Consciousness can be studied in many ways on various levels. Contributing to most of these inquiries would be a better understanding of how consciousness relates to brain function, that is,an explanation of consciousness in anatomico-physiologic terms. Following this approach I consider in this essay a wide variety of information including neuropathology and clinical neurology as well as neuroanatomy and neurophysiology.

Table of Abbreviations

THREE BASIC FACTS AND THEIR COROLLARIES

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 mesencephalic reticular formation ( MRF) or the thalamic intralaminar nuclei(ILN).[these and other letter symbols are listed at the end of the text just before the references]

Corollary; 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 thr 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 ...".(p 484 of Kolb and Wishaw, 4th edition, 6th printing 2000). People who want to understand consciousness will be badly led astray if they believe these two incorrect statements.

2. The larger the lesion, the more widespread the diaschisis and the more longlasting the deficit.

Corollary: the effects on consciousness of appropriately placed focal lesions follow the same rules as the effects of focal lesions on other CNS functions.The assertion that eventual recovery from partial lesions of ILN shows that they are not essential for consciousness (Smythies,1997,p468) is tantamount to asserting, a priori, that consciousness is not a brain property like language,vision,motor control, etc. all of which tend to partial recovery depending upon the size of the appropriately placed lesions.

3. So long as the lesion is unilateral, there will be no loss of consciousness. This is true even for lesions in excess of 400 grams grams(i.e. an entire hemisphere).

Corollary;the mechanisms for consciousness are paired, existing in duplicate, a conclusion consonant with the bilaterallity 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" (including cortex, underlying white matter and basal ganglia). Of the four patients reported by Austin and Grant(1958,ref 29)one patient 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 consciousness, the anatomy exists in duplicate. That only one suffices for consciousness is clear from hemispherectomy in humans.30-1 as well as hemicerebrectomy in monkeys and cats.32-4 From time to time it is asserted by insufficiently inforned persons that the term " hemispherectomy" is applied to an operation more properly termed"hemidecortication" as well as to disconnection procedures called "functional hemispherectomy" and for this reason such procedures do not show that only one member of each structural pair is enough to maintain consciousness, This assertion is correct for a majority of so-called hemispherectomies but is not true of many others, particularly those called "total hemispherectomy" or "hemicerebrectomy".

Because the anatomy subserving consciousness exists in duplicate, one might expect that there can be doubling of consciousness, and this has indeed has been inferred from split-brain cats and monkeys35 as well as humans.36 How this structural duality is negotiated by an assortment of integrating mechanisms in the intact cerebrum is a fascinating and important question;37--40 but it is not the issue here. [{See the publications listed in this website in the table of contents entitled The Other Side of the Brain}]. [{See also in the main table of contents for this website,The Human Split Brain-Significance.}]

Because an individual needs only one hemisphere to be conscious, our 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 how misleading is the assertion of certain philosophers

(e.g. Dennett, Flanagan) who have argued against an anatomically specifiable mechanism necessary for consciousness on the ground that no suitable anatomic structure is present in the middle of the head. What is plainly evident on any horizontal or frontal section of the cerebrum is the duality of any and all reasonable candidates; these are present in pairs, either member of the pair being in the middle of its respective hemisphere, only one of which is necessary for consciousness. Their confusion on this point may arise in part from the common custom of speaking of "the" thalamus or "the" amygdala or "the" limbic system which inclines people to forget that there are two of all of these, one in each hemisphere.

THE CRUCIAL CENTRAL CORE OF CONSCIOUSNESS

Once we understand that clarifying the physiology of consciousness is more likely to be worked out one hemisphere at a time, our problem is considerably simplified. That is,we can avoid confronting that question simultaneously with the question of interhemispheric integration. It will also be helpful if we do not try to explain too much. That is, we need to restrict our search to a manageable notion of consciousness; trying to explain everything that anybody wants to include is a fundamental mistake.[ For an extensive discussion of this important point,please see my Con and Cog II(1995)].

