Visual Agnosia is a comprehensive and up-to-date review of disorders of higher vision that relates these disorders to current conceptions of higher vision from cognitive science, illuminating both the neuropsychological disorders and the nature of normal visual object recognition.Brain damage can lead to selective problems with visual perception, including visual agnosia the inability to recognize objects even though elementary visual functions remain unimpaired. Such disorders are relatively rare, yet they provide a window onto how the normal brain might accomplish the (...) complex task of vision. Visual Agnosia reviews a century of case studies of higher-level visual deficits following brain damage, places them in the general context of current neuroscience, and draws relevant conclusions about the organization of normal visual processing. It is unique in drawing on research in cognitive psychology, computational vision, visual neurophysiology, and neuropsychology to interpret the agnosias and draw inferences from them about visual object recognition.Following a historical account of agnosia research, Visual Agnosia offers a taxonomy of a wide range of agnosia syndromes, describing and interpreting the syndromes in terms of the latest theoretical models of visual processing and ultimately bringing them to bear as evidence on a variety of questions in the study of higher vision.Martha J. Farah is Associate Professor of Psychology at Carnegie Mellon University. Visual Agnosia is included in the Issues in Biology of Language and Cognition series, edited by John Marshall. (shrink)

Patients with right parietal lesions often deny their paralysis , but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task vs a unimanual one . They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis . Second, I used a "virtual reality box" (...) to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM′s left ear canal with cold water, a procedure that is known to shift that patient′s spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also emply a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift". A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor. (shrink)