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Normative theories of reasoning distinguish two kinds of persuasive arguments depending on the inferential connection between premises and conclusion. If the truth of an argument's premises guarantee that of its conclusion, the argument is called valid, whereas if the premises merely enhance the plausibility of the conclusion, the argument is probabilistically strong. Human intuition about validity and probability is limited to inferences of moderate size and reveals systematic imperfections even when applied to simple cases. Nonetheless, starting from adolescence both forms of reasoning are recognizable approximations to their normative counterparts [3, 6, 11].
What is the psychological relation between deductive and probabilistic reasoning? One influential theory conceives both kinds of reasoning as involving the manipulation of ‘mental models’. In this view, an argument is evaluated by constructing alternative models of its premises, where each model is a representation of potential circumstances that would render the premises true. The argument is then judged to be probabilistically strong in case a large proportion of the models generated for the premises render the conclusion true as well; the intuition of validity arises from the limiting case in which this proportion reaches one. Within epistemology, such an account of the relation between validity and probability was proposed by Wittgenstein [[41], §5.15], and followed up by de Finetti [9] and others. A psychological version of the same idea has recently been proposed by Johnson-Laird [23], where it receives detailed and persuasive defense.
We used [18F]FDG and PET in patients with obsessive–compulsive disorder (OCD) to evaluate cerebral metabolic involvement before and after treatment with serotonin-specific reuptake inhibitors.
Method
In 11 untreated, drug-free adults, regional cerebral metabolic rate for glucose (rCMRglu) was compared with that of 15 age-matched normal controls.
Results
rCMRglu values were significantly increased in the cingulate cortex, thalamus and pallidum/putamen complex. After treatment a significant improvement in obsessive–compulsive symptoms on the Y-BOC scale (t = 3.59, P < 0.01) was associated with a significant bilateral decrease of metabolism in the whole cingulate cortex (P < 0.001). Clinical and metabolic data were significantly intercorrelated (Kendall's τ = 0.65; P < 0.01).
Conclusions
These findings indicate that OCD is associated with functional hyperactivity of a selected neuronal network and that treatment to reduce symptoms may have a selective neuromodulatory effect on cingulate cortex.
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