Pain is a complex experience that includes sensory, emotional, autonomic and motoric components, and each of these components can differ among various pain states. Despite the many qualitative differences of clinical and experimental pain states, they all share a common aversive nature, leading us to characterise each as “pain.” This talk will present evidence showing a common cortical network that, when activated, leads to the perception of pain. Activation of this circuit can result from direct stimulation of peripheral nociceptors or from the disruption of endogenous modulatory circuits in the CNS that allows normally nonpainful stimuli to access the cortical pain system. Using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), we find that a network of cortical regions is reliably activated by experimental pain and chronic clinical pain states, including the primary and secondary somatosensory cortices (S1 and S2), the anterior cingulate cortex (ACC) and the insular cortex (IC). This network is activated during pain produced by stimuli as divergent as cutaneous heat, visceral pain produced by esophageal distension, or tactile allodynia produced by capsaicin application. Our imaging data show that allodynia related to peripheral or CNS damage activates the same cortical pain system as that activated during acute pain states. Other experiments suggest that these various cortical regions have a differential role in processing the sensory and affective dimensions of pain. Experimental manipulations that selectively alter the affective component of pain predominantly modulate activity in ACC, whereas those that alter the sensory component of pain modulate activity in the other cortical regions, particularly S1 cortex. Finally, whether the cortical areas are activated by experimental pain or by aberrant chronic pain states, the pain-evoked activation can be modulated by cognitive factors, such as direction of attention.