# Consciousness Studies/Neuroscience 1#More about Models

## The cortex and consciousness

The cerebral cortex consists of a set of specialised areas that process
different aspects of sensation and motor control. There are about ten
times as many nerve fibres going from the cortex to the thalamus as
there are from the thalamus to the cortex (Destexhe 2000).

![](constudconn.gif "constudconn.gif")

Histologically the cerebral cortex is a layer of greyish neurons
overlying a huge mass of white nerve fibres, the cerebral medulla. The
cortex consists of six main layers. The upper layers receive input from
the relays in the thalamus such as the lateral geniculate, from the
thalamus in general and from other areas of cortex plus a few
specialised inputs from other locations. The lower layers give rise to
output fibres that largely connect with the thalamus and other areas of
cortex although particular specialised processors in the cortex may also
have direct connections elsewhere such as to motor nuclei.

![](Constudcortex2.png "Constudcortex2.png")

The cerebral cortex has many functions and is divided up into numerous
separate processors. The most important function of the cortex from the
point of view of consciousness studies is that it creates models. As was
seen in Part I, philosophers debate whether these models are actually
experienced consciously but in the neurophysiological literature it is
normally assumed that we do experience models and rehearsals such as
inner speech and imaginings. There is considerable evidence that the
parts of the brain that deal with imagining (modelling) things are also
the parts that deal with perception (i.e.: modelling the world). The
overlap between imagination and normal perception is not complete
because, as Tong(2003), in a review of visual consciousness, put it:
\"Internally generated experiences share some, but not all, of the
phenomenal properties of actual perception\". There is also considerable
overlap between the areas used for imaginary speech (thought) and actual
speech, areas dealing with the control of sensation and of the tongue
etc. being used in actual speech but not in imagined speech (Fu *et al.*
2002). Kreiman *et al.* (2000) investigated the activity of single
neurons in humans and also found that the brain activity evoked by
visual imagination overlapped that which occurs upon direct stimulation
by the same image.

Our conscious experience consists of the output of the cortical
modelling and perceptual processes. The cerebral cortex itself appears
to be non-conscious. The evidence for the non-conscious nature of the
cerebral cortex consists of lesion studies in which large amounts of
cortex can be removed without removing consciousness and physiological
studies in which it is demonstrated that the cerebral cortex can be
active without conscious experience.

Lesion studies have shown that up to 60% of the cerebral cortex can be
removed without abolishing consciousness (Austin and Grant 1958). An
entire hemisphere can be removed or much of the front or back of the
cerebral cortex can be cut off yet consciousness persists.

Fiset *et al.* (1999) and Cariani (2000) have shown that cortical
activity can be normal or even elevated during the unconscious state of
general anaesthesia. Alkire *et al.* (1996) also showed that cortical
activity related to word recognition occurred during general
anaesthesia.

Libet *et al.* (1967) found that there could be cerebral cortical
activity in response to weak stimulation of the skin without any
conscious awareness of the stimulus. This work provides a
neurophysiological basis for subliminal (non-conscious) perception and
also shows that large areas of the cerebral cortex can be active without
conscious experience. The insensitivity of experience to cortical
activity has been further confirmed by Libet *et al.* (1979). They
electrically stimulated the cerebral cortex of conscious patients and
discovered that the stimulus must be continued for about 0.5 seconds for
subjects to report a conscious experience of the stimulation. Libet\'s
findings have been analysed at length but there still appears to be a
0.25 to 0.5 secs delay (Klein 2002).

It has been demonstrated that cerebral cortical activity is not
synonymous with conscious experience but why should there be a delay of
up to 0.5 seconds or so between cortical stimulation and a conscious
percept? What is the cortex doing in the 0.5 seconds between the start
of stimulation and the report of awareness of the stimulation? It is
probably synchronising its various processors and creating a waking
dream, a structured set of events that accounts for the activity. The
synchronisation of cerebral cortical processes will be discussed later,
but what evidence is there for the cerebral cortex constructing a waking
dream, or model, to describe the world?

