William Hirstein

Neurological syndromes in which consciousness seems to malfunction, such as temporal lobe epilepsy, visual scotomas, Charles Bonnet syndrome, and synesthesia offer valuable clues about the normal functions of consciousness and ‘qualia’. An investigation into these syndromes reveals, we argue, that qualia are different from other brain states in that they possess three functional characteristics, which we state in the form of ‘three laws of qualia’. First, they are irrevocable: I cannot simply decide to start seeing the sunset as green, or feel pain as if it were an itch; second, qualia do not always produce the same behaviour: given a set of qualia, we can choose from a potentially infinite set of possible behaviours to execute; and third, qualia endure in short-term memory, as opposed to non-conscious brain states involved in the on-line guidance of behaviour in real time. We suggest that qualia have evolved these and other attributes because of their role in facilitating non-automatic, decision-based action. We also suggest that the apparent epistemic barrier to knowing what qualia another person is experiencing can be overcome by using a ‘bridge’ of neurons; and we offer a hypothesis about the relation between qualia and one's sense of self.

[This is a response to a target article in BBS]. Although the art-historical context of a work of art is important to our appreciation of it, it is our knowledge of that history that plays causal roles in producing the experience itself. This knowledge is in the form of memories, both semantic memories about the historical circumstances, but also episodic memories concerning our personal connections with an artwork. We also create representations of minds in order to understand the emotions that artworks express

Recent evidence points to widespread underconnectivity in autistic brains owing to deviant white matter, the fibers that make long connections between areas of the cortex. Subjects with autism show measurably fewer long-range connections between the parietal and prefrontal cortices. These findings may help shed light on the current debate in the consciousness literature about whether conscious states require both prefrontal and parietal/temporal components. If it can be shown that people with autism have conscious states despite such underconnectivity, this would constitute an argument for the claim that conscious states can exist in posterior cortex without associated prefrontal activity. This in turn lends support to a class of theories according to which microconsciousness is possible—consciousness in small areas of cortex without active connections to the prefrontal cortex, as opposed to the higher-order thought (HOT) theory of consciousness, according to which conscious states can only occur when posterior cortical areas (in the parietal or temporal lobes) have active connections to the prefrontal cortex. In this chapter, after listing several candidate examples of consciousness without accompanying prefrontal connections, I will argue that autism provides yet another such example. I will also examine a recent version of the higher-order theory that acknowledges these cases of consciousness without prefrontal activity and, instead depicts consciousness as requiring higher-order thoughts located in posterior cortex. In the final section, I will examine the consequences of these views for our understanding of the metaphysical nature of consciousness itself—the classic mind-body problem.

Cases in which people are self-deceived seem to require that the person hold two contradictory beliefs, something which appears to be impossible or implausible. A phenomenon seen in some brain-damaged patients known as confabulation (roughly, an ongoing tendency to make false utterances without intent to deceive) can shed light on the problem of self-deception. The conflict is not actually between two beliefs, but between two representations, a 'conceptual' one and an 'analog' one. In addition, confabulation yields valuable clues about the structure of normal human knowledge-gathering processes. [The hypothesis defended here is significantly altered and greatly expanded in my book Brain Fiction.]

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.'

One of the final obstacles to understanding consciousness in physical terms concerns the question of whether conscious states can exist in posterior regions of the brain without active connections to the brain's prefrontal lobes. If they can, difficult issues concerning our knowledge of our conscious states can be resolved. This paper contains a list of types of conscious states that may meet this criterion, including states of coma, states in which subjects are absorbed in a perceptual task, states in brains with damaged prefrontal lobes, states of meditation and conscious states of some infants and animals. Recent evidence also suggests that conscious states of some people with autism may meet this criterion.

According to several current theories, executive processes help achieve various mental actions such as remembering, planning and decision-making, by executing cognitive operations on representations held in consciousness. I plan to argue that these executive processes are partly responsible for our sense of self, because of the way they produce the impression of an active, controlling presence in consciousness. If we examine what philosophers have said about the "ego" (Descartes), "the Self" (Locke and Hume), the "self of all selves" (William James), we will find that it fits what is now known about executive processes. Hume, for instance, famously argued that he could not detect the self in consciousness, and this would correspond to the claim (made by Crick and Koch, for instance) that we are not conscious of the executive processes themselves, but rather of their results

Contrary to the widely-held view that our conscious states are necessarily private (in that only one person can ever experience them directly), in this paper I argue that it is possible for a person to directly experience the conscious states of another. This possibility removes an obstacle to thinking of conscious states as physical, since their apparent privacy makes them different from all other physical states. A separation can be made in the brain between our conscious mental representations and the executive processes that manipulate them and are guided by them in planning and executing behaviour. I argue here that these executive processes are also largely responsible for producing our sense of self in the moment. Our conscious perceptual representations themselves reside primarily in the posterior portions of the brain's cortex, in the temporal and parietal lobes, while the executive processes reside primarily in the prefrontal lobes. We can imagine an experiment in which we sever the association fibers that connect the posterior regions with these prefrontal regions and, instead, connect the posterior regions to the prefrontal regions of another person. According to my hypothesis, this would produce in the latter person the direct experience of the conscious perceptual states of the first person.

The patient with Capgras’ syndrome claims that people very familiar to him have been replaced by impostors. I argue that this disorder is due to the destruction of a representation that the patient has of the mind of the familiar person. This creates the appearance of a familiar body and face, but without the familiar personality, beliefs, and thoughts. The posterior site of damage in Capgras’ is often reported to be the temporoparietal junction, an area that has a role in the mindreading system, a connected system of cortical areas that allow us to attribute mental states to others. Just as the Capgras’ patient claims that that man is not his father, the patient with asomatognosia claims that his arm is not really his. A similar account applies here, in that a nearby brain area, the supramarginal gyrus, is damaged. This area works in concert with the temporoparietal junction and other areas to produce a large representation of a mind inside a body situated in an environment. Damage to the mind-representing part of this system (coupled with damage to executive processes in the prefrontal lobes) causes Capgras’ syndrome, whereas damage to the body-representing part of this system (also coupled with executive damage) causes asomatognosia.