Theorists are converging from quite different quarters on a version of the global neuronal workspace model of consciousness, but there are residual confusions to be dissolved. In particular, theorists must resist the temptation to see global accessibility as the cause of consciousness (as if consciousness were some other, further condition); rather, it is consciousness. A useful metaphor for keeping this elusive idea in focus is that consciousness is rather like fame in the brain. It is not a privileged medium of (...) representation, or an added property some states have; it is the very mutual accessibility that gives some informational states the powers that come with a subject's consciousness of that information. Like fame, consciousness is not a momentary condition, or a purely dispositional state, but rather a matter of actual influence over time. Theorists who take on the task of accounting for the aftermath that is critical for consciousness often appear to be leaving out the Subject of consciousness, when in fact they are providing an analysis of the Subject, a necessary component in any serious theory of consciousness. (shrink)

A broad consensus has developed in recent years in the cognitive and neurosciences that the cognitive functions of the mind arise out of the activities of an extensive and diverse array of specialized processors operating as a parallel, distributed system. A theoretical perspective is presented which expands upon this "society" model to include globally integrative infuences upon this arrary of processors. This perspective serves as the basis for an explicit neural model of a "global workspace within a system of distributed (...) specialized processors". Anatomical and physiological evidence are reviewed which suggest that this parallel, modular architecture is superceded by a more diffuse, tangential intracortical network capable of integrating underlying modular activites into increasingly global cognitive representations. There follows an explication of the role of this "neural global workspace" in providing the essential basis for the central control of attention and the generation of unified, conscious percepts. Finally the role of thalamic and brainstem activation systems in these integrative processes is discussed. (shrink)

This introductory chapter attempts to clarify the philosophical, empirical, and theoretical bases on which a cognitive neuroscience approach to consciousness can be founded. We isolate three major empirical observations that any theory of consciousness should incorporate, namely (1) a considerable amount of processing is possible without consciousness, (2) attention is a prerequisite of consciousness, and (3) consciousness is required for some specific cognitive tasks, including those that require durable information maintenance, novel combinations of operations, or the spontaneous generation of intentional (...) behavior. We then propose a theoretical framework that synthesizes those facts: the hypothesis of a global neuronal workspace. This framework postulates that, at any given time, many modular cerebral networks are active in parallel and process information in an unconscious manner. An information becomes conscious, however, if the neural population that represents it is mobilized by top-down attentional amplification into a brain-scale state of coherent activity that involves many neurons distributed throughout the brain. The long-distance connectivity of these `workspace neurons' can, when they are active for a minimal duration, make the information available to a variety of processes including perceptual categorization, long-term memorization, evaluation, and intentional action. We postulate that this global availability of information through the workspace is what we subjectively experience as a conscious state. A complete theory of consciousness should explain why some cognitive and cerebral representations can be permanently or temporarily inaccessible to consciousness, what is the range of possible conscious contents, how they map onto specific cerebral circuits, and whether a generic neuronal mechanism underlies all of them. We confront the workspace model with those issues and identify novel experimental predictions. Neurophysiological, anatomical, and brain-imaging data strongly argue for a major role of prefrontal cortex, anterior cingulate, and the areas that connect to them, in creating the postulated brain-scale workspace. (shrink)

Four detailed cases of delusions of misidentification (DM) are presented: two cases of misidentification of the reflected self, one of reverse intermetamorphosis, and one of reduplicative paramnesia. The cases are discussed in the context of three levels of interpretation: neurological, cognitive and phenomenological. The findings are compared to previous work with DM patients, particularly the work of Ellis and Young (1990; Young, 1998) who found that loss of the normal affective response to familiar faces was a contributing factor in the (...) Capgras delusion. The four cases presented suggest that this particular deficit is not a critical factor in the development of other forms of DM. (shrink)

Logothetis, N.K.: Single units and conscious vision. Philosophical Transactions of the Royal Society of London Series B-Biological Sciences 353, 1801-1818 (1998) Abstract.

We describe some of the signs and symptoms of left visuo-spatial neglect. This common, severe and often long-lasting impairment is the most striking consequence of right hemisphere brain damage. Patients seem to (over-)attend to the right with subsequent inability to respond to stimuli in contralesional space. We draw particular attention to how patients themselves experience neglect. Furthermore, we show that the neglect patient's loss of awareness of left space is crucial to an understanding of the condition. Even after left space (...) has been brought into the patient's consciousness (either by local cueing on the left or by an emphasis on global properties of the scene as a whole), this awareness of left space rapidly declines. We suggest that much of the symptomology of left neglect can be interpreted as a disconnection between brain mechanisms that are relatively specialized for local (detail) visual processing and global (panoramic) processing. This failure of communication between functional (subpersonal) mechanisms then has consequences for how perceptual and representational content enters into awareness. Failure of the local contents of left space to be consciously accessed is, in turn, an important aspect of why left neglect is so difficult to remediate. Patients can ''know'' that they have neglect but are cut off from the perceptual awareness that would enable them to overcome their attentional bias to the right. (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)