The \'Attentional Blink\' (Raymond *et al.* 1992) is consistent with the
concept of the cerebral cortex being a device that creates models. In
the \'Attentional Blink\' the identification of an object impairs the
identification of a second object that is presented within 0.5 seconds
of the first. Raymond *et al.* used a stream of letters (11 letters per
second) and the identification of a first letter impaired the
identification of a subsequent \'probe\' letter in the stream. If the
probe letter followed the first letter within about 180 msecs it could
easily be identified, suggesting that chunks of about 180 msecs of data
stream are modelled together. Christmann & Leuthold (2004) have
theorised that the \'Attentional Blink\' involves perceptual and central
components of visual processing. This is supported by the fMRI studies
of Marois *et al.* (2004) who presented subjects with faces mounted on
scenes of places. The scenes of places often went undetected by subjects
but they activated regions of the medial temporal cortex involved in
high-level scene representations, the parahippocampal place area (PPA).
When the scenes of places were detected by the subjects there was
activity in the frontal cortex and the PPA activity was increased. These
experiments are consistent with the idea of a cerebral cortex that is a
multiprocessor system that creates consistent models of the environment.

Bregman\'s (1990) auditory continuity illusion is another example of how
sensory events are modelled. If a pure tone is followed by broadband
noise and the noise followed by the same pure tone it seems as if the
tone occurs throughout the period of noise. If the noise is not followed
by the pure tone there is no sound of the tone during the period of
noise. This effect is similar to the results found by Libet because a
delay of several hundred milliseconds between sensory stimulation and
conscious experience is needed to account for the apparent rewriting of
history after the second tone appears.

Dennett and Kinsbourne (1992) argued strongly against modelling as the
source of conscious experience. They discussed two illusions, the
\"cutaneous rabbit illusion\", in which the subject is tapped
successively in such a way that some illusory taps appear and the \"phi
illusion\" in which successively illuminated lights appear as a motion
of the light. Dennett and Kinsbourne declared that there should be no
cerebral cortical filling in of the gaps in the these illusions. Both
these illusions have now been investigated. Blankenburg *et al.* (2006)
found that cerebral cortical activity occurred at the locations expected
for the missing taps in the \"cutaneous rabbit\" illusion and Larsen *et
al.* (2006) found that the areas of cerebral cortex that would be
stimulated by a moving light were active during the \"phi illusion\".

## The delay before consciousness of \"voluntary\" actions

The 0.5 second delay required for the cortex to model an event has
implications for the role of conscious experience in the control of our
lives. If experience is about 0.5 seconds behind the true present
instant then how can we be said to control anything? The brain must be
acting automatically whilst performing most tasks. The 0.5 second delay
also seems to contradict our everyday experience. We certainly feel like
we are aware of things in less than 0.5 seconds, for example, the direct
stimulation of sense organs seems to be experienced much more rapidly
than the delayed experience of cortical stimulation. In fact subjects
report that they are conscious of stimuli, such as being touched or
seeing flashing lights, within 0.1 to 0.2 seconds of the event. So how
can subjects report events within 0.2 seconds even though it seems to
take 0.5 seconds for the cortex to generate activity that can be
experienced? The simplest explanation is that the reaction occurs
automatically within 0.2 seconds and then the conscious experience of
this reaction occurs 0.3 seconds later. This gives a total 0.5 seconds
delay before conscious experience whilst allowing fast reactions.

Libet *et al.* extended their experiments by stimulating a \"relay
nucleus\" in the thalamus that intercepts signals from the senses before
they reach the somatosensory cortex. It was found that when this nucleus
was stimulated for 0.5 seconds the subjects reported that the stimulus
occurred 0.2 seconds after it had begun. When the nucleus was stimulated
for less than 0.5 seconds the subjects did not report any sensation.
This supports the concept of a 0.5 second delay whilst the cortex puts a
stimulus in context before it is experienced.

These experiments show that our experience is an output of cortical
processing rather than the processing itself. If our conscious
experience is non-cortical then this raises the possibility that the
non-conscious cerebral cortex can perform actions without conscious
control. Of course, the cortex does this all the time when we are
indulging in skilled or routine behaviour. The ability of the
non-conscious cortex is quite remarkable; for instance car drivers
sometimes discover that they have driven for several miles without
conscious experience of driving, even at the level of having no
recollection of the route.

