Psychopathology : Biological Approach to OCD (explaining) Flashcards
Whats DNA?
• Found in the nucleus, wound into tightly packed structures (chromosomes)
• Humans have 23 pairs of chromosomes
• DNA is made of 4 nucleotides (A, T and C, G) and a double helix backbone
Whats a gene?
specific sequence of nucleotides and acts as a blueprint for making proteins that influence characteristics (eg. eye colour)
Whats an allele?
variations in nucleotides within a gene. Contributes to variation among humans, affecting how genes function (can be good or bad)
Whatre monozygotic twins?
Identical - 1 egg released, fertilised then splits into two zygotes that share 100% of DNA
Whatre dizygotic twins?
Fraternal - 2 eggs released, both fertilised, 2 zygotes that share 50% of their DNA
Advs of the biological approach to treating OCD
• increased concordance between monozygotic vs dizygotic twins → Nestadt (2010) shows there’s a higher concordance rate for OCD in MZ twins (68%) vs DZ twins (31%), supporting the roll of genetics in OCD, since MZ and DZ twins grow up sharing similar environments like food, upbringing, education and life events like bereavement or parental divorce. But, increased concordance rates doesn’t necessarily indicate genetics’ role: MZ may be treated more similarly as they’re identical vs Dz. Also, because concordance was 68% not 100% there must be some environmental component.
Whats a neurotransmitter?
How the brain cells (neurons) communicate → electrochemically
How do neurones communicate?
• electrical signal (nerve impulse) → action potential, passes through neurone to reach axon terminal or the pre-synaptic terminal
• it causes a chemical (neurotransmitter) to release across the synapse as the vecickles containing the neurotransmitter binds with the membrane of the pre-synaptic neurone and released the neurotransmitters
• on the other side, post-synaptic receptors receive the neurotransmitters and they bind together with the receptors that fit
• the post synaptic neurone is activated and generates an electric signal that passes on to the next neurone
Genetic Explanations - Family Studies
Nestadt et al. (2000) found that first degree relatives of OCD sufferers had a higher chance of developing the disorder → 12% chance 1st degree, 3% in control group
Marini & Stebnick (2012) found that a person with a family member with OCD is about 4x more likely to develop it than someone without
Candidate genes - COMt gene
Causes low levels of the enzyme catchecol-o-methyltransferase. Enzymes break down/metabolise other molecules (eg neurotransmitters). This enzyme regulates the amount of dopamine in the brain. Low levels of the COMt enzyme = high levels of dopamine. Turkel et al. (2013) found that low-activity version of coMt gene was more common in patients with OCD compared to controls.
Candidate genes - SERt gene
creates a protien (serotonin transporter) which removes serotonin by detecting the amount of neurotransmitter in the synapse and taking it back into the synapse after it’s released. When a mutation makes too much serotonin transporter, serotonin levels go down. Ozaki et al (2003) found 2 families with the high-activity version of the gene (made too much): 6/7 people had OCD.
Is OCD polygenic?
Taylor (2013) found evidence of up to 230 candidate genes- OCD is liken to be polygenic (caused by more than one gene)
Is OCD aetiologically heterogenous?
different combinations of genes cause different types of OCD in different people
Whats the diathesis/ stress model?
‘genetic vulnerability’ ‘environment’ - certain genes leave some people more likely to suffer a mental disorder but it’s not certain as some environmental stress is necessary to trigger the condition
Disadvs of the genetic explanation of OCD
• environmental → Cromer et al (2007) found over half of OCD patients in their sample experienced a traumatic life event, and that OCD was more severe in these - suggesting a diathesis-stress model. This supports that OCD doesn’t have solely genetic origins
• there are credible alternative explanations for the development of OCD (eg. two process model) that suggest learning is crucial → support for this is found in the success of behavioural treatments for OCD where symptoms of patients are improved for 60-90% of adults (Albucher et al, 1998). Initial learning of feared stimulus could occur through classical conditioning’s associative process where, for example, dirt is paired with anxiety. This behaviour pattern would be maintained through operant conditioning and negative reinforcement where the stimulus is avoided so anxiety is removed, resulting in an obsession linked to the development of a compulsion
Neural explanations - how is serotonin involved in OCD?
serotonin is important for the regulation of mood - it has a calming effect. Low levels mean the brain doesn’t communicate info about mood effectively. This reduction in functioning seems to be linked to OCD. Low levels of serotonine have been associated with w symptoms of anxiety. Piggot et al (1990) reported that SSRis (reduce uptake of serotonin, so prolong it’s actions at the synapse) are effective in treating OCD.
How is dopamine involved in OCD?
maintains interest and motivation. High levels of dopamine help maintain compulsive thoughts or behaviours, leading to some symptoms of OCD (compulsive behaviours)
Whats the orbitofrontal cortex?
a region which converts sensory info to thoughts + actions. PET scans found higher activity in the orbitofrontal cortex with OCD when they’re asked to challenge a belief obsession compulsion, increasing conversion of sensory into to actions - resulting in compulsions
Advs of the neural explanation
• empirical evidence from structural + functional imaging studies → Menzies et al (2007) found OCD suffers + their family had reduced grey matter in key regions of the brain (inc. OFC). Plus, several neuroimaging studies using PET scanners have shown hyperactivity in the OFC and caudate nucleus in people w OCD both while scanning brain at rest and when stimulated.
• empirical evidence from effects of SSRIs that neurotransmitters do play a role-meta analysis by Soomro et al (2008) demonstrated SSRis are more effective vs placebos, suggesting serotenergic involvement. The drugs reduce OCD symptoms by increasing neurotransmitter levels by blocking serotonin reuptake process, suggesting serotonin does play a part.
Disadvs of the neural explanation
• However, researchers can’t be sure it hyperactivity is caused or a consequence of OCD → Maia et al. (2008) reviewed evidence which permitted stronger casual inferences (inc. development of OCD) following brain injury, paediatric autoimmune neuropsychiatric disorders associated with stereotypical infection
• But, despite altering levels within hours, drugs take weeks to reduce symptoms (40-60% of patients show no or partial symptom improvement)
Whats the basal ganglia?
a cluster of neurones, including the caudate nucleus (base of forebrain) which is involved in multiple processes including the coordination of movement
Whats the worry circuit? → corticostriatal thalamocortical circuit
- OFC sends ‘worry signal’ to thalamus to report on things which should cause worry
- in normal functioning, the basal ganglia filters out minor worries, but if It’s hyperactive, even small worries get to the thalamus, then passed back to the OFC, forming a loop (recurring obsessive thoughts)
- repetitive motor functions (compulsions) attempt to break the loop. Carrying it out may give temporary relief, but the basal ganglia will soon resume the worry circuit
Whats the parahippocmal gryus?
area of cortex close to hippocampus (underside), linked w OCD. Responsible fer regulating + processing unpleasant emotions + has functioned abnormal w OCD
