CONSCIOUSNESS (AROUSAL)

We can try and explain many brain functions in a mechanical way as with our
computer simile but as in all the major disciplines of science one eventually comes
upon a brick wall :- what is space, time, energy, what initiated the big bang, what was
there before it, and in the case of the biological sciences what is consciousness ?. This
is the only enigma that remains allowing philosophy to reign over neuroscience.
Nevertheless consciousness as we know it cannot exist without a brain and is lost
forever in brain disease or brain death. Even our deepest emotions such as love and
hate, happiness or deep depression can only exist in the conscious brain.
Consciousness is very difficult to define, Descartes dictum "I think therefore I am “
(Cogito Ergo Sum) falls short in defining consciousness since the converse is not true,
if I cant think I may be demented, deluded or hallucinated but I am not unconscious. If
unconscious for a prolonged time do I exist as a person with a mind, if for ever
unconscious and so brain stem dead do I exist. We all know when we are conscious
and aware of self existence and the passage of time and we can recognise
consciousness in others based upon their responses. We do not however know what is
going on in the conscious mind of another person if they do no communicate with us.
It is very difficulty to measure conscious awareness or level of arousal, we know when
someone is asleep or awake and absence of sleep wake cycles can be used to define
coma. Scales such as the Glasgow coma scale do not in fact measure consciousness but
behavioural responses to stimulation. If one gives a non anaesthetised person curare
they are fully conscious but how does an outsider determine that there is a personal
inner awareness. Is a newborn infant conscious ? most people would agree that it is
conscious in that it shows sleep wake cycles and shows arousal to stimuli such as
hunger. Is a baby conscious in utero before birth or does consciousness appear at
birth, they certainly show sleep wake cycles in utero, when does that consciousness
appear during development of the foetus when brain stem develops, diencephalon or
cortex, has it any content ?. Are we conscious in REM sleep when dreaming and
immediately aware but memory is switched off so there is usually no recall. Clinical
diffrentiation of different disorders with absent responses may be impossible ie.
Coma
Persistent vegetative state
Sleep
Anaesthesia or drug overdose
Akinetic-mutism
Dystonia with non communication
An absence seizure or fugue state
Brain stem death

No one would doubt that their pet dog or horse was conscious shows recognition and
could remember people and places as well as understanding a limited vocabulary ( or
intonation pattern). Are all vertebrates conscious, are all animals with a rudimentary
cerebral cortex such as a shark or dogfish. Is consciousness, even a
microconsciousness a feature of all living cells and a huge protoplastmic conglomerate
such as the brain merely amplifies it into a macroconsciousness ?. If consciousness is a
feature of all living cells then an amoeba or any individual body cell has
microconsciousness and trees would be conscious The brain could amass a large
amount of consciousness by joining billions of cells in the form of what Graham
Cannon in Manchester used to call "organismal control " and death is simply the
permanent loss of this organismal control via the reticular formation and a return to a
mass cellular microconsciousness.
Do we simply need a nerve net such as the reticular formation linking millions of cells
as one unit to give us consciousness. Does the size of the cerebral cortex merely store
more information for the content of consciousness ( a human with gigabytes of
cerebral hard disc and a fish or bird megabytes, invertebrates with only a ganglion a
kilobyte ? !). Some experts in artificial intelligence have claimed that a computer if
made powerful enough would automatically become conscious. Apart from being a
frightening concept, the biggest argument against this is that loss of intelligence in
man in mental handicap or severe dementia does not mean a proportionate loss of
consciousness only diminution in its content.

The idea that consciousness, like self replication, is simply a property of some
macromolecules once they achieve a particular size and configuration is as equally
frightening as the computer model. It perpetuates the saga of ignoring the whole cell as
the unit of life. In neurology we have been obsessed by synapses, neurotransmitters
and nerve nets and have forgotten the actual living part of the brain ie the neuron. If
we believe that nerve networks achieve consciousness then there would appear to be
no sensible reason not to accept that a computer’s electronic networks could achieve
consciousness. We now know that the cell consists of organelles which are themselves
as complex as the organs of a whole body one can localise any cellular function to a
prescribed sub - cellular unit or organelle. Even accepting this we have completed the
circular argument to return to the idea of consciousness being a property that develops
in certain self replicating large molecules eg. DNA.