!Typical recording of the readiness
potential.{width="150"}Although
it might be accepted that much of our everyday behaviour is automatic is
there any behaviour that is definitely initiated by conscious
experience? This is probably a pointless question because consciousness
is about observation, not action; however, despite this there have been
several experiments that have attempted to determine the relationship
between consciousness and action.

In 1964 Kornhuber and Deecke performed a series of experiments that
measured the electrical activity from the scalp (EEG) during voluntary
actions. They averaged many EEG\'s from subjects who were about to move
a finger and discovered that there is an increase in scalp potential
before the movement takes place. The increase in potential can start as
long as 2 seconds or so before the movement and is known as the
\"readiness potential\" (Bereitschaftspotential). The readiness
potential is strange because it seems to contradict our conscious
experience; we do not decide to move a hand and then wait 2 seconds
before the hand moves. It seems that the non-conscious brain may be
taking things into its own hands.

Libet *et al.* (1983) extended the readiness potential experiments by
asking subjects to observe a Wundt clock whilst flexing a finger. The
Wundt clock had a spot of light that moved around a circle every 2.56
seconds and allowed the subjects to obtain timings that were related to
their mental experiences. When the subjects flexed a finger it was found
that the readiness potential occurred about 0.5 seconds before the
finger moved and the subjects reported they were going to move the
finger about 0.2 seconds before the movement. This suggested that a
subject\'s cerebral cortex was preparing for the movement about 0.3
seconds before the subject was conscious of this. Libet\'s experiments
have been reproduced elsewhere (see Keller & Heckhausen 1990). (It is
important to note that the subjects in Libet\'s experiment were asked to
wait until they felt the urge to move the finger.) These results are
consistent with the idea of the cortex as a modelling system that
constructs a consistent model of events to pass on to whatever mediates
conscious experience.

More recently fMRI and direct electrode recording have borne out the
readiness potential experiments. Soon *et al.* (2008) allowed subjects
to decide to press either a left or right button. They used fMRI to show
that there was spatially organised activity in the polar frontal cortex
and parietal cortex (from precuneus into posterior cingulate cortex)
that predicted the conscious left/right decision and preceded it by
about **seven seconds**. Rektor *et al.* (2001) used direct electrode
recordings to show a 2 second latency. Haggard & Eimer (1999) and also
Trevena and Miller (2002, 2009) have identified a \"Lateralized
Readiness Potential\" that is correlated with the movement of a
particular hand (left or right) in their EEG experiments and Trevena and
Miller claim that this potential always follows the making of a
conscious decision and precedes the actions being studied. However, Soon
*et al.* (2008) showed that fMRI can predict which button will be used
well before any conscious decision is reported. (See Haggard (2008) for
a review of conscious volition).

## Perception, Imagination, Memory and Dreams

### More about Models

Our dreams are clearly models that form a \'dreamworld\' but the idea
that perception might be like a dream that is updated by sensation is
not so obvious. Experience seems to be an active model of the world
(virtual reality) based on sense data rather than a simple mapping of
retinal and other sensory data. This is demonstrated by visual illusions
such as the Ames Room, Spoke Illusion and Muller Lyer illusions shown
below:

![](Constudame.png "Constudame.png")

Notice how the circle is distorted without any distortion in the
\'spokes\', it is as if the circle has been treated as a separate object
by the processes in the brain that rearranged it. In all of these
illusions the brain has rearranged large areas of the visual field and
has managed the input as a collection of \'objects\' that are
manipulated separately. Even movement seems to occur in some figures
showing that the brain models the position of things:

![](Constudcafe.png "Constudcafe.png")

The creation of a model is also demonstrated by the illusion of movement
experienced when we watch the cinema or television. This is due to the
cortical modelling that is known as \'short-range apparent motion\'
rather than flicker fusion or persistence of vision. It is intriguing
that, although it has been known for decades that the joining together
of static images in our minds is due to modelling activity in the brain
the myth that it is due to persistence of vision or flicker fusion is
universal. As Anderson and Anderson (1993) noted:

`Indeed, in the past decade, psychoanalytic-Marxist film scholars `\
`have retained the  model implied by persistence of vision: theirs `\
`is a passive viewer, a spectator who is "positioned," unwittingly `\
`"sutured" into the text, and victimized by excess ideology.`

Our experience of the cinema is like a dream updated by sensation rather
than sensation updated by interpretation. In fact the most compelling
evidence for the modelling power of the brain is the existence of
dreams; our dreams are often models of worlds that do not exist and
involve little or no sensory input yet can involve effects as powerful
as any television drama.

Short range apparent motion occurs when the interval between
presentations of an object is brief (c. 50-100 msecs). Motion modelling
in response to longer intervals is known as long range apparent motion.
There is evidence that the modelling in short range apparent motion is
enhanced if the moving patterns are similar to moving human forms (such
as patterns of dots outlining a person)(Thornton *et al.* 1998). The
accuracy of predicting movement can actually improve if the interval
between presentations is increased when human forms are used.

Motion modelling can also be seen in visual illusions such as the
*Waterfall Illusion* (motion aftereffect). The waterfall illusion is
commonly seen after viewing a sequence of scrolling credits on the
television; when the credits stop rolling it appears as if they briefly
move in the opposite direction. Tootel *et al.* (1995) have used fMRI to
show that this is correlated with activity in the motion modelling area
of visual cortex (area MT/V5). The waterfall illusion is also associated
with an intriguing aftereffect known as **storage of the motion
aftereffect**. Normal motion aftereffects last for up to about ten
seconds after the stimulus, however, if the subjects close their eyes
for the normal duration of the aftereffect then reopen them they see the
illusion for almost the normal duration. Culham *et al.* (1999) used
fMRI to show that activity in area MT/V5 was low during the period when
the eyes were closed then increased dramatically when the eyes were
opened. This is strongly suggestive of a modelling mechanism outside
MT/V5 that has adapted to motion and then models stationary data with
movement in the wrong direction.

Visual area MT/V5 is also involved in the separation of moving visual
scenes into *sprites* or objects that move together as a whole within a
scene (Muckli *et al.* 2002).

The way that mental models may be the basis of ordinary reasoning was
outlined by Johnson-Laird (1980), based on earlier work by Kenneth
Craik.

Studies of \'change blindness\' and \'inattentional blindness\', where
subjects fail to spot outrageous changes in their environment, also
demonstrate that we experience a model and suggest that the brain must
analyse an object to incorporate it fully into the model (See for
instance Rensink (2000), Simons & Rensink (2005)).

### Brain areas used in perception overlap those used in imagination and recall

Functional Magnetic Resonance Imaging (fMRI) has shown that similar
areas of brain are used during perception involving the senses as during
imagination (Tong 2003, Kosslyn and Thompson 2003). The substrate of the
mental images that occur in both modes of brain activity has not yet
been found. This overlap of the brain areas used in perception with
those used in imagination, memory and recall has been demonstrated in a
wide range of experiments.

Ganis *et al.* (2004) used fairly complex perceptual and imagination
tasks that activated large areas of the brain, they found an overlap
between the brain areas activated during perception and imagery. The
principle areas that were different in the two tasks were found in the
primary sensory areas of the visual cortex. Other areas in the visual
cortex and activity in the rest of the brain showed a remarkable degree
of overlap. The authors suggested that the differences in the activity
of primary visual cortex may have been due to differences between the
perceptual and imaginary stimuli such as speed of onset etc. The
hippocampus was not activated.

It is intriguing that, contrary to object imagery, spatial imagery such
as predicting when a cross on a screen would fall on an imaginary letter
actually seems to inhibit activity in sensory visual cortex (Aleman *et
al.*). Both fMRI and blocking with transcranial magnetic stimulation
(TMS) showed that the posterior parietal cortex was involved in the
spatial imagery.

