AN APPROACH TO THE PHYSIOLOGY of CONSCIOUSNESS
by
Joseph E. Bogen
Clinical Professor of Neurologic Surgery
University of Southern California
and
Adjunct Professor of Behavioral Neuroscience
University of California at Los Angeles
and
Visiting Professor of Biology
California Institute of Technology
ABSTRACT Consciousness can be investigated in a variety of ways on different levels, including the physiological level. Exploring consciousness physiologically is facilitated by recognizing that the many meanings of "consciousness" almost all have in common (as their intersection ) a crucial core here called C also referred to as subjectivity, awareness, phenomenonal experience, sentience, consciousness-as-such or consciousness per se. A sharp distinction can be made between the property C and the contents of consciousness. Significant loss of contents without loss of C is typical of cerebro-cortical lesions. By contrast, loss of C from quite small lesions occurs only in certain subcortical sites which appear therefore to play a particularly important role in the manifestation of consciousness. Because the neuronal mechanism required for C also acts as an attention-action coordinator, it must have widespread connectivity. It is hypothesized that these requirements are best met by the thalamic intralaminar nuclei (ILN). The anatomic and neurologic evidence together with a variety of physiologic evidence is the main content of this essay. Also discussed are some implications for volition and emotion. It is urged that further study of the ILN is particularly apt to yield a clearer understanding of the neuronal substrate for consciousness.
CONSCIOUSNESS EXISTS: The first question about consciousness is whether there is such a thing. Claims to the contrary arise at least three ways: 1. Although we often can reach considerable agreement as to who or what is conscious, there are many indeterminate examples, e.g. sleepwalking. In answer to this: First, as pointed out by T.Sullivan (in discussion), it is fallacious to argue that, "if it is unclear in some cases whether something has C, then there is no such thing as having C." Second although indeterminate and partial states of consciousness no doubt occur I follow here the advice that, at our present state of knowledge, we do best to contrast the extreme examples, those about which we generally agree that the entities either are or are not conscious [Crick and Koch,1990, 2000]. Partial states such as sleepwalking are discussed by a number of authors[see e.g. Churchland,1986 and 2002; Revonsuo et al 2000].
2. The basis on which we attribute consciousness is not always the same-there seems to be no single universally applicable criterion [Allport,1988]. For example, we often use accurate eye tracking of a moving object as an indicator that someone is consciousness, but this can be fallible as well as often inappropriate. I follow Hempel [1966] and Goldman [1993] in their view that insisting on a single criterion for a supposedly unitary property has in science been "long since given up"; a standard example is length, which is measured in different ways depending on the context.
3. The word "consciousness" is used in many ways[Natsoulas,1983; Galin,1992; Guzeldere,1997; Hardcastle,2001; Zeman, 2001; Chalmers 2002]. The variety of usages led to the opinion of G. Rey [1997] that , "... there would seem to be no actual thing or process that our past usages have been getting at." [p473]. Related are assertions that it is necessary to define precisely as well as measure what we are talking about. But formal definitions and precise measurement typically emerge after we understand a subject, not before. These issues are discussed further in Appendix A for those interested.
THE CRUCIAL CORE (C) OF CONSCIOUSNESS .
One way to consider consciousness physiologically begins by recognizing that the many usages of "consciousness" have in common a crucial, central core which I have called C [Bogen, 1993a,1995a]. The property C has many other names including: 1st person experience[Fessard,1954], subjectivity[Flanagan,1992; Chalmers, 2002], awareness[Goldman,1993] , sentience[Searle,1993,1998], phenomenal consciousness [Block,1995], primary consciousness [Edelman,1992; Revonsuo,1995], consciousness-as-such[Baars1988,1993], consciousness per se [Gray,1995], consciousness itself [Moscovitch.1995], core consciousness [Parvisi and Damasio,2001] or simply, consciousness [G.E.Moore,1922; Grossman,1980].
Appendix A describes some philosophical considerations concerning the meaning of C, especially Naess's notion of precisation. For the moment, it may suffice to say that C is a much narrower concept than many people's usage of "consciousness"; it is intended to include the ascription of self or “me-ness” to some percept or affect. Examples include: “It hurts me,” “I see red,” “I feel thirsty.” Whatever else one might want to include in consciousness (e,g planning, control, awareness of self, monitoring, language, higher thoughts, sociality), C is at the core of most people's concept of consciousness.
The view urged here is that we are well served by making a sharp distinction between the property C and the contents, potentially enormous, of consciousness. Appendix A has more on this, including references to others who have urged the same distinction. One fact motivating this approach is that partial, specific loss of contents is typical of cerebro-cortical lesions which leave C otherwise intact. A useful first step is to look for a process or mechanism providing the property C, without trying to explain everything else that "consciousness" might include.
C ARISES FROM BRAIN.
A persistent question about consciousness is: where does it come from? I take it for granted in this essay that C depends upon specific brain processes. I assume that every sensation, thought, feeling, memory, expectation is represented in brain by a neuronal activity pattern (NAP). This view, while explicitly mechanistic, is not necessarily materialistic or completely deterministic, as discussed in Appendix C [and in Bogen,1998] for those who care about the metaphysics.
This approach allows an experimental approach to several questions: First, what is the change in a NAP that occurs when it is endowed with C? This question implies that recording from brain cells (electrically or chemically or both) will provide information which distinguishes, in the words of Marcel[1988], "processing without consciousness from processing which is also describable as conscious"(p126). Second, is there an identifiable mechanism that produces the change in a NAP? Such a mechanism, which endows NAPs with C, is named in this essay Mc. A third question is: what determines which NAP will be endowed with C at any particular time?
Regarding the first question, one possibility is that the change in a NAP is simply a sufficient increase in activity as measured by neuronal firing rates [Fuster,2002]; a problem with this suggestion is that, under some circumstances, recordings from neurons known to respond to a specific stimulus sometimes show a decrease in firing rate when the subject (a monkey) indicates it is aware of that stimulus [Leopold and Logothetis,1996; see also Rees et al, 2002; Kreiman et al,2000]. Later in this essay, we can briefly consider the possibility that the change in NAPs might include increased synchrony [Singer,1998;Fries et al 1999a]. Regarding the third question, the answers are usually expressed in such psychological terms as "salience" or "attention"; I will address these important aspects sparingly, instead focusing on the second question, characterizing Mc, the mechanism that can endow a NAP with C.
WE ARE LOOKING FOR Mc RATHER THAN C.
C is provided by some cerebral mechanism, Mc. It is this mechanism which we hope to identify and ultimately analyze. Trying to point to C may turn out to be like pointing to the wind. We can point to the effects of the wind, and we can usually give a good account of what causes the wind, the causes often being quite distant (in miles) from the effects. We do not actually see the wind itself, only leaves fluttering, or material such as dust or smoke being carried by the wind. Similarly with C, we detect its presence by its effects. Which effects might be considered most typical of "consciousness" is important. However, in this essay I assume the specific effects depend mainly upon the contents which are endowed with C; since the contents vary with species, individuals and surounding context, considering the effects is not apt to tell us what is common to all of these, that is the neuronal basis of Mc.
While looking for Mc, we keep in mind some relevant points to be discussed next: that cognition can occur without C, that endowment with C is transient, that C is emergent, and that C depends upon some anatomical structures more than others.
.
COGNITIVE PROCESSING UNACCOMPANIED BY C.
Although mentation, either thinking or feeling, was for centuries described as synonymous with consciousness, it is now established that complex, purposeful mentation occurs without our being conscious of it. That is, although C facilitates mentation and is necessary for much of it, we nevertheless recognize that the NAPs corresponding to much mentation need not be endowed with C. Earlier experiments to show that meaningful contents requiring neocortical activity can influence behavior without being conscious were subject to a variety of methodological criticisms [Hollender, 1986]. However, considerable evidence since has made clear the existence of nonconscious sensorially guided and precisely monitored action [ Kihlstrom, 1987; Landis and Regard,1988: Taylor & McCloskey, 1990; Berti and Rizzolatti, 1992; Bar & Biederman, 1998,1999; Libet, 1993; Henke et al, 1993; Castiello et al 1991; Jeannerod, 1992; Wexler et al, 1992; Zaidel et al,1995; Milner and Goodale,1996]. See also the reviews by Weiskrantz,1997; Zeman,2001 and Koch,2003).
C REQUIRES A TIME DEPENDENT PROCESS.
Most discussants agree that NAPs which are potentially conscious make up a restricted fraction of the NAPs possible in a brain. And of those NAPs which sometime or other can acquire C, a very small fraction is endowed with C at any one moment. There is considerable debate as to how long a "moment" is, possibly varying with the NAP involved. The exact time is not essential for most hypotheses about consciousness: most views currently advocated seem compatible with a metaphor of Pavlov[1928], "if the place of optimal excitability were luminous, then we should see [it] playing over the cerebral surface"[p222]. I believe that the "hot spot" can involve the depths as well as the surface. As mentioned in the previous paragraph, "optimal excitability" does not necessarily mean "increased excitability". Evidence will be presented here that specific, wired-in anatomical structures are needed for Mc; in addition, there needs to be some active process that transiently involves each NAP for the brief time it is endowed with C. This implies an affirmative answer to the question, "Does time help to understand consciousness?" [Engel et al,1999b].
C IS AN EMERGENT PROPERTY
A question not always explicitly addressed is whether C is an aggregative or an emergent property. A property possessed by a combination of parts is said to be aggregative if it results from combining smaller amounts of the same property; common examples are mass or electrical charge. An emergent property arises not from an accumulation of smaller amounts possessed by each part, but from the particular way in which the parts are put together; a common example is the rolling of a wheel. Whether it is made of wood, steel, plaster-of paris, or clay fired in a kiln, a wheel can roll. The property of "rollness' is largely independent of the properties of the parts, although not entirely; one cannot very well make a wheel out of jello, or oatmeal.
Another example of emergence is from Wimsatt (2002], "Many cases were classically considered as involving emergence—cases motivating claims that “the whole is more than the sum of the parts.”—like an electronic oscillator circuit. There’s nothing anti-reductionistic, mysterious, or inexplicable about being an oscillator. You can make one by hooking up an inductance, a capacitor, and a resistor in the right way with a voltage source. The system has the property of being an oscillator although none of its parts in isolation exhibit properties at all like this".
If as I maintain here, C is an emergent property, there may well be restrictions on the sort of parts that can be assembled for this purpose. At present, most of us believe that neurons are the essential constituents [McCulloch,1951]. An open mind on this issue involves remembering that real brains also have an abundance of glial cells [ Fields and Stevens-Graham,2002] and lots of different juices surrounding the neurons. (The wetness of brains is one of the big differences between brains and all known manmade computers).
That C is aggregative has had many advocates, one of the more prominent being R.Llinas [2001] who suggests that each individual neuron has, "a sliver of qualia" so that when many are added together there is a substantial amount. A similar view was expressed earlier by K.S.Lashley [1954] who spoke of "consciousness quanta" possessed even by simple reflexes.[p437]. Related is the suggestion of Greenfield[1998] that the intensity of subjective experience may correlate with the size of a nonspecialized neuronal network.
Until we have a more widely agreed upon understanding of C, this question remains open. The view in this essay is that Mc requires a specific arrangement of nerve cells, probably including or inducing specific chemical environments [Fuxe and Agnati, 1991;Bunin and Wightman,1999; Marder and Bucher,2001]. C DEPENDS UPON AN ANATOMICALLY LOCALIZABLE MECHANISM.
Once we agree that C depends upon brain, a next question is: are some brain parts more important than others? One can approach a physiologic understanding at anatomic levels from the microscopic to the most encompassing. That is, C might be supposed to appear at the subcellular level [e..g. the microtubules, as in Hameroff,1998]. Another approach is to attribute C to specific neurons.. Related is the view that processing of information is best described as depending upon a large number of nodes and each of these nodes is capable of generating its own "microconsciousness" [Zeki and Bartels, 1999]. The "nodes" may depend upon a special kind of cell, or special collections of cells. The idea that consciousness is generated independently in different places is supported by the finding that color and motion occurring at the same time can sometimes be perceived at different times [Zeki and Bartels,1999]. Hopefully, the reader will find that this phenomenon is also explicable by the hypothesis of this essay.
Special cells or circuits seem implied by the idea that C can accompany the ventral stream but not the dorsal stream. This last was proposed by Milner and Goodale [1996]; it derives from the proposal that visual information flows forward from the primary visual area in two directions: the ventral stream into the temporal lobe, giving rise to knowledge of what an object is, and the dorsal stream into the parietal lobe, giving rise to where it is [Ungerleider and Mishkin,1982]. Milner and Goodale prefer to regard the ventral and dorsal streams as serving perception and action respectively(p178) and suggest that processing in the dorsal stream is not normally available to awareness(p200).
A different approach emphasizing specialized cells was offered by E.G. Jones (1998). He pointed out that in each thalamus there are some cells, staining for the presence of parvalbumin, that project focally to cortex. Others which he calls matrix cells and which stain for calbindin project more diffusely. He suggests that it is the diffusely projecting matrix cells that contribute to "the binding of all aspects of sensory experience into a single framework of consciousness".(p69). Some hope to understand C in terms of much larger frameworks; these include the Extended Reticular Thalamocortical Activating System (ERTAS) of Baars and Newman [Newman,1995] which can act as a "global workplace" or "theatre of consciousness"[Baars,1997]
Claims that an entire brain must be involved are sometimes called "global" theories. What seems to be such a view was expressed by Lycan (1997) when he wrote,"The central nervous system is as central as it gets"(p762). More restricted, but nonlocalized hypotheses include the "integrated field theory of consciousness" of Kinsbourne[1988] and the complexity theory of Tonini and Edelman[1998] which proposes a highly mobile "dynamic core" of activity whose composition "can transcend traditional anatomic boundaries".
By contrast with much of the foregoing, I present below evidence for the hypothesis that C is better understood in terms of centrally located, hardwired circuits which embody what I have called Mc [Bogen,1993,1995,1997]. That is, Mc is supposed to depend upon a specific arrangement of neurons so organized, so centrally located, and so widely connected to other brain parts, that it can transiently endow a NAP elsewhere in brain with the property C. Kinsbourne, [1995] has criticized this concept, jocularly referring to what I call Mc as "the subjectivity pump"; this describes indeed what we are trying to find.
NAPs which are potentially conscious undoubtedly number in the billions. However, only a few can have C at any one moment. Probably relevant here is the process of "sparsening" by which complex, distributed material can be rapidly and specifically retrieved using only a fraction of the material to be retrieved [Kanerva,1988 concisely explained by Laurent,2002]. Because Mc, as conceived here, needs to reflect only a very small set of NAP at any one moment, Mc need not be very large as would be required in a socalled "Cartesian theatre", that is, "a place where it all comes together" [Dennett and Kinsbourne,1992].
EVIDENCE FOR LOCALIZATION OF Mc.
The usual localizationist argument involves two findings: first, a large deficit in some function (f) is produced by a small lesion in the “center” or "node" for that f. [this does not imply that the representation of f is wholly contained within some sharp boundary (Bogen & Bogen, 1976; Bogen 1976, Bogen and Berker,2002). Second, a large lesion elsewhere results in very little if any disturbance of f. A familiar example is the profound disturbance of speech beginning with "a complete linguistic suppression" [Lecours et al,1983] often leading to what is called agrammatism, from relatively small lesions in and around Broca's area of the left hemisphere[Henderson,1990]. By contrast, a very large lesion, even complete removal, of the right hemisphere rarely affects the syntactic competence of a right hander. With respect to C, quite small lesions involving the intralaminar nuclei (ILN) typically impair Mc (see below). By contrast, very large bicortical lesions typically do not (Damasio & Damasio, 1989; Benson, 1994). Anatomy, both what is required for C, as well as much that is dispensable, is discussed below, and in more detail in Appendix B.
NEOCORTEX PROVIDES CONTENT, NOT THE PROPERTY C.
That C is not produced by cerebral cortex was particularly urged by Penfield and Jasper (1954). Their views derived largely from observations of epilepsy, including that consciousness could be absent during complex behavior (requiring neocortex). Conversely, severe disturbances of function either from cortical removals or cortical hyperactivity need not be accompanied by loss of consciousness. There is more on this in Appendix B.
As early as 1937, Penfield expressed the main point of this chapter, “All parts of the brain may well be involved in normal conscious processes but the indispensable substratum of consciousness lies outside of the cerebral cortex, probably in the diencephalon..” (Penfield, 1937). (Diencephalon includes both thalamus and hypothalamus). It is an interesting fact that this view has largely been ignored by recent theorizers on consciousness, many of whom are almost exclusively fixated on neocortical function. We would do well to keep in mind the point of Steriade et al [1997] that for cortical information processing, "... at each step of this information flow, corticothalamic volleys engage synaptically the intrathalamic networks..."(p13). These authors go so far as to suggest that thalamus acts as a "switchboard" for the cerebrum. A slightly more up-to-date metaphor was offered by J.Schlag (in conversation) when he ventured that the ILN of thalamus acts as, "the brain's CPU" (central processing unit).
CONSCIOUS CONTENT INCLUDES PRIMITIVE, NONCOGNITIVE COMPONENTS.
To Penfield and Jasper's reasons can be added the observation that some important contents of consciousness are unneedful of cortical processing. Some potential contents of consciousness are quite primitive, that is, unneedful of neocortical discrimination, association or learning. Examples are nausea,shortness of breath, unelaborated pain (for example, the "electric" jabs of trigeminal neuralgia), thirst, and the like. It may be that Mc evolved to give these percepts greater potency, either to facilitate learning or to provide another layer of control over the stopping of ongoing action. In either case, it would appear that Mc was only subsequently recruited to serve so-called “higher functions” and more elaborate responses. We understand that Mc of humans routinely endows with C patterns of complex cortical activity describable as “representations of representations” or “higher order thoughts”[Rosenthal,1993;Rolls, 2000]. But these are special contents, not the crucial core of consciousness.
.AN HISTORICAL ANTECEDENT; THE CENTRENCEPHALON
When Penfield and Jasper [1954] argued against cerebral cortex as the source of C, they introduced the concept of a “centrencephalon”. When considering the possible anatomy embodying this psychological concept, they particularly stressed the role of ILN. Why was this concept, quite popular at the time, subsequently ignored for many years? At least three reasons can be readily seen:
1) The centrencephalon was supposed to be not only a mechanism for consciousness, but also a source of seizures which were “generalized from the start.” The concept of “centrencephalic seizures” has been largely abandoned by epileptologists. However, that Penfield and Jasper combined these two ideas does not require that we do so; arguments for an ILN role in C can be made quite independently of theories about seizure origin and spread.
2) Cerebral commissurotomy (the split-brain) reinforced doubts about the existence of a centrencephalon (Doty, 1975). However, the problem of localizing Mc can be approached in terms of a single hemisphere (which we know can have C), postponing to the future the problem of integrating two Mc, and how this bears on the “unity of consciousness.”
3)When Penfield and Jasper emphasized the ILN, there was considerable doubt of ILN projections to cortex, because unilateral decortication did not produce rapid degeneration in the ILN as it did in the principal nuclei. However, more recent tracer techniques have shown that ILN do indeed project to cortex, and widely.
The concept of a “centrencephalon” tried to explain too much. But it contained a germ of truth which now needs to be nourished in terms of ILN as a major constituent of the mechanisms which provide us, and creatures like us, with consciousness.
DIFFERENT KINDS OF EVIDENCE THAT Mc REQUIRES THE ILN.
Evidence for the hypothesis presented in this chapter comes from clinical neurology, from neuroanatomy. from electrophysiology and from other studies including experiments with functional magnetic resonance imaging(fMRI). Before getting to this evidence, some introductory anatomy may be helpful.
SIMPLIFIED IMAGE OF A THALAMUS.
Within each cerebral hemisphere, close to the midline, sits the thalamus of that hemisphere. When the hemispheres are separated and each is viewed from the medial aspect, each thalamus looks somewhat like a large pearl in an opened oyster. The human thalamus has about the size and shape of a pecan in the shell, with a bulbous swelling at the back end called the pulvinar (meaning: pillow).. The neurons in each thalamus are in clusters called nuclei. According to Netter[1953], long a favorite of medical students, each thalamus contains 11 nuclei. According to Hassler [in Schaltenbrand and Wahren,1977], long favored by neurosurgeons who operate on thalami, there are about 80 different nuclei. According to Jones[1985,1995], whose views reflect modern staining techniques, there are about 40.
We can restrict our attention to just a few nuclei. Of particular concern when emotion is discussed later in this essay is the medial dorsal nucleus(MD). MD is an ellipsoid about the size and shape of a Virginia peanut (out of its shell)located inside the pecan. MD is nestled up against the roof of the thalamus and against the medial wall. The ILN are collections of nerve cells draped like a blanket all over the MD, top and bottom, front and back and all along the side. In rats, cats and monkeys similar cells also cover the medial surfaces of both right and left MD; these clusters are merged in the midline and are given a separate name, the midline nuclei. In humans the midline nuclei are minimal and for the most part the two thalami are cleanly separated. In addition to the "blanket", it is customary to include in the ILN the centre mediane (CM) which resembles a soybean up against the "blanket", adjoining it just below the back end of MD. The CM seems to have a different function as judged by the fact that it stains differently from the rest of the ILN. It is notably bigger in primates than in most animals, and more so in humans, a fact to which we will return when discussing volition.
.
THE DEFINITION OF ILN HAS CHANGED.
Modern thalamic terminology was greatly influenced by LeGros Clark[1932]. He wrote, "Broadly speaking, the thalamic nuclei may be divided into two groups: principal nuclei and intralaminar nuclei". Further on, "Among the principal nuclei and outlining them are fiber tracts which form the medullary laminae. These laminae are strewn with cells[which] form the intralaminar nuclei."(p418) That is, the "intralaminar nuclei" originally got their name from their association with the laminae, whether actually inside them or close by outside them. Anatomists have argued about what should be included; most nowadays accept the view that they are defined by their projection to the striatum [Jones,1985,1989, 1998]. The considerable importance of this projection will come up later on with respect to volition. First, we consider some evidence that Mc depends on the ILN.SOME NEUROLOGIC EVIDENCE:THREE CLINICAL FACTS.
1.There are two levels in the CNS where very small lesions (less
than 1 gram) placed bilaterally can abruptly abolish consciousness: these
are either in the brainstem reticular formation (BSRF) or in the thalamic intralaminar nuclei (ILN). These facts are discussed in more detail, with appropriate references, further on. [see also appendix B].
Corollary: the effect on consciousness of brain damage depends crucially on its location. One of the most widely used textbooks on human
neuropsychology states:”There are no reports that individuals, who have lost
a certain restricted portion of the brain have lost their consciousness. The
idea that consciousness is a property of a single system or brain area
receives no support from clinical studies of people who have suffered brain
damage ...”.[Kolb and Wishaw,2000,p484].
People who want to understand consciousness can be led astray by these two sentences. Perhaps the authors had in mind cortical "system or brain area"; if so they were undoubtedly correct.
2. The larger the thalamic lesion, the more widespread the diaschisis (the shock effect depressing nerve cell function) [Szelies et al,1991]. Also, the larger the lesion, the more longlasting the deficit. This follows a basic principle of behavioral neurology (and of neuropsychology):that is, the location of the lesion commonly determines the nature of the behavioral deficit whereas the size of the lesion is usually the main determinant of the time and extent of recovery[Kertesz,1993]
.
Corollary: the effects on consciousness of appropriately
placed focal lesions follow the same rules as the effects produced by focal lesions on other brain functions. The fact that responsiveness returns after a small ILN lesion is not evidence against the necessity of ILN for C [Petit et al,1981;Smythies,1997], anymore than rapid recovery from a small lesion in Broca's area [Moutier,1908;Mohr,1973,1976; Dronkers,2000] means that this cortical area is irrelevant for aphasia, as once claimed by Pierre Marie[1906]. The ability of brains to recover significantly (though rarely ever completely) from structural damage is, along with wetness, an important property distinguishing brains from known artefacts.