The word "consciousness" is used in many different ways by different people . It is not now feasible to look for the neural correlates of all those innumerable things of which we may at some time be conscious. An anatomico-physiologic approach in the spirit of Crick & Koch1 requires that we severely constrain what we hope to explain.2,3

The crucial, central core of the many, various concepts of consciousness includes what is sometimes called subjectivity, the ascription of self or "me-ness" to some percept or affect. Examples include: "It hurts me," "I see red," "I feel thirsty." This central core of subjectivity is here called "C." That is, whatever else consciousness involves(e,g,language, higher thoughts, sociality) without C there is no consciousness. [{ see the figure, accompanying the Abstract, which represents this central intersection of most usages and motivates the distinction between the property of consciousness and the contents thereof }]

Reaffirmed here[as earlier affirmed in Con and Cog I,1995] is that C, the central core of consciousness is engendered by neuronal activity in and immediately around the intralaminar nuclei (ILN) of each thalamus. One reason to consider this proposal plausible is that many informed persons have believed it, or something like it, for decades [this includes Wilder Penfield and Herbert Jasper, of whom more later; see also Llin s & colleagues].4,5 Falsification of this proposal is straightforward: find someone with essentially complete, bilateral destruction of ILN whom we would consider conscious.

C is provided by some cerebral mechanism, Mc. We provisionally assume that despite the great variety of contents there can be a single, common mechanism. It is this mechanism which we hope to locate and ultimately analyze. Pointing to C itself may turn out to be like trying to point to the wind. We can point to the effects of the wind, and we can often give a good account of the mechanism that causes the wind, the causes often being quite distant (even hundreds of miles) from the effects. We expect that Mc will be identifiable within and as part of cerebral anatomy. This view, while explicitly mechanistic, is not necessarily materialistic, fully deterministic or solely reductionistic.3 We need assume only that Mc necessarily involves neural activity whose specific nature is discoverable.

An ongoing argument is between advocates of a localizable mechanism and advocates of a more global phenomenon.6 The former view is adopted here and it is suggested that the mechanism crucially depends upon the thalamic intralaminar nuclei (ILN). If this is even partially correct, we need to be better informed as to the neurophysiology of ILN; some of what little we do know is described further on.

The Nature of C

Consciousness involves both a property C of varying intensity, and a great variety of contents. The content (often of cortical origin) is not our main concern here. Rather, we are concerned with Mc which can (serially) endow with C very small fractions of a wide variety of contents. It is essential to make this distinction and to focus on the neural substrate for intensity, rather than the content which is typically transient and often idiosyncratic. This assumption closely resembles the distinction made between "consciousness as such" and "different contents of consciousness" by Baars.7 The same distinction has been made by others.8-10

It is assumed here that each and every percept, affect, memory, or expectation is represented by a pattern of nerve cell activity. We are conscious of only a few neuronal activity patterns (NAP) at any one time, although the number of NAP which are potentially available to consciousness is enormous. How Mc momentarily endows with C percepts or affects represented by NAP situated elsewhere is more likely to be solved when the structures subserving Mc are located. [{In previous papers I used the symbol Pi for what are here called NAP}].

Some specific mechanism is responsible for endowing NAP with subjectivity. How to identify such a mechanism (called a "subjectivity pump" by Kinsbourne11) is discussed below. Meanwhile it is essential to understand that a NAP can affect behavior before or even if it never reaches awareness.12-19

LOCATING Mc

One clue to the anatomical basis of Mc is that when a NAP in one network acquires C, it simultaneously acquires increased access to other networks. In other words, C is associated with widespread dissemination of information. Hence, structures providing Mc must have widespread, reciprocal connections with most cerebral regions. Second, Mc needs direct, robust efference into motor systems, since being endowed with C ordinarily gives a NAP significant influence on behavior. These anatomical requirements are best met by the thalamic intralaminar nuclei (ILN) as discussed further on. Meanwhile, there is a third clue, that minor damage to Mc causes serious impairment of C, contrasting with minimal depression of C by quite massive damage elsewhere. We consider these clinical observations next.

The usual localizationist argument involves two findings: first, a large deficit in some function (f) is produced by a small lesion in the "center" for that f. [this does not imply that the representation of f is wholly contained within some sharply circuscribed region19a). Second, a large lesion elsewhere (the right hemisphere in the example of syntactic competence of a right hander) results in a small (or no) loss of f. With respect to C, quite small bithalamic lesions involving both ILN typically impair Mc (see below), whereas very large bicortical lesions typically do not20,21.

Support of the proposal that ILN subserve Mc includes the results of thalamic occlusive strokes. Simultaneous bimedial thalamic infarction 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 infarction of the two sets of ILN, unresponsiveness typically ensues (see Table 2 in Guberman and Stuss22). 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.23 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.24

Unresponsiveness after incomplete , paired thalamic lesions varies in duration, usually being longer in direct proportion to the size of the smaller lesion. Emergence from unresponsiveness 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.22-3,24-7. Patients with extensive ILN lesions may survive for many months in a persistent vegetative state even with relatively intact brainstem and cerebral cortex.28

PREFRONTAL CORTEX IS NOT NECESSARY FOR C.