Imagery involving places and faces activates the place and face areas
that are activated during perception (Ishai *et al.* 2000).

The recall and recognition of things also seems to involve very similar
brain areas to those used during perception. Wheeler and Buckner (2003)
showed that areas involved in perception were also involved in the
recall of the perceptual stimuli.

Recall causes activation of areas used in perception but also seems to
use areas that may be particularly related to the process of recall
iself, such as the left parietal cortex (Konishi *et al.* 2000)
(Brodmann\'s area 40/39). Frontal and parietal regions are involved in
the recognition of whether stimuli have been experienced before.

Image generation during sleep seems to differ from that during
imagination and recall. In particular it seems to involve a few well
defined areas of cortex and considerable activation of the posterior
thalamus.

Sleep studies have shown that people dream throughout sleep. However,
dreams are more frequent during the REM (rapid eye movement) periods of
sleep than the NREM (non-REM) periods. Dreams are reported after 70-95%
of awakenings in REM sleep and 5-10% of awakenings in NREM sleep. REM
dreams are more visual than NREM dreams which are more \'thoughtlike\'
(Solms 2000). Thoughtlike events (mentation) are reported after 43% of
awakenings from NREM sleep.

Solms (1997) found that patients who had lesions in the
parietal-temporo-occipital junction reported a cessation of visual
images in dreams. Solms also found that patients with lesions in the
white matter inferior to the frontal horns of the lateral ventricles, in
the ventromesial quadrant of the frontal lobes, also reported loss of
dreaming. Loss of dreaming is also reported by leucotomised patients
with frontal ventromesial damage. Damasio *et al.* (1985) and Solms
(1997) also reported that some patients with damage to the medial
prefrontal cortex, the anterior cingulate cortex, and the basal
forebrain became confused about what was real life and what was dreaming
(waking dreams occurred).

Studies using fMRI show that the sensory occipital lobe (BA 18) and
posterior thalamus, especially the lateral geniculate nuclei, are
activated in REM sleep, weaker activations of the posterior cingulate,
putamen and midbrain were also found (Wehrle *et al.* 2005, Loveblad *et
al.* 1999). These findings are consistent with activation of the
ponto-geniculo-occipital system (PGO) during REM.

So dreams may be more like primary activations of sensory cortex than
imagining or recall. This suggests that dreams have a thalamic origin or
are managed via connections from the cortex through the thalamus to the
visual cortex.

Hallucinations seem to differ from dreams. In Charles Bonnett Syndrome
patients can have clear hallucinations. These, like imaginations, seem
to involve areas of the visual cortex that deal with processed data, for
instance hallucinations of faces activate the \"face area\" rather than
visual cortical area V1 (Ffytche *et al.* 1998).

### Suppression of data acquisition during saccades - perception as a patchwork

If you look at yourself in the mirror you will not see your eyes moving
even though they will be darting all over the view of your face. Even
when you deliberately look from place to place your eyes will appear
steady. The natural darting of the eyes from place to place as you view
a scene is known as \"saccadic\" movement of the eyes. The suppression
of the visual image during the motion of the eyes is known as \"saccadic
suppression\" or \"saccadic masking\". The suppression of the
acquisition of image data extends to suppression of awareness of flashes
of light during saccades, this effect is known as \"flash suppression\",
however, flash suppression seems to apply only to rather dull flashes
(Volkman (1962). The suppression during saccades is probably due to
suppression of the magnocellular pathway (the motion sensitive pathway)
in the lateral geniculate nucleus (Burr *et al.* (1996).

The most intriguing feature of this suppression of data acquisition
during saccades is that each snapshot that is obtained between saccades
can only contain a relatively small amount of information. This is
because the fovea, which is the most sensitive area of the eye, is tiny
(about 1mm diameter) and only receives input from a few degrees of the
visual field. As a result what we consider to be a uniform scene in our
minds is actually a patchwork of intersaccade snapshots.