3. So long as the lesion is unilateral, there will be no loss
of consciousness. This is true not only for a small lesion of a few grams in one of the two thalami but even for very large damage or removals (e.g. the removal of an entire hemisphere,in excess of 400 grams ).
Corollary;the mechanism for consciousness is paired,
existing in duplicate, a conclusion consonant with the bilaterality of the
anatomy and experimentally supported by the results of hemispherectomy and
the split-brain.
BILATERALITY OF THE MECHANISM
A striking example of loss of cerebral tissue is “total hemispherectomy” also called "hemicerebrectomy" (including cortex, underlying white matter and basal ganglia). Of the four patients reported by Austin and Grant[1958]one was stuporous preoperatively. The other three continued speaking and were “acutely aware” of their surroundings throughout the operation which was done under local anesthesia. Whatever the anatomical basis for producing C the anatomy exists in duplicate. That only one of the pair suffices for C is clear from hemispherectomy in humans[Austin and Grant,1958;Smith and Burklund,1900;Smith and Sugar,1975;Peacock,1996;Bogen et al 1999]. The same conclusion follows from hemicerebrectomy in monkeys and cats.[White et al,1959;Koskoff et al,1959; Kruper et al, 1971; Bogen and Campbell,1962;Bogen,1974]. And the same conclusion follows from temporarily anesthetizing a hemisphere (in humans)rather than removing it[Lesser et al, 1986].
Because the anatomy subserving Mc exists in duplicate, one might expect that there can be doubling of C, and this has indeed been inferred from the behavior of split-brain cats and monkeys[Sperry,1961] as well as humans.[Sperry, Gazzaniga and Bogen,1969]. How this duality is negotiated by an assortment of integrating mechanisms in the intact cerebrum is a fascinating and important question[Sperry,1968;Bogen,1969,1977,1990,1993;Kinsbourne and Smith,1974; Trevarthen,1974;Landis and Regard, 1988; Iacoboni & Zaidel, 1996;Zaidel et al, 2003).
However, because an individual needs only one hemisphere to be conscious, our immediate problem can be much simplified by restricting our attention to how C is engendered in someone with a single cerebral hemisphere.
It is worth emphasizing at this point that it is a mistake to argue against the possibility of an anatomically specifiable mechanism necessary for consciousness on the ground that no suitable anatomic structure is present in the middle of the head [Dennett and Kinsbourne ,1992; Flanagan,1991]. What is evident on any horizontal or frontal section of the cerebrum is the duality of any and all reasonable candidates; these are all present in pairs. The hemispherectomy data have established that either member of a pair is, in general, sufficient for C. If one is looking for a structure located "in the middle" of the hemisphere, one obvious place is in the thalamus of that hemisphere.
Many people are so accustomed to speak of “the” thalamus or “the” amygdala or “the” limbic system that they easily forget that there are two , one in each hemisphere.
THE ILN SUBSERVE Mc: BITHALAMIC PARAMEDIAN STROKES.
Support of the proposal that ILN subserve Mc includes the results of
thalamic obstructive strokes involving the thalamoperforating (paramedian)
arteries [Tatu et al,1998]. Simultaneous bimedial thalamic damage can
occur because the medial parts of both thalami are occasionally supplied by
a single arterial trunk which branches, one branch to each thalamus. If the
trunk is occluded before it branches, both thalami will be affected. When
there is simultaneous, partial damage of the two sets of ILN,
unresponsiveness typically ensues (see Table 2 of Guberman & Stuss, 1983).
Sudden onset of coma can occur even when the lesions are only a few cubic
centimeters in volume, as in case 4 of Graff-Radford et al [1990]. This is
in contrast to retention of responsiveness with very large infarctions
elsewhere. Even a quite large lesion involving one (and only one) thalamus
rarely if ever causes coma (Plum & Posner, 1985).Correlating thalamic damage with behavioral deficit is more precise with strokes from occlusion of blood supply than from bleeding or from tumors, so that emphasis is given here to cases of occlusion.
Classical autopsy examples of bithalamic occlusion often had extension of the damage downward into subthalamus [Facon et al 1958 ;Castaigne et al 1981]. Many cases carried uncertainties inherent in now outdated imaging techniques. In the past few years, published cases typically have crisp MRI images of quitesmall lesions whose extent is well demonstrated[Graff-Radford et al,1990; Tatemichi et al, 1992;Domburg et al, 1996; Wiest et al, 2000]; in these cases it has again been reported that onset of the bilateral damage was accompanied by abrupt loss of responsiveness.
Emergence from unresponsiveness after incomplete bithalamic lesions depends on the size of the lesion, taking only a few hours if the lesions are tiny, as in case 4 of Graff-Radford et al[1990].
When the lesions are larger it takes longer for the patient to arouse. With larger lesions, the recovery is commonly accompanied by mental impairments variously described as confusion, dementia, amnesia and/or hypersomnia. Which of these impairments dominates depends on precise lesion site as well as size [Mills and Swanson,1978;Schott et al 1980;Michel et al,1982;Guberman & Stuss, 1983; Graff-Radford et al,1990; Plum & Posner, 1985;Bewermeyer et al,1985; Gentilini,et al, 1987;Meissner et al,1987;Yasuda et al,1990;Bogousslavsky et al,1991;Malamut et al,1992; Markowitsch et al,1993;Abe et al,1993;Pasquier et al, 1995: Bogousslavsky & Caplan, 1995;Bassetti et al,1996].
With quite large bilateral lesions the patients usually remain in coma until they die. However, a patient with extensive ILN lesions may survive for many years, if medically supported, in a persistent vegetative state. That is, such a patient remains unresponsive in spite of relatively intact brainstem and cerebral cortex, as in the case (widely publicized at the time) of Karen Ann Quinlan [Kinney et al ,1994].
THE ILN SUBSERVE Mc.: THE WIDESPREAD CONNECTIONS.
Experiments using anatomical tracers have shown that with small lesions in almost every cortical region these regions project to ILN. It was pointed out by Koch (Koch, 1995) that inferotemporal cortex in the monkey has not been shown to connect with ILN. If further search for this specific connection fails, our attention will be increasingly focused on the pulvinar because it is widely connected to all of post-rolandic cortex and is thought to be essential to the determination of the salience of visual stimuli (Robinson & Cowie, in pressssss]. Groenewegen and Berendse [1994] reviewed evidence that ILN are more specific than the traditional term “non-specific” might suggest. They concluded that, “. . . the major role of the midline-intralaminar nuclei presumably lies in the regulation of the activity and the ultimate functioning of individual basal-ganglia-thalamocortical circuits” (p. 56), and that, “the midline-intralaminar nuclei are positioned in the forebrain circuits like a spider in its web” (p. 57).
Ascending input to ILN can help explain C of primitive percepts. The input to ILN includes a large fraction of the ascending output of the brainstem reticular formation, which subserves arousal but also contains information about other bodily states. Other input comes from a phylogenetically old spinothalamic system (conveying temperature and nociceptive information) and from the dentate nuclei in the cerebellum. There are also ascending inputs to ILN from deep layers of the superior colliculus, periacqueductal gray, substantia nigra, amygdala, trigeminal complex, and vestibular nuclei [McGuiness & Krauthamer, 1980; Kaufman & Rosenquist, 1985;Royce et al,1991].
THE ILN SUBSERVE Mc: MULTIPLE FUNCTIONAL ROLES.
In addition to clinical cases and use of anatomical tracers, information on the ILN has come from recording and stimulation. By 1966, Ervin and Mark [Ervin & Mark, 1966] were stimulating the ILN in pain patients, obtaining diffuse dysphoria, and making lesions which produced “a striking loss of the clinical pain.” When recording, they found neurons responding to visual and auditory as well as somesthetic stimuli. When Albe-Fessard and Besson published their monumental review [Albe-Fessard & Besson, 1978] they emphasized the polysensory functions of the ILN although admitting “a role to play” in the appreciation of pain. By 1980, McGuinness and Krauthamer [1980] concluded that the ILN acted not only as a thalamic pacemaker and as a relay for cortical arousal, but was characterized also by presence of cells responding to visual, auditory and somesthetic stimuli. They found further that at least part of the ILN was active in central pain mechanisms and in addition acted as a modulator of both striatal output and input, hence could be considered part of the motor apparatus. Similar conclusions were reached by Schlag and Schlag-Rey [1971,1984] after nearly twenty years of experiments on thalamic function. In addition, they had established a major role for ILN in the control of eye movements and visual attention[Orem et al,1973].
Purpura and Schiff [1997] concluded that a wide range of data, "suggest that in the state of wakefulness, the ILN neurons promote the formation of an "event-holding" function in the cortex". An abundance of neurologic, anatomic and functional evidence was subsequently reviewed by Schiff and Plum[1999] who wrote,"cortical and subcortical innervations of the ILN place them in a central position to influence distributed networks underlying arousal, attention, intention, working memory, and sensorimotor integration, including gaze control.".
SHORTNESS OF BREATH .
What may be the most primitive of subjective sensations is the experience of shortness of breath (SOB), sometimes called breathlessness, or air hunger or dyspnea. The usual cause of SOB is increased CO2 in the blood, whether from exertion, inadequate ventilation, lung disease or direct introduction of CO2 into the subjects inspired air. Extensive investigations have made it clear that SOB does not depend on feedback from respiratory muscles or rib cage; it is directly related to "respiratory drive", that is, the frequency of neuronal firing in the respiratory centers of the medulla [Eldridge and Chen, 1996]. The amount of respiratory drive is typically measured by recording the frequency of nerve impulses descending the phrenic nerve, rather than recording directly from the medulla. Since the sensation of SOB is not from bodily sensations (SOB occurs even when these are interrupted as in spinal cord injury) the likely source is a corollary discharge travelling upward from the medulla. Search of midbrain and of thalamus has disclosed neurons whose activity is closely correlated with phrenic nerve activity, as CO2 levels are manipulated. In thalamus the neurons becoming active with increased CO2 appear to be in the ILN [Eldridge and Chen,1996].
When CO2 is elevated, the pulse rate and respiratory rate rise along with increased respiratory effort. These compensatory reactions occur automatically. So what advantage is there in also having a subjective experience? The answer is not altogether clear; it may increase the likelihood of remembering what circumstances brought on the problem, or it may serve mainly to encourage the individual to change whatever else is occurring at the time.
Other questions remain since the experiments of Eldridge and Chen lacked histologic controls and have not been replicated to my knowledge. When they are repeated, it would be of interest to know if the ILN neurons apparently correlated with SOB are the same as those known to be responsive to pain, somesthetic and visual stimuli.
ASCENDING ACTIVATION.
It is important to distinguish Mc from the ascending activating influences arising from several sources in the brainstem reticular formation(BSRF). First, some background.
It has been known since work by Berger (1930) that transitions from resting to behavioral alertness are reflected in the electroencephalogram (EEG) as transitions from high-voltage low frequencies (HVLF) to lower-voltage higher frequencies (LVHF). This has since been considered to be a "desynchronization" of the EEG. When Bremer (1935,1936)transected the neuraxis at C1 ( the top end of the spinal cord) he found that the isolated brain (encéphale isolé) alternated between HVLF and LVHF. In addition, the cat's pupils alternated between small, as in sleep, and dilated as in the aroused animal. In other words, the isolated cat brain alternated between sleep and wakefulness in spite of being disconnected from the body below the neck and in spite of the head being fixed in a frame so the EEG could be recorded. From my own personal experience with the encephale isole I can also add that when the cat is awake, as judged by EEG criteria and pupil size, it accurately tracks with its eyes objects or persons moving about the room.
By contrast, Bremer found that after midbrain transection (the socalled Sherringtonian decerebration) the isolated cerebrum (cerveau isolé) stayed in the HVLF state. That is, without the brainstem the cerebrum was apparently unarousable. Subsequently, Moruzzi and Magoun [1949] found that stimulation within the brainstem reticular formation (BSRF) produced the EEG desynchronization typical of arousal. As was pointed out above, small (bilateral) lesions in the BSRF can cause immediate unresponsiveness. Together with relevant autopsy studies of coma in humans, this line of research led to the widely accepted notion of an ascending reticular activating system (ARAS) (Magoun, 1952).
A case of medullary infarction in human described by Plum and Posner [1985] indicates that transections even higher than C1, that is near the level of cranial nerve VIII (the auditory nerve) are compatible with, as they put it, “the behavioral appearance of consciousness.” Cats with an even higher transection of the brain stem at the level of cranial nerve V which carries sensory infomation from the head, are arousable. That is , although without sensory input including deafness, brains can respond to olfactory or visual input with the EEG characteristics and tracking eye movements we recognize as concomitants of awareness (Batini et al, 1959).
By 1960 it was generally accepted not only 1) that for consciousness, the cerebrum must remain attached to the upper end of the brainstem, but 2) this fact depended upon
ascending activating influences from the BSRF.
As the anatomic and chemical complexities of the BSRF became more apparent, the simple view of an ARAS came under attack; among other complexities was the growing awareness that the ascending influences arose from a number of different cell groupings [Brodal,1969]. And there were suggestions that both stimulation and lesions of BSRF might be affecting fibers of passage rather than BSRF cells. Moreover, when decerebrated cats were kept alive long enough, the isolated cerebrum could show transitions to the LVHF (“desynchronized”) state [Jouvet, 1967). This last finding is important since it indicates that the thalamocortical activity required for C (whether waking or in the REM state) can occur by itself even though it ordinarily depends upon ascending activation from the BSRF. In support of this, Alemà et al [1966] concluded from their experiments (see Appendix B for details) that ,"In man the most important subcortical structures ultimately responsible for maintenance of the level of consciousness are located rostral to the brain stem, perhaps in the diencephalon.”
For several decades, roughly 1965 to 1995, the concept of ascending activation was thought to be outdated. However, with the improvement of techniques there has been a reemergence of the concept. One example of a new technic is the use of ibotenic acid to make BSRF lesions. This excitatory poison does not act on nerve fibers, only on nerve cell bodies. Use of ibotenic acid showed that stimulation and lesion effects were indeed attributable to BSRF cellular components. As put by Steriade [1996] the concept of activation ascending from the BSRF, “has been rescued from oblivion.” Furthermore it now appears that the BSRF stimulation which desynchronizes the EEG can facilitate synchrony in the gamma range (20-70 ~/sec) (Munk,1996]. This is important because synchrony in the gamma range has been thought to underlie aspects of cognition, so this finding fits the idea that arousal facilitates thinking (see the section on synchrony below). An imaging study found that procedures that called for focusing attention caused increased activation of both BSRF and the thalamic ILN [Kinomura et al, 1996].THE ILN ARE NOT SIMPLY RELAYS FOR ACTIVATION.
When the concept of ascending activation was first popular, the arrival at cortex of activating influences appeared attributable to an "unspecific thalamocortical system" including the ILN [Jasper,1954]. Since then, it has often been supposed that the function of the ILN is best understood as relaying to cortex the activation originating in the brainstem. Perhaps the most explicit expression of this is the ERTAS advocated by Baars and Newman[Newman,1995]. Considering the ILN to act principally as relays for activation seems inadequate for several reasons:
First, the view that thalamic nuclei act mainly as relays (and are often labeled "relay nuclei" in introductory texts) is no longer tenable [Guillery and Sherman,2002]. In this connection we note that only 10 to 20% of LGN synapses are from the eyes (LGN is the visual "relay" nucleus of thalamus). Necessarily implied is that information arriving from the eyes is subject in LGN to modification from a variety of sources. Moreover, fibers from visual cortex back to LGN are about 10 times as numerous as the fibers carrying information from LGN up to visual cortex [Sherman and Koch,1986]. The ILN are not simply "relays".
Second, the internal organisation of the ILN implies selective processing. Although Molinari et al [1993] recognized that ,"The circuitry of the ILN is quite complex with afferent systems arising from many different sources and efferent fibres reaching the entire cortical mantle .... supported the idea of the ILN as a melting pot", their analysis of the micro structure led them to conclude that the ILN , "present a precise structural organisation capable of highly specific integration of the different inputs."(p205). In this connection see also Groenewegen and Berendse [1994].
Third, the output of the ILN is not only to cortex, but more prominently to striatum, which suggests a role of ILN in volition, as discussed below.
Fourth, activation of cortex occurs independently of ILN as evidenced by rare cases of nearly complete destruction of the ILN but relative sparing of cortex; the resulting vegetative state includes cycling between "sleep" and "wakefulness" i.e.states with and without cortical arousal [Kinney et al,1994;Schiff and Plum,1999].
THALAMIC CONTRIBUTION TO ATTENTION.
Considering how consciousness and attention are related is made difficult by the various usages of both words. “Attention” can be synonymous with an orientation of head and eyes to a brief stimulus, attributable to midbrain function and occurring well before awareness of the stimulus. What we see may or may not correspond to the "spotlight of attention" [Jung,1954; He et al,1997]. Or, “attention” may refer to an individual’s keeping some location “in mind” while fixating vision elsewhere (Treue & Maunsell, 1996) as evidenced, for example, by faster response to that location than to others. It is not surprising then, that multiple mechanisms have been implicated in attention, including an assortment of cortical regions (Posner & Rothbart, 1992).
It has been suggested that the reticular nucleus of thalamus (R) affords part of the physiologic basis for selective attention [Scheibel & Scheibel, 1966; Yingling & Skinner, 1976, 1977; Crick, 1984; Mitrofanis & Guillery, 1993; Guillery et al, 1998]. Briefly, a physiologic mechanism for attention is ascribed to R because (1) each R envelops, in a thin layer, most of the thalamic nuclei; the thalamocortical fibers, as well as the fibers returning from cortex to thalamus, when passing through R give off collaterals as they pass through. (2) R efferents terminate in the immediately underlying thalamic nuclei, and (3) R efferents are GABAergic (the neurons in R are exclusively inhibitory, using GABA as their transmitter). The likelihood exists, therefore, that thalamocortical communication can be simultaneously inhibited overall with highly selective noninhibition. Such localized gating could provide a mechanism for selective attention in cognition. The fact that focal attention can be influenced by C could in part have its anatomical basis in known connections from the ILN to R .
Associated with R is a plausible theory of C which should be mentiioned though it seems inadequate for several reasons. It assumes that the thalamocorticothalamic (TCT) activity passing through R can grow, in one small locale, so large that it shuts down other TCT activity by a sort of surround inhibition; this would account for the focus of attention. Meanwhile, the level of activity in the small locale could rise above the “threshold for consciousness.” Problems with this view include: 1) it does not account for C of primitive content; 2) reaching consciousness is not simply a matter of increased activity; 3) focal attention can be dissociated from C [Braun,1997; Koch,2003]; and 4) it makes no provision for an immediate inhibition (or release) of a developing motor plan.APPROPRIATE INTERACTION
ILN efferents, some of them collaterals of the ILN projection to striatum, are widely and sparsely distributed to most of neocortex. One can see how ILN could directly influence ideation, insofar as ideation depends upon cortex. This implies that awareness of content depends upon some as yet unspecified “appropriate interaction” between ILN and the neural representation of that content. The possibility that what I call the “appropriate interaction” involves synchronization of neuronal activity at 40 Hz, gamma synchrony as it is called, will be discussed further on.
As an example of “appropriate interaction” between ILN and a specific cortical area, we can consider awareness of the direction of motion of a stimulus. It is now widely understood that motion direction information (MDI) is represented in cortex of the superior temporal sulcus (STS), especially area V5, also called MT (Allman & Kaas, 1971; Zeki, 1974; Maunsell & Newsome, 1987; Rodman, Gross & Albright, 1990; Zeki, 1993)
According to the present hypothesis, for the MDI to have a subjective aspect (i.e., to acquire C) there must occur the “appropriate interaction” between STS neurons and Mc. We keep in mind that the MDI in STS might well be available for adaptive behavior whether or not it acquires C.
In the neurally intact individual, the “appropriate interaction” can be on, or off, or in between, and is quickly adjustable. However, when V1 (striate cortex) has been ablated, the “appropriate interaction” for vision typically does not occur. That is, the MDI in STS is not available to verbal output (the individual denies seeing the stimulus). At the same time, the MDI may be available for some other behavior. This is an example of “blindsight” (Weiskrantz,1986,1997;Grüsser & Landis, 1991; Ptito et al, 1991; Stoerig and Cowey,1995; Stoerig ). When we accept availability to verbal output as the index of C (which we commonly do) it appears that the “appropriate interaction” between STS and ILN cannot readily occur without an essential influence from striate cortex (V1). One explanation for the fact that C usually does not accompany the processing of visual information in the absence of V1 may be that the excitatory drive of the extrastriate regions by striate cortex may be the essential ingredient[Bullier et al,1994;Koch,2003]. More feeble input from subcortical sources (such as pulvinar) might enable some low level processing by MT without awareness [but cf Celesia et al, 1991].
When visual processing in the absence of V1 is accompanied by C [Stoerig and Barth,2001] this may indicate stronger than usual input from pulvinar. Alternatively, Zeki and Bartels [1999] consider visual C without V1 to be evidence for their theory of multiple microconsciousnesses.
BINOCULAR RIVALRY
When a NAP in neocortex is engaged in “appropriate interaction” with Mc we might expect the NAP neurons to exhibit different behavior than when not endowed with C. A conceptually straightforward, but experimentally demanding approach is to record from a neuron participating in a percept both when the subject is consciousness of the percept and when it is not. One way to show that a cortical neuron is participating in a conscious percept is to exploit the phenomenon of binocular rivalry.
Binocular rivalry arises when two different stimuli are presented simultaneously, one to each eye. Rather than seeing both superimposed, the subject typically is aware of first one and then the other, alternating every few hundred msec or so. In an ingenious experiment, Logothetis and Schall (1989) used gratings of horizontal bars drifting vertically, up for one eye and down for the other (and they alternated which eye viewed the upward motion). Monkeys were trained to glance rightward if they saw upward motion and to the left if they perceived the downward drifting grating. [On half the interleaved trials, both gratings moved in the same direction, to confirm that the monkeys were following the rule.] With electrodes chronically implanted, it was possible to record from neurons in STS which preferentially responded to either upward or downward motion, as reflected in the cell’s response (spiking) when the two gratings were moving in the same direction. When there was binocular rivalry the cell responded with rapid spiking only on the trials in which the monkey indicated motion in the cell’s preferred direction (up or down). When the monkey responded oppositely, the cell’s activity was suppressed although in both cases the cell was exposed (through one eye or the other) to its preferred direction.
Although we must keep in mind that complex, seemingly thoughtful behavior can occur without concomitant subjectivity, the Logothetis experiment seems most simply interpreted as showing us motion direction cells that are involved in a conscious percept. [Logothetis,2002]. Similar results have since been obtained in V4 [Leopold & Logothetis, 1996] and for shapes in inferior temporal cortex [Sheinberg and Logothetis,1997].
NEURONAL SYNCHRONY
There has been increased interest in the extent to which neuronal activity is synchronized. One reason to consider this important is that when neurons having a common downstream target fire synchronously, they will have a greater effect on the target. A well described example has been shown in the locust where neuronal synchrony in p----- is necessary for the correct read-out of olfactory information by downstream neuronal populations in the mushroom body [Macleod et al,1998].
NEURONAL SYNCHRONY AND BINDING.
One of the prominent features of cerebro-cortical organization is the different locations of cerebral representations. A common example is that the color, shape and motion of an object are processed via different channels and areas in cerebral cortex [Allman and Kaas,1971; Livingstone and Hubel,1988; Felleman and Van Essen,1991; Zeki,1974,1993]. When information is developed simultaneously in disparate places these different features must be brought together in order to represent some single object or entity; this is an example of the so-called "binding problem". One mechanism for coordination in time could be synchronous neuronal firing[von der Malsburg,1995]. There are numerous examples of rhythmic nerve cell activity exhibiting coherence among segregated neuronal populations (Steriade, McCormick & Sejnowski, 1993; Gray, 1994; Desmedt & Tomberg, 1994; Singer & Gray, 1995; Gray,1999). Of particular interest are synchronous discharges in the gamma range (20-70 Hz), most often around 40 Hz. Although originally described in anesthetized animals, the gamma synchrony (at least for vision) is more evident in the alert state, is enhanced by arousal (as mentioned above), and is related to the presence and properties of experimental stimuli [Munk et al, 1996; Gray & Viana di Prisco,1997;Fries et al,2001].