There is a long history of assertions that consciousness depends on the frontal lobes.41 When we describe "frontal lobe symptoms" or "frontal lobe functions," we have in mind a large expanse of cortex more precisely termed "prefrontal."42-3 We do not mean "frontal lobe" as it is used incontemporary 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.44-5 This is in keeping with the conclusion of Jones46 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."47. The term "IQ" can be misleading as a measure of cognitive ability.48 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.20-21,42-5 Prefrontal cortex is extremely valuable; it is essential for planning and for conscience, but it is not required for C.

ASCENDING ACTIVATION

It has been known since work by Berger that transitions to behavioral alertness are reflected in the 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 transected the neuraxis at C1, he found that the isolated brain (enc‚phale isol‚) alternated between HVLF and LVHF. By contrast, after intercollicular transection the isolated cerebrum (cerveau isol‚) stayed in the HVLF state, apparently unarousable. Moruzzi and Magoun49 found that stimulation within the brainstem reticular formation (BSRF) produced EEG desynchronization. Coupled with relevant neuropathological studies of coma, this line of research lead to the widely accepted notion of an ascending reticular activating system (ARAS).50

A case of medullary infarction described by Plum and Posner24 indicates that transections higher than C1, i.e., near the level of cranial nerve VIII are compatible with, as they put it, "the behavioral appearance of consciousness." A cat with an even higher transection of the brain stem (at the level of cranial nerve V) although deaf, is able to respond to olfactory and visual input with the EEG characteristics and tracking eye movements we generally recognize as concomitants of awareness.51

As the anatomic and chemical complexities of the BSRF became more apparent, the simple view of an ARAS came under attack, including suggestions that both stimulation and lesions of BSRF might be affecting fibers of passage rather than BSRF cells. Moreover, when the intercollicularly decerebrated cats were maintained chronically, the isolated cerebrum could show transitions to the LVHF ("desynchronized") state.52 This last finding is important since it suggests that the thalamocortical activity required for C (whether waking or in the REM state) can occur sui generis even though it ordinarily depends upon ascending activation from the BSRF. Alem… et al53 injected barbiturate into the vertebral circulation of nineteen humans, producing loss of pupillary light reflex, corneal reflex and both facial and eye movements for three to four minutes. 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 seconds. 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."

With the improvement of techniques there has been a reemergence of the concept of ascending activation after a two decade eclipse. One example is the use of ibotenic or kainic acid to make BSRF lesions. These excitatory poisons do not act on nerve fibers, only on somata. Their use showed that stimulation and lesion effects were indeed attributable to BSRF cellular components. As recently put by Steriade54, the concept of activation ascending from the BSRF, "has been rescued from oblivion." It now appears that the BSRF stimulation which desynchronizes EEG activity below 20 HZ can facilitate synchrony in the gamma range (20-70 Hz)55 which has been thought to underlie aspects of cognition (see below). A recent imaging study found that focusing attention caused increased activation of both BSRF and the thalamic ILN.56

Mc IS THALAMIC

C is not produced by cerebral cortex, a view particularly urged by Penfield and Jasper.57 Their views derived largely from observations of epilepsy, including the fact 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. As early as 1937, Penfield noted, "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."58

To their reasons for this auxiliary conclusion can be added the following: some potential contents of consciousness are quite primitive, that is, unneedful of neocortical discrimination, association or learning. Examples are nausea, fatigue, unelaborated pain (for example, the jabs of trigeminal neuralgia), thirst, and the like. It may be that Mc evolved to give these percepts greater potency, another layer of control over the starting and stopping of ongoing action. If so, it would appear that Mc was only subsequently recruited to serve so-called "higher functions" and more elaborate responses. We understand that Mc might endow with C patterns of complex cortical activity describable as "representations of representations" or "higher order thoughts." But these are special contents, not the crucial core of consciousness. Moreover, such special contents may influence behavior without involving consciousness.12-19

Widespread Connections

Experiments with small lesions in almost every cortical region provide evidence that these regions project not only to their principal nuclei but also to ILN. It was pointed out by Koch59 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 behavioral salience of visual stimuli.60 Groenewegen and Berendse61 recently 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 afference 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.62-4