Another aspect of saccades is that the timing of events is referred back
to the beginning of the saccade. This effect is known as \"saccadic
chronostasis\". For example, if an object changes colour during a
saccade the observer feels as if the colour change occurred at the
beginning of the saccade, so extending the amount of time that the
object possesses the changed colour. This effect can extend apparent
durations by up to 500 ms and is consistent with the idea that the
visual system models events prior to perception (see Yarrow *et al.*
2006).

Burr D, Morrone M, Ross J. (1996) Selective suppression of the
magnocellular visual pathway during saccades\]\'\', Behavioral Brain
Research 80 1-8 (1996)
<http://www.pisavisionlab.org/downloads/BBRReview96.pdf>

Volkman, F. (1962). Vision during voluntary saccadic eye movements. J.
Opt Soc. Am. 52:571-578. 1962.

Yarrow, K, Whiteley, L, Rothwell, J.C & Haggard,P. (2006) Spatial
consequences of bridging the saccadic gap. Vision Res. 2006 February;
46(4): 545--555.
<http://www.hexicon.co.uk/Kielan/papers/Moving_chrono.pdf>

## Blindsight

Blindsight studies illuminate the relationship between the cerebral
cortex and our experience. When the visual cortex is removed subjects
become almost totally blind. If the visual cortex on one side is removed
subjects become relatively blind in the contra-lateral hemifield. One of
the most revealing studies of blindsight is Marcel\'s 1998 paper: \"
Blindsight and shape perception: deficit of visual consciousness or
visual function?\".

It is useful when considering blindsight to contemplate for a while the
appearance of the world with both eyes closed and then with one eye
closed. When both eyes are closed our experience is of a darkish space
radiating out from our heads, with one eye closed we tend to ignore the
darkish areas that cannot be seen even though they are still present.
Marcel notes that patients who have a right blind field still have an
underlying visual field on the right side and that this can even contain
conscious visual experience. This sounds a bit like the darkish space
that we all experience if deprived of visual input on one side. As
Marcel says: \"A question that naturally arises is whether the loss is a
\'total\' loss of visual consciousness in the blind field. It is often
assumed to be so, especially by those who discuss blindsight without
carefully reading the literature or working with the subjects. One can
immediately respond negatively to the question..\"

The consciousness of the completion of Kanizsa figures in blindsight
patients is particularly indicative of the preservation of the field
even though the content was largely missing. A Kanizsa figure is shown
below:

![](Whiter_than_white_illusion.jpg "Whiter_than_white_illusion.jpg")

If we put Marcel\'s observations together with cortical anatomy and
function it seems that the space of our experience is located outside of
the cerebral cortex. The cortex generates much of visual and other
content but it does not generate the space.

## The Role of the Thalamus

The thalamus is connected to the entire bottom layer of the cerebral
cortex. It is the nexus of the various cortical processors as well as a
recipient of independent input from most of the rest of the brain.

![](Constudbrain.png "Constudbrain.png")

The thalamus is subdivided into numerous small and medium sized nuclei
that between them receive inputs from every process in the nervous
system (the white fibres in the illustration above largely penetrate the
thalamus). The thalamic nuclei are interconnected which means that any
of them could, potentially host activity from anywhere in the body or
brain. Although the founders of neurology such as Hughlings Jackson and
Penfield & Jasper located conscious experience in the diencephalon,
including the thalamus, this is no longer the conventional wisdom. The
small size of the thalamic nuclei means that they cannot support the
processes that are assumed to compose access consciousness, however,
even some of the smallest thalamic nuclei host millions of synapses so
size would not be an obstacle if the thalamus contains the substrate of
phenomenal consciousness. Indeed, the diencephalon and the thalamus in
particular can be shown to be excellent candidates for a possible
location of phenomenal experience.