It has been suggested that 40 Hz synchrony might characterize consciousness because consciousness requires temporal coordination, i.e.binding of disparate NAPs [Crick & Koch, 1990; Linás & Ribary, 1993; Singer,1998,2001; Engel et al 2002]. This might be part of the answer to the question of how a NAP changes when it is endowed with C. However, even if gamma synchrony helps with the feature binding problem, and may well be necessary for C, it is not sufficient for C because: first, perception and the use of percepts in complex behavior can proceed without C (as mentioned above), and second, although more evident in the alert state, the existence of gamma synchrony during anesthesia renders it an ambiguous sign of C. Nevertheless, stimulus dependent synchronization of cortical cells with ILN cells at 40 Hz could be a persuasive example of C plus content (Steriade, Curró Dossi & Contreras, 1993).
INTERRUPTION OF ACCESS TO C.
The hypothesis of this essay suggests that for some content represented by NAPs in cortex to be endowed with C, there must be a connection between the ILN and the region(s) of cortex containing those NAPs. Years ago it was suggested that unawareness of one's bodily derangement (called anosognosia) could be caused by an interruption between thalamus and parietal cortex [Sandifer.1946]. The disconnection of ILN from cortex should result in the unavailability to consciousness of some content; the more extensive the disconnection, the greater the loss of content. An extreme example would be the vegetative state in which there is eye opening to minimal stimuli, cycling between sleeping and waking states, and preservation of many brainstem functions but little if any evidence of mental function [Plum and Posner,1985]. The undetectability of mental function is accompanied by loss of metabolic activity and decreased blood flow in the cerebrum. Although the vegetative state may follow widespread cerebral damage it can also appear either from damage solely to the thalami [Szirmai et al, 1977] or from interruption of thalamocortical connections with relatively little damage to either thalami or cortex [Kinney et al, 1994;Schiff et al, 2002]. A PET study (measuring blood flow) done by Laureys et al [2000] showed thalamocortical disconnection as the cause of a reversible vegetative state. These authors concluded, "restoration of consciousness seems to be paralleled by the resumption of the functional relation between thalami and associative cortices". The next sections discuss interference with the ILN-cortex connections which are physiologic (functional) rather than anatomic.
LOSS OF FUNCTION FROM UNBALANCED INHIBITION.
An important principle of neuropsychology is that loss of some ability is not necessarily the result of destruction of a brain part essential to that ability. A fairly common example is the loss of a stroke patient's ability to look toward the side of a cortical lesion; this deficit sometimes subsides in a few hours but may take much longer. The problem is not primarily in the midbrain circuits controlling eye movement; the problem is that these circuits are receiving from one hemisphere influences no longer balanced by those from the damaged hemisphere. There are multiple influences, both inhibitory and facilitatory. As some of these influences subside, the ability to gaze in either direction returns. Recovery from a brain injury results from a variety of processes; one of these is a rebalancing of the facilitatory and inhibitory influences. When performance has been lost because the competence has lost some facilitation, reemergence of the performance can result simply from subsidence of inhibition [Sherrington, 1932]. Much the same suggestion was made by von Monakow [1911].
To the extent that neuronal synchrony is important, as discussed above, so much more is an appropriate balance of inhibitiory influences. This follows from the fact that inhibition is crucial for both the appearance and the spatial extent of neuronal synchrony {Steriade et al ,1993].
The main point is that a loss of performance is not necessarily the result of damage to the competence for that performance; it may result from unbalanced or excessive inhibition of the competence.
INHIBITION OF ACCESS TO C.
The concept of an appropriate interaction between ILN and a NAP elsewhere implies that C of some representations can be lost not only when the representations are damaged, or when anatomical connections are severed. In addition, contents (represented by various NAPs) which are ordinarily available to consciousness can be unavailable because the interaction is inhibited. An example may be found in some cases of parietal hemineglect.
C AND THE NEGLECT OF LEFT HEMISPACE.
A subject(S) with hemineglect from a right parietal lesion ignores stimuli toward the left. This may be an ignoring of objects located to the S's left, or ignoring the left half of a seen object, or ignoring sounds from the left side as well as other stimuli, sometimes including the left side or parts of S's own body. Related to hemineglect, and often considered a lesser form of the same condition, is extinction, in which stimuli to the left are readily recognized when they occur alone but are not when some other stimulus simultaneously appears to the right of the first stimulus. There are innumerable variations, and different degrees of recovery [Brain,1941; Paterson and Zangwill,1944; Albert,1973; Weinstein and Friedland,1977;Jeannerod,1987;Heilman et al, 1993; Halligan and Marshall, 1998;Driver and Vuilleumier,2001].
In a simple but eloquent experiment by Bisiach and Luzzati [1978], patients with right hemisphere lesions were asked to imagine themselves at one end of the Piazza del Duomo in Milan and describe all the places of business on the plaza. They failed to recall shops, cafes, etc., on the left. Remarkably, when imagining themselves at the other end of the plaza, they named the previously neglected places but omitted those recalled before. It is clear that the information regarding each side of the plaza was possessed by the subjects, and that it was available to consciousness, or not, depending upon its relation to the subjects’ imagined body-centered coordinates. Another way to show in hemineglect patients that information is present, although not available to C, is to temporarily abolish the neglect by using cold water to stimulate the inner ear on one side [Rubens,1985]. Neglect can also be briefly improved by stimulatiom of one side of the neck [Guariglia et al ,1998]. Or one can use mirrors to make left sided stimuli appear to be on the right [Ramachandran and Blakeslee,1998]. A standard explanation in psychological terms for these phenomena is that the parietal lesion has produced an imbalance or bias of attention[Kinsbourne,1970]. An explanation in physiological terms is that access to consciousness of information from the left is actively inhibited in the damaged brain, and that this inhibition can be overcome by various temporary maneuvers. Such inhibition, although continually present in the normal state, would not be apparent since it is normally overcome by facilitatory influences from other sources. This way of explaining parietal neglect means that the parietal lesion removes facilitation rather than damaging the competence for representing and processing left sided information. If this way of explaining parietal neglect is correct, some addendum would seem appropriate to the view that, "the ultimate cause of neglect is the loss of neurons which selectively represent certain parts of space for specific functions." [Driver and Vuilleumier,2001].
In considering this inhibition theory of neglect and/or extinction, it deserves emphasis that hemineglect Ss effectively process information of which they are not conscious. Earlier evidence [e.g. Volpe et al,1979] that neglect was due to an inability of perceptually processed information to reach consciousness was methodologically criticized [Farah et al,1991]. However, considerable evidence has accumulated since, as summarized by Driver and Vuilleumier[2001], that stimuli which are not available to verbal output are nevertheless processed up to a semantic level. In general the processing does not proceed as fully as for consciously perceived material. The increased cerebral activation when the stimuli are consciously perceived is dramatically evident in fMRI studies [Rees et al,2000; Vuilleumier et al, 2001]. These studies make quite clear the considerable neuronal response to stimuli not endowed with C (as judged by the S's verbal output]; the nonconsciousness activation even included the amygdala and orbital cortex when the stimuli were "fearful faces" [Vuilleumier et al 2002]. One way to demonstrate that a performance deficit is the result of unbalanced inhibition (rather than destruction of the underlying competence) is to make a second lesion. That is, after the first lesion has resulted in loss of performance, a second lesion strategically placed is abruptly followed by reemergence of the performance. Two-stage procedures to suppress performance with a first lesion and then to eliminate inhibition with a second operation have been done in cats [Bogen & Campbell, 1962; Bogen, 1974; Sprague, 1966; Wallace et al,1990]. It is unlikely that treating hemineglect with a second lesion will be tried in humans. However, an analogous “experiment of nature” was reported by Vuilleumier et al [1996]. Their right-handed patient had the sudden onset of a right parieto-occipital infarct. The patient’s left hemineglect, “remained unvaryingly severe” for ten days, until an angiogram resulted in a left frontal infarct with abrupt disappearance of all signs of left hemineglect.
A result related to the above was obtained by Payne et al[1996] who produced contralateral hemineglect in cats with cold applied to one parietal region; then they showed that cold simultaneously applied to the opposite parietal region resulted in abolition of the hemineglect. A similar effect in humans was recently reported by Brighina et al [2002]. They applied transcranial magnetic stimulation (TMS) to the left side of the heads of two patients with left neglect from right temporoparietal lesions. The patients' improvement (p<.00005) was still present 15 days after the end of the treatment. Somewhat similar was an improvement in tactile extinction from right hemisphere damage when treated with left frontal TMS.[Oliveri et al,1999].
There are as yet no data to tell us the place where the inhibition occurs. However, explaining hemineglect as the result of inhibition of a cortico-thalamic connection implies a definite prediction: that hemineglect from a thalamic lesion [Watson et al,1981] would not be reversed by either a second lesion or relieved temporarily by mirrors or by inner ear, neck or TM stimulation..
THE CONVICTION OF VOLITION
The existence of connections to ILN from globus pallidus suggests a monitoring of motor systems, as do the cortical projections to ILN from sensorimotor and premotor cortex. A role for ILN in the control of motor output can be inferred from the very substantial projections from ILN to striatum. "Damage to the striatum results in major defects in voluntary movement" [Graybiel et al,1994]. Is the ILN projection to striatum a pathway for the inhibition (or release from inhibition) of motor plans which have been developing for several hundred msec? Is this the basis for a “volitional” decision?
Closely related to or synonymous with “volitional” are such adjectives as voluntary, discretionary, conative, spontaneous, intentional, deliberate, and the like. We need not consider here how these concepts differ, nor mire down in the centuries old problem of free will versus either theological or materialistic determinism. We need recognize only the fact that each of us has a conviction of volition that we attach to some of our acts (those for which we feel responsible) but not to some other acts, and that our conviction of volition has a neurophysiological explanation. It helps to consider first acts which are nonvolitional. A common example of an act for which people do not consider themselves responsible is the pupillary constriction to light. Probably the commonest example of incessant activity for which we do occasionally take responsibility is breathing. Many activities carry on in the absence not only of voluntary control but of any awareness: we understand that most bodily adaptations (including postural adjustments, sensorimotor coordination, phoneme generation during speech, as examples, as well as most autonomic regulation) not only can proceed independently of C but, more often than not, are unavailable to C.
The philosopher Velmans (Velmans, 1991) and the psychologist Gray (Gray, 1995) have reviewed a range of processes in which awareness follows rather than precedes the information processing. A famous experiment (Libet et al,1983;Libet, 1993) showed that an intent to act develops, as evidenced by development of the readiness-potential (RP) several hundred milliseconds before the subject decides to act, as noted by the subject who is watching an indicator sweeping a large clock face marked in milliseconds. This experiment of Libet has been furiously discussed for 20 years, sometimes regarding the method but mainly with respect to the interpretation. Much of the argumentation has stemmed from suspicions that the experiment has or has not some significance for certain metaphysical issues; these are irrelevant to my suggestion here that the experiment tells us something about the conviction of volition. The methodological criticisms have probably been laid to rest by replication of the original findings [Keller and Heckhausen,1990; Trevena and Miller,2002]. Trevena and Miller did point out that the lateralized readiness potential (LRP) appeared at the time indicated by the subjects, probably concordant with activation of motor cortex. Their article is part of a thorough discussion in Consciousness and Cognition vol.11, #2. The discussion largely concluded with the statement by Pockett[2002] who is in most respects critical of Libet; she wrote."Thus by no means all of the time difference between the start of the RP and the consciousness of initiating an action can be accounted for by measurement errors. Clearly there is at least some form of unconsciousness preparation going on well before a subject consciously initiates a voluntary action."(p323).
The foregoing does not mean that intent plays no role in what happens because, although conscious intent appears well after the intent to move has been developing, it appears some 150 milliseconds before the action (pushing of a button). There exists, therefore, time for the subject to either stop the process or allow it to continue. Moreover, motor plans can be voluntarily formulated and stored, the storage probably involving the motor areas in medial frontal cortex[Libet, 1993; Passingham, 1993; Tanji & Shima, 1994]. Stored motor plans can be subsequently released by a triggering stimulus which acquires C after the action has been initiated. Indeed, the action may be triggered by stimuli which never are “perceived,” that is, acquire C (Taylor & McCloskey, 1990).
The proposal here is that a motor plan develops over time, that part way through this development, or while it is held in readiness but not yet executed, we become aware of it [Libet,1993]. We can readily suppose that “appropriate interaction” between premotor cortex and ILN occurs early enough (i.e., 150 msec) before action so that “self” is associated with the developing motor plan. There would thus be time for ILN to exert an inhibition that would stop the action, or to overcome any tonic inhibition and thus allow the action. If the motor plan is permitted to run to completion, “self” or “me-ness” would be associated with the action and the individual would feel responsibility precisely because there had been an opportunity to abort the plan.
THE AUTONOMOUS HAND (AH).
The autonomous (aka alien,aka anarchic) hand refers to well-coordinated, seemingly purposeful activity which is disclaimed by certain neurologic patients. The AH seems to tell us something about the nature of will or volition. It has been ascribed to hemispheric independence due to callosal injury [Goldstein,1908;Brion and Jedynak,1972,1975;Bogen 1979,1993; Feinberg et al,1992; Geschwind et al,1995;Baynes et al,1997; Zaidel et al, 2003]. On the other hand, the AH may result from failure to attach “me-ness” (that is, subjectivity) to the behavior because a lesion has disconnected the ILN from the cortical NAP representing the motor plan [Bogen, 1993; Della Sala et al,1994; Goldberg & Bloom, 1990; Feinberg et al, 1992; Goldberg, 2000;].
The term "alien hand" was first used by me in 1979. it was a mistake because
I did not read Brion and Jedynak carefully enough; they used the term "la
main etranger' for a sensory phenomenon resulting from callosal
disconnection and they used several different terms(in different papers and their book) to refer to a motor phenomenon also attributable to callosal
disconnection. The sensory phenomenon appeared when the subject's left hand
was out of sight and being felt by the S's right hand (connected to S's
speaking left hemisphere). the left hand was not recognized by the S who
considered it to belong to someone else, i.e. a stranger. this is simply
explained as the result of a failure of interhemispheric transfer;the
sensory information from the left hand is not transferred to the speaking
left hemisphere. The motor phenomenon is much more interesting and consists
of well coordinated, seemingly purposeful movements of left hand (and arm)
for which the S does not accept responsibility, as in the frequently heard
comment from recently operated split-brain Ss, "I didn't do that, it was my
hand". The phenomenon seems to tell us something about the ability of the
nonspeaking right hemisphere to exhibit wellcoordinated movement which seems
purposeful (picking something up,for example); that is, it seems as if the
right hemisphere has a will of its own, disconnected from the speaking left
hemisphere. It was subsquently pointed out by Goldberg et al[1981]that this could not be the explanation when AH occurred in the right hand of
a righthander. One explanation is to say that the movements are carried out
by cortical regions under the guidance and monitoring of other (sensory)
cortical areas, both sensory and motor areas lacking the usual connections
with Mc[in ILN per my hypothesis]. It is possible that one or the other of these mechanisms is involved in different
cases, as proposed by Feinberg et al(1992). Meanwhile the term "alien hand"
became quite popular and some neurologists started using it for all sorts of
involuntary movements such as writhing, elevation, flinging and other
movements long known to result from basal ganglia damage. Using the term this way obscures the main interest of the phenomenon as originally described, since these basal ganglia abnormalities are neither well coordinated nor purposeful. Moreover, they have
commonly been accepted as motor machinery gone awry without any implications
for our concepts of volition. Meanwhile, as many neurologists were reporting
cases of alien hand, Della Sala et al recognized that the term had been
incorrect from the beginning. Della Sala and colleagues were kind enough
not to point out my deficiencies in translating from the French; they
suggested that a better term would be the "anarchic hand" because the Ss,
although denying intent, do not deny that it is their hands doing these
things. In one case the S, fully recognizing possession of the hand,
claimed it was being controlled by the man in the moon [Geschwind et al.,1995].
The term "anarchic" also seems slightly off the mark because what was originally and now usually intended are movements which are well coordinated and not simply disruptive in
their effect. I prefer the term "autonomous hand", but it is probably
too late to change common usage. A well informed, brief word on all this is in an editorial by Goldberg [2000].
A PATHWAY FOR VOLITION?
If we assume that the anatomical requirement for subjectivity involves ILN, the large ILN to striatum projection could be the substrate for inhibition (or release) of a developing motor plan. This hypothesis therefore suggests that activity in the ILN-to-striatum pathway is the trigger for actions which we call volitional. What do we know of this pathway?
In primates, the predominant origins of the ILN-striatum projection are the parafascicular nucleus (Pf) and the centromedian nucleus (CM, aka centre médian aka centrum medianum) [Jones, 1989]. This is not to be confused with nucleus centralis medialis, usually abbreviated CeM and often called “centralmedian nucleus,” a term sometimes, unfortunately, applied to CM [Rinaldi et al 1991]. The projection from Pf is mainly to associative-limbic portions of striatum, largely caudate and accumbens, whereas the projection from CM is mainly to sensorimotor portions of striatum [Sadikot et al,1992]. It has been found [Sidibé & Smith, 1996] that the CM projection, most likely excitatory, preferentially innervates the direct inhibitory pathway from striatum to globus pallidus interna (GPi). This would result in disinhibition both of ventrolateral thalamus and of CM (via collaterals to CM from GPi). The positive feedback loop could result in a sudden burst of excitation, overcoming any ongoing inhibition. If the ILN to striatum pathway is important for willed movement, we can see that it is probably important for the acquisition of procedural memories [Knowlton et al, 1996]. Procedural memories are established by multiple, willful repetitions unlike episodic memories which are commonly acquired on single exposure [Tulving,1983,1985; Schacter,1989] and are discussed further on.
ENDOWING EMOTIONS WITH C.
The present hypothesis, including that a NAP can be converted to CNAP by Mc implies that the NAPs representing emotions can exist (and cause behavioral signs of emotion) while nonconscious. This is consonant with the common dictionary definition of affect as the conscious aspect of emotion. Attributing Mc to the ILN provides a tangible mechanism for the conscientiation of emotion, i.e. turning a nonconscious emotion into an affect. Before considering the anatomy, it helps to explore briefly the notion that being conscious of emotions may be more fundamental than being conscious of ideas [Panksepp,1988;Damasio 1999; Watt,2000].
The C of nausea, thirst, fatigue and the like are at least as typical of being conscious (having qualia) as having C of time, place, person, meanings, memories and expectations. In all likelihood, C of emotions antedated C of cognition in phylogeny, and so too in ontogeny. An excessive emphasis on the consciousness attending cognition by many current students of consciousness may derive, as do so many attitudes, from Descartes who claimed: I think, therefore I am. A neurobiological understanding of C might come more quickly if we were to aver: I feel, therefore I am [Bogen, 1997]. (E. Robkin has pointed out to me that Graham Greene anticipated this point; in the first line of A Burnt Out Case the cabin-passenger wrote in his diary ,"I feel discomfort, therefore I am alive". T.Sullivan has pointed out that what Descartes meant by "thinking'' likely included feelings as well as thoughts.).
Looking for the mechanism endowing emotions with C involves finding connections between structures subserving C and structures subserving emotion. The latter are, roughly speaking, the constituents of the limbic system, including the amygdala, orbital cortex and, connected to both of these, the medial dorsal nucleus of the thalamus. As pointed out above, the ILN are draped over and around the MD like a blanket. This relationship is particularly well demonstrated by staining for the compound calretinin , which is for the most part restricted to the ILN [Fortin et al,1998; Cicchetti et al.1998; Munkle et al,1999,2000;]. So striking is this relationship that one is tempted to suggest it as the anatomical basis for the statement, "I feel, therefore I am".
IMPORTANCE OF C FOR DECLARATIVE(INCLUDING EPISODIC) MEMORY.
One function of consciousness(C), perhaps the phylogenetically earliest, is
to facilitate certain aspects of learning, hence the importance of the ILN for C implies a role in these aspects [Bogen, 2001]. A possible example is the case of trace conditioning (TC). TC of the blink reflex to a puff of air is said to be dependent on the subject becoming aware of the relationship between the unconditioned stimulus (US) and the conditioning stimulus (CS) [Clark and Squire, 1998; Clark et al, 2001). Conditioning involves following a conditioning stimulus(CS) such as a tone by an unconditioned stimulus(US), which for the blink reflex is a puff of air directed at the cornea. In the usual Pavlovian conditioning there is an overlap because the US begins before the CS ends. By contrast, trace conditioning(TC), is characterized by a time gap which intervenes between the end of the CS and the start of the US. The gap may be as much as several seconds in duration. By contrast, awareness is not required for acquisition of conditioning when the US and CS overlap. The blink reflex has been studied extensively in rabbits as well as humans [Thompson and Logan,1996; LaBar and Disterhoft,1998; Disterhoft et al,2002].
It seems to me likely that C is also essential to learning the delayed nonmatch to sample(DNMS). Delayed nonmatch-to-sample is a form of what is called operant conditioning, that is the subject makes a choice which produces either a reward or not. In order to be rewarded in the DNMS, a monkey must choose one of a pair of symbols; each symbol covers a well. In one of these there is a reward, e.g. a raisin or nut. The monkey finds the reward only if it picks the symbol which was not not rewarded on the immediately previous trial. The delay between trials can be made longer to increase the memory requrement [Mishkin and Appenzeller,1987].
The anatomy of memory has become progressively better understood over the past several decades [Milner et al, 1998]. Both TC and DNMS are dependent on neuronal circuits that include the entorhinal cortex (EC), which is the principal bottleneck for information to and from the
hippocampus. . If is correct that both TC and DNMS require consciousness , then they evidently depend not only on EC but also on a connection between EC and at least one other structure relevant to C. The most likely candidate is the ILN, not only because of the considerable evidence presented in this chapter that the ILN are essential to C , but also because it is known that damage to the ILN impairs DNonMS as well as match-to sample [Burk and Mair,1998]). So far as I am aware, no one has yet examined whether lesions of the ILN would prevent trace conditioning; this should be a rewarding experiment.
If it is correct that an EC-ILN pathway underlies either DNMS learning or TC learning or both, this hypothesis can be tested by making a lesion in the inferior thalamic peduncle, thus severing the known pathway between EC and ILN. [It is possible that production of the learning deficit would require a prior section of the fornix]. To avoid the difficulties of making symmetrical lesions and to avoid seriously incapacitating the animal subject(AS), the experiment can be done in a split-brain AS so the AS serves as its own control (Sperry, 1961). To counter the expected criticism that the
lesion interferes by destruction of local neurons rather than of fiberscoursing through the isthmus, a lesion at least as large and of similarlocation could then be made with ibotenic acid, thus destroying the localneurons while sparing both the fibers of passage and the learning ability.
The experiment can be done with either TC or DNMS, clarifying simultaneously
a function of C and the neural structures underlying that function.
There has recently appeared evidence that the anterior cingulate cortex in mice is important for trace conditioning(Han et al, 2002); this suggests that additional pathways, possible sites for further experimentation, are involved besides those already mentioned. Since the consolidation of memories involves protein instantiation ,i.e. engrams, elsewhere than in either thalamus or hippocampus (probably the neocortex), engrams for trace conditioning may be laid down in anterior cingulate cortex, at least in mice trained with an electric shock used as the US. This is suggested by the importance of anterior cingulate for emotional aspects of pain

OVERALL CHAPTER SUMMARY
An anatomico-physiologic approach to consciousness is facilitated by recognizing that the various meanings of consciousness have in common a crucial core C sometimes called consciousness-as-such, or consciousness per se. A sharp distinction is made between the property C and the contents of consciousness. The neuronal mechanism producing C also acts as an attention-action coordinator, hence must have specific connectivity requirements. These requirements are best met by the thalamic intralaminar nuclei (ILN). Whereas large lesions elsewhere leave C undisturbed, quite small bilateral lesions in ILN engender immediate unresponsiveness. This combination of anatomic and neurologic evidence is bolstered by a variety of physiologic evidence, which leads to the conclusion that further investigations of the ILN, and their interaction with lower centers as well as cerebral cortex, are most apt to yield a better understanding of consciousness.APPENDIX A; CONSTRAINING THE SEMANTICS.
