articles Emotional, cognitive and physical behaviors mediated by the central nervous system are integrated with peripheral changes in bodily states. Moreover, physiological changes in bodily state directly influence emotional expression 1,2 and cognitive functions such as decision-making 3 and memory 4 . At a broader level, emotions may be subsumed within homeostatic mechanisms that underlie survival of the organism 2,5 . In a theoretical model 5 based on neurological observations, prime emphasis is given to the cerebral representation of bodily states as a substrate for emotions and conscious awareness. Fundamental components of the model are first-order autoregulatory mappings and second-order re-mappings of bodily states consequent upon behavioral experience. The dorsal pons is proposed to support first-order mapping of bodily state, because of its involvement in homeostatic regulation mediated via afferent information from the body. The model also proposes that somatosensory areas, the somatosensory cortices and insula, contribute to this primary representation of bodily states. In contrast, cingulate and medial parietal cortices are critical components in second-order mappings of experience-dependent changes in body states.Here we tested specific predictions arising from these theoretical considerations. We compared the state-dependent regional brain activity in healthy human subjects with activity in subjects with pure autonomic failure (PAF) 6 . PAF is an idiopathic disorder acquired in middle age that only affects the peripheral autonomic nervous system. Subjects with PAF cannot modulate their bodily state via the autonomic nervous system because of peripheral autonomic denervation, but have no other neurological deficit (sensory or motor). Consequently, there is no integrated central feedback of information concerning autonomic changes that are normal accompaniments of ongoing behavior 6 . Peripheral autonomic denervation results in a failure of neurogenic control of circulation, the cardinal feature of which is orthostatic (postural) hypotension due to an inability to activate sympathetic pathways to engender vasoconstriction during gravitational challenges [6][7][8] . Additionally, subjects with PAF do not generate heart rate and blood pressure increases during effortful exercise or mental arithmetic (stressor tasks) 6 and do not increase circulating catecholamines during physical or emotional challenge 6 . These subjects have absent sympathetic skin conductance responses to emotive and orienting stimuli 9 , and have diminished pupilliary reflexes 10 . Through histological evidence, PAF has been associated with Lewy bodies in peripheral autonomic ganglia 11 , but its cause is unknown 6 . PAF is distinguished from central neurodegenerative causes of autonomic failure (such as multiple system atrophy or Parkinson's disease with autonomic failure) by normal life expectancy 6,7 , and by the absence of clinical and hormonal 12 indicators of central neurological degeneration. Similarly, gross and pervasive...