Anatomy of Consciousness
Consciousness depends upon the reticular activating system and septal nuclei being
intact. One may have a gross lower brainstem, ie lower pons and medulla, lesion as
with a pontine glioma so that all body movement, speech and swallowing are
paralysed and yet the child may be fully conscious and can think normally. One may
equally remove a whole cerebral hemisphere thus limiting the content of consciousness
and yet the child is fully conscious. Extensive disease of both cerebral hemispheres
will cause severe mental defect or dementia and so limit or even abolish all cognitive
learning (as in post - traumatic persistent vegetative state) and thus grossly restricting
the content of consciousness (thought processes) and yet the child is still conscious.
That is to say there is a relatively small area of upper brain stem, thalamus and septum
which appears to be necessary to sustain consciousness and a small lesion here as with
tentorial herniation secondary to raised intracranial pressure, primary midbrain injury
in trauma, localised encephalitis or tumour may cause prolonged coma. An irreversible
lesion in the brainstem eg central ischaemic neuronal necrosis, can result in permanent
failure of cortical arousal and consciousness, hence the concept of brain death depends
upon brain stem function rather than cortex.

The mesencephalic reticular formation leads to continuous sleep and lesions in the
medullary reticular formation to constant wakefulness. The reticular formation is a
continuous network of small interconnected cells which have a basketwork of axons,
dendrites and side connections form ascending and descending pathways. The
dendrites are long and straight. The axons run upwards and downwards coveing many
levels from the same cell. The reticular formation starts caudally in the central grey
matter of the spinal cord and is then present in medulla as the medial and lateral
reticular nuclei which give rise to the reticulospinal pathways. There are some very
large cells in the medulla and pons ie the gigantocellular nucleus. The midbrain,
thalamic reticular nucleus and intralaminar thalamic nuclei all form part of the system
There are also the specific neurotransmitter pathways which influence the cerebral
cortex and basal ganglia eg.
Nor adrenaline from the locus coeruleus
Serotonin - from the median raphe nucleus ( plate of neurones in middle of
midbrain and pons)
Dopaminergic from the substantia nigra
Cholinergic from Meynherts nucleus.

Reticular Activating System.

Fibres to the cortex arise from the intralaminar thalamic nuclei, locus coeruleus and
Raphe nuclei. Possibly switch on specific areas via the cartridge on the apical dendrite.
Cuses arousal and wakefulness or vigilance, changes respiration and blood pressure
There is tonic activity of the arousal system.

The EEG desynchronises with reticular activating stimulation causes the synchronised
slow waves of sleep to disappear with lower amplitude asynchronous fast activity
appearing. It takes only 10 seconds of ischaemia to flatten the EEG and impair
consciousness but 4 minutes ro irreversibly damage the cortex. Even after reanimation
there is often consciousness with sleep wake cycles but little content or
communication. Consciousness depends upon energy from oxygenation but is not
permanently lost by periods of hypoxia,
Consciousness
Thought is the content of consciousness
Short term memory is the capacity of consciousness
Attention maintains the current content of consciousness
Distraction clears current content.

QuickTimeª and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

No one would doubt that their pet dog or horse was

conscious shows recognition and could remember people and
places as well as understanding a limited vocabulary ( or
intonation pattern). Are all vertebrates conscious, are all
animals with a rudimentary cerebral cortex such as a shark
or dogfish. Is consciousness, even a microconsciousness a
feature of all living cells and a huge protoplastmic
conglomerate such as the brain merely amplifies it into a
macroconsciousness ?. If consciousness is a feature of all
living cells then an amoeba or any individual body cell has
microconsciousness and trees would be conscious The brain
could amass a large amount of consciousness by joining
billions of cells in the form of what Graham Cannon in
Manchester used to call "organismal control " and death is
simply the permanent loss of this organismal control via the
reticular formation and a return to a mass cellular
microconsciousness.