A PHYSIOLOGY OF CONSCIOUSNESS NEEDS SEMANTIC SPECIFICATION.
While elucidation of consciousness at a physiological level is desirable, an immediate difficulty arises from the heterogeneity of "consciousness" as discussed by different authors, sometimes differing from time to time or even page to page in the same author. As Natsoulas (1983) put it,
"No individual familiar with the history of psychology will be surprised that, at the present time, conceptual confusions and difficulties in mutual comprehension attend scientific discussions of consciousness, even where the participants are relatively sophisticated students of the topic."
Finding the physiology of everything that anybody might mean by "consciousness" is clearly impossible. An essential step, therefore, is to sharpen or constrain our description, a step to some extent separable from showing the physiology. These two steps are not entirely separable because increased physiological knowledge can suggest some of the constraints to be adopted.
The program suggested here is to take what often appears to be a rather diffuse, intuitive notion (i.e., "consciousness") and narrow it down, by stripping off various layers of implication and connotation, to what I believe is at the core (which I call C) of this notion. In other words, C is intended to be a highly constrained concept suitable for neurologizing and, at the same time, reasonably representative of what is both indispensable about "consciousness" and is part of what is meant by most users of the term.
We can keep in mind, as the characterization of C proceeds, to take note of the comment by Donald MacKay (1969, p. 83)
"... in the early stages particularly, the technical equivalent of a common term should conform as far as possible with common usage. The technician's effort to sharpen the concept should at least in principle allow the technical equivalent to be substituted for the term, without violation of basic sense or grammar, in as many contexts as possible."
One way in which I diverge from MacKay's advice is to use the symbol C, rather than asking the reader to keep constantly in mind that the word "consciousness" is being used in a narrow, more technical way.
The goal described here involves decisions both as to what must be included in C and what needs to be avoided.
1. C MUST INCLUDE SUBJECTIVITY
Your subjective experience is different from mine, ours from a monkey's or a cat's, and all of these from a bat's. But do they not all have something crucial in common? Thomas Nagel's oft-cited essay (1974) asserted the unreasonableness of attempting an objective (i.e., scientific) explanation of the subjective. He wrote, "With consciousness it [the mind-body problem] seems hopeless." It may have seemed hopeless to him, but it does not seem hopeless to others, including me. This is a question, probably, of what one judges might be a productive line of inquiry.
Nagel went on to say, "Conscious experience is a widespread phenomenon. It occurs at many levels of animal life." Here we are in agreement. That is, I believe that phenomenal awareness is possessed by many animals, although the things of which they are aware may differ widely. [Both bats and dolphins are both apparently aware of auditory information unavailable to humans]. This chapter ignores the variety in content of consciousness which is dependent upon species differences and variation in individual experiences, as well as alterations by drugs, hypnosis, etc. These are all satellite diversions which eventually (but not this early on) deserve exploration.
2. C NEED NOT BE FORMALLY DEFINED TO BE USEFULLY CONSIDERED
You are likely conscious (hence, endowed with C) while reading this and you probably believe that I was conscious when I wrote it. Although there are troublesome exceptions (Allport, 1988), we commonly think we know consciousness when we see it. As an example, consider the importance of consciousness for a neurosurgical decision whether or not to operate upon an acutely brain-sick patient, and when. In spite of CAT scans, PET scans, magnetic resonance imaging and angiography, quantitative EEG, Doppler sonography, and other "hi tech" methods now clinically available, it is still the case that in the neurosurgeon's multifactorial equation, the level of consciousness (rather, its rate of change) is the major variable. If the patient's level of consciousness is decreasing, aggressive intervention is needed, and the more rapid the decrease, the more urgent the need. Widely accepted among neurosurgeons for the labeling of lower levels of consciousness (because of its interobserver reliability) is the Glasgow Coma Scale [GCS](Teasdale & Jennett, 1974). It might be objected that the GCS provides numerical labels for levels of reactivity and not of consciousness. I believe this objection misunderstands how measurement often works. For example, we do not measure the temperature of room air by trying to determine the average kinetic energy of the air molecules; we look at the length of a column of mercury because experience has led us to believe the latter is reasonably related to what concerns us. The GCS is undoubtedly cruder than we would like, but is better than the Torino scale for the risk from near-earth objects or the Beaufort scale used for many years by the British navy to label numerically levels of wind velocity.
Our ability to label levels of consciousness is largely the result of ostention. Ostention means that I convey what I mean by ''x'' by saying "x'' when pointing to n objects, and "not x" when pointing to m others. A problem with ostention is that it does leave considerable room for misunderstanding. Ostention contributes both to our having some common understanding and to our uncertainty about (and disagreement with) what others mean. But in spite of some inevitable ambiguity, ostention works, not only for people but also for artefacts. Quite often, the training of artificial networks involves the presentation of a large number of examples from which categories are eventually abstracted. Indeed, the success of both people and artificial networks suggests that this approach can at times be better than beginning with a formal definition.
By a "formal definition," I mean a statement which includes conditions which are both necessary and sufficient. Such a definition usually needs rather than precedes an adequate theory (Edelman, 1989, p. 19). As Weiskrantz (1986, p. 166) put it, "Definitions are more helpful after one considers the body of background knowledge to a concept than before." P. S. Churchland (1988, p. 284) pointed out,
"The idea that if only we could get the words correctly defined then we would understand the phenomenon is seductive but misguided. The words will come to have a more precise meaning as they are more deeply embedded within the framework of an empirical theory ... some philosophers have called the "define-the-words-first" strategy the heartbreak of premature definition." [The italicized passage she attributes to D.Dennett.]
As we come to understand C better, we will approach a formal definition. Meanwhile, we must content ourselves with a characterization which, while insufficient for a formal definition, is sharper than that given solely by ostention .
It was pointed out to me by Professor Asa Kasher that the process I am advocating here was discussed in detail by Rudolf Carnap (1950) who called it "explication." He wrote,
"By the procedure of explication we mean the transformation of an inexact, prescientific concept [the datum] into a new exact concept ... since the datum is inexact, the problem itself is not stated in exact terms; and yet we are asked to give an exact solution. This is one of the puzzling peculiarities of explication. It follows that, if a solution for a problem of explication is proposed, we cannot decide in an exact way whether it is right or wrong. Strictly speaking, the question whether the solution is right or wrong makes no good sense because there is no clear-cut answer. The question should rather be whether the proposed solution is satisfactory, whether it is more satisfactory than another one, and the like."
I would include in "satisfactory" that the new concept lend itself to experimentally testable hypotheses. For example, experiments are immediately suggested by the hypothesis that consciousness crucially depends upon the ILN or, as proposed in this chapter, that episodic memory depends upon anatomical connection between entorhinal cortex and the ILN.
Carnap attributed to Arne Naess a related concept: precisation. In paraphrase, the concept of Naess seems to be: the formulation "C" is more precise than "consciousness" if there are properties of "consciousness" which are not properties of "C," but there are no properties of "C" which are not also properties of "consciousness." What I pursue might better be called "precisation" than "explication" since C cannot yet be made "exact" in Carnap's sense, although C will be more sharply characterized than the amalgamate datum (consciousness) with which we begin. 3. C INVOLVES SOME BACKGROUND PRESUPPOSITIONS
A program of precisation is inevitably affected by preconceptions. I will try to make explicit a few of mine. Already mentioned is my bias for constraining C in the light of and with an emphasis on neuroanatomy. Three others will be discussed next.
3.1 C Can Have (but Need Not Have) a Causal Role in Our Behavior
Some suppose that consciousness (including C) is an epiphenomenon, like the sounds of a beating heart which can inform us about the state of the heart although having no influence on the heart's functions. When we reject this view (of C as epiphenomenon) it may be, at least in part, for personal reasons. It seems to challenge our selfhood or in some such way makes us feel uncomfortable. But there are less self-serving rebuttals; in his monograph on consciousness, Baars (1988) devotes Chapter 10 to this question. One reason which many find compelling is the appearance and persistence of C under selective pressure during mammalian (and other?) evolution.
When someone honestly says, "I am thinking it over," this need not be simply a report of what is happening. Rather, the person's C of what is happening can itself affect what happens. More specifically, when the neuronal circuits generating C are active concurrently with the activity of circuits involved in some decision, the decision is often (certainly not always) affected one way or another by the concurrence. When a pattern of nerve cell activity becomes endowed with C, that pattern of activity so endowed has an increased likelihood of influencing other neuronal activity. This might well cause some change in ongoing behavior. At times this may be as simple a matter as inhibiting further action while detailed processing occurs elsewhere.
3.2. We Are Looking for Mc, Not C
C is provided by some cerebral mechanism, Mc. It is this mechanism which we hope to locate and ultimately analyze. Pointing to C may turn out to be like pointing to the wind. We can point to the effects of the wind, and we can often give a good account of what causes the wind, the causes often being quite distant (in miles) from the effects. An objective here is to constrain C sufficiently that Mc will be identifiable within and as part of cerebral physiology. The effects of C, when it is generated by Mc, will depend on the nature of the things potentially affected by Mc.
3.3. C Is an Emergent Property of Mc
The term "emergent" is used variously (Wimsatt, 1976, 1985). What I mean here is a property of a set of elements, which is neither explicable nor predictable solely on the basis of the properties of those elements together with some simple aggregative operation such as addition, multiplication, or integration (in the math sense). Understanding of an emergent property (generally not present in what we call "collections") requires specification of the particular way in which the elements are configured and the particular way they communicate elsewhere. [Some collections might acquire a new property just by being big enough, an example being a "critical mass" of particle emitters].
Knowledge of the configurational properties can sometimes give us predictability (sometimes even constructability) in the absence of a complete description of the parts making up the whole. Two common examples are a wheel and an oscillator, as described in the main text. Note that how the emergent properties of a wheel are manifested also depends upon how it is connected; sometimes wheels turn without rolling.
With respect to the importance of internal arrangements, examples abound in organic chemistry. A particularly notorious example is thalidomide. The left-handed form of thalidomide is a fairly safe, mild sedative whereas the right-handed form (when taken in early pregnancy) causes severe congenital defects such as absent or deformed limbs (Atkins, 1987). Simple emergent properties may require only minimal specification of internal arrangements. It was shown by Hopfield (1982) that certain emergent properties could arise within a system whose only specification is that it be composed of a large number of nonlinear, richly interconnected components. For example, associative memory is likely a "natural--almost spontaneous-property of neuron ensembles" (Tank & Hopfield, 1987).
On the other hand, when specific problems are to be solved, efficient computation is favored by the introduction of specific configurational properties (such as introducing an appropriate pattern or "syntax" of inhibitory relations) and by "forward engineering," the provision of a restricted set of hypothetical solutions (Hopfield & Tank, 1986).[ The words in quotes are also in quotes in Hopfield and Tank (1986)].
To reiterate, C should not be expected to result from the simple piling up of decision elements, neuronal or otherwise.
And we need a specification of how Mc is connected to elsewhere in a brain; how the emergent properties of the wheel are manifested depends upon how it is connected. The stationary but rotating wheel exemplifies the importance of external connections. Neurophysiologic examples exist in the functions of various cerebrocortical areas. It has been found that the areas in temporal lobe which ordinarily have an auditory function can be converted to visual function by manipulations in very early development (the manipulations consist in removing the source of auditory input combined with removing the usual targets for neurons carrying visual information [Sur, Garraghty, and Poe, 1988]). The variations in types and distribution of neurons in various brain areas are to considerable extent dependent upon where they receive and send information[Schlaggar and O'Leary,1991]. Cells which have longer axons have, in general, larger cell bodies. [Understanding this point helps us to understand better the cytoarchitectonic variations in neocortex].
That we can to some extent ascertain the function of some brain part by knowing how it is connected is an essential aspect of our search for Mc. As pointed out in the main text, the external connections of ILN are part of the evidence that ILN provide the best candidate for Mc.
4. CONSCIOUSNESS INCLUDES BOTH A PROPERTY (C) OF VARIABLE INTENSITY AND A GREAT VARIETY OF CONTENTS
We can consider the intensity of C without, at the same time, worrying about the specific contents of consciousness.. Besides the great variety, contents are typically transient and often idiosyncratic. As noted in Part I, this important distinction has already been made by Baars[1993].
The same distinction has been made by others. Grossman [1980] wrote: "We can also introspectively discriminate between the contents of consciousness ... and the quality of being conscious." And there is a resemblance here to the distinction made by G. E. Moore between "the sensing, which alone is distinctively mental, from the sense datum sensed" [Peters & Mace, 1967]. Landesman [1967], quotes Moore as follows,
"The sensation of blue differs from that of green. But it is plain that if both are sensations they also have some point in common.... I will call this common element "consciousness".... We have then in every sensation two distinct terms, (I) "consciousness," in respect of which all sensations are alike, and (2) something else [the object], in respect of which one sensation differs from another." [Philosophical Studies, London, 1922].
Moore's usage of 'consciousness' is akin to what I call C, whereas many people expect "consciousness' to include much more. Probably relevant here is Edelman's [1992] distinction between "primitive" and "higher" consciousness.
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5. AVAILABILITY TO VERBAL OUTPUT (AVO) NEED NOT ACCOMPANY C
When dealing with human subjects, availability to verbal output is commonly taken as evidence for subjective states. If a subject denies feeling a pressure on the skin, we ordinarily assume it was not "felt," i.e., had no accompanying C, even if we see correlated voltage changes (evoked potentials) when recording from the subject's head. If someone says of a wound suffered in midst of battle, "I didn't feel it at the time," we believe. The reasons we believe include the person's behavior at the time, and/or because we ourselves have on occasion sustained a wound without feeling it.
But C does not depend upon availability to verbal output, nor need it involve any linguistic competence. We need only ascribe subjective states (e.g., pain, thirst) to monkeys to establish this point. Whether or not the monkey's subjective states can encompass "higher thoughts" is not essential to possessing the property C. The phenomenon of automatic utterance shows us that availability to verbal output (AVO) need not be accompanied by C. On the other hand, what we ordinarily take as signs of C (certain nonverbal behaviors) can be produced by neural activity which does not have AVO. These facts may help us by stimulating some questions, such as: what are the connections between C and AVO? One hint seems to come from the AVO of much right hemisphere information when the corpus callosum is intact, rather than severed. This AVO depends on communication over long distances via collections (tracts) of nerve fibers. One might suppose that AVO of information already in the left hemisphere (of a right hander) is often similarly communicated, i.e., by long tracts. If so, various kinds of cerebral processing could lose AVO by interruption of nerve fiber tracts, i.e., by disconnection [Geschwind, 1965]. This sort of disunification may tell us something about AVO, but it does not explain C or Mc.
6. C INVOLVES ONLY A SMALL PART OF WHAT IS COMMONLY MEANT BY "SELF".
The word "self" seems to be used even more variously than the word "consciousness." My Webster's Collegiate Dictionary has about 350 usages spread over three and a half pages.
As a possible example of a relatively narrow usage, Dennett [1991] refers to the "self as the center of narrative gravity." This is a felicitous phrase; but linguistic ability (good or bad) is not essential to the C we share with so many other species. At another extreme, Galin [1992] proposed that "self" be defined as ". .. the overall organization that makes a person a unity." A similar concept of "self" was recently discussed by Churchland[2002]. This may not be the most inclusive usage possible, but it is surely a contender, there being such a multitude of hormonal and neural unifying mechanisms. We need not define "self" nor attempt a catalogue of what it might contain, in order to point to one aspect which is typically implied when the word "consciousness" is used. Flanagan [1991, p. 352] quotes William James as saying, "Whatever I may be thinking of, I am always at the same time more or less aware of myself, of my personal existence." Flanagan goes on to observe,
"This low level sense of "me-ness," of "something happening here" does seem to underlie all conscious experience. All conscious experiences are, in addition to being experienced, experienced as attached to the subject of these very experiences." (emphasis added).
There may be exceptions (extreme absorption or certain meditative states). But Flanagan describes what I intend to be a characteristic of C. That is, "attachment [of an experience] to the subject of the experience" is part of what I have described earlier as "endowing with C some particular content." If we use NAP to mean a particular pattern of neuronal activity then "endowing with C" includes "giving subjectivity to a NAP." This can be symbolized as CNAP. This makes explicit two questions: 1. In what way is a NAP changed when it is made conscious? and 2. what is the mechanism[Mc}which causes this change?
According to Hart and colleagues[Hart and Whitlow,1995] the sense of self has 5 facets: one of these, subjective selfawareness seems closest to what Flanagan calls "me-ness"; this contrasts with Hart's other 4 facets including objective selfawareness, memories, representations and theories of self. That the subjective awareness of Hart is not as low level as Flanagan ( and I) have in mind is indicated by Hart and Whitlow[1995] maintaining that monkeys do not have even this aspect of self. It may help to emphasize that the me-ness ascribed to C is neither an aspect of cognition nor does it require cognition; it is, in T. Sullivan's
term, subconceptual. Taylor[2002] offers a nice summary of recent papers advocating the concepts of "primitive self" or "minimal self" or "pre-reflective self" or "ipseity". See also article on this subject by Galin [2002].
7. C DOES NOT REQUIRE THE SELF-NONSELF DISTINCTION
A particularly prominent aspect of consciousness which I intend NOT to be a property of C, but rather a particular content, is the self-nonself distinction (S/NS-D) .
First, the S/NS-D is commonly made without C. The S/NS-D is routinely made by our immune systems. And it is made by creatures (e.g., amoebae) without any central nervous system. The S/NS-D does not require C. (There is a multiauthor discussion entitled "Reflections on Self" in the 12 April 2002 issue of Science 296:297-316).
Does C require the S/NS-D? Considering reports of an "oceanic" state, a feeling of "oneness with the world," the answer is immediately "no." This is because the "oceanic" feeling is an example of a subjective state without the S/NS-D.
More compelling perhaps is the existence of pathologic states in which the S/NS-D is grossly erroneous but C persists with the same dynamic range and most of the usual potential contents. First, there are brain lesions in which a subject's limbs (more often the left limbs) are not considered part of the subject's self [Bisiach et al,1986; McGlynn & Schacter, 1989; Bisiach & Geminiani, 1991]. And there are states without demonstrable brain lesion, as with phantom limbs, in which things nonexistent for others are felt as part of the self[Melzack, 1989]. In addition to the foregoing, there are reports of people "identifying" their "selves" with external objects, or other persons, or even all persons, or maybe even all living things. These observations exemplify how idiosyncratic (highly personal) the S/NS-D can sometimes be. Hence, we should not consider the S/NS-D as an integral part of C. Rather, it is one more example of content which must be brought into consciousness by the "appropriate interaction" between Mc and the neural activity responsible for the S/NS-D.
Certain disorders of "selfhood" are associated with lesions of parietal cortex [Critchley, 1953; Hecaen & Albert, 1978; Benton & Sivan, 1993; Stein, 1992]. For example, when someone has an occipital lesion resulting in hemianopia, unawareness of the visual loss typically means that the lesion extends into parietal cortex [Koehler et al, 1986;Grusser & Landis, 1991]. It is likely that parietal cortex plays a special role in the S/NS-D (Damasio, 1994). If so, awareness of the S/NS-D would require the "appropriate interaction" between parietal cortex and Mc.
We can consider a specific example whose physiology is somewhat understood; we adopt temporarily the view that "self" means everything in one's body. Compare the report, "I feel thirsty" with a second report, "I smell something burning." Most of the time, the first statement ("I feel thirsty") means "I am aware of a brain state ascribable to some goings-on in my body proper." (By "body proper'' I mean the body exclusive of brain.) The goings-on are usually either an increase in blood osmolality (detected in the hypothalamus) or a significant decrease in intravascular volume (detected in the right atrium and great veins). Sometimes the subjective state (thirst) reflects a brain state attributable to dryness of the tongue, or to elevated body temperature, or any combination of the above. Rarely, the feeling of thirst arises from a brain lesion. Whatever the cause, thirst typically reflects something within one's self.
The second verbal report, "I smell something burning," also reflects a particular brain state. This may, on quite rare occasions, arise spontaneously in brain, as in the variety of epilepsy called "uncinate fits." Also rarely, it may reflect some condition in the nose (part of the body proper). But most of the time, by far, it reflects a brain state best ascribable to conditions outside the body. When it does not, we tend to consider it pathologic, i.e., suggestive of some disease process. Whatever the loci of the neural activity making the S/NS-D, making this decision is not a function of Mc. The neural activity making the S/NS-D need not be endowed with C; indeed, much of the time it probably is not.
8. C DOES NOT NECESSARILY INVOLVE AWARENESS OF THE SELF.
One of the properties commonly ascribed to consciousness, especially in higher primates, is "awareness of self." Does this mean one's own body image, body boundaries, state of health? Does it include hopes, intentions or recollections of long-past experiences? All of these can be contents of consciousness. They may be endowed with C from moment to moment. But none of them is necessary for C. Note that if awareness of self begins with an awareness of the self/nonself distinction, then proposition 7 entails this proposition 8. When we refer to ourselves, it can reflect quite different contents. This was the subject of a lengthy discussion by
Ryle [1949,pp183-198] on what he called "the systematic elusiveness of 'I'" and the "elasticities in the uses of' 'I' and 'Me'. .. ." He distinguished among usages of "logically different types." The distinctions I would emphasize depend upon differences in neuronal referents. In particular, there is a difference between awareness (endowment with C) of ascending (sensory) information(e.g." I feel x") versus awareness of descending (motor) information(e.g. I intend x").
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9. THE CONTENTS ENDOWED WITH C ARE VERY RESTRICTED AT ANY ONE TIME
In common use nowadays is the metaphor of a "spotlight" or "searchlight" of consciousness, a small circle of bright light, surrounded by a halo of lesser illumination (the penumbra). The contents brightly illuminated, as well as the penumbra, are at any one time a very small fraction of what is potentially available to C. When the spotlight was first pictured (so far as I am aware) by Richard Jung [1954], he called the penumbra a "fringe" and said it was "hazy"; in a discussion by Crick and Koch [1990], the penumbra is considered hazy and treated in part as the result of an inhibitory surround. According to Julesz [1991], "the single searchlight metaphor originated with Helmholz [1896]. William James [1890/1925], according to Julesz, "opened up an entirely new field of inquiry called divided attention." Calling the penumbra a "fringe" is different from James' views on what he called the "fringe" as has recently been pointed out by Mangan [1993] and by Galin [1993, 1994]. Galin [1994] noted that James' fringe is not the dim or fuzzy fringe of the spotlight metaphor. "James' fringe represents a separate class of information than the nucleus, not just the same kind of information at a lower resolution'' . Defects of the spotlight metaphor include the image of a sharp, closed boundary between what is illuminated and what is not[He et al,1997]. A bit better in this respect is the description by Wigner (1967),
"There always seems to be some single sensation or thought at the center of my attention, but there are other sensations which cast shadows on the center, as if they were just outside my field of vision." (p. 190)
To whatever extent the spotlight metaphor may be helpful, the main point is that what is "endowed with C" at any one time is picayune compared to what is potentially available. One importance of this fact (relatively little content at any one time) is that it allows us to consider structures which are small (relative to a cerebral hemisphere) as candidates for Mc.
10. THE NEURAL SUBSTRATE FOR Mc MUST HAVE IMMEDIATE ACCESS TO MOTOR SYSTEMS.
This anatomic requirement follows from the common observation that the "crucial core of consciousness" not only includes subjective awareness of various contents (sensations, feelings, etc. which are often described as "sensory") but must also have a means to influence action. Mc must be so connected as to take account of the subjective experience that one is responsible for an action. The large efference from ILN to the striatum is an important reason for attributing Mc to the ILN, particularly CM.
