Understanding the physical basis of psychosomatic processes, including the so-called mind-body problem, will require a detailed understanding the psychobiology of interoception.

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A dissociation between human neural systems that participate in the encoding and later recognition of new memories for faces was demonstrated by measuring memory task-related changes in regional cerebral blood flow with positron emission tomography. There was almost no overlap between the brain structures associated with these memory functions. A region in the right hippocampus and adjacent cortex was activated during memory encoding but not during recognition. The most striking finding in neocortex was the lateralization of prefrontal participation. Encoding activated left prefrontal cortex, whereas recognition activated right prefrontal cortex. These results indicate that the hip-pocampus and adjacent cortex participate in memory function primarily at the time of new memory encoding. Moreover, face recognition is not mediated simply by recapitulation of operations performed at the time of encoding but, rather, involves anatomically dissociable operations. In humans and nonhuman primates, damage to the hippocam-pus and adjacent cortex produces a profound anterograde amnesic syndrome that impairs the ability to form and store new explicit memories (1-5). Although recall for previously stored information can remain largely intact (1, 4, 6), the retrieval of recently formed memories may be impaired (3). Thus, for a limited time after initial storage, access to memories does depend on the integrity of the medial temporal structures, suggesting that these structures may actively participate not only in memory storage but also in the retrieval of recently stored memories. Despite this clear evidence of memory impairment after medial temporal lesions, functional brain imaging studies of human memory have been mostly unsuccessful in demonstrating the participation of the hippocampus and adjacent cortex in either the encoding or the retrieval of new long-term memories (7-12). These same studies, however, consistently demonstrate that the frontal lobes participate in episodic memory encoding and retrieval, although studies of the effects of frontal lobe lesions suggest these areas do not play a critical role in episodic memory processing (13-18). Most previous functional brain imaging studies of memory have used verbal materials and have demonstrated a functional dissociation between left and right prefrontal areas. Whereas left prefron-tal areas are activated during episodic verbal memory encoding , right prefrontal areas are activated during retrieval. Although some studies suggest that right prefrontal areas might also be involved in the retrieval of nonverbal long-term memories, no studies of nonverbal memory encoding have been reported. To clarify the roles played by these brain structures in episodic memory, we investigated memory for a different type The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. of information-namely faces-using an experimental design t...

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These results demonstrate the involvement of specific brain regions as well as hemispheric laterality of function in visceral perception, and they suggest that during emotional reactions involving changes in visceral organ function, activation of some of the brain regions observed could be due specifically to interoceptive processes.

Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.

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