This pattern of activation accords with other fMRI studies of people who binge-eat. Increased motor responses to food images may reflect an anticipated desire for food consumption, as these regions are also activated in BIBW2992 healthy people who have fasted and report a craving for food. Furthermore, activation of the caudate and motor regions are implicated in addictive behaviour and thus might suggest that there are some similarities in neural systems between addiction and binge eating. Our data suggest that women with BN have an elevated neural appetitive response to food images, combined with activation of motor areas, when thinking about eating food. We also observed an increased right dorsolateral prefrontal cortex response to the food versus non-food images, but this was comparable in both eating disordered groups. The DLPFC forms part of the cognitive control network, and is associated with restriction of appetitive responses. Activation of a “top-down�?cognitive control network, which interacts with “bottom-up�?appetitive responses might be expected when women, who have a pathological desire to be thin and to control their food intake, think about eating food. This is likely to be sporadic in women with BN, who attempt to control their food intake but who are prone to yield to binge eating. In line with this notion, it is plausible that, in women with BPAN, intermittent activation of appetitive systems impinge on attempts at top-down control, but to a lesser extent than those with BN. It is currently unclear however, whether it would be greater top-down control or weaker bottom-up activation that prevents a person with BPAN from gaining weight and/or developing BN symptoms. The balance between these behaviours is likely dependent on the level of bottom-up impingement on cognitive control, as has been shown in two studies with conflicting results: one shows greater, while the other reduced DLPFC activation. Both studies examined response inhibition in females with BN, one study using the ‘Go/ No-Go�?task, the other using the ‘Simon Incompatibility�?task, which may activate different levels of arousal, and which would account for differential disruption to PFC networks. Additionally, women who have recovered from BN continue to show an aberrant pattern of activation in the striatum in response to reward and also a reduced pattern of activation in PFC regions to the taste of glucose. It could be that as a woman with BN recovers, the arousal system in the brain, albeit aberrant, is tamed and causes less impingement on PFC cognitive networks. Furthermore, there could be different aetiologies for women with AN and BN, in that the former is driven by excessive activation of PFC cognitive inhibition systems, whereas the latter is driven by excessive arousal in reward regions.