C is necessarily of the present; some form of immediate memory is necessary but not long term memory or even most of what is usually called working memory. And C needs no aspect of the future such as anticipation. Consider holding one's breath, feeling pain or thirst, tasting something sweet, or feeling sad. Each of these may be accentuated by or even mainly arise from anticipation. But the neural activity subserving C is distinguishable from the neural activity responsible for the specific content of C, including the neural activity associated with anticipation. I appreciate that this is a severe constraint. However, experience, both my own and that reported by others, with bifrontal lobectomies and lobotomies has led me to conclude that anticipation (indeed, any concern for future consequences) is dissociable from C, hence anticipation is only one of many specific contents to which C can attach.
H
ow c evolved is an important question-in broad terms, C does play an important role in certain kinds of learning, hence it would have important survival value. that is how I believe C originally survived, assuming a chance appearance, whereas the role of C in action appeared later; and the role of C in planning for action appeared even later than that, and in ideation even later.
11. THE CONTRIBUTION OF C TO BEHAVIORAL UNIFICATION SHOULD NOT BE OVERESTIMATED
By behavioral unification, I mean what is sometimes called "organismal unity," i.e., parts of the organism function to further the survival, and success otherwise, of the whole organism. Well-known examples can be seen in plants where the unification is mainly hormonal (Thimann, 1977; Jones, 1994). Hormonal integrations are important in mammals also, but they generally proceed at a much slower pace than the unifications effected by the central nervous system (CNS).
An essential aspect of "unification" is a selection or choice among alternative responses to a specific stimulus; this depends as much upon the ongoing state at the time of stimulation as it does upon the nature of the stimulus. In the CNS, the "ongoing state" is largely a function of the neuropil, the feltwork of interwoven nerve cell processes, and locally connected interneurons. Neuropil is prominent throughout the neuraxis from top (cortex) to bottom (tip of the spinal cord). Hence, alternative responses are available even at the spinal reflex level.
As a particularly simple example of neuropil function we can consider the withdrawal reflex. A sharp stimulus to the toe of a spinal frog typically results in one of two movements: flexion of the leg if the tip of a toe is stimulated when the leg is extended, but extension of the leg if it is already flexed. The "switching mechanism," as Magnus (1924) called it, as well as the circuits for coordinated motion of one leg (while suppressing the other), are present in the spinal cord of a mammal, as well as a frog.
In Magnus' words (describing hind limb behavior in a paraplegic dog),
"If, therefore, one and the same sensory stimulus brings about at one time flexion and at another time extension, a specific switching process must take place each time in the spinal cord centers" (p. 32).
A withdrawal response typically results from a noxious stimulus. However, if you are aware that you are about to be stimulated, a pattern of descending cerebrofugal inhibition can often prevent any observable response.
As more levels of CNS are added above, the behavioral alternatives available are altered and, in general, expanded. This is particularly evident with enlargement of the cerebrum, including an increase in the cortical connections with Mc. However, the alternatives influenceable by C remain a relatively small part of the overall expansion. "Adding above" to the neuraxis can be understood both in a phylogenetic (evolutionary) sense and in terms of how much CNS is left attached to the spinal cord when the neuraxis is truncated. For example, a midbrain animal (all nerve tissue removed above the midbrain) has a larger repertoire of behavior than an animal decerebrated at a lower level such as by a cut through the midbrain (the so-called intercollicular decerebration). The reverse ("subtracting from above") occurs with cerebral lesions. The effects of cerebral lesions depend upon lesion site, but they almost all have the effect of simplifying the subject's behavior (i.e., reducing the repertoire of potential alternatives).
As Danto (1985) put it:
"Choosings between alternative courses of action, in the preponderance of motor acts we perform, occur as the outcome of deliberations of which we are barely conscious, if at all. ... Happily, we are so wired that deliberation may occur without the mediation of consciousness .. ."
The same point was made by Purves and Lichtman (1985),
"Consciousness, after all, is only a small corner of our neural universe. Man's view tends to be biased because our minds have no direct access to the myriad neural mechanisms that allow us to function successfully in daily life ... (p. 355).
It is essential to understand that most bodily adaptations (including postural adjustments, sensorimotor coordination, phoneme generation during speech, as examples, as well as most autonomic regulation) not only can proceed independently of C but, more often than not, are unavailable to C. The pupillary constriction to light is one of the most familiar. An interesting partial exception is the regulation of body temperature. When we are cold enough to shiver, usually we feel cold and we feel the shivering. In this case we are directly aware of aspects of an ongoing bodily adjustment; of both its cause (lower body temperature) and its result (rapid muscle contractions), However, we probably do not have direct awareness of the brainstem neural activity producing the muscle activity. Awareness of shivering contributes little (if at all) to the ongoing adaptive processes. This seems to me to be a circumstance in which C can appear to be merely epiphenomenal.
Breathing is different. When people say, "I was shivering," the meaning of "I" is quite different from its meaning in "I was holding my breath" .Both the control of and the sensory feedback from respiratory movement are ordinarily without C. But both can easily be endowed with C, (Again, this probably does not include awareness of the neural activity in the respiratory centers in the brain stem.) It is difficult (although seemingly obtainable by lots of practice) to be aware of one's own breathing without affecting it. In breathing, as opposed to shivering, epiphenomenality seems to require a lot of practice!
An epiphenomenalist might say that the report, "I am holding my breath," reflects an awareness of something happening in which the awareness has no more causal effect than it does in "I am shivering." But I believe there is a significant difference. The difference is in the neurophysiology; it goes something like this:
The verbal report, "I am shivering," reflects an awareness of proprioceptive information ascending from the spinal cord, and conceivably but improbably some collateral information from the brain stem neurons which are generating the motor output which produces (via spinal cord) the shivering. The verbal report (written at the time) "I am holding my breath," reflects an awareness not only of ascending information from spinal cord (and possibly brain stem) but in addition reflects a thalamic (ILN) contribution to the descending (cerebrofugal) control of brainstem respiratory mechanisms.
One can also be aware of holding one's breath, but without doing it deliberately (when frightened, for example). That could be epiphenomenal.
By "directly aware," I mean that feeling cold and feeling shivery are qualia (as some philosophers call them). As Daniel Dennett (1988) noted, the words qualia (plural) and quale (singular) are not transparently clear. Even pain seems sometimes to be an elaborated rather than pure percept, although some types of pain (e.g., trigeminal neuralgia) are probably as pure as contents of "direct awareness" can get, because it has the same electric quality in everbody who has it, irrespective of age, sex, education or other cultural variables. One of Dennett's arguments against the existence of qualia is that what was thought to be a single quale or "raw feel" (e.g., the sensation elicited by a specific musical chord) can be heard, after musical training, as distinct tones, simultaneously present; i.e., qualia are often divisible. My reaction is, so what? What we are directly aware of no doubt depends on our education--it does not mean we were unaware of the chord before the education. This is the argument made by Paul Churchland (1989) on this point, if I understand him correctly.
OVERALL SUMMARY OF APPENDIX A :
A physiologic understanding of consciousness is desirable and will be facilitated, at this stage, by adopting severe constraints on what aspects are to be explained. The constraints employed should reflect our anatomic and neurologic knowledge.The aspects here considered essential require a mechanism (Mc) for the generation of subjectivity. The main text of this chapter presents evidence that Mc is mainly subserved by the thalamic intralaminar nuclei.
.APPENDIX B: BRAIN PARTS NEEDED, AND NOT NEEDED FOR C.
1. C CAN EXIST IN BRAIN DISCONNECTED FROM MOST OF THE BODY.
When an individual has had a high spinal injury, such as a C, (first cervical segment) transection, C remains, as in a case I attended of an athletic father of four who fell from a backyard trapeze onto his head. In such cases, movement is lost below the face. To be kept alive, such individuals need artificial respiration. Also lost are somatic sensory inputs from below the throat and ears. Yet, such individuals are convincingly conscious in their responses to questions; although what they say reflects their distressing circumstance, their capacity for awareness seems no less than before.
A case of medullary infarction described by Plum and Posner (1985, p. 29) indicates that transections even higher than C,, i.e., near the level of cranial nerve VIII are compatible with, as they put it, "the behavioral appearance of consciousness."
"Intermittently during those final days, she had brief periods of unresponsiveness, but then awakened and signaled quickly and appropriately to questions demanding a yes or no answer and opened or closed her eyes and moved them laterally when commanded to do so. There was no other voluntary movement."(p29)
A cat with the pretrigeminal transection of the brain stem (in front of cranial nerve V) although deaf, is able to respond to olfactory and visual input with the EEG characteristics and tracking eye movements we recognize as concomitants of awareness (Battini et al,1959; Zernicki,1986).
It is generally recognized that in the intact mammal, activation is ordinarily provided by the upper brainstem core, as discussed in the main text. This has been confirmed for h¨mans by many autopsy studies; for a recent confirmatory MRI study see Parvizi et al[ 00].
Although the necessary activation is mainly associated with the upper brainstem core, there is evidence that even without it, aroused states are possible. As pointed out in the main text, the cerveau isole cat eventually arouses if maintained long enough in the chronic state. There is also the result of Alema et al(1966); they injected barbiturate into the vertebral circulation of 19 humans, producing loss of pupillary light reflex, corneal reflex, and both facial and eye movements for 3 to 4 min. However, loss of button presses to acoustic or visual signals and verbal responses to questions were only occasionally affected and in those cases for no more than 10 s. There was never slowing of the EEG. The authors concluded,
"In man the most important subcortical structures ultimately responsible for maintenance of the level of consciousness are located rostral to the brain stem, perhaps in the diencephalon."
Complementing the above cases with thalami intact are cases with severe, bilateral thalamic damage. In spite of relatively intact brainstem and cerebral cortex and in spite of alternating states of drowsy and awake, such patients can remain in a persistent vegetative state for many years as in the widely publicized case of Karen Ann Quinlan (Kinney,1994).
2. HUMAN C DOES NOT REQUIRE TEMPORAL STRUCTURES INCLUDING THE HIPPOCAMPUS.
This fact is is now widely understood by those concerned with consciousness so that an extensive review is unnecessary here; the Kluver-Bucy syndrome exemplifies the massive cognitive loss with retention of C following bitemporal damage. Particularly well known by now is the case of HM [Scoville and Milner,1957; Corkin,1984]. An even greater bilateral loss including both temporal lobers is the patient Boswell (DRB)[see fig. 2.13 in Damasio and Damasio,1989].
3.HUMAN C DOES NOT REQUIRE PARIETAL LOBE FUNCTION.
Parietal neurons respond both to the position of the arm as felt and as seen [Graziano et al, 2002]. Maps are present in the posterior parietal cortex for both visualized space including seen objects, and for the positional information from muscle(proprioceptive)afferents [Anderson 2002]. Parietal cortex is an essential part of the cortical networks for attention [Posner and Rothbart,1992]. Note also the disorders of "self" from parietal lesions as discussed in Appendix A part 7. Taylor [2001]concluded that in the inferior parietal cortex occurs," the confluence of information on salience, episodic memory, high level coding of inputs and information on body state to create consciousness"(p404).
A problem with attributing C to parietal cortex is that extensive bilateral damage there leaves C for simpler contents seemingly normal [Jeannerod et al,1994]. The patient of Uyama et al,1993] with adrenoleukodystrophy gradually developed a biparietal lesion sparing most of the cerebrum, culminating in a near absence of cognition without loss of C. The striking syndrome of Balint [Husain and Stein, 1988] includes a disability of voluntary gaze (reflex eye movements remaining intact), a problem seeing more than one object at a time (simultanagnosia), and optic ataxia, a difficulty reaching for objects the patient can see. The optic ataxia seems directly attributable to the patient's failure to coordinate the visual and proprioceptive maps. At least some of the devastating disability may be explicable in terms of an attentional deficit [Rizzo and Vecera, 2002]. Other unfortunate problems may also be present, but nobody claims the Balint patients are not conscious.
4. HUMAN C DOES NOT REQUIRE PREFRONTAL CORTEX.
There is a long history of assertions that consciousness depends on the frontal lobes [Markowitsch, 1995]. When we describe “frontal lobe symptoms” or “frontal lobe functions,” we have in mind a large expanse of cortex more precisely termed “prefrontal” [Levin, Eisenberg & Benton, 1991; Damasio & Anderson, 1993]. We do not mean “frontal lobe” as it is used in current anatomy texts where “frontal lobe” includes everything anterior to the central (Rolandic) sulcus. Prefrontal cortex has come to be precisely defined as the large expanse of each frontal lobe which is reciprocally connected with the mediodorsal nucleus (MD) of the thalamus [Divac, 1988: Fuster, 1989]. This is in keeping with the conclusion of Jones [1987] that the most useful guide to delimiting cortical areas is their thalamic connections.
A half-century ago it was shown that normal IQ could be present after bifrontal lobectomy “despite the loss of somewhere around 15 percent by weight of the total mass of the cerebrum.” (Hebb, 1959). The common tests for“IQ” can be misleading as a measure of cognitive ability Lezak,1998]. However, it is hard to believe that someone does well on so-called IQ tests without possessing C. Humans from whom the prefrontal cortex has been removed or disconnected bilaterally appear to be both subjectively aware and volitional, whatever the extent to which they are neglectful, shortsighted, unconcerned, apathetic, perseverative, impulsive, or even explosive (Eslinger and Damasio,1985; Damasio & Damasio, 1989; Benson, 1994; Levin, Eisenberg & Benton, 1991; Damasio & Anderson, 1993; Divac, 1988; Fuster, 1989).In one study, both IQ and good psychiatric recovery were actually found to correlate positively with the amount of frontal lobe damage from lobotomies done 25 years or so before (Stuss & Benson, 1986, p. 10).
The reciprocal connections between MD and prefrontal cortex make up the white matter in the medial inferior aspect of each frontal lobe. These tracts can be easily severed by inserting a spatula through two burr holes in the top of the skull. This procedure (bimedial leukotomy) has occasionally been used to treat excruciating pain caused by head or neck cancer; it is remarkably reliable. Postoperatively the patient's conversation, food preferences, memories, and awareness of current events remain intact. And both verbal and bodily signs of distress are absent. When specifically asked if they have "pain," they typically say that they do, and in the same location as before. But they express no concern about this, and rarely if ever request pain medication. The main drawback of the procedure is that the patients also evidence minimal concern for the future consequences of their behavior which on some notorious occasions has included urinating or defecating in public. The connections between MD and prefrontal cortex are valuable, but required for C they are not.
C is necessarily of the present; some form of immediate memory is necessary but not long term memory or even most of what is usually called working memory. And C needs no aspect of the future such as anticipation. Consider holding one's breath, feeling pain or thirst, tasting something sweet, or feeling sad. Each of these may be accentuated by or even mainly arise from anticipation. But the neural activity subserving C is distinguishable from the neural activity the neural activity associated with anticipation. Experience, both my own and that reported by others, with bifrontal lobectomies and lobotomies has led me to conclude that anticipation (indeed, any concern for future consequences) is dissociable from C, hence anticipation is only one of many specific contents to which C can attach.
I point to the nonnecessity for C of prefrontal cortex for two reasons: as a further illustration of how neurologic experience has contributed to my proposed precisation of C and to illustrate how otherwise knowledgeable people have been misled because they lack personal experience with humans who have had massive bifrontal damage. For example, a famous astrophysicist with whom I had dinner, a man also known for his ability to explain difficult material to the general public, opined: "Consciousness depends on the frontal lobes." "How so?" I asked. "Because (1) they are for the anticipation of consequences [probably true] and (2) anticipation of consequences is a defining characteristic of consciousness." (This second claim is the source of his error--if his circle of acquaintances were wider he might have met many persons whom he would consider conscious but who minimally consider consequences.) I then asked, "What would you say if someone had severe frontal damage and was still conscious?" "Is that so?" he replied, and changed the subject.
C IS NOT "TIME BINDING"
One of the most reliable signs of a bilateral prefrontal lobectomy in monkeys is their inability to do delayed-alternation tasks (Jacobsen & Nissen, 1937; Mishkin, 1957; Iversen & Mishkin, 1970; Pribram, Plotkin, Anderson, & Leong, 1977; Markowitsch, Pritzel, Kessler, Guldin, & Freeman, 1980; Fuster, 1989; Sawaguchi & Goldman-Rakic, 1991).
In this task, the monkey must remember, during a brief delay, which of two otherwise identical containers held the reward (e.g., a banana chip) on the immediately preceding trial. To obtain a reward on the current trial, the monkey must choose the other container.
Similar impairment of delayed responses was found following frontal lobectomy in humans (Prisko, 1963). Milner and Corsi (Milner, 1971) went on to use "recency" tasks to show in these patients a disturbance in the temporal ordering of events (Milner, Corsi, & Leonard, 1991; McAndrews & Milner, 1991). Luria's (1966) frontal lobe patients had "memory disorders" most evident when two tasks requiring recollection were given sequentially; the items from one task interfered with those from the other. Hecaen and Albert (1978) pointed out that most of Luria's findings were based on cases of large frontal tumors which likely affected other brain parts as well as prefrontal cortex. This methodologic problem qualifies ascription of the timing deficit solely to damage of prefrontal cortex , but it does not affect the important conclusion that patients unable to properly order recent events can be conscious. Moreover, deficits in temporal organization have been found in patients whose frontal lesions were not caused by tumors (Petrides & Milner, 1982; Shimamura, Janowski, & Squire, 1990; Verin et al,1993; Levin et al,1994].
When Taylor [2001] located the essential circuits for consciousness, he argued that the patient of Ackerly and Benton showed the non-necessity of most frontal cortex for consciousness. This case is qualified by the likelihood of some compensatory alterations because the tissue loss occurred early in life. The same cannot be said however of the Brickner case. [Both of these cases are well described in Damasio and Anderson,1993].
Appendix C: METAPHYSICS: PHYSICALISM WITHOUT MATERIALISM.
The hypothesis presented here implies that C requires normally functioning brain. As pointed out in the main text , this view, while explicitly mechanistic, is not necessarily materialistic, a point elaborated here in this appendix C.
Some writers imply, or assert outright, that a full account of consciousness includes the belief that Self or Soul can exist without body. Falsification of such beliefs seems to me impossible, hence arguing either for or against the existence of the nonmaterial is not a scientific question. What I believe is that to the degree that something nonmaterial, if it exists, has observable effects, these effects can be exerted only through functioning brain. This does not entail materialism since it is also consistent with any form of dualism which recognizes that mental occurences have their origin in brain occurrences and that nonmaterial forces, if any, can act ONLY through brain. That is, I hold that one can be a cerebralist without being a materialist.(In Bogen,1998 I argued that physicalism did not require materialism. Discussions since, especially with T.Sullivan, have persuaded me that the word "physicalism" has a history that makes its usage complicated by unnecessary connotations. I have therefore reverted to the word "cerebralism" which conveys straightforwardly my belief that consciousness depends upon and needs explanation in terms of properly functioning cerebrum). The main point is that the usual ontologic questions are orthogonal (i.e. not at all correlated) with progress in neuroscience, as evidenced by the success of many dualists. Let's consider a few:-
Ontologic dualism was the creed of many past creators of neuroscience. Fritsch and Hitzig [1870] were prominent pioneers in cortical localization. Summing up some experimental results, they said,
"... one might express himself thus: there was some motor connection between the soul and the muscle, while the connection from muscle to soul was somewhere interrupted."
This quotation is from the translation by Gerhardt von Bonin [1960, p. 96]. In the translation by Wilkins [1965, p. 27] the word "Seele" is translated "psyche" instead of "soul". This reflects the fact that in previous years, the word "Seele" could be used to mean either mind or soul, a conflation of two distinguishable concepts. That the two were conflated by Descartes was one source of Ryle's [1969] condemnation of the "ghost in the machine"; this sort of conflation is not pecuiarly European; both meanings also attach to the Chinese character commonly pronounced 'shin'.
Hughlings Jackson was forthrightly dualistic and went so far as to say,
"We cannot understand how any conceivable arrangement of any sort of matter can give mental states of any kind ... I do not trouble myself about the mode of connection between mind and matter." [Taylor, 1931, Vol. I, p. 52].
At one time, Jackson went so far as to say, "Psychical states are never states of the organism." [Taylor, 1931, Vol. II, footnote on p, 95].
Sir Charles Sherrington closed the introduction to his classic on Integrative Action [1947,p. xxiv] as follows,
"Of these two views Cajal tells how he was for a time a zealous disciple of the former, and noticed that to his practical life adherence neither to the one nor to the other seemed to make any difference whatever. ... that our being should consist of two fundamental elements offers I suppose no greater improbability than that it should rest on one only."
Sir Francis Walshe was one of the more profound thinkers of 20th century clinical neurology, When criticizing Karl Lashley's metaphysics he said,
"Yet, when not on this subject, no one could be a more penetrating student of the nature of cerebral organization than he was. This, surely is the proper business of the physiologist, and it is not facilitated by attaching to it, like a sinker, an irrelevant materialist ideology." [Walshe, 1965, p. 208].
Walshe might have added, if he had been so inclined, that a humane clinical neurology can be practiced without attaching to it a dualistic metaphysics.
The achievements of the foregoing historical figures (and many others) show that a dualistic metaphysics need not impede scientific success. The best minds of the Western world have long argued on both sides the problem of monism versus dualism, especially after, in the words of L. J. Rather [1965, p. 5], "Descartes' rediscovery of and emphasis on the primacy of awareness." Rather's 16-page discussion is a gem; among other things, he points out that, "the problem is not likely to be resolved within the set of presuppositions that helped generate it."
Is it unfruitful that so many engage in this unending controversy? (Rather slyly called it "intellectual tauromachy").There is no need here to either affirm or deny ontologic dualism; physicalism can work with either ontologic view, as follows:
We can say that a small subset of cerebral processes maps onto (not just "into") mentation. (The word "onto" means that the target of the mapping is exhausted by the mapping, so that nothing is left over. And an even smaller subset of cerebral processes has the potential to be endowed with C. No one now knows how the set of brain states specifically maps onto mental states, but it is surely not one-to-one for each individual brain state [Sperry, 1952, p. 309]. A variety of distinguishable brain states likely correspond to a small number of mental states, in a many-to-few mapping analagous to the dynamics of the network described by Hopfield : "The flow is not entirely deterministic, and the system responds to an ambiguous starting state by a statistical choice between the memory states it most resembles" (p. 2557). This is one example of a probabilistic many-to-few mapping; such a brain-onto-mind mapping imposes some limitation on the reverse, a mind-to-brain reduction. To speak of a "brain/mind relation" is to suppose that we obtain information from our own mentation which needs to be correlated with information about brain states. That is, for the foreseeable future, our knowledge of what goes on inside a human head will come from two sources, introspection and observation. This is epistemologic dualism but is ontologically neutral. That is, cerebralism is compatible with either ontologic dualism or materialism. Moreover, for the foreseeable future, cerebralism is much less likely to be eliminative of folk psychology than to be revisionary [cf. P. S. Churchland, 1995, her footnote 13; see also Horgan & Woodward, 1985]. In view of the "near completeness" of physics, how something without spatial extent (e.g., the Soul) could affect brain is, and has long been, a problem: the "nexus problem." But this is not the same as the "mapping problem," i.e., how brain maps onto mind. Some superlative scientists ,e.g., Sperry [1980], Edelman [1992], Crick [1994] have explicitly denied ontologic dualism, thus denying the existence of any nexus problem. Others, e.g., Popper & Eccles [1981], MacKay [1980], Eccles [1989] being dualists, have explicitly explored the nexus problem. Unclear is how either attitude, whatever other virtues they possess, contributes to the mapping problem. Many people have mistakenly conflated these two problems.
RECAPITULATION OF APPENDIX C.
0. I do not start with all the terms and all the assumptions typical of the monism/dualism debate of the last 400 years. I am aware that many people, having laboriously familiarized themselves with these previous usages and issues, might be offended by views which are not cast in familiar terms.