![](constudintralam.jpg "constudintralam.jpg")

`<font size=1>`{=html} The Intralaminar Nuclei of the thalamus. The
white space above and to the left of RN is the third ventricle.
MD=mediodorsal nucleus. CM=Centromedian nucleus, RN=red nucleus (not
part of thalamus) The black areas are stained white fibres. Picture
from: <http://www.neurophys.wisc.edu/> University of Wisconsin and
Michigan State Comparative Mammalian Brain Collections. Preparation of
image has been funded by the National Science Foundation, as well as by
the National Institutes of Health. May only be used with these
acknowledgements.`</font>`{=html}

If the thalamus contains a location for conscious experience then
lesions should abolish this experience. Unlike the cerebral hemispheres,
lesions of the thalamus do indeed seem to abolish consciousness. The
area that is most sensitive to lesions contains the Intralaminar Nuclei,
especially the Parafascicular and Centromedian Nuclei. If these are
damaged bilaterally patients suffer death, coma, akinetic mutism,
hypersomnia, dementia and other equally serious impairments of
consciousness that depend upon the size and placement of the lesions
(Bogen 1995, Schiff & Plum 1999). In cases of fatal familial insomnia,
in which patients exhibit many of these symptoms, there is marked neuron
loss in the Intralaminar Nuclei (Budka 1998).

The effect of interrupting the blood supply to the medial thalamus
depends upon the severity of the damage. There is frequently initial
coma. The recovery after coma is often incomplete, Krolak-Salmon *et
al.* (2000) described bilateral paramedian thalamic infarcts as normally
being \"followed by persisting dementia with severe mnemic disturbance,
global aspontaneity and apathy.\" The symptoms of bilateral damage to
the ILN can be so severe that it is possible that, even after recovery
from coma, some patients may cease to be conscious and are being
coordinated by automatic cortical processes.

Bjornstad *et al.* (2003) and Woernera *et al.* (2005) both reported
that the initial coma after bilateral paramedian infarct was accompanied
by a similar pattern of EEG activity to stage 2 sleep. Woernera *et al.*
(2005) also discovered that painful stimuli gave rise to a range of EEG
activity, transiently breaking the stage 2 sleep pattern but without
recovery of consciousness. Unfortunately even in those patients who
recover consciousness Kumral *et al.* (2001) report that \"Cognitive
functions in patients with bilateral paramedian infarction did not
change significantly during the follow-up, in contrast to those with
infarcts in varied arterial territories\" although Krolak-Salmon *et
al.* (2000) did report a single patient who made a total recovery.

Laureys *et al.* (2002) investigated recovery from \'persistent
vegetative state\' (wakefulness without awareness). They found that
overall cortical metabolism remained almost constant during recovery but
that the metabolism in the prefrontal and association cortices became
correlated with thalamic ILN and precuneus activity. Again confirming
that thalamo-cortico-thalamic activity is required for consciousness and
that cortical activity by itself is not conscious. Yamamoto *et al.*
(2005) investigated persistent vegetative state and found that deep
brain stimulation (25Hz) of the centromedian-parafascicular complex (19
cases) or mesencephalic reticular formation (2 cases) resulted in 8 of
the patients emerging from persistent vegetative state. It is
interesting that zolpidem, a GABA agonist, has recently been found to
reverse PVS in some patients (Claus & Nel 2006). The effect is rapid and
might be used to demonstrate the correlations that occur on recovery
from PVS.

As Bogen(1995) demonstrates, the ILN receive inputs, either directly or
indirectly, from every part of the CNS but what do they do?

Interest in the thalamus has recently been revived by the theories of
Newman & Baars (1993), Baars, Newman, & Taylor1998) and Crick & Koch
(1990). In Baars, Newman and Taylors\' (1998) theory it is suggested
that \"The brain stem-thalamocortical axis supports the state, but not
the detailed contents of consciousness, which are produced by cortex\".
They also propose that the \"nucleus reticularis thalami\" (Thalamic
Reticular Nucleus, TRN), which is a thin sheet of neurons that covers
the thalamus, is involved in a selective attention system. This concept
is reinforced by the way that point stimulation of the TRN causes focal
activity in the overlying cortex (MacDonald *et al.* 1998) and the way
the TRN is organised topographically (i.e.: has activity that is like an
electrical image of receptor fields).

The thalamus is ideally placed for integrating brain activity, if tiny
parts of the thalamus are removed consciousness is abolished and the
thalamus is involved in attention and the global integration of cortical
activity. Any impartial judge might pronounce that the site of conscious
experience has been found, possibly in the ILN of the thalamus, but no
one can say how it works.

