Johan Carlin reports on a fascinating investigation into the neural substrates of cognitive flexibility. This experiment led to a counterintuitive finding. Lesions to either the orbitofrontal cortex or the amygdala in isolation caused impairment on a cognitive flexibility task, but no impairment was observed when both structures were experimentally damaged.
Carlin concludes this well-written post:
the take-home message for those studying humans is that there is an entire range of complex interactions in the brain that fMRI, with its blurry temporal resolution and lack of experimental manipulation, can only hint at. We know much about functional localisation in the human brain, but the issue of how these areas connect and interact is largely uncharted territory.