Attention

Considering how consciousness and attention are related is made difficult by the various usages of both words. "Attention" can be synonymous with the orientation of head and eyes to a brief stimulus, attributable to midbrain function and occurring well before awareness of the stimulus. Or, "attention" may refer to an individual's keeping some location "in mind" while fixating vision elsewhere,65 (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.66

It is now widely thought that the reticular nucleus of thalamus (R) affords part of the physiologic basis for selective attention.67-70 Briefly, a physiologic mechanism for attention is ascribed to Rbecause (1) each R envelops, in a thin layer, most of the ipsilateral thalamic nuclei, so that the thalamocortical fibers pass through R, (2) R efferents terminate in the immediately underlying thalamic nuclei, and (3) R efferents are GABAergic. The likelihood exists, therefore, that thalamocortical communication can be generally inhibited simultaneously with highly selective noninhibition; such localized gating could thus provide a mechanism for selective attention in cognition. That focal attention can be influenced by C could in part have its anatomical basis in collaterals of ILN efferents that terminate in R.71 [the anatomy discussed here is represented in the drawing accompanying the Con table of contents]

Associated with R is a plausible theory of C which 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) There may well be focal attention without C (and possibly vice versa); and 3) it makes no provision for an immediate inhibition (or release) of a developing motor plan.

MULTIPLE FUNCTIONAL ROLES

In addition to anatomical tracers and lesions of ILN, information has come from recording and stimulation. By 1966, Ervin and Mark72 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,73 they emphasized the polysensory functions of the ILN although admitting "a role to play" in the appreciation of pain. By 1980, McGuinness and Krauthamer62 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, moreover 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-Rey74 after nearly twenty years of experiments on thalamic function. In addition, they established a major role for ILN in the control of eye movements.

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 is a function of cortex. This implies that awareness of content depends upon some as yet unspecified "appropriate interaction" between Mc and the neural representation of that content. It has been suggested1,4 that the "appropriate interaction" involves synchronization of neuronal activity at 40 Hz; this proposal will be discussed further on.

As an example of "appropriate interaction" between Mc 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 available in cortex of the superior temporal sulcus (STS), especially area V5, commonly called MT.75-9

We expect that 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."81-2 It seems (when we accept availability to verbal output as the index of C) that the "appropriate interaction" between STS and ILN cannot readily occur in the absence of influences from ipsilateral striate cortex.

When NAP in neocortex are engaged in "appropriate interaction" with Mc, we might expect the involved neurons to exhibit different behavior than when not endowed with C. Approaches to this problem include neuronal gamma synchrony, and neuronal selectivity during binocular rivalry.

BINOCULAR RIVALRY

One way to show that a cortical neuron is participating in a conscious percept is to exploit the phenomenon of binocular rivalry. This 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 hundred msec or so (depending on the individual). In an ingenious experiment, Logothetis and Schall83 used gratings of horizontal bars drifting vertically, up for one eye and down for the other (and alternating 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 (rapid 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 which STS cells are involved in a conscious percept of motion direction. An analogous result has since been obtained for V4 cells responding to orientation.84

GAMMA SYNCHRONY

There is an increasing emphasis among neuroscientists on the widely distributed nature of many cerebral functions. We should expect to find mechanisms for coordination in time. There are, in fact, many examples of rhythmic nerve cell activity exhibiting coherence among segregated neuronal populations.85-88 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.55,89 It has been suggested that 40 Hz synchrony might characterize consciousness because consciousness requires temporal coordination of disparate NAPs. In particular, gamma synchrony could help with the visual feature binding problem,88 that is the problem of getting together into a single percept such properties as motion, color, outline and location, which are now believed to be detected in different regions of prestriate neocortex. Even if this is so, however, it need not tell about 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, however important it may be for sensory feature binding. On the other hand, stimulus dependent synchronization of cortical cells with ILN cells could be a persuasive example of C plus content.90

INHIBITION OF ACCESS TO C

Endowing NAP with C is subject to inhibition. We readily recognize that material (various NAP) ordinarily available to consciousness can be unavailable momentarily, or even longer. Clues as to how this happens may be found in some cases of hemineglect.

The patient with hemineglect from a right parietal lesion ignores stimuli in left hemispace. In a simple but eloquent experiment by Bisiach and Luzzati,91 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 available to consciousness, or not, depending upon its relation to the subjects' imagined body-centered coordinates. A likely explanation, in physiological terms, is that access to consciousness of information from the left was actively inhibited. Such inhibition, although existing in the normal state, would not be apparent because it is normally overcome by facilitatory influences from the cerebral regions damaged in the neglect patients.

