Two long-standing traditions have highlighted cortical decision mechanisms in the parietal and prefrontal cortices of primates, but it has not been clear how these processes differ, or when each cortical region may influence behaviour. Recent data from ventromedial prefrontal cortex (vmPFC) and posterior parietal cortex (PPC) have suggested one possible axis on which the two decision processes might be delineated. Fast decisions may be resolved primarily by parietal mechanisms, whereas decisions made without time pressure may rely on prefrontal mechanisms. Here, we report direct evidence for such dissociation. During decisions under time pressure, a value comparison process was evident in PPC, but not in vmPFC. Value-related activity was still found in vmPFC under time pressure. However, vmPFC represented overall input value rather than compared output value. In contrast, when decisions were made without time pressure, vmPFC transitioned to encode a value comparison while value-related parameters were entirely absent from PPC. Furthermore, under time pressure, decision performance was primarily governed by PPC, while it was dominated by vmPFC at longer decision times. These data demonstrate that parallel cortical mechanisms may resolve the same choices in differing circumstances, and offer an explanation of the diverse neural signals reported in vmPFC and PPC during value-guided choice.
These data suggest that a specific functional inhibition of trigemino-cortical projections is one of the reasons that triptans, unlike pain killers, act highly specifically on headache and migraine but not pain as such.
BackgroundAcetylsalicylic acid is one of the most used analgesics to treat an acute migraine attack. Next to the inhibitory effects on peripheral prostaglandin synthesis, central mechanisms of action have also been discussed.MethodsUsing a standardized model for trigeminal-nociceptive stimulation during fMRI scanning, we investigated the effect of acetylsalicylic acid on acute pain compared to saline in 22 healthy volunteers in a double-blind within-subject design. Painful stimulation was applied using gaseous ammonia and presented in a pseudo-randomized order with several control stimuli. All participants were instructed to rate the intensity and unpleasantness of every stimulus on a VAS scale. Based on previous results, we hypothesized to find an effect of ASA on central pain processing structures like the ACC, SI and SII as well as the trigeminal nuclei and the hypothalamus.ResultsEven though we did not find any differences in pain ratings between saline and ASA, we observed decreased BOLD signal changes in response to trigemino-nociceptive stimulation in the ACC and SII after administration of ASA compared to saline. This finding is in line with earlier imaging results investigating the effect of ASA on acute pain. Contrary to earlier findings from animal studies, we could not find an effect of ASA on the trigeminal nuclei in the brainstem or within the hypothalamic area.ConclusionTaken together our study replicates earlier findings of an attenuating effect of ASA on pain processing structures, which adds further evidence to a possibly central mechanism of action of ASA.
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