Biological accounts of OCD have sought to explain OCD in terms of general deficits in specific areas of the brain or in differences in neurotransmitters. Studies have focused particularly on serotonin, the neurotransmitter that is known to modulate mood, emotion, sleep and appetite and is implicated in the control of numerous behavioural and physiological functions. The finding that particular medications which act as serotonin reuptake inhibitors (SSRIs) can be effective in reducing OCD symptoms led to the initial hypothesis that there may be an abnormality in serotonin and studies have reported different levels of serotonin in OCD (e.g. Insel et al., 1985; Zohar et al., 1988). In addition, brain scanning studies have been used to suggest that there are biological differences in OCD, such as differing metabolic rates in the part of the brain known as the fronto-striatal system (e.g. Baxter et al., 1988). However, just because differences are found does not necessarily mean that there is a deficit or abnormality. Baxter et al. (1992) demonstrated that the anomalies detected through brain scanning can resolve through medication or behaviour therapy, suggesting that any neurological changes are reversible.
If OCD is caused by biological factors, theories need to be able to account for the effectiveness of treatment and to explain how psychological therapy may work. Theories must also be able to account for the phenomenology of OCD more broadly, such as why memory and decision-making problems only occur in situations linked to the obsessional problem. To progress our understanding, biological accounts of OCD need to be able to generate specific predictions based on the phenomenology of OCD and must be able to provide evidence to evaluate them.
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