A straightforward 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. This two-stage procedure has been accomplished in cats,both with respect to paw contact placing reactions33-4,and to visual attention92-3, It is unlikely that surgical,treatment of hemineglect will be tried in humans. However, an analogous "experiment of nature" was recently reported by Vuilleumier et al94 . Their right-handed patient had left hemineglect from 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.

Once we understand that access to consciousness as well as performance deficits consequent to cortical lesions can reflect imbalance rather than loss of competence,95a we can better appreciate the idea, put forward by C. S. Sherrington96 in his 1932 Nobel lecture, that recovery from CNS lesions can often be attributable to subsidence of inhibition.

THE CONVICTION OF VOLITION

The existence of connections to ILN from globus pallidus (thought to be collaterals of pallidal projections to VL and VA of thalamus) suggests a monitoring of motor systems, as do the cortical projections to ILN from sensorimotor and premotor cortex. A role in control of motor output is evident in the very substantial projections from ILN to striatum. Is this 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 well known 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.

Both the philosopher Velmans97 and the psychologist Gray11 have reviewed a range of processes in which awareness follows rather than precedes the information processing. Both Velmans and Gray cite the classic experiment of Libet15 in which it was found that a voluntary act develops (as evidenced by a readiness-potential) several hundred milliseconds before the subject decides to act. This does not mean that intent plays no role in what happens because, although conscious intent appears well after the motor plan 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, probably involving the SMA,15,98-9 and then 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.14

The proposal here is that a motor plan develops over time, that part way through this development, or while it is held in readiness, we become aware of it. 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. 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. Failure to attach "me-ness" (that is, subjectivity) because a lesion has disconnected the ILN from the cortical NAP representing the motor plan may explain the phenomenon of the alien hand.40,100-2

If we assume, as proposed in this review, that the anatomical requirement for subjectivity involves ILN, the large ILN to striatum projection would 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 major origins of the ILN-striatum projection are the parafascicular nucleus (Pf) and the centromedian nucleus [CM, aka centre m‚dian aka centrum medianum.72,103 This is not to be confused with nucleus centralis medialis, usually abbreviated CeM and often called "centralmedian nucleus," a term sometimes104 applied to CM]. 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. It has recently been reported105 that the CM projection, most likely excitatory although the transmitter is still unknown, 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.

THE CENTRENCEPHALON REVISITED

When Penfield and Jasper7 advocated the concept of a "centrencephalon," they particularly stressed the role of ILN. Why was this concept largely abandoned? 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.106 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) Forty (even twenty) years ago, there was considerable doubt of ILN projections to cortex, because unilateral decortication did not produce rapid degeneration in the ILN as it did in most of the ipsilateral thalamus. Another exception to rapid degeneration was nRt which, indeed, we now believe does not project to cortex.68,72 However, more recent tracer techniques have shown that ILN do project to cortex, and widely.

The "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 conscious awareness.

SUMMARY

An anatomico-physiologic approach to consciousness is facilitated by recognizing that the various meanings of consciousness have in common a crucial core C variously called subjectivity, consciousness-as-such, or consciousness per se. A sharp distinction is made between the property C and the contents of consciousness, partial loss of which is typical of cerebro-cortical lesions. The neuronal mechanism producing subjectivity 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.

ABBREVIATIONS            Return to top

ARAS    ascending reticular activating system.
BSRF    brainstem reticular formation.
C       crucial core of consciousness. subjectivity.
CL      n. centralis lateralis thalami.
CeM     n. centralis medialis thalami
CM      centrum medianum (aka centre median).
GPe     globus pallidus externus
GPi     globus pallidus internus.
ILN     intralaminar nuclei or thalamus including CL, CM and Pf
Me      cerebral mechanism producing C
MD      n. medialis dorsalis thalami.
MDI     motion direction information
MRF     midbrain reticular formation (upper end of BSRF)
NAP     neuronal activity patterns (singular same as
R       n. reticularis thalami.
Pf      n. parafascicularis thalami.
REM     rapid eye movement.
SMA     supplementary motor area.
SPN     a specific nucleus of thalamus such as VA, VL, or MD
STN     subthalamic nucleus
STS     superior temporal sulcus.
TCT     thalamocorticothalamic connections
VA      n. ventralis anterior thalami
VL      n. ventralis lateralis thalami

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