1. By mentation I mean either thought or emotion (or a combination) each instance of which is called an m. Each thought or emotion is associated(see below) with a NAP(NEURONAL ACTIVITY PATTERN) which in practice I expect to be represented by a vector.. Note that there are a great many NAP (singular same as plural like sheep) that can never be an m. What makes this "identity" theory different from most is that a number of different NAP (hence different vectors) can be associated with the very same m. Also, a particular NAP can correspond to more than one m. [This is what I mean by a probabalistic many-to-few mapping which we know can occur even in a relatively simple neural net]. As a result, given a NAP, the corresponding(associated) m can only be partially predicted, i.e. a range of m each with a certain probability. Inversely, given an m, it is even harder to predict which associated NAP will be detected because there are so many possibilities. This situation comes about,in part, because we identify (detect) NAP and m in two distinctly different ways.
2. Every NAP is potentially available to external monitoring given sufficient technical advances [a huge multielectrode array, or an fMRI with remarkable resolution].
3. By contrast, only a fraction of NAP are potentially available (in the form of m) to the internal monitoring we call consciousness, and only a few at a time.
4. When I say a NAP is "associated with" an m, I mean that a NAP "is" an m in the sense that the relation occurs naturally, i.e. is an aspect of Nature built into brains by evolution. I don't mean "is" in the sense that 2+2 is 4 which follows by deduction from the definitions of 3 and of 4 In other words, the association is a "natural kind"- or, to put it differently, that's just the way it is, just as it is a property of stars that they give off light.
5. We are at a stage resembling those days when people knew a star gives off light [ big rocks do not and are seen only because they reflect light] but people did not not yet have a good explanation for why stars shine. Similarly, I claim that certain NAP "give off" C-and our problems are to figure out what is different about them, and what mechanism makes them be different transiently.
6. To continue the analogy: As for measuring consciousness, we are not yet even at a stage comparable to the measurement of light 100 years ago. Nowadays by "photometer" we mean an instrument that counts photons per minute. 100 years ago a photometer was a setup for comparison by some human observer of the intensity of a light source with a "standard candle". According to The New International Encyclopedia of 1926, "The candle in use in the United States and England for photometric tests is the standard spermaceti candle, which burns 120 grains of material per hour and six of which weigh one pound [and when it] burns with a flame 45 millimeters in height, the light emitted is considered unity;". In those days the slight scientific understanding of light is reflected in the same encyclopedia's definition," The sensation of which one becomes conscious through the optic nerves [caused by] the entrance into the eye of ether waves whose wave numbers lie between certain limits;". Nowadays we know that although the optic nerves are usually involved in light perception, they are neither sufficient nor necessary. I claim that to have visual consciousness it is necessary and sufficient to have the "appropriate interaction" between a piece of extrastriate cortex and the ILN; and that this claim is 1. experimentally testable and 2. neither requires nor negates anybody's faith in the nonmaterial, the existence(or not) of which is orthogonal to the brain/mind problem.
REFERENCES

Abe, K, Yokoyama, R, and Yorifuji, S. (1993). Repetitive speech
disorder resulting from infarcts in the paramedian thalami and midbrain. J
Neurol, Neurosurg Psychiatry. 56, 1024-1026.
Abel, T, Nguyen, PV, Barad, M, Deuel, TAS, Kandel, ER and Bourtchauladze,
R. (1997). Genetic demonstration of a role for PKA in the late phase of LTP
and in hippocampus-based long-term memory. Cell. 88, 615-626.
Adams, JH, Graham, DI, and Jennett, B. (2000). The neuropathology of
the vegetative state after an acute brain insult. Brain. 123, 1327-1338.
Adrian, ED, Bremer, F and Jasper, HH (eds.) (1954). Brain mechanisms and
consciousness. Springfield, IL: C.C. Thomas
Albe-Fessard, D, and Besson, JM (1978). Convergent thalamic and cortical
projections, the non-specific system. In A. Iggo (ed.). Handbook of Sensory
Physiology: Somatosensory System. New York: Springer.
Albert M. A simple test of visual neglect. (1973) Neurology 23:658-664.
Alemà, G, Perria, L, Rosadini, G, Rossi, GF, and Zattoni, J. (1966).
Functional inactivation of the human brain stem related to the level of
consciousness. J Neurosurgery. 24, 629-639.
Allman, JM, and Kaas, JH (1971). A representation of the visual field in
the caudal third of the middle temporal gyrus of the owl monkey (Aotus
trivirgatus). Brain Res. 31, 85-105.
Allport, A. (1988). What concept of consciousness? In A. J. Marcel and
E. Bisiach (eds.). Consciousness in contemporary science. Oxford: Clarendon
Press.
Atkins, PW. (1987). Molecules. New York: Sci. Am.
Austin, GM, and Grant, FC (1958). Physiologic observations following total
hemispherectomy in man. Surgery. 38, 239-258.
Baars, BJ. (1988). A cognitive theory of consciousness. Cambridge,
England: Cambridge Univ. Press.
Baars, BJ (1993). How does a serial, integrated and very limited stream of
consciousness emerge from a nervous system that is mostly unconscious,
distributed, parallel and of enormous capacity? In G. Broch & J. Marsh
(eds.). Experimental and Theoretical Studies of Consciousness. New York:
John Wiley and Sons.
Baars, BJ (1997). In the theatre of consciousness. New York: Oxford
Univ. Press.
Bar, M & Biederman, I (1996). Subliminal visual priming. Psychological
Science. 9, 464-469.
Bar, M and Biederman, I. (1999). Localizing the cortical region
mediating visual awareness of object identity. Proc Natl Acad Sci USA. 96,
1790-1793.
Basetti, C, Mathis, J, Gugger, M, Lovblad, KO, and Hess, CW (1996).
Hypersomnia following paramedian thalamic stroke: a report of 12 patients.
Ann Neurol. 39, 471-80.
Batini, C, Moruzzi, G, Palestini, M, Rossi, GF, and Zanchetti, A. (1959).
Effects of complete pontine transections on the sleep-wakefulness rhythm:
the midpontine pretrigeminal preparation. Arch Ital Biol. 97, 1-12.
Bayley, PJ, and Squire, LR. (2002). Medial temporal lobe amnesia:
Gradual acquisition of factual knowledge by non-declarative memory. J
Neurosci. 22, 5741-5748.
Baynes K, Tramo, MJ, Reeves AG, and Gazzaniga MS. (1997). Isolation of a right hemisphere cognitive system in a patient with anarchic (alien) hand sign. Neuropsychologia. 35, 1159-173.
Benson, DF. (1994). The Neurology of Thinking. New York: Oxford Univ. Press.
Benton, AL, Sivan, AB. (1993). Disturbances of the body schema. In K. M. Heilman & E. Valenstein (eds.). Clinical neuropsychology. New York: Oxford Univ. Press.
Berger, H. (1930) Uber das Elektrenkephalogram des Menschen, II. Arch Psychol Neurol. (Lpz.), 40, 160-169. Cited in Adrian et al, op cit.
Berti, A, and Rozzolatti, G. (1992). Visual processing without
awareness: Evidence from unilateral neglect. J Cognitive
Neuroscience. 4, 345-351.
Bewermeyer, H, Dreesbach, HA, Rackl, A, Neveling, M. and Heiss, W-D. (1985). Presentation of bilateral thalamic infarction on CT, MRI and PET. Neuroradiology. 27, 414-419.
Bisiach, E and Geminiani, G. (1991). Anosognosia related to hemiplegia and hemianopia. In G. P. Prigatano & D. L.. Schacter (eds.). Awareness of deficit after brain injury. New York: Oxford Univ. Press.
Bisiach, E, and Luzzatti, C. (1978). Unilateral neglect of representational space. Cortex. 14, 129-133.
Bisiach, E, Vallar, G, Perani, D, Papagno, C, and Berti, A. (1986).
Unawareness of disease following lesions of the right hemisphere: Anosognosia for hemiplegia dnd anosognosia for hemianopia. Neuropsychologia. 24:471-482.
Bloch, N. (1995). On a confusion about a function of consciousness. Brain Behav Sci. 18, 227-287.
Bogen, JE. (1969). The other side of the brain. II: An appositional mind. Bull Los Angeles Neurol Soc. 34, 135-162.
Bogen, JE. (1974). Hemispherectomy and the placing reaction in cats. In M. Kinsbourne and W L. Smith, (eds.). Hemispheric Disconnection and Cerebral Function. Springfield: C. C. Thomas.
Bogen, JE. (1976).
Bogen, JE. (1977). Further discussion on split-brains and hemispheric capabilities. Br J Phil Sci. 28, 281-286.
Bogen, JE. (1979). The callosal syndrome. In K. Heilman & E.
Valenstein (eds.). Clinical Neuropsychology. New York: Oxford Univ. Press.
Bogen, JE. (1990). Partial hemispheric independence with the neocommissures
intact, in C. Trevarthen, (ed.). Brain circuits and functions of the mind. Cambridge, England: Cambridge University Press.
Bogen, JE. (1993a). Intralaminar nuclei and the where of awareness. Proc Soc Neurosci 19, 1446.
Bogen, JE. (1993b). The callosal syndromes. pp. 337-381 in K. Heilman & E. Valenstein (eds.). Clinical Neuropsychology. 3rd ed. New York: Oxford Univ. Press.
Bogen JE. (1995a). On the Neurophysiology of Consciousness. I. An Overview. Consciousness and Cognition. 4, 52-62.
Bogen JE. (1995b). On the Neurophysiology of Consciousness. II. Constraining the semantic problem. Consciousness and Cognition. 4, 137-158.
Bogen, JE. (1997). The crucial central core of consciousness does not require cognition. Proc Soc Neurosci. 23:1926.
Bogen JE. (1997). Some neurophysiologic aspects of consciousness. Seminars in Neurology. 17, 95-103.
Bogen JE. (1998). My developing understanding of Roger Wolcott Sperry's philosophy. Neuropsychologia. 36, 1089-1096.
Bogen JE. (2001) An experimental disconnection approach to a function of consciousness. Int J Neurosci 111:135-6.
Bogen JE and Berker E. (2002) Face module, face network. Neurology 59:652-653.
Bogen JE, Berker E, van Lancker D, Sudia S, Lipstad B, Sadun A and Weekes N. (1998). Left hemicerebrectomy: Vision, olfaction and mentation 45 years later. Proc Soc Neuroscience. 24, 173.
Bogen, JE and Bogen, GM. (1976). Wernicke's Region—Where is it? Ann N Y Acad. Sci. 280, 834-843.
Bogen, JE and Campbell, B. (1962). Recovery of foreleg placing after ipsilateral frontal lobectomy in the hemicerebrectomized cat. Science. 135, 309-10
Bogousslavsky, J, Miklossy, J, Regli, F, Deruaz, JP, Assal, G, and Delaloye,
B. (1988). Subcortical neglect: Neuropsychological, SPECT, and
neuropathological correlations with anterior choroidal artery territory infarction. Ann Neurology. 23 (5), 448-452.
Bogousslavsky, J. Regli, F, Delaloye, B, Delaloye-Bischof, A, Assal, G, and Uske, A. (1991). Loss of psychic self-activation with bithalamic
infarction; Neurobehavioural, CT, MRI and SPECT correlates. Acta Neurol Scand. 83, 309-316.
Bogousslavsky, J. and Caplan, L. (1995). Stroke syndromes. Cambridge: Cambridge Univ Press.
von Bonin, G. (1960). The cerebral cortex. Springfield, IL: C. C.
Thomas.
von Bonin, G. (1960). Some papers on the cerebral cortex. Springfield, IL: C. C. Thomas.
Brain, WR. (1941). Visual disorientation with special reference to
lesions of the right hemisphere. Brain. 64, 244-272.
Braun, J. (1997). Divided attention: Narrowing the gap between brain and behavior. In R. Parasuman (ed.). The attentive brain. Cambridge, MA: MIT Press.
Bremer, F. (1935). Cerveau isolé et physiologie du sommeil. C. R. Soc. Biol. 118, 1235-1242.
Bremer, F. (1936). Nouvelles recerches sur le mécanisme du sommeil. C. R. Soc. Biol. 122, 460-464.
Brighina, F, Bisiach, E, La Bua, V, Piazza, A, and Fierro, B. (2002).
Low-Frequency repetitive transcranial magnetic stimulation of left parietal cortex ameliorates contralesional visuospatial hemineglect. Neurology 58, 222.
Brion, S and Jedynak, CP. (1972). Troubles du transfer
interhémisphérique (callosal disconnection). A propos de trois observations de tumeurs du corps calleux. Le signe de la main étrangère. Rev Neurologie. 126, 257-266.
.
Brion, S and Jedynak, CP. (1974). Semeiologie calleuse dans les tumeurs et malformations vasculaires. In F. Michel and B. Schott (eds.). Les syndromes de disconnexion calleuse chez l'homme. Lyon: Hopital Neurologique.
Brion, S and Jedynak, CP. (1974). Les troubles du transfer
interhemispherique. Masson; Paris.
Brodal, A. (1969). Neurological anatomy. 2nd ed. London: Oxford Univ.
Press.
Brothers, L, Ring, B, and Kling, A. (1990). Responses of neurons in the macaque amygdala to complex social stimuli. Neurosciences. 41, 199-213.
Brun, VH, Otnaess, MK, Molden, S, Steffenach, H-A, Witter, MP, Moser, M-B, and Moser, EI. (2002). Place cells and place recognition maintained by direct entorhinal-hippocampal circuitry. Science. 296, 2243-2246.
Bullier J, Girard P and Salin P. (1994) The role of area 17 in the transfer of information to extrastriate visual cortex. in A. Peters and K.S.Rockland (eds.) Cerebral cortex vol.10 New York:Plenum.
Bunin, MA, and Wightman, RM. (1999). Paracrine neurotransmission in the CNS: involvement of 5-HT. Trends Neurosci. 22, 377-382.
Burk JA and Mair RG (1998) Thalamic amnesia reconsidered: excitotoxic lesions of the intralaminar nuclei, but not the mediodorsal nucleus, disrupt place delayed matching-to-sample performance in rats (Rattus norvegicus). Behav. Neurosci. 112:54-67.
Canli, T, Sivers, H, Whitfield, SL, Gotlib, IH, and Gabrieli, JDE.
(2002). Amygdala response to happy faces as a function of extraversion.
Science. 296, 2191.
Carnap, R. (1950). Logical foundations of probability. London:
Routledge & Kegan Paul.
Castaigne, P, Lhermitte, F, Buge, A, Escouroile, R, Hauw, JJ, and
Lyon-Caen, O. (1981). Paramedian thalamic and midbrain infarcts; clinical and neuropathological study. Ann Neurol. 10, 127-148.
Castiello, U, Paulignan, Y, and Jeannerod, M. (1991). Temporal dissociation of motor responses and subjective awareness; A study in normal subjects. Brain. 114, 2639-2655.
Chalmers DJ. (1998) On the search for the neural correlate of consciousness. in SR Hameroff, AW Kaszniak and AC Scott (eds.) Toward a science of consciousness ll Cambridge,MA: MIT Press
Chalmers DJ. (2002). The puzzle of conscious experience. Sci Amer. 12, 90-98.
Churchland PM. (1989). A neurocomputational perspective. Cambridge: MIT Press.
Churchland PS. (1986). Neurophilosophy: toward a unified science of the mind-brain. Cambridge, MA: MIT Press.
Churchland PS. (1988). Reduction and the Neurobiological Basis of Consciousness. pp 273-304 in A .J. Marcel and E. Bisiach (eds.),
Consciousness in Contemporary Science. New York: Oxford Univ. Press.
Churchland PS. (1995). Can neurobiology teach us anything about consciousness? In H. Morowitz & J. Singer (eds.). The mind, the brain and complex adaptive systems. New York: Addison Wesley.
Cicchetti, F, Lacroix, S, Beach, TB, Parent, A. (1998). Calretinin gene expression in the human thalamus. Mol. Brain Res. 54, 1-12.
Clark RE and Squire LR (1998) Classical conditioning and brain systems: the role of awareness. Science 280:77-81.
Clark RE, Manns JR and Squire LR (2001) Trace and delay eyeblink conditioning: contrasting phenomena of declarative and nondeclarative memory. Psychol.Sci. 12:304-8.
von Cramon, DY, Hebel, N, and Schuri, U. (1985). A contribution to the anatomical basis of thalamic amnesia. Brain. 108, 993-1008.
Crick, F. (1984). Function of the thalamic reticular complex: The
searchlight hypothesis. Proc Natl Acad Sci USA. 81, 4586-4590.
Crick, FHC. (1994). The astonishing hypothesis: The scientific search for the soul. New York: Scribner's.
Crick, F., & Koch, C. (1990). Towards a neurobiological theory of
consciousness. Seminars in the Neurosciences, 2, 263-275.
Crick, F., & Koch, C. (2000). The problem of consciousness. Sci Amer. 12, 10-17.
Critchley, J. (1966, originally 1953). The parietal lobes. New York: Hafner.
Damasio, A. (1994). Descartes' error. New York: Putnam.
Damasio, A. (1999). The feeling of what happens: Body and emotion in the making of consciousness. New York: Harcourt Brace.
Damasio, AR and Anderson, SW. (1993). The frontal lobes. In K. M. Heilman and E. Valenstein (eds.), Clinical Neuropsychology, 3rd ed. New York: Oxford Univ. Press.
Damasio, H and Damasio, AR. (1989). Lesion Analysis in Neuropsychology. New York: Oxford Univ. Press.
Danto, AC. (1985). Consciousness and motor control. Behavioral and Brain Sciences. 8, 540-541.
Daum, I, and Ackermann, H. (1994). Dissociation of declarative and nondeclarative memory after bilateral thalamic lesions: A case report. Intern J Neuroscience. 75, 153-165.
Della Sala, S, Marchetti, C. and Spinnler, H. (1994). The anarchic hand: a fronto-mesial sign. In F. Boller & J. Grafman (eds). Handbook of Neuropsychology, Vol 9. Amsterdam: Elsevier.
Dennet, DC. (1988) Quining qualia. In A. J. Marcel & E. Bisiach (eds.). Consciousness in contemporary science. Oxford: Clarendon Press.
Dennet, DC. (1991). Consciousness explained. Boston: Little, Brown.
Desmedt, JE, and Tomberg, C. (1994). Transient phase-locking of 40-Hz
electrical oscillaations in prefrontal and parietal human cortex reflects a
conscious somatic perception process. Neurosci Lett. 1168:126-129.
Disterhoft JF, Carillo MC, Fortier CB, Gabrieli JDE, Knuttinen MG, McGlinchey-Berroth R, Preston A and Weiss C. (2002) Impact of temporal lobe amnesia, aging and awareness on human eyeblink conditioning. in D.Schacter and L.Squire (eds.) Neuropsychology of memory 3rd ed. New York: Guilford.
Divac, I. (1988). A note on the history of the term "prefrontal." IBRO News. 16:2.
Doty, RW. (1975). Consciousness from neurons. Acta Neurobiol. Exp. 35, 791-804.
Dronkers, NF. (2000). The gratuitous relationship between Broca's aphasia and Broca'a area. Behav Brain Sci. 23:30-31.
Eccles, JC. (1989). Evolution of the brain: Creation of the self. New York: Routledge, Chapman & Hall.
Edelman, GM. (1989). The remembered present: A biological theory of
consciousness. New York: Basic Books.
Edelman, GM. (1992). Bright air, brilliant fire. New York: Basic
Books.
Engel, AK, Fries, P, König, P, Brecht, M, and Singer, W. (1999).
Temporal binding, binocular rivalry, and consciousness. Consciousness and
Cognition. 8, 128-151.
Engel, AK, Fries, P, König, P, Brecht, M, and Singer, W. (1999). Does time help to understand consciousness? Consciousness and Cognition. 8,
260-268.
Ervin, F. R., & Mark, V. H. (1966). Studies of the human thalamus: IV.
Evoked responses. Ann New York Acad Sci. 112, 81-92.
Eslinger, P, & Damasio, AR. (1985). Severe cognitive disturbance of
higher cognition after bilateral frontal lobe ablation. Neurology. 35,
1731-1741.
Façon, E, Steriade, M, and Wertheim, N. (1958). Hypersomnie prolongée
engendrée par des lésions bilatérales du systéme activateur médial le
syndrome thrombotique de la bifurcation du tronc basilaire. Rev Neurol. 98,
117-133.
Farah, MJ, Monheit, MA, and Wallace, MA. (1991). Unconscious perception
of "extinguished" visual stimuli: Reassessing the evidence.
Neuropsychologia. 29,949-958.
Feinberg, TE, Schindler, RJ, Flanagan, NC and Haber, LD. (1992). Two
alien hand syndromes. Neurology. 42, 19-24.
Felleman, DJ, and Van Essen, DC. (1991). Distributed hierarchical
processing in the primate cerebral cortex. Cerebral Cortex. 1, 1-47.
Fessard, AE. (1954). Mechanisms of nervous integration and conscious
experience. pp. 200-236. In E. D. Adrian, F. Bremer, H. H. Jasper (eds.).
Brain mechanisms and consciousness. Springfield, IL: C. C. Thomas.
Flanagan, O. (1991). The modularity of consciousness. Behav Brain Sci.
14, 446-447.
Flanagan, O. (1991). The science of the mind, 2nd ed. Cambridge, MA:
MIT Press.
Flanagan, O. (1992). Consciousness reconsidered. Cambridge, Mass.: MIT
Press.
Fortin M, Asselin M-C, Gould PV and Parent A. (1998) Calretinin-immunoreactive neurons in the human thalamus. Neuroscience 84:537-48.
Freeman, WJ. (1997). Three centuries of category errors in studies of
the neural basis of consciousness and intentionality. Neural Networks. 10,
1175-1183.
Fries, P, Reynolds, JH, Rorie, AE and Desimone R. (2001). Modulation of
oscillatory neuronal synchronization by selective visual attention. Science.
291, 1560-1563.
Fritsch, G and Hitzig, E. (1870). On the electrical excitability of the
cerebrum. Arch f. Anatomie, Physiologie und Wissenschaftliche Medicin,
300-332. [English translation in von Bonin, 1960.]
Fuster, JM. (1989). The Prefrontal cortex: anatomy, physiology and
neuropsychology of the frontal lobe. New York: Raven Press.
Fuster J (1995) Memory in the cerebral cortex. Cambridge,MA:MIT Press.
Fuster J (2002) Cortex and mind:unifying cognition. New York:Oxford U. Press.
Fuxe, K and Agnati, LF, (eds.). (1991). Volume transmission in the
brain: Novel mechanisms for neural transmission. New York: Raven Press.
Galin, D. (1992). Theoretical reflections on awareness, monitoring, and
self in relation to anosognosia. Consciousness and Cognition. 1, 152-162.
Galin, D. (1993). Beyond the fringe. Consciousness and Cognition. 2,
113-118.
Galin, D. (1994). The structure of awareness: Contemporary applications
of William James' forgotten concept of "the fringe." J Mind and
Behavior. 15, 375-400.
Galin, D. (In press 2002). The concepts "self," "person" and "I" in
Buddhism and in western psychology. In B. A. Wallace (ed.). Breaking new
ground: Essays on Tibetan Buddhism and modern science. New York: Columbia
Univ. Press.
Gentilini, M, De Renzi, E, and Crisi, G. (1987). Bilateral paramedian
thalamic artery infarcts: Report of eight cases. J Neurol, Neurosurg &
Psych. 50, 900-909.
Geschwind, DH, Iacoboni MD, Mega MS, Zaidel DW, Cloughesy T, and Zaidel
E. (1995). Alien hand syndrome: Interhemispheric motor disconnection due to
a lesion in the midbody of the corpus callosum. Neurology. 45, 802-808.
Geschwind, N. (1965). Disconnexion syndromes in animals and man.
Brain. 88, 237-294, 585-644.
Goldberg, G. (2000). When aliens invade; multiple mechanisms for
dissociation between will and action. J Neurol Neurosurg Psychiatry. 68
(1):7.