## General Anaesthesia and the Thalamus

General anaesthesia should result in a profound depression of activity
in the ILN if these are indeed the sites of the conscious state. White &
Alkire (2003) administered halothane or isoflurane to volunteers and
used positron emission tomography (PET) to monitor brain activity. They
found severe depression of activity in the thalamus. The depression
appeared to be higher in the non-specific nuclei than in the relay
nuclei of the thalamus. In other words the anaesthesia is neither
turning off the cortex nor turning off the input to the cortex but it is
turning off an important part of the thalamus. Fiset *et al.* (1999)
have also demonstrated a similar pattern of medial thalamic inactivity
and cortical activity in propofol anaesthesia. Suppression of cortical
activity is not the cause of unconsciousness; for instance, the
anaesthetic agent chloralose leads to increased neural activity in the
cortex relative to conscious patients (Cariani 2000).

## The function of consciousness

When we walk our conscious experience does not contain data about the
control of the spinal, cerebellar and vestibular reflexes that keep us
on an even keel. When we reach out for a cup our conscious experience
only contains data related to the need for the cup, not data about the
elaborate control system that enables the action. When we talk the words
just come into mind, we do not painstakingly control the syntax and
vocal chords. When our attention shifts the conscious experience
containing the shift happens after the attention has shifted. This
passive nature of experience recurs throughout the neuroscience of
consciousness from the \"readiness potential\" to the \"auditory
continuity illusion\". So what does conscious observation do? The
medical evidence of the lack of consciousness in some forms of delirium,
mutism, PVS etc. suggest that the role of conscious observation is to
stabilise the brain so that it acts as a coordinated whole. Conscious
observation is an orderly arrangement of events, a stable groundform
that reflects the environment and composes the stage for action. It
could be speculated that if quantum events were prominent in brain
function then such a groundform would be essential but even a classical
brain might require a stabilising form that could be continuously
compared with the world beyond the body.

A stable form of neural information that contains bound data from the
senses and internal neural processes is likely to have a role in the
functioning of the organism. There is now an *integration consensus*
that proposes that phenomenal states somehow integrate neural activities
and information-processing that would otherwise be independent (see
review in Baars, 2002).

However, it has remained unspecified which kinds of information are
integrated in a conscious manner and which kinds can be integrated
without consciousness. Obviously not all kinds of information are
capable of being disseminated consciously (e.g., neural activity related
to vegetative functions, reflexes, unconscious motor programs, low-level
perceptual analyses, etc.) and many kinds can be disseminated and
combined with other kinds without consciousness, as in intersensory
interactions such as the ventriloquism effect.

Morsella (2005) proposed a *Supramodular Interaction Theory* (SIT) that
contrasts the task demands of consciously penetrable processes (e.g.:
those that can be part of conscious experience such as pain, conflicting
urges, and the delay of gratification) and consciously impenetrable
processes (e.g.: intersensory conflicts, peristalsis, and the pupillary
reflex). With this contrastive approach, SIT builds upon the integration
consensus by specifying which kinds of interaction require conscious
processing and which kinds do not (e.g., some intersensory processes).
SIT proposes that conscious processes are required to integrate
high-level systems in the brain that are vying for (specifically)
skeletomotor control, as described by the principle of *parallel
responses into skeletal muscle* (PRISM). Accordingly, regarding
processes such as digestion and excretion, one is conscious of only
those phases of the processes that require coordination with
skeletomotor plans (e.g., chewing or micturating) and none of those that
do not (e.g., peristalsis). From this standpoint, consciousness
functions above the level of the traditional module to "cross-talk"
among high-level, specialized and often multi-modal, systems.

**References**

Baars, B. J. (2002). The conscious access hypothesis: Origins and recent
evidence. *Trends in Cognitive Sciences, 6,* 47 -- 52.

Morsella, E. (2005). The function of phenomenal states: Supramodular
interaction theory. *Psychological Review, 112,* 1000 - 1021.

 More\... Click here for Rivalries and synchronisation, bibliography
and references

