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)

Localizing the self in the brain has been the goal of consciousness research for centuries. Recently, there has been an increase in attention to the localization of the self. Here we present data from patients suffering from a loss of self in an attempt to understand the neural correlates of consciousness. Focusing on delusional misidentification syndrome , we find that frontal regions, as well as the right hemisphere appear to play a significant role in DMS and DMS related disorders. These (...) data are placed in the context of neuroimaging findings. (shrink)

In spite of enormous recent interest in the neurobiology of the self, we currently have no global models of the brain that explain how its anatomical structure, connectivity, and physiological functioning create a unified self. In this article I present a triadic neurohierarchical model of the self that proposes that the self can be understood as the product of three hierarchical anatomical systems: The interoself system, the integrative self system, and the exterosensorimotor system. An analysis of these three systems and (...) their functional features indicates that the neural hierarchy possesses features of both non-nested and nested hierarchies that are necessary for the creation of a unified consciousness and self. These functional properties also make the central nervous system a biologically unique entity unlike anything else in nature. (shrink)

We provide a battery of examples of delusions against which theoretical accounts can be tested. Then, we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher’s view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second factor in the (...) aetiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows. But we point out some problems that confront any attempt to say more about the nature of this second factor. (shrink)

Article copyright 2002. We provide a battery of examples of delusions against which theoretical accounts can be tested. Then we identify neuropsychological anomalies that could produce the unusual experiences that may lead, in turn, to the delusions in our battery. However, we argue against Maher's view that delusions are false beliefs that arise as normal responses to anomalous experiences. We propose, instead, that a second factor is required to account for the transition from unusual experience to delusional belief. The second (...) factor in the etiology of delusions can be described superficially as a loss of the ability to reject a candidate for belief on the grounds of its implausibility and its inconsistency with everything else that the patient knows, but we point out some problems that confront any attempt to say more about the nature of this second factor. (shrink)

Anosognosia is literally ‘unawareness of or failure to acknowledge one’s hemi- plegia or other disability’ (OED). Etymology would suggest the meaning ‘lack of knowledge of disease’ so that anosognosia would include any denial of impairment, such as denial of blindness (Anton’s syndrome). But Babinski, who introduced the term in 1914, applied it only to patients with hemiplegia who fail to acknowledge their paralysis. Most commonly, this is failure to acknowledge paralysis of the left side of the body following damage to (...) the right hemisphere of the brain. In this paper, we shall mainly be concerned with anosognosia for hemiplegia. But we shall also use the term ‘anosognosia’ in an inclusive way to encompass lack of knowledge or acknowledgement of any impairment. Indeed, in the construction ‘anosognosia for X’, X might even be anosognosia for some Y. (shrink)