Goldberg, G and Bloom, KK. (1990). The alien hand sign: localization,
lateralization and recovery. Amer J Med Rehab.. 69, 228-38
Goldberg G, Mayer NH, and Toglia JU. (1981). Medial frontal cortex
infarction and the alien hand sign. Arch Neurol. 38, 683-686.
Goldman, AI. (1993). Consciousness, folk psychology and cognitive
science. Consciousness and Cognition. 2, 364-382.
Goldstein, K. (1908). Zur lehre von der motorischen Apraxie. J
Physiologie und Neurologie. XI, 169-187. Cited by Brion and Jedynak, 1975).
Goodale, MA, Milner, AD, Jakobson, LS, et al. (1991). A neurological
dissociation between perceiving objects and grasping them. Nature. 349,
154-156.
Graff-Radford, N, Tranel, D, Van Hoesen, GW, and Brandt, JP. (1990).
Diencephalic amnesia. Brain. 113, 1-25.
Gray, CM. (1994). Synchronous oscillations in neuronal systems: mechanisms
and functions. J Comput Neurosci. 1, 11-38.
Gray, CM. (1999). The temporal correlation hypothesis of visual feature
integration: still alive and well. Neuron. 24, 31-47.
Gray, CM, and Viana di Prisco, G. (1997). Stimulus dependent neuronal
oscillations and local synchronization in striate cortex of the alert cat. J Neurosci. 117, 3239-3253.
Gray, JA. (1995). The contents of consciousness: a neuropsychological
conjecture. Behavioral and Brain Sciences. 18, 659-722.
Graybiel, AM, Aosaki, T, Flaherty, AW, and Kimura, M. (1994). The basal
ganglia and adaptive motor control. Science. 265, 1826-?
Graziano, MSA, Cooke, DF, and Taylor, CSR. (2000). Coding the location
of the arm by sight. Science . 290, 1782-1786.
Greenfield, SA. (1998). A rosetta stone for mind and brain? In S. R.
Hameroff, A. W. Kazniak and A. C. Scott, op. cit.
Groenewegen, JJ and Berendse, HW. (1994). The specificity of the
"nonspecific" midline and intralaminar thalamic nuclei. TINS. 17, 52-57.
Grossman, RG. (1980). Are current concepts and methods in neuroscience
adequate for studying the neural basis of consciousness and mental activity?
In H. M. Pinsker & W. D. Willis, Jr. (eds.). Information processing in the
nervous system. New York: Raven Press.
Grüsser OJ and Landis, T. (1991). Visual agnosias and other disturbances of
visual perception and cognition. London: Macmillan & Co.
Guariglia, C, Lippolis, G and Pizzamiglio, L. (1998). Somatosensory
stimulation improves imagery disorders in neglect. Cortex. 34, 233-242.
Guberman, A and Stuss, D. (1983). The syndrome of bilateral paramedian
thalamic infarction. Neurology. 33, 540-546.
Guillery, RW, Feig, SL and Loszadi, DA. (1998). Paying attention to the
thalamic reticular nucleus. TINS. 21, 28-32.
Guillery, RW and Sherman, SM. (2002). Thalamic relay functions and
their role in corticocortical communication: generalizations from the visual
system. Neuron. 33, 163-175.
Güzeldere, G. (1997). The many faces of consciousness: A field guide.
In N. Block, O. Flanagan & G. Güzeldere (eds.). The nature of consciousness.
Cambridge, Mass.: MIT press.
Halligan, PW and Marshall, JC. (1998). Neglect of awareness. Con &
Cog. 7:356-380.
Hameroff, SR. (1998). Did consciousness cause the Cambrian explosion?
In S. R. Hameroff, A. W. Kazniak and A. C. Scott (eds.). Toward a science of
consciousness II: The second Tucson discussion and debates. Cambridge,
Mass.: MIT Press.
Hardcastle, VG. (2001). Consciousness: chili of the brain. Con & Cog.
10, 418-420.
Haugeland, J. (1982). Weak supervenience. American Philosophical
Quarterly. 19, 93-103.
He S, Cavanagh P and Intriligator J. (1997). Attentional resolution.
TINS. 1, 115-121.
Hebb, DO. (1959). Intelligence, brain function and the theory of mind.
Brain. 82, 260-275.
Hecaen, H, and Albert, ML. (1978). Human neuropsychology. New York:
Wiley.
Heilman, KM, Watson, RT, and Valenstein, E. (1993). Neglect and related
disorders. In K. M. Heilman & E. Valenstein (eds.). Clinical
neuropsychology. 3rd ed. New York: Oxford Univ. Press.
von Helmholtz, H. (1896). Handbuch der physiologischen optik. Dritter
abschnitt, zweite au Jlage. Hamburg: Voss. [Published in English as
Helmholtz's treatise on physiological optics, by J. P. C. Southall, 1924.
(The Optical Society of America); republished by Dover, New York, 1962.)
(Cited in Julesz, 1991)
Hempel, CG. (1966). Philosophy of natural science. Englewood Cliffs,
NJ: Prentice Hall. Cited in Goldman, AI. (1993).
Henderson, VW. (1990). Alalia, aphemia, and aphasia. Arch Neurol. 47,
85-88.
Henke, K, Landis, T and Markowitsch, HJ. (1993). Subliminal perception
of pictures in the right hemisphere. Con & Cog. 2, 225-236.
Heilman, KM and Valenstein, E. (eds.). (1993). Clinical neuropsychology.
New York: Oxford Univ. Press.
Heilman, KM, Watson, RT and Valenstein, E. (1993). Neglect and related
disorders. In K. M. Heilman and E. Valenstein (eds.). Op. cit.
Holender, D. (1986). Semantic activation without conscious
identification in dichotic listening, parafoveal vision, and visual masking:
A survey and appraisal. Behav Brain Sci. 9, 1-66.
Hopfield, JJ. (1982). Neural networks and physical systems with
emergent collective computational abilities. Proc Nat Acad Sci USA. 79,
2554-2558.
Hopfield, JJ. (1991). Physics, computation and biology. In M. Suzuki
and R. Kubo (eds.). Evolutionary trends in the physical sciences. Berlin:
Springer-Verlag.
Hopfield, JJ, and Tank, DW. (1986). Computing with neural circuits: A
model. Science. 233, 625-633.
Horgan, T, and Woodward, J. (1985). Folk psychology is here to stay.
Philosophical Review. 94, 197-226.
Husain M and Stein J (1988) Rezso Balint and his most celebrated case. Arch. Neurol. 45:89-93.
Iacoboni, M and Zaidel, E. (1996). Hemispheric independence in word
recognition: Evidence from unilateral and bilateral presentations. Brain and
Language. 53, 121-140.
Iverson, SD, and Mishkin, M. (1970). Perseverative interference in
monkeys following selective lesions of the inferior prefrontal convexity.
Exp Brain Research. 11, 376-386.
Jacobsen, CF, and Nissen, HW. (1937). Studies of cerebral function in
primates. IV: The effects of frontal lobe lesions on the delayed alternation
habit in monkeys. J Comp Physiol Psychol. 23, 101-112.
James, W. (1925). The principles of psychology. New York: Dover.
[Original work published 1890.]
Jasper, HH. (1954). Functional properties of the thalamic reticular
system. pp 374-401 in Adrian et al, op. cit.
Jeannerod, M. (ed.). (1987). Neurophysiological and neuropsychological
aspects of spatial neglect. Amsterdam: North-Holland.
Jeannerod, M. (1992). The where in the brain determines the when in the
mind. Behav. Brain Sci. 15, 212-213.
Jeannerod, M, Decety, J, and Michel, F. (1994). Impairment of grasping
movements following a bilateral posterior parietal lesion. Neuropsychologia,
32, 369-380.
Jones, AM. (1994). Surprising signals in plant cells. Science. 263,
183-184.
Jones, EG. (1985). The Thalamus. New York: Plenum Press.
Jones, EG. (1987). Brodmann's areas. In G. Adelman (ed.). Encyclopedia of
Neuroscience. Boston: Birkhauser.
Jones, EG. (1989). Defining the thalamic intralaminar nuclei in primates.
In G. Gainotti, M. Bentivoglio, P. Bergonzi, & F. M. Ferro (eds.).
Neurologia e Scienze de Base: Scritti in Onore di Giorgio Macchi. Milan:
Università Cattolica del Sacro Cuore.
Jones, EG. (1998). A new view of specific and nonspecific
thalamocortical connections. In H. H. Jasper, L. Descarries, v. F.
Castellucci, and S. Rossignol (eds.). Consciousness: At the frontiers of
neuroscience, Advances in Neurology, Vol. 77. Philadelphia: Lippincott-Raven
Publishers.
Jones, EG. (1998). The thalamus of primates. pp. 1-298. In A.
Björklund and T. Hökfelt. Handbook of chemical neuroanatomy. Amsterdam:
Elsevier.
Jones, EG. (1998). The thalamus of primates. In A. Björklund and T.
Hökfelt, (eds.). The Primate Nervous System. Amsterdam: Elsevier.
Jouvet, M. (1967). Neurophysiology of the states of sleep. Physiol. Rev.
47, 117-177.
Julesz, B. (1991). Early vision and focal attention. Rev modern
Physics. 63, 735-767.
Jung, R. (1954). Correlation of bioelectrical and autonomic phenomena
with alterations of consciousness and arousal in man. In E. D. Adrian, F.
Bremer, & H. H. Jasper (eds.). Brain mechanisms and consciousness.
Springfield, IL: C. C. Thomas
Kalin, NH, Shelton, SE, Davidson, RJ, and Kelley, AE. (2001). The
primate amygdala mediates acute fear but not the behavioral and physiological
components of anxious temperament. J Neuroscience. 21 (6),
2067-2074.
Kanerva P (1988) Sparse distributed memory. Cambridge,MA (cited in Laurent,2002)
Kaufman, EFS and Rosenquist, AC. (1985). Afferent connections of the
thalamic intralaminar nuclei in the cat. Brain Research. 335, 281-296.
Kennedy, F. (1939). The inter-relationship of mind and body. In F.
Kennedy, A. M. Frantz, & C. H. Hare, (eds.). ARNMD, Vol. 19. The
inter-relationship of mind and body.
Kihlstrom, JD. (1987). The cognitive unconscious. Science. 237,
1445-1452.
Kinney, HC, Korein, J, Panigrahy, A, Dikkes, P, and Goode, R. (1994).
Neuropathological findings in the brain of Karen Ann Quinlan: The role of
the thalamus in the persistent vegetative state. New Eng J. Med. 330,
1469-1475.
Kinomura, S, Larsson, J, Gulyás, and Roland, P E. (1996). Activation by
attention of the human reticular formation and thalamic intralaminar nuclei.
Science. 271, 512-515.
Kinsbourne, M. (1970). A model for the mechanism of unilateral neglect of
space. Trans Amer Neurol Assoc. 95, 143-146.
Kinsbourne, M. (1993). Integrated cortical field model of consciousness.
In Ciba Symposium on Experimental and Theoretical Studies of Consciousness.
Chister, West Sussex: Wiley & Sons.
Kinsbourne, M. (1995). The intralaminar thalamic nuclei: subjectivity pumps
or attention-action coordinators? Consciousness and Cognition. 4, 167-171.
Kinsbourne, M. and Smith, WL. (1974). Hemispheric disconnection and
cerebral function. Springfield, IL: C. C. Thomas.
Koch, C. (1995). Visual awareness and the thalamic intralaminar nuclei.
Consciousness and Cognition. 4, 163-166.
Koch, C. (2003). The quest for consciousness: A scientific approach. (Forthcoming).
Koehler, PJ, Endtz, LJ, Te Velde, J, and Hekster, REM. (1986). Aware or non-aware: On the significance of awareness for the localization of the lesion responsible for homonymous hemianopia. J Neurol Sci. 75, 255-262.
Kolb, and Wishaw, (2000). Fundamentals of Human Neuropsychology, 4th
ed., 6th printing. USA: W. H. Freeman and Co.
Koskoff YD, Patton R, Migler B and Kruper D. Hemicerebrectomy in the rhesus monkey:surgical technique and preliminary behavioral observations. Cerebral palsy review Sept-Oct 1959.
Kreiman G, Koch C and Fried I (2000) Category-specific visual responses of single neurons in the human temporal lobe. Nature Neuroscience 3:946-953.
Kruper D, Patton RA and Koskoff YD. (1971) Visual discrimination in hemicerebrectomized monkeys. Physiol.Behav.7:173-179.
LaBar KS and Disterhoft JF (1998) Conditioning, awareness and the hippocampus. Hippocampus 8:620-626.
Landesman, C. (1967). Consciousness. In P. Edwards (ed.). Encyclopedia of
Philosophy. 2, 191-195.
Landis, T and Regard, M. (1998). The right hemisphere's access to lexical meaning: A function of its release from left hemisphere control? In C. Chiarello (ed.). Right hemisphere contributions to lexical semantics. New York: Springer.
Laurent G (2002) Olfactory network dynamics and the coding of multidimensional signals. Nature Reviews Neuroscience 3:884-995.
Laureys, S, Faymonville, ME, Luxen, A, Lamy, M, Franck, G, and Maquet, P. (2000). Restoration of thalamocortical connectivity after recovery from persistent vegetative state. The Lancet. 355, 1790-1791.
Lecours, AR, Lhermitte, F, and Bryans, B. (1983). Aphasiology. London:
Balliere Tindall.
LeGros Clark, WE. (1932). The structure and connections of the
thalamus. Brain. 55, 406-470.
Leopold, DA, and Logothetis, NK. (1996). Activity changes in early visual cortex reflect monkeys' percepts during binocular rivalry. Nature. 379:549-553.
Lesser, RP, Dinner, DS, Lüders, H, and Morris, HH. (1986). Memory for objects presented soon after intracarotid amobarbital sodium injections in patients with medically intractable complex partial seizures. Neurology. 36, 895-899.
Levin, HH, Eisenberg, HM, and Benton, AL. (1991). Frontal lobe function and
dysfunction. New York: Oxford Univ. Press.
Levin, HS, Culhane, KA, Fletcher, JM, Mendelsohn, DB, Lilly, MA, Harward, H, Chapman, SB, Bruce, DA, Bertolino-Kusnerik, L, and Eisenberg, HM. (1994). Dissociation between delayed alternation and memory after pediatric head injury: Relationship to MRI findings. J Child Neurology. 9, 81-89.
Lezak, M. D. (1988). IQ: R.I.P. J Clin Exper Neuropsychol. 10, 351-361.
Libet, B. (1993). Neurophysiology of Consciousness. Boston: Burkhäuser.
Libet B,Gleason CA, Wright EW, and Pearl DK (1983) Time of conscious intention to act in relation to onset of cerebral activity (readiness potential). Brain 106:623-642.
Livingstone M and Hubel D. (1988) Segregation of form, color, movement, and depth:anatomy, physiology, and perception. Science 240:740-749.
Llinas R (2001) I of the vortex: from neurons to self. Cambridge,MA:MIT Press
Llinás R and Ribary U. (1993). Coherent 40-Hz oscillation characterizes
dream state in humans. Proc Natl Acad Sci USA. 90, 2078-2081.
Logothetis NK. (2002) Vision: a window on consciousness. Sci.Amer. Special Ed. 12:18-25.
Logothetis NK and Schall JD. (1989). Neuronal correlates of subjective
visual perception. Science. 245, 761-63.
Luria, AR. (1966). Higher cortical function in man. New York: Basic
Books.
Lycan WG. (1997). Consciousness as internal monitoring. In Block,
Flanagan and Guzeldere (eds.). op. cit..
MacKay, DM. (1969). Information, mechanism and meaning. Cambridge: MIT
Press.
MacKay, DM. (1980). Brains, machines and persons. Grand Rapids:
William B. Eerdmans.
MacLeod, K, Bäcker, A, and Laurent, G. (1998). Who reads the temporal
information in synchronized spike trains? Nature. 395, 693-698.
Magnus, R. (1924). Korperstellung. Berlin: Springer-Verlag. [Reissued
in English translation by W. R. Rosanoff and Franklin Book Programs.
Available from the U.S. Dept. of Commerce, Springfield, VA.]
Magoun, HW. (1952). An ascending reticular activating system in the
brainstem. Arch Neurol Psychiatry. 57, 145-154.
Malamut, BL, Graff-Radford, N, Chawluk, J, Grossman, RI, and Gur, RC.
(1992). Memory in a case of bilateral thalamic infarction. Neurology. 42,
163-169.
von der Malsburg, C. (1995). Binding in models of perception and brain
function. Curr Opinion in Neurobiol. 5, 520-526.
Mangan, B. (1993). Theoretical focus; Taking phenomenology seriously:
The "Fringe" and its implications for cognitive research. Consciousness and
Cognition. 2, 89-108.
Marcel, AJ. (1988). Phenomenal experience and functionalism. pp.
121-158 in A. J. Marcel and E. Bisiach, op. cit.
Marder, E, and Bucher, D. (2001). Central pattern generators and the
control of rhythmic movements. Current Biology. 11, 986-996.
Marie, P. (1966). Revision de la question de l'apahsie: la troisième
circonvolution frontale gauche ne joue aucun rôle special dans la fonction du
langage. Sem Med. 26, 241-247.
Markowitsch, HJ. (1995). Cerebral bases of consciousness: a historical
view. Neuropsychologia. 33, 1181-1192.
Markowitsch, HJ, Pritzel, M, Kessler, J, Guldin, W, and Freeman, RB. (
1980). Delayed alternation performance after selective lesions within the
prefrontal cortex of the cat. Behavioral and Brain Research. 1, 67-91.
Markowitsch, HJ, von Cramon, DY, and Schuri, U. (1993). Mnestic performance
profile of a bilateral diencephalic infarct patient with preserved
intelligence and severe amnesic disturbances. J Clin Exper Neuropsychol.
15, 627-652.
Maunsell, JHR, and Newsome, WT. (1987). Visual processing in primate
extrastriate cortex. Ann. Rev. Neurosci. 10, 363-.
McAndrews, MP, and Milner, B. (1991). The frontal cortex and memory for
temporal order. Neuropsychologia. 29, 849-859.
McCulloch, WS. (1951). Why the mind is in the head. In L. A. Jeffress
(ed.). Cerebral mechanisms in behavior. New York: Wiley.
McGlynn, SM, and Schacter, DL. (1989). Unawareness of deficits in
neuropsychological syndromes. J Clini Exper
Neuropsychol. 11, 143-205.
McGuiness, CM, and Krauthamer, GM. (1980). The afferent projections to the
centrum medianum of the cat as demonstrated by retrograde transport of
horseradish peroxidase. Brain Research. 184, 255-269.
Meissner, I, Sapir, S., Kokmen, E, and Stein, SD. (1987). The
paramedian diencephalic syndrome: A dynamic phenomenon. Stroke. 18,
380-385..
Melo, M, Carod-Artal, FJ, Medeiros, MSM, Dias, EC, and Brenner, C.
(2001). Thalamic dementia resulting from a bilateral paramedian thalamic
infarction. J InternatNeuropsychol Soc. 7, 403-436.
Melzack, R. (1989). Phantom limbs, the self and the brain. Canadian
Psychology/Psychologie Canadienne. 30, 1-16.
Mesulam, MM. (1998). From sensation to cognition. Brain. 121,
1013-1052.
Michel, D, Laurent, B, Foyaher, N. Blanc, A, and Portafaix, M. (1982).
Infarctus thalamique paramèdian gauche: Ètude de la mémoire et du langage.
Rev Neur. 138, 533-550.
Mills, RP, and Swanson, PD. (1978). Vertical oculomotor apraxia and
memory loss. Ann Neurol. 4, 149-153.
Milner, AD, and Goodale, MA. (1996). The visual brain in action.
Oxford: Oxford Univ. Press.
Milner, B. (1971). Interhemispheric differences in the localization of
psychological processes in man. Brit Medi Bull. 27, 272-277.
Milner, B, Corsi, P, and Leonard, G. (1991). Frontal-lobe contribution
to recency judgments. Neuropsychologia. 29, 601-618.
Milner, B, Squire, LR, and Kandel, ER. (1998). Cognitive Neuroscience
and the Study of Memory. Neuron. 20:445-468.
Mishkin, M. (1957). Effects of small frontal lesions on delayed
alternation in monkeys. J Neurophysiology. 20, 615-622.
Mishkin M and Appenzeller T (1987) The anatomy of memory. Sci. Amer. 256:80-89.
Mitrofanis, J, and Guillery, RW. (1993). New views of the thalamic
reticular nucleus in the adult and the developing brain. TINS. 16, 240-245.
Mohr, JP. (1973). Rapid amelioration of motor aphasia. Arch Neurol.
28:77-82.
Mohr, JP. (1976).
Mohr, JP. (1977). Broca's area and Broca's aphasia. In H. Whitaker &
H. A. Whitaker, (eds.). Studies in neurolinguistics. : Academic
Press.
Molinari M, Leggio MG, Dell'anna ME, Giannetti and Machi G. (1993) Structural evidence in favor of a relay function for the anterior intralaminar nuclei. in D Minciacchi,M Molinari, G Macchi and EG Jones (eds.) Thalamic networks for relay and modulation. New York:Pergamon.
von Monakow, C. (1911). Localization of brain functions. Trans. In
von Bonin, op. cit.
Moore, GE. (1922). Philosophical studies [cited by C. Landesman (1967) op.
cit.]
Moutier, F. (1908). L'aphasie de Broca. ?: Steinhell.
Moruzzi, G, and Magoun, HW. (1949). Brain stem reticular formation and
activation of the EEG. EEG Clin Neurophysiol. 1, 455-473.
Moscovitch, M. (1995). Models of consciousness and memory. In M. S.
Gazzaniga (ed.). The Cognitive neurosciences. Cambridge, Mass.: MIT Press.
Moutier, F. (1908). L'aphasie de Broca. Paris: Steinheil.
Muller, A, Baumgartner, RW, Rohrenbach, C, and Regard, M. (1999).
Persistent Kluver-Bucy syndrome after bilateral thalamic infarction.
Neuropsychiatry Neuropsychol Behav Neurol. 12,(2), 136-139.
Munk MHJ, Roelfsema PR, König P, Engel AK, and Singer W. (1996). Role of reticular activation in the modulation of intracortical synchronization Science. 272, 271-274.
Münkle, MC, Waldvogel, HJ, and Faull, RLM. (1999). Calcium-binding
protein immunoreactivity delineates the intralaminar nuclei of the thalamus
in the human brain. Neuroscience. 90, 485-491.
Münkle, MC, Waldvogel, HJ, and Faull, RLM. (2000). The distribution of
calbindin, calretinin and parvalbumin immunoreativity in the human thalamus.
J Chem Neuroanatomy. 19, 155-173.
Nagel, T. (1974). What is it like to be a bat? Philosophical Review.
[Reprinted in D. R. Hofstadter & C. D. Dennett (eds.). (1981). The mind's
I. New York: Basic Books.
Natsoulas, T. (1983). Concepts of consciousness. J Mind and
Behavior. 4, 13-59.
Netter, FH. (1953). The Ciba collection of medical illustrations, Vol.
I. Nervous system. Summit, NJ: Ciba.
Oliveri, M, Rossini, PM, Traversa, R, Cicinelli, P, Filippi, MM,
Pasqualetti, P, Tomaiuolo, F, and Caltagirone, C. (1999). Left frontal
transcranial magnetic stimulation reduces contralesional extinction in
patients with unilateral right brain damage. Brain. 122, 1731-1739.
Orem, J, Schlag-Rey, M, and Schlag, J. (1973). Unilateral visual
neglect and thalamic intralaminar lesions in the cat. Experimental
Neurology. 40, 784-797.
Panksepp, J. (1998). Affective neuroscience. New York: Oxford Univ.
Press.
Paré, F, and Llinás, R. (1995). Conscious and pre-conscious processes as
seen from the standpoint of sleep-waking cycle neurophysiology.
Neuropsychologia. 33, 1155-1168.
Parvizi J and Damasio A. (2001) Consciousness and the brainstem. Cognition 79:135-160
Pasquier F,Lebert F and Petit H. (1995) Dementia, apathy and thalamic infarcts. Neuropsychiat.. Neuropsychol. Behav. Neurol. 8:208-214.
