formation of OCD outside of biological factors - overly deterministic also
- Also could be a limitation of the neural explanation
Evaluation of the biological approach to explaining OCD - Strengths and Weaknesses of the Neural explanation
Strength 1) There is evidence to support the the role of some neural mechanisms in OCD, such as antidepressants that alter levels of serotonin showing to be effective in reducing OCD symptoms
- This suggests that the explanation has real-world applications and external validity, as it can help target treatments to help alleviate OCD symptoms
Weakness 1) Research has identified that other brain systems beyond the decision-making systems may sometimes be involved in OCD, and no system has been found to always play a role in OCD
- Too narrow of an explanation to accommodate for the range of neural factors that may be causing OCD - it also weakens the explanation, as the specific areas identified by the approach may not actually be relevant to OCD - more holistic than specific circuitry, lacks generalisability
Weakness 2) There is evidence to suggest that various neurotransmitters and brain systems do not function normally in patients with OCD, however this does not necessarily mean that this abnormal functioning caused the OCD
- This suggests that the explanations hold a lack of causality; they help us to understand what is abnormally functioning but does not confirm it causes OCD
Treating OCD - the biological approach; Drug therapies with SSRI
Anti-depressants - SSRIs
- Selective serotonin reuptake inhibition
- The most commonly used drug for depression and OCD, and it is used to increase serotonin levels and correct abnormal worry circuitry which are impacted by low serotonin levels
- It works by blocking the reuptake of serotonin in the synaptic knob, increasing serotonin levels to regulate mood and anxiety
- Examples of an SSRI - Prozac, Zoloft and Paxil
1) Serotonin is released by certain neurons in the brain
2) Serotonin is released by the presynaptic neurons and travels across the synapse
3) Serotonin binds to the receptor sites on the post-synaptic neuron and conveys the signal from the presynaptic neuron to the post-synaptic neuron
4) Normally -> Serotonin is reabsorbed by the presynaptic neuron where is it broken down and reused
5) On drugs -> SSRIs prevent the reabsorption and breakdown of serotonin
6) This effectively increases the levels of serotonin in the synapse and they continue to simulate the post-synaptic neuron
7) This compensates for whatever is wrong with the serotonin system in OCD
