explanations of ocd Flashcards
(11 cards)
outline the neural explanation of ocd.
the orbifrontal cortex converts sensory information into thoughts + emotions (obsession / distress) - the caudate nucleus suppresses “worry signals” from the orbifrontal cortex. if it is damaged, it sends worry signals on a loop, meaning high anxiety is repeated + compulsions are a temporary relief until distress starts again.
how do low levels of serotonin cause ocd?
low levels means there are less levels of mood-relevant info which means mental processes are affected. SSRIs reduce ocd symptoms.
what are the 4 ways that the caudate nucleus can be damaged?
- high levels of dopamine
- low levels of serotonin
- inherited genes
- brain trauma
who found that ocd is poly genetic?
taylor (2013) - there are at least 230 genes involved in ocd.
how do high levels of dopamine cause ocd?
high levels lead to over activity in the basal ganglia which respond + process thoughts (motivation+reward= compulsions)
how is the COMT gene relevant in the development of ocd?
it regulates the production of dopamine and has been found to be more common in people with ocd.
how is the SERT gene relevant in the development of ocd?
it affects the transport of serotonin which therefore creates lower levels. ozaki (2003) found a mutation of this gene in two unrelated families where 6/7 members had ocd.
what did carey (1981) find in his twin study?
mz twins show 87% concordance and dz twins had 31% concordance in ocd diagnosis.
what did nestadt (2000) find?
people with first-degree relatives with ocd were 5x more likely to develop ocd compared to the general population.
what is one strength of the genetic explanation for ocd?
it has support from twin studies - carey (1981) and nestadt (2000)
what is the diathesis stress model?
states that genes create inherited vulnerabilities for ocd development but stressors in our environment determine whether the illness develops.