Passingham, R. (1993). The Frontal Lobes and Voluntary Action. Oxford:
Univ. of Oxford Press.
Paterson, A, and Zangwill, OL. (1944). Disorders of visual space
perception associated with lesions of the right cerebral hemisphere. Brain.
67, 331-358.
Pavlov, IP. (1928). Lectures on conditioned reflexes. (W. H. Gantt, trans.). New York: Liveright Pub. Corp.
Payne BR, Lomber SG, Villa AE and Bullier J (1996) Reversible deactivation of cerebral network components. TINS 19:535-542.
Peacock WJ. (1996). Hemispherectomy for intractable seizures in children:
a report of 58 cases. Child's Nerv Syst. 12, 376-84
Penfield, W. (1937). The cerebral cortex and consciousness. The Harvey Lectures. Reprinted (1965) in R. H. Wilkins (ed.). Neurosurgical Classics. New York: Johnson Reprint Corp.
Penfield, W, & Jasper, HH. (1954). Epilepsy and the Functional Anatomy of the Human Brain. Boston: Little, Brown and Co.
Peters, RS, and Mace, CA. 91967). Psychology. In P. Edwards (ed.).
Encyclopedia of Philosophy. Vol. 7, p. 27. New York: Macmillan.
Petit, et al (1981).
Petrides, M, and Milner, B. (1982). Deficits on subject-ordered tasks after frontal- and temporal-lobe lesions in man. Neuropsychologia. 20, 249-262.
Plum, F and Posner, JB. (1985). The Diagnosis of Stupor and Coma. 3rd ed. Philadelphia: F. A. Davis.
Popper, KS, and Eccles, JC. (1981). The self and its brain. Berlin:
Springer-Verlag.
Posner, MI, and Rothbart, MK. (1992). Attentional mechanisms and conscious experience. In A. D. Milner & M. D. Rugg (eds.). The Neuropsychology of Consciousness. San Diego: Academic Press.
Pribram, KH, Plotkin, HC, Anderson, RM, and Leong, D. (1977).
Information sources in the delayed alternation task for normal and frontal monkeys. Neuropsychologia. 15, 329-340.
Prisco, LH. (1963). Short-term memory in focal cerebral damage.
Unpublished Ph.D. thesis, McGill University. [Cited in Milner, et al, 1991).
Ptito, A, Leporé, F, Ptito, M, and Lassonde, M. (1991). Target detection and movement discrimination in the blind field of hemispherectomized patients. Brain. 114, 497-512.
Purpura, KP and Schiff, ND. (1997). The Thalamic intralaminar nuclei: A
Role in visual awareness. The Neuroscientist. 3, 8-15.
Purves, D, and Lichtman, JW. (1985). Principles of neural development. Sunderland, MA: Sinauer.

Rainville, P, Duncan, GH, Price, DD, Carrier, B, and Bushnell, MC.
(1997). Pain affect encoded in human anterior cingulate but not
somatosensory cortex. Science. 277, 968-971.
Ramachandran, VS and Blakeslee, S. (1998). Phantoms in the brain: Probing the mysteries of the human mind. New York: William Morrow.
Rather, LJ. (1965). Mind and body in eighteenth century medicine. Berkeley: Univ. of California Press.
Rees G, Wojciulik E, Clarke K, Husain M, Frith C and Driver J. (2000) Unconscious activation of visual cortex in the damaged right hemisphere of a parietal patient with extinction. Brain123:1624-1633.
Rees G, Kreiman G and Koch C (2002) Neural correlates of consciousness in humans. Nature Reviews Neuroscience 3:261-27.
Revonsuo, A. (1995a). Conscious and nonconscious control of action. Behav Brain Sci. 18, 265-266.
Revonsuo, A. (1995b). On the nature of consciousness. Turku, Finland: Turun Ydiopisto.
Revonsuo, A, Johanson, M, Wedlund, JE and Chaplin, J. (2000). The zombies among us: Consciousness and automatic behaviour. Pp 331-351. In Y. Rossetti and A. Revonsuo (eds.). Beyond dissociations: Interaction between conscious and nonconscious processing. Amsterdam: John Benjamins.
Rey, G. (????). A question about consciousness. pp. 461-482. In Bloch, Flanagan and Güzeldere, op. cit.
Rinaldi, PC, Young, RF, Albe-Fessard, D, and Chodakiewitz, J. (1991). Spontaneous neuronal hyperactivity in the medial and intralaminar thalamic nuclei of patients with deafferentation pain. J. Neurosurg. 74, 415-421.
Rizzo, M, and Vecera, SP. (2002). Psychoanatomical substrates of Bálint's syndrome. J Neurol Neurosurg Psychiatry. 72, 162-178.
Robinson, DL, and Cowie, RJ. The primate pulvinar: structural, functional and behavioral components of visual salience. In D. A. McCormick, M. Steriade & E. G. Jones, (eds.). Thalamus: Organization in Health and Disease. Amsterdam: Elsevier.
Rodman, HR, Gross, CG., and Albright, TD. (1990). Afferent basis of visual response properties in area MT of the macaque. II. Effects of superior colliculus removal. J. Neurosci. 10, 1154-1164.
Rolls, ET. (2000). The brain and emotion. Behavioral and Brain Sci. 23, 177-234.
Rosenthal, DM. (1990). Two concepts of consciousness. In D. M.
Rosenthal (ed.). The Nature of Mind. Oxford: Oxford Univ. Press. Cited in Rolls, op. cit.
Rosenthal, DM. (1993). Thinking that one thinks. In M. Davies and G. W. Humphreys (eds.). Oxford: Blackwell.
Royce, GJ, Bromley, S, and Gracco, C. (1991). Subcortical projections to the centromedian and parafascicular thalamic nuclei in the cat. J. Comp. Neurol. 306, 129-155.
Rubens, AB. (1985). Caloric stimulation and unilateral visual neglect.
Neurology. 35, 1019-1024.
Ryle, G. (1949). The concept of mind. New York: Barnes & Noble.
Sandifer, PH. (1946). Anosognosia and disorders of body scheme. Brain.
69, 122.
Sadikot AF, Parent A, Smith Y and Bolam JP. (1992) Efferent connections of the centromedian and parafascicular thalamic nuclei in the squirrel monkey: a light and electron microscopic study of the thalamostriatal projection in relation to striatal heterogeneity. J Comp Neurol 320:228-42.
Sawaguchi, T, and Goldman-Rakic, PS. (1991). D1 dopamine receptors in
prefrontal cortex: Involvement in working memory. Science. 251, 947-950.
Schacter, DL. (1989). On the relation between memory and consciousness: Dissociable interactions and conscious experience. In H. L. Roediger, and F.I. M. Craik, (eds.). Varieties of memory and consciousness: Essays in honour of Endel Tulving. Hillsdale, NJ: Lawrence Erlbaum Associates.
Schaltenbrand, G and Wahren, W. (1977). Atlas for stereotaxy of the
human brain, 2nd ed. Stuttgart: Thieme.
Scheibel, ME, and Scheibel, AB. (1966). The organization of the nucleus
reticularis thalami: A Golgi study. Brain Research. 1, 43-62.
Schiff, ND, and Plum, F. (1999). Target article: The neurology of
impaired consciousness: global disorders and implied models. Association for
Scientific Study of Consciousness. Electronic Seminar Series. Accessible at
http://athena.english.vt.edu/cgi-bin/netforum/nic/a/1.
Schiff, ND, Ribary, V, Moreno, DR, Beattie, B, Kronberg, E, Blasberg, R,
Giacino, J, McCagg, D, Fins, JJ, Llinás, R and Plum, F. (2002). Residual
cerebral activity and behavioral fragments can remain in the persistently
vegetative brain. Brain. 125, 1210-1234.
Schlag J and Schlag-Rey M (1971). Induction of oculomotor responses from thalamic internal medullary lamina in the cat. Brain Res. 22:1-13.
Schlag J and Schlag-Rey M. (1984). Visuomotor functions of central
thalamus in monkey. II. Unit activity related to visual events, targeting,
and fixation. J. Neurophysiol. 51, 1175-1195.
Schlaggar, BL, and O'Leary, DDM. (????). Potential of visual cortex to
develop an array of functional units unique to somatosensory cortex.
Science. 252, 1556-9.
Schott, B, Mauguière, F, Laurent, B, Serclerat, O., and Fischer, C.
(1980). L'amnésie thalamique. Rev Neurol. 136, 117-130.
Searle, JR. (1993). The problem of consciousness. Consciousness and
Cognition. 2, 310-319.
Searle, JR. (1998). How to study consciousness scientifically. Phil
Trans R Soc Lond. 353, 1935-1942.
Sheinberg, DL, and Logothetis, NK. (1997). The role of temporal
cortical areas in perceptual organization. Proc Natl Acad Sci USA. 94,
3408-3413.
Sherman, SM, and Koch, C. (1986). The control of retinogeniculate
transmission in the mammalian lateral geniculate nucleus. Exp Brain Res.
63, 1-20.
Sherrington, CS. (1947). The integrative action of the nervous system.
Cambridge: Cambridge Univ. Press. [Original work published 1906.]
Sherrington, CS. (1965 originally 1932). Inhibition as a coordinative
factor. In Nobel Lectures in Physiology or Medicine 1922-1941. Amsterdam:
Elsevier.
Shimamura, AP, Janowsky, JS, and Squire, LR. (1990). Memory for the
temporal order of events in patients with frontal lobe lesions and anmesic
patients. Neuropsychologia. 28, 803-813.
Sidibé, M, & Smith, Y. (1996). Differential synaptic innervation of
striatofugal neurones projecting to the internal or external segments of the
globus pallidus by thalamic afferents in the squirrel monkey. J Comp
Neurol. 365, 445-465.
Singer, W. (2001). Consciousness and the binding problem. In P. C.
Marijuán (ed.). Cajal and consciousness: Scientific approaches to
consciousness on the centennial of Ramón y Cajal's Textura. Ann
New York Acad Sci. 929:123-146.
Singer, W, and Gray, CM. (1995). Visual feature integration and the
temporal correlation hypothesis. Annu. Rev. Neurosci. 18, 555-86.
Slotnick, SD, Moo, LR, Kraut, MA, Lesser, RP, and Hart J. (2002).
Interactions between thalamic and cortical rhythms during semantic recall in
human. Proc Natl Acad Sci. 99, 6440-6443.
Smith, A and Sugar, O. (1975). Development of above-normal language and
intelligence 21 years after left hemispherectomy. Neurology. 25, 813-818.
Smythies, J. (1997). The functional neuroanatomy of awareness: With a
focus on the role of various anatomical systems in the control of intermodal
attention. Consciousness and Cognition. 6, 455-481.
Sperry, RW. (1952). Neurology and the mind-brain problem. American
Scientist. 40, 291-312.
Sperry, RW. (1961). Cerebral organization and behavior. Science. 133,
1749-1757.
Sperry, RW. (1968). Mental unity following surgical disconnection of
the cerebral hemispheres. Harvey Lecture Series 62. New York: Academic
Press.
Sperry, RW. (1980). Mind-brain interaction: Mentalism, yes; dualism,
no. Neuroscience. 5, 195-206.
Sperry, RW, Gazzaniga, MS, and Bogen, JE. (1969). Interhemispheric
relationships: The neocortical commissures; syndromes of hemisphere
disconnection. Handbook Clin Neurol. 4, 273-290.
Sprague, JM. (1966). Interaction of cortex and superior colliculus in
mediation of visually guided behavior in the cat. Science. 153, 1544-47.
Stein, JF. (1992). The representation of egocentric space in the
posterior parietal cortex. Behavioral and Brain Sciences. 15, 691-700.
Steriade, M. (1996). Arousal: Revisiting the reticular activating system.
Science. 272, 225-226.
Steriade, M, Contreras, D, Amigica, F, Timofe??, I. (1996). S. . ?? of
fast (30-40-Hz) . . . Neurosci 16, 2788-2808.
Steriade, M, Curró Dossi, R, and Contreras, D. (1993). Electrophysiological
properties of intralaminar thalamocortical cells discharging rhythmic ( 40
Hz) spike-bursts at 1000 Hz during waking and rapid eye movement sleep.
Neuroscience. 56, 1-9.
Steriade, M, Jones, EG, and McCormick, DA. (1997). Thalamus I:
Organization and function. New York: Elsevier.
Steriade, M, McCormick, DA, & Sejnowski, TJ. (1993). Thalamocortical
oscillations in the sleeping and aroused brain.. Science. 262, 679-685.
Stoerig, P..
Stoerig, P. and Barth, E. (2001). Low-level phenomenal vision despite
unilateral destruction of primary visual cortex. Consciousness and
Cognition. 10, 574-587.
Stoerig, P, and Cowey, A. (1995). Visual perception and phenomenal
consciousness. Behavioral Brain Research. 71, 147-156.
Stuss, DT, and Benson, DF. (1986). The frontal lobes. New York: Raven
Press.
Stuss, DT, Guberman, A, Nelson, R, and Larochelle, S. (1988). The
neuropsychology of paramedian thalamic infarction. Brain and Cognition. 8,
348-378.
Sur, M, Garraghty, PE, and Roe, AW. (1988). Experimentally induced
visual projections into auditory thalamus and cortex. Science. 242,
1437-1441.
Szelies, B, Herholz, K, Pawlik, G, Karbe, H, Hebold I, and Heiss, W-D.
(1991). Widespread functional effects of discrete thalamic infarction. Arch
Neurol. 48, 178-182.
Szirmai, I, Guseo, A, and Molnár, M. (1977). Bilateral symmetrical
softening of the thalamus. J Neurol. 217, 57-65.
Tanji, J, and Shima, K. (1994). Role for supplementary motor area cells
in planning several movements ahead. Nature. 371, 413-416.
Tank, DW, and Hopfield, JJ. (1987). Collective computation in
neuronlike circuits. Scientific American Special Issue on Trends in
Computing. 54-61.
Tatemichi, TK, Steinke, W, Duncan, C, Bello, JA, Odel, JG, Behrens, MM,
Hilal, SK, and Mohr, JP. (1992). Paramedian thalamopeduncular infarction:
Clinical syndromes and magnetic resonance imaging. Ann Neurol. 32, 162-171.
Tatu, et al
Taylor, J. (1931). Selected writings of John Hughlings Jackson, Vols. I
& II. London: Hodder and Stoughton.
Taylor JG. (2001). The central role of the parietal lobes in
consciousness. Con & Cog. 10, 379-417.
Taylor, JG. (2002). Paying attention to consciousness. Trends Cog Sci.
6, 206-210.
Taylor, JL, and McCloskey, DI. (1990). Triggering of preprogrammed
movements as reactions to masked stimuli. J. Neurophysiol. 63, 439-446.
Teasdale, G, and Jennett, B. (1974). Assessment of coma and impaired
consciousness: A practical scale. The Lancet. 2, 81-84.
Thimann, KV. (1977). Hormone action in the whole life of plants.
Amherst, MA: Univ. of Massachusetts Press.
Thompson RF and Logan CG (1996) Memory and learning. in R.Greger and V.Windhorst (eds.) Comprehensive human physiology. Berlin:Springer
Treue, S, and Maunsell, JHR. (1996). Attentional modulation of visual
motion processing in cortical areas MT and MST. Nature. 382, 539-541.
Trevarthen, C. (1974). Functional relations of disconnected hemispheres with the brain stem, and with each other: Monkey and man. In M. Kinsbourne and W. L. Smith (eds.). op. cit.
Tulving E. (1983) Elements of episodic memory. New York:Oxford Univ. Press
Tulving E. (1985). Memory and consciousness. Canadian Psychology. 26,
1-12.
Ungerleider, LG, and Mishkin, M. (1982). Two cortical visual systems.
In D. J. Ingle, M. A. Goodale, and R. J. W. Mansfield (eds.). Analysis of
visual behavior. pp. 549-586. Cambridge, MA: MIT Press.
Uyama, E, Ewagoe, H, Maeda, J, Nakamura, M, Terasaki, T, and Ando, M.
(1993). Presenile-onset cerebral adrenoleukodystrophy presenting as Balint's
syndrome and dementia. Neurology. 43, 1249-1251.
Velmans, M. (1991). Is human information processing conscious? Behavioral
Brain Sciences. 14, 651-726.
Verin, M, Partiot, A, Pillon, B, Malapani, C, Agid, Y, and Dubois, B.
(1993). Delayed response tasks and prefrontal lesions in man—Evidence for
self-generated patterns of behaviour with poor environmental modulation.
Neuropsychologia. 31, 1379-1396.
Volpe, BT, Ledoux, JE, and Gazzaniga, MS. (1979). Information
processing in an "extinguished" visual field. Nature. 282, 722-724.
Vuilleumier, P, Hester, D, Assal, G, and Regli, F. (1996). Unilateral
spatial neglect recovery after sequential strokes. Neurology. 19, 184-189.
Vuilleumier P, Armony JL, Clarke K, Husain M, Driver J and Dolan RJ. (2002) Neural response to emotional faces with and without awareness: event-related fMRI in a parietal patient with visual extinction and spatial neglect. Neuropsychologia 40:2156-66.
Vuilleumier P, Sagiv N, Hazeltine E, Poldrack RA, Swick D, Rafal RD and Gabrieli JDE.(2001) Neural fate of seen and unseen faces in visuospatial neglect: a combined event-related functional MRI and event related potential study. PNAS 98:3495-3500.
Wallace, SF, Rosenquist, AC, and Sprague, JM. (1990). Ibotenic acid lesions of the lateral substantia nigra restore visual orientation behavior in the hemianopic cat. J Comp Neurol. 296, 222-252.
Walshe, FMR. (1965). Further critical studies in neurology. London: E. & S. Livingstone.
Watson, RT, Valenstein, E, and Heilman, KM. (1981). Thalamic neglect: The possible role of the medical thalamus and nucleus reticularis thalami in behavior. Arch Neurol. 38, 501-507.
Watt, DF. (2000). Emotion and consciousness. J Consciousness Studies. 7, 72-84.
Weinstein, EA and Friedland, RP. (1977). Hemiinattention and hemisphere specialization. New York: Raven Press.
Weiskrantz, L. (1986). Blindsight: A Case Study and Implications.
Oxford: Clarendon Press
Weiskrantz, L. (1997). Consciousness lost and found. Oxford: Oxford Univ. Press.
Wexler, BE, Warrenburg, S, Schwartz, GE, and Janer, LD. (1992). EEG and EMG responses to emotion-evoking stimuli processed without conscious awareness. Neuropsychologia. 30, 1065-1079.
White, RJ, Schreiner, LH, Hughes, RA, MacCarty, CS and Grindlay, JH. (1959). Physiologic consequences of total hemispherectomy in the monkey. Neurology. 9, 149-159.
Wiest, G, Mallek, R, and Baumgartner, C. (2000). Selective loss of vergence control secondary to bilateral paramedian thalamic infarction. Neurology. 54, 1997-1999.
Wigner, EP. (1967). Symmetries and reflections. Cambridge, MA: MIT Press.
Wilkins, RH. (1965). Neurosurgical classics. New York: Johnson Reprint
Corp.
Wimsatt, WC. (1976). Reductionism, levels of organization, and the mind-body problem. In G. G. Globus, G. Maxwell & I. Savodnik (eds.). Consciousness and the brain. New York: Plenum.
Wimsatt, WC. (1985). Forms of aggregativity. In A. Donagan, NPerovich & M. Wedin (eds.). Human nature and natural knowledge. pp. 259-293. Dordrecht: Reigel.
Yasuda, et al (1990). JNNP
Yingling, CD, and Skinner, JE. (1976). Selective regulation of
thalamic sensory relay nuclei by nucleus reticularis thalami.
Electroencephalography and Clinical Neurophysiology. 41, 476-482.
Yingling, CD, and Skinner, JE. (1977). Gating of thalamic input to cerebral
cortex by nucleus reticularis thalami. In J. E. Desmedt (ed.). Attention,
Voluntary Contraction and Event-related Cerebral Potentials. Basel: Karger.
Zaidel, DW, Hugdahl, K, and Johnsen, BH. (1995). Physiological responses to
verbally inaccessible pictorial information in the left and right
hemispheres. Neuropsychology. 9, 1-6.
Zaidel, et al (2003). The callosal syndromes. In K. M. Heilman and E.
Valenstein, (eds.). op. cit.
Zeki, S. (1974). Functional organization of a visual area in the superior
temporal sulcus of the rhesus monkey. J. Physiol. 236, 549.
Zeki, S. (1993). A vision of the brain. Oxford, England: Blackwell
Scientific Pubs.
Zeki, S, and Bartels, A. (1999). Toward a theory of consciousness. Con & Cog. 8, 225-259.
Zernicki, B. (1986). Pretrigeminal preparation. Arch Ital Biol. 124:133-196.

Albert M. A simple test of visual neglect. (1973) Neurology 23:658-664.
Fuster J (2002) Cortex and mind:unifying cognition. New York:Oxford U. Press.
MacLeod, K., Bäcker, A. & Laurent, G.: Who reads the temporal
> information in synchronized spike trains? Nature 395, 693 - 698 (1998).
Kanerva P (1988) Sparse distributed memory. Cambridge,MA (cited in Laurent,2002)
Kreiman G, Koch C and Fried I (2000) Category-specific visual responses of single neurons in the human temporal lobe. Nature Neuroscience 3:946-953.
Laurent G (2002) Olfactory network dynamics and the coding of multidimensional signals. Nature Reviews Neuroscience 3:884-995.
Libet B,Gleason CA, Wright EW, and Pearl DK (1983) Time of conscious intention to act in relation to onset of cerebral activity (readiness potential). Brain 106:623-642.
Leopold DA and Logothetis NK (1996) Activity changes in early visual cortex reflect monkeys' percepts during binocular rivalry. Nature 379:549-553.
Goldberg et al 1981
Payne BR, Lomber SG, Villa AE and Bullier J (1996) Reversible deactivation of cerebral network components. TINS 19:535-542.
Rees G, Wojciulik E, Clarke K, Husain M, Frith C and Driver . (2000) Unconscious activation of visual cortex in the damaged right hemisphere of a parietal patient with extinction. Brain 123:1624-1633.
Vuilleumier P, Armony JL, Clarke K, Husain M, Driver J and Dolan RJ. (2002) Neural response to emotional faces with and without awareness: event-related fMRI in a parietal patient with visual extinction and spatial neglect. Neuropsychologia 40:2156-66.
Vuilleumier P, Sagiv N, Hazeltine E, Poldrack RA, Swick D, Rafal RD and Gabrieli JDE. Neural fate of seen and unseen faces in visuospatial neglect: a combined event-related functional MRI and event related potential study. PNAS 98:3495-3500.
Squire ref and date!for procedural. Schacter? zaidel et al 2003. Stoerig recent.
Celesia GG, Bushnell D, Toleikis SC and Brigell MG (1991) Cortical blindness and residual vision. Neurology 41:862-869.
Bogen J (1997) The crucial central core of consciousness does not require cognition. Proc.Soc Neurosci
Bogen JE and Berker E (2002) Face modules, face network Neurology 59:652-653.
Tulving,E (1985) Memory and consciousness. Canadian Psychology 26,1-12.
Rees G, Kreiman G and Koch C (2002) Neural correlates of consciousness in humans. Nature Reviews Neuroscience 3:261-270.
Landis,T. and Regard, M. (1988) The right hemisphere's access to lexical
> meaning: a function of its release from left hemisphere control? in
> C.Chiarello (ed.) Right hemisphere contributions to lexical semantics. New
> York: Springer
Zeman A. (2OO1) Consciousness. Brain 124:1263-1289.
Mechanisms of Cortical Electrical Activation and Emergence of Gamma
>> Rhythm. J. Theo. Biol. (In press)
>> C. J. Rennie , J. J. Wright, P. A. Robinson (2002)
> Weinstein, EA and Friedland, RP. (1977). Hemiinattention and hemisphere
specialization. New York: Raven Press.