Almost everyone who has a limb amputated will experience a phantom limb--the vivid impression that the limb is not only still present, but in some cases, painful. There is now a wealth of empirical evidence demonstrating changes in cortical topography in primates following deafferentation or amputation, and this review will attempt to relate these in a systematic way to the clinical phenomenology of phantom limbs. With the advent of non-invasive imaging techniques such as MEG (magnetoencephalogram) and functional MRI, topographical reorganization can also be demonstrated in humans, so that it is now possible to track perceptual changes and changes in cortical topography in individual patients. We suggest, therefore, that these patients provide a valuable opportunity not only for exploring neural plasticity in the adult human brain but also for understanding the relationship between the activity of sensory neurons and conscious experience. We conclude with a theory of phantom limbs, some striking demonstrations of phantoms induced in normal subjects, and some remarks about the relevance of these phenomena to the question of how the brain constructs a 'body image.'

Several recent lines of inquiry have pointed to the amygdala as a potential lesion site in autism. Because one function of the amygdala may be to produce autonomic arousal at the sight of a signi¢cant face, we compared the responses of autistic children to their mothers' face and to a plain paper cup. Unlike normals, the autistic children as a whole did not show a larger response to the person than to the cup. We also monitored sympathetic activity in autistic children as they engaged in a wide range of everyday behaviours. The children tended to use self-stimulation activities in order to calm hyper-responsive activity of the sympathetic (`¢ght or £ight') branch of the autonomic nervous system. A small percentage of our autistic subjects had hyporesponsive sympathetic activity, with essentially no electrodermal responses except to self-injurious behaviour. We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes.

SUMMARYPatients with Capgras syndrome regard people whom they know well such as their parents or siblings as imposters. Here we describe a case (DS) of this syndrome who presents several novel features. DS was unusual in that his delusion was modality-specific : he claimed that his parents were imposters when he was looking at them but not when speaking to them on the telephone. Unlike normals, DS's skin conductance responses to photographs of familiar people, including his parents, were not larger in magnitude than his responses to photographs of unfamiliar people. We suggest that in this patient connections from face-processing areas in the temporal lobe to the limbic system have been damaged, a loss which may explain why he calls his parents imposters. In addition, DS was very poor at judging gaze direction. Finally, when presented with a sequence of photographs of the same model's face looking in different directions, DS asserted that they were ' different women who looked just like each other '. In the absence of limbic activation, DS creates separate memory ' files ' of the same person, apparently because he is unable to extract and link the common denominator of successive episodic memories. Thus, far from being a medical curiosity, Capgras syndrome may help us to explore the formation of new memories caught in flagrante delicto.

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