Do we simply need a nerve net such as the reticular

formation linking millions of cells as one unit to give us
consciousness. Does the size of the cerebral cortex merely
store more information for the content of consciousness ( a
human with gigabytes of cerebral hard disc and a fish or bird
megabytes, invertebrates with only a ganglion a kilobyte ? !).
Some experts in artificial intelligence have claimed that a
computer if made powerful enough would automatically
become conscious. Apart from being a frightening concept,
the biggest argument against this is that loss of intelligence
in man in mental handicap or severe dementia does not
mean a proportionate loss of consciousness only diminution
in its content.

The idea that consciousness, like self replication, is simply a

property of some macromolecules once they achieve a
particular size and configuration is as equally frightening as
the computer model. It perpetuates the saga of ignoring the
whole cell as the unit of life. In neurology we have been
obsessed by synapses, neurotransmitters and nerve nets
and have forgotten the actual living part of the brain i.e. the
neuron. If we believe that nerve networks achieve
consciousness then there would appear to be no sensible
reason not to accept that a computer’s electronic networks
could achieve consciousness. We now know that the cell
consists of organelles which are themselves as complex as
the organs of a whole body one can localise any cellular
function to a prescribed sub - cellular unit or organelle. Even
accepting this we have completed the circular argument to
return to the idea of consciousness being a property that
develops in certain self replicating large molecules eg. DNA.

The thalamus and neocortex maintain a continuous dialogue

through a vast number of complex connections (Jones, 1985;
Steriade et al., 1990; Guillery, 1995; Steriade et al., 1997).
Depending on the interactions established in the network
different states of vigilance will be generated, such as
wakefulness and sleep (Steriade et al., 1990; McCormick and Bal,
1997). The neural mechanisms that give rise to changes from one
conscious state to another operate in the thalamocortical
network. During wakefulness, sensory inputs gain access to the
cortex only after substantial processing in the thalamus (Steriade
et al., 1990) and, when falling asleep, the thalamus functionally
disconnects the cortex from ascending sensory inputs and
generates slow rhythms characteristic of sleep (Steriade et al.,
1990).
A key structure involved in all these mechanisms taking place in
the thalamocortical network is the thalamic reticular (RE)
nucleus. For long years regarded as a diffusely organized
structure, having global rather than localized actions on
thalamocortical pathways (Scheibel and Scheibel, 1966), the RE
nucleus is known today to be divided into several distinct sectors,
each related to a particular functional group of thalamocortical
pathways (Jones, 1985; Crabtree, 1989, 1992, 1996); and
showing a crucial role in promoting sleep and waking activity
(Steriade et al., 1990). There are, as yet, no morphological
correlates of the two populations of RE nucleus described with
different bursting properties (Contreras et al., 1992), one of
which typically generates low-threshold spikes and is able to
switch from tonic to burst firing, the other apparently lacking the
low-threshold calcium conductance and firing only tonically
(Contreras et al., 1992). Thus, bursting mode is exhibited during
EEG-synchronized sleep, while tonic discharge is detected during
waking and rapid eye movement sleep (Mukhametov et al.,
1970; Steriade and Wyzinski, 1972; Steriade et al., 1986). The
two firing modes depend on the membrane potential of the cell
(Contreras et al., 1992; Bal and McCormick, 1993; Gentet and
Ulrich, 2003). At depolarized membrane potentials (positive to
-65 mV), intracellular injection of a positive current pulse results
in the activation of a train of action potentials (Bal and
McCormick, 1993). In contrast, intracellular injection of the same
current pulse at hyperpolarized membrane potentials (negative to
-65 mV) results in the generation of a high-frequency (300-500
Hz) burst of action potentials (Bal and McCormick, 1993).
Barbiturate anesthesia depresses the cortical network activity and
turns the membrane potential of RE neurons to hyperpolarized
levels, favoring the generation of spike-bursts.

Neurons from the RE nucleus are all gabinergic exhibit a

prominent tendency to generate rhythmic oscillations in the 10
Hz-band range, Spindles are the distinct EEG correlate of sleep
onset and the only rhythm, during the transition from wake to
sleep, which involves the synchronous activity of a large number
of thalamic neurons and of their cortical targets (Contreras and
Steriade, 1996; Contreras et al., 1997), so that it can be
recorded on the scalp. This means that electrical synapses might
synchronize oscillations in the range of spindles, which are
mediated by LTSs.
Keeping awake
These structures are the posterior hypothalamus, the basal
telencephalon, and the intralaminar nuclei of the thalamus.
Together they are often referred to as the “executive
network”. Stimulating the posterior hypothalamus
produces a state of wakefulness comparable to that induced
by stimulating the reticular formation in the brainstem. The
activity of the posterior hypothalamus diminishes naturally
during sleep, when it releases less histamine, a molecule
that it uses as a neurotransmitter. The antihistamines that
people take for allergy symptoms are known to cause some
sleepiness, by reducing the activity of histamine. he
intralaminar nuclei of the thalamus contain thalamocortical
neurons that send projections throughout the cortex. The
activation of these thalamocortical neurons causes them to
release excitatory amino acids such as aspartate and
glutamate, thus contributing to excitation of the cortex and
to wakefulness. During wakefulness, these neurons generate
single action potentials at regular intervals, but as the
individual falls asleep, these neurons begin firing in bursts
instead, thus causing the cortex to display the synchronized
EEG pattern that is typical of sleep.
http://thebrain.mcgill.ca/flas

midbrain reticular formation projects massively into the

thalamic nuclei, which in turn influence the entire cortex. The
role of this formation is to desynchronize the cortex in the
broad sense, thus facilitating not only wakefulness but REM
sleep as well. Formerly known as the ascending reticular
formation, it is now regarded simply as part of the
wakefulness network.

cholinergic mesopontine nuclei project to the thalamus.

The acetylcholine produced by these nuclei has two effects:
it reduces the activity of the thalamic reticular nucleus,
which is part of the sleep system, and it activates the
thalamocortical neurons involved in wakefulness. For
example, the neurons of the mesopontine cholinergic nuclei
of the ascending pathway, which are located in the rostral
part of the pons, project their axons to the thalamus. There
they make cholinergic connections not only in its sensory
areas, but also in its reticular nucleus, a layer of neurons
that surrounds the thalamus like a skin and exerts a general
inhibiting effect on it by means of the neurotransmitter
GABA. ( the thalamic reticular nucleus has nothing to do with
the reticular formation.)
The cholinergic neurons from the pons sensitize the sensory
thalamus but inhibit the reticular nucleus. How can this be
so? The answer is that these two structures have different
kinds of receptors for acetylcholine and hence respond to it
differently. The sensory thalamus is sensitized by the
activation of its nicotinic receptors for acetylcholine,
whereas the reticular thalamus is inhibited by the activation
of its muscarinic receptors for this same neurotransmitter.
Note that these pyramidal cells receive direct nicotinic
cholinergic excitation directly from the basal nucleus of
Meynert as well as from the thalamocortical neurons.

Central cholinergic pathways are ideally suited to

regulate global functions that rely upon the cerebral
cortex; such functions include attention, arousal,
motivation, memory and consciousness (Woolf,
1991; Woolf, 1996). The basal forebrain contains two
groups of cholinergic neurons: (1) the medial septal
group (medial septal nucleus and vertical diagonal
band: ms and vdb) that project cholinergic axons to
the hippocampus and parahippocampal gyrus and
(2) the nucleus basalis group (nucleus basalis,
substantia innominata and horizontal diagonal band:
bas, si, hdb) that project cholinergic axons to all
parts of the neocortex, parts of limbic cortex and to
the amygdala. The cholinergic pontomesencephalon
neurons (laterodorsal tegmental and
pedunculopontine tegmental nuclei: ldt and ppt)
project onto hindbrain, thalamus, hypothalamus and
basal forebrain.

magnocellular medullary reticular nuclei, whose

neurons are cholinergic or aspartergic/glutamergic, are the
origin of both the reticulo-thalamic-cortical pathway and the
reticulo-hypothalamic-cortical pathway. Their projections
therefore run to the midbrain reticular formation and the
cholinergic mesopontine nuclei, as well as to the basal
telencephalon and the posterior hypothalamus.

nuclei of the locus coeruleus are located in the dorsal

part of the pons, and their noradrenergic projections
influence brain structures such as the thalamus, the
hippocampus, and the cortex. The locus coeruleus is at its
most active when an individual is awake and active. It is less
active during calm wakefulness, even less active during non-
REM sleep, and completely quiescent during REM sleep.

serotonergic nuclei of the anterior raphe (also known as

the superior raphe) send serotonin to the hypothalamus and
the cortex. These nuclei are active during wakefulness. Their
overall effect is to support wakefulness, and, unlike with
other groups of aminergic neurons, lesions to these nuclei
cause prolonged insomnia that lasts several days. The likely
reason for this apparent contradiction is that this system,
which innervates the anterior hypothalamus both in the
preoptic area and in the circadian clock circuits of the
suprachiasmatic nucleus, seems to measure the duration
and intensity of wakefulness. This antiwaking system is set in
motion by serotonin one of the neurotransmitters secreted
during waking periods:..

GABAergic neurons, sometimes described as non-REM (or

NREM) sleep-on neurons, are at their most active during
deep (non-REM) sleep and are inactive during wakefulness
and REM sleep. Electrical stimulation of these neurons
quickly causes sleep, and their destruction causes insomnia.
This insomnia can be interrupted, however, by the injection
of muscimol (a GABA analogue) into the posterior
hypothalamus, where several components of the
wakefulness system converge

suprachiasmatic nucleus, which is the main component of

this biological clock, is thus also involved in triggering sleep.
When its neurons are damaged, the normally long periods of
wakefulness shorten and become randomly distributed
across the day. These neurons influence wakefulness
through one of their neuropeptides: vasopressin. (Note that
the effects that the vasopressin synthesized by the
suprachiasmatic nucleus has on the brain are completely
different from those of the vasopressin produced by the
posterior pituitary gland, which acts mainly on kidney
function and blood pressure.) Back to serotonin, however.
This neurotransmitter plays a specific dual role. On the one
hand, it is produced in large amounts during wakefulness
and contributes importantly to this state. But on the other
hand, serotonin also plays a fundamental role in the process
of falling from wakefulness into non-REM sleep.The
explanation for this contradiction took scientists a while to
find. They had even long regarded serotonin as the “sleep
hormone”, because in animal experiments, destroying the
neurons that synthesized it, or inhibiting its synthesis in
other ways, caused periods of sleeplessness that lasted
several days, but the same animals could sleep again if the
immediate precursor of serotonin was then injected into the
preoptic area of their anterior hypothalamus. The expression of
robust circadian rhythms depends on the integrity of the biological
clock and on the integration of thousands of individual
cellular clocks found in the clock. Neurotransmitters are
required at all levels, at the input, in the clock itself, and in
its efferent output for the normal function of the clock
Since, then, scientists have obtained a far better
understanding of why a lack of serotonin in the anterior
hypothalamus prevents the onset of sleep. This improved
understanding led to the hypothesis that the preoptic area of
the anterior hypothalamus did not operate as a “sleep
centre”, but rather as an area that imposed an inhibition on
wakefulness. This hypothesis was subsequently confirmed
electrophysiologically. It was found that the measured unit
activity of the serotonergic raphe neurons is at its greatest
during wakefulness, declines at the onset of non-REM sleep,
and ceases during REM sleep. This gradual onset of electrical
silence as someone moves from non-REM sleep into REM
sleep thus indicates that the raphe neurons stop releasing
serotonin into the synapses because it has done its work of
inhibiting wakefulness, and its levels can therefore be
allowed to decline.

When the brain is awake, its cholinergic, histaminergic, and

noradrenergic networks thus activate the thalamus in two
ways: directly, by facilitating the sensory thalamus, and
indirectly, by inhibiting the reticular nucleus and thus
suppressing its general inhibiting effects on the thalamus.
Note that these pyramidal cells receive direct nicotinic
cholinergic excitation directly from the basal nucleus of
Meynert as well as from the thalamocortical neurons. During
the minutes when an individual is falling asleep (Stage 1 non-
REM sleep), the firing frequency of the noradrenergic,
cholinergic, and serotonergic neurons of the activating
system in the brainstem decreases, so that the thalamus is
less activated.

Stage 2 of non-REM sleep, the cortex goes into an automatic

activity pattern of thalamic origin, characterized by sleep
spindles on the EEG. These spindles are caused by the
process just described: the rhythmic firing of the reticular
neurons produces cyclical hyperpolarizations in the
thalamocortical neurons, followed by bursts of action
potentials. These potentials are received by the cortical cells,
where they generate the sleep spindles. The slow, high-
amplitude waves produced in stages 3 and 4 of non-REM
sleep result from the hyperpolarization of the pyramidal cells
of the neocortex, which is triggered by local GABAergic
interneurons, most likely under the influence of the preoptic
neurons of the anterior hypothalamus. The thalamic neurons,
whose membrane potential is then even more negative than
during sleep spindles (seen mainly in Stage 2) probably also
contribute to these slow cortical waves.

Anatomy of Consciousness
Consciousness depends upon the reticular activating system
and septal nuclei being intact. One may have a gross lower
brainstem, ie lower pons and medulla, lesion as with a
pontine glioma so that all body movement, speech and
swallowing are paralysed and yet the child may be fully
conscious and can think normally. One may equally remove
a whole cerebral hemisphere thus limiting the content of
consciousness and yet the child is fully conscious. Extensive
disease of both cerebral hemispheres will cause severe
mental defect or dementia and so limit or even abolish all
cognitive learning (as in post - traumatic persistent
vegetative state) and thus grossly restricting the content of
consciousness (thought processes) and yet the child is still
conscious. That is to say there is a relatively small area of
upper brain stem, thalamus and septum which appears to be
necessary to sustain consciousness and a small lesion here
as with tentorial herniation secondary to raised intracranial
pressure, primary midbrain injury in trauma, localised
encephalitis or tumour may cause prolonged coma. An
irreversible lesion in the brainstem eg central ischaemic
neuronal necrosis, can result in permanent failure of cortical
arousal and consciousness, hence the concept of brain death
depends upon brain stem function rather than cortex.
The mesencephalic reticular formation leads to continuous
sleep and lesions in the medullary reticular formation to
constant wakefulness. The reticular formation is a continuous
network of small interconnected cells which have a
basketwork of axons, dendrites and side connections form
ascending and descending pathways. The dendrites are long
and straight. The axons run upwards and downwards coveing
many levels from the same cell. The reticular formation
starts caudally in the central grey matter of the spinal cord
and is then present in medulla as the medial and lateral
reticular nuclei which give rise to the reticulospinal
pathways. There are some very large cells in the medulla
and pons ie the gigantocellular nucleus. The midbrain,
thalamic reticular nucleus and intralaminar thalamic nuclei
all form part of the system
There are also the specific neurotransmitter pathways which
influence the cerebral cortex and basal ganglia eg.

The EEG desynchronises with reticular activating stimulation

causes the synchronised slow waves of sleep to disappear
with lower amplitude asynchronous fast activity appearing. It
takes only 10 seconds of ischaemia to flatten the EEG and
impair consciousness but 4 minutes ro irreversibly damage
the cortex. Even after reanimation there is often
consciousness with sleep wake cycles but little content or
communication. Consciousness depends upon energy from
oxygenation but is not permanently lost by periods of
hypoxia,
This study sought to determine whether electrical stimulation of
the amygdaloid central nucleus (ACe) produces cholinergically
mediated neocortical arousal manifested in the suppression of
frontal cortex delta wave (1-4 Hz) activity.

QuickTimeª and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

The components of these ascending systems can be divided

into two major pathways, one ventral, the other dorsal,
both of which arise from the reticular nucleus in the medulla
oblongata. In addition to maintaining wakefulness, several of
the nuclei of these two pathways use acetylcholine and
glutamate as neurotransmitters and are partly responsible
for the cortical activation that occurs during

The ventral pathway is called the reticulo-hypothalamic-

cortical pathway. It projects to the posterior hypothalamus
and to the nucleus of Meynert, which consists of cholinergic
neurons and is located in the basal telencephalon.

The dorsal pathway is called the reticulo-thalamic-

cortical pathway. It activates the cholinergic mesopontine
nuclei, the aspartergic and glutamergic neurons of the
midbrain reticular formation, and the thalamus.

1 Ventrolateral nucleus – motor from Cerebellum (motor cortex) and

basal ganglia (supplementary motor area)
2 VPL and VPM – sensory information from spinothalamic and
posterior column / medial lemniscus
3 Vision – lateral geniculate- Visual Cortex area 17
4 Hearing – medial geniculate – Heschl’s gyrus
5 Intralaminar thalamic N - Reticular formation – arousal & attention.
6 Nucleus reticularis – surface rim Gabinergic cells and controls all
thalamic nuclei – attention
7 Dorso medial N major input to prefrontal lobe from Amygdala
reticular formation and hypothalamus and reciprocal frontal.
8 Anterior Nucleus project to Cingulate Gyrus. (Papez) from Mamillary
body

Reticular Inhibiting system.

Links limbic, hypothalamic, amygdala and cortex.

Causes of Unconsciousness.
Most cases of coma are due to
a) Tentorial herniation with midbrain compression from raised
intracranial pressure, Duret haemorrhages
b) Trauma with primary midbrain injury
b) Hypoxia
c) Drugs affecting the reticular formation including general
anaesthetics.

Primary upper brain stem tumours and infarcts are uncommon, upper brain stem
infarcts and haemorrhages are most commonly secondary to raised intracranial
pressure. Trauma can cause primary brainstem injury without any raised pressure. Loss
of cerebral perfusion as in syncope or any other transient ischaemic attack will cause
rapid loss of consciosness.

Hypnotic drugs have specific actions on the reticular activating system there may be
natural endogenous hypnotics such as natural benzodiazipines in the same way that
there are natural endogenous opoids. Toxic substances accumulate in renal and hepatic
failure or inborn errors in metabolism appear to work in the same way on the high
metabolic activity of this multisynapse system, it is for the same reason that hypoxia
or hypoglycaemia can also rapidly produce coma.. Another way to very rapidly make a
person unconscious is to give them a general anaesthetic. These substances are usually
alcohols or ethers of fatty acids such as chloroform, ether and Halothane. They are
postulated to work through GABA receptors causing inhibition of the cell.

The brain forms 2% body weight (1.5 / 70 Kg) but takes 20% oxygen consumption.
The most sensitive way to reduce consciousness and flatten the EEG is to reduce the
cells metabolism by hypoxia. This suggests that consciousness requires a constant
energy supply and is an active process in the cell. The reticular formation,
hippocampus and basal ganglia have the highest oxygen uptake.
 QuickTimeª and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Inhaled anaesthetic agents act in different ways at the level of the central
nervous system. They may disrupt normal synaptic transmission by
interfering with the release of neurotransmitters from pre-synaptic nerve
terminal (enhance or depress excitatory or inhibitory transmission), by
altering the re-uptake of neurotransmitters, by changing the binding of
neurotransmitters to the post-synaptic receptor sites or by influencing the
ionic conductance change that follows activation of the post-synaptic
receptor by neurotransmitters. Both pre- and post-synaptic effects have
been found.Direct interaction with the neuronal plasma membrane is very
likely, but indirect action via production of a second messenger also remains
possible. The high correlation between lipid solubility and anaesthetic
potency suggