The Neurology of Consciousness, Second Edition

Book Preface

Looking back is often disappointing and not really a good way of deciding what to do next. But in cognition research we can’t help but muse on those who claimed as little as 25 years ago that consciousness was not a subject respectable neuroscientists should concern themselves with. The problem was too complex, the concept too ill-defined, the level of organization unreachable and so on. Predicting the future is a difficult game, which is presumably why, as a community, scientists prefer experimentation based on models, peer review, and evaluation. Happily so, this book clearly demonstrates that not only is consciousness a viable subject for scientific study but also that the diverse meanings of the word “consciousness” firm up as new measuring instruments and experimental methods become available.

As a word, “consciousness” is rich, means too many things and requires deconstruction to become tractable. There are, for example, the contents of consciousness, mechanisms that access them, issues of awareness, implicit and explicit ways of recovering conscious events and so on. In common language, all these are subsumed in one way or another under the single term, consciousness. A simple analogy might be with the term “memory”—understood by all, but dissection of that concept by science into various types and mechanisms has enriched its comprehension considerably. An initial division into normal “conscious access” and its disorders in humans is potentially helpful. It is a universal experience to oscillate daily between sleep and wakefulness, thereby regularly to experience loss of conscious access. Similarly, general anesthesia systematically manifests by a chemically elicited and reversible “loss of consciousness,” a widely accepted use of the word consciousness in a medical context.

From the neurological standpoint, it is commonly held that to lose consciousness (in the sense of a global loss of conscious access) it is necessary to suffer bilateral hemispheric damage or a midbrain lesion. Certainly this is true, but there are states in which apparent changes in consciousness are found that are limited to bilateral thalamic damage; so, bi-hemispheric, but limited in extent to critical regions. Consciousness can be impaired by large intracerebral lesions, such as hemorrhages, tumors, or aneurysms, that distort the brain by occupying space and impinging directly on both hemispheres, or pushing down onto the midbrain or by disease of local origin that spreads to involve these regions, as in focal epilepsies. It can also result from metabolic starvation as in hypoxia or with poisoning, for example, with gases such as carbon dioxide, carbon monoxide, or nitrous oxide. These phenomena have been known for a long time and, though dramatic, they give little insight into the neurobiology of consciousness, other than by providing the gross anatomical substrate described above.

Generally disturbed consciousness can occur in milder form, sometimes manifesting as confusion, and can also be caused by poisoning or metabolic insults from various pharmacological or toxic agents. Sometimes these are taken voluntarily; often they can modify the contents of consciousness in a repeatable and predictable manner. Alcohol is a clear example and various psychoactive drugs can either alter consciousness by instilling a negative state (such as opiates) while others distort consciousness, invoking hallucinations or heightened awareness that is often imaginary but easily communicated to others (e.g., LSD, magic mushrooms, and the like). In this latter situation, the disturbances of consciousness are not just due to altered access but also to an interaction with the contents of consciousness.

As mentioned, an unconscious state that resembles slow-wave sleep can be induced in a controlled fashion by infusion of general anesthetics, with remarkable precision. Propofol, for instance, can induce a loss of consciousness and subsequent recovery in seconds by manipulating intravenous doses, indicating a precise threshold effect. The mechanisms by which drugs such as propofol, barbiturates, and benzodiazepines act are known in detail at the molecular level, and their sites have been explored by photo-labeling and X-ray crystallography at the atomic level. They act as positive allosteric modulators of receptors and ion channels, such as the GABAA receptor (the ionotropic receptor of the inhibitory neurotransmitter gamma-aminobutyric acid). By enhancing inhibition in the brain at this level, they depress a general excitation of the cerebral cortex that seems necessary for conscious access. But the precise sub-cellular and neuronal targets at which they cause a loss of consciousness are still not fully identified.

The unconscious state that has been the most intriguing and that, it must be said, has caused the most difficulty is that of sleep. For example, sleep, in which we are considered unconscious, can be associated with total muscle atony but also with muscular activity, be it of the eyes or manifesting as more general movements. It is a state into which one can “drop,” or awaken from with a startle. One cause of ambiguity is the observation that we dream in sleep and at times are able to recount some of the substance of those dreams when awake again. If an account of a dream can be given, is a subject conscious whilst unconscious? The awareness of spontaneous inner states implies access to content and hence consciousness, while unresponsiveness to the external world implies the opposite. Is a recounted dream episode a form of deferred consciousness, or is it the product of an interaction between level of awareness and access to the contents of consciousness? Different phenomenological features co-occur in different ways to produce a rich tapestry of sleep states, which is why we struggle with understanding a unitary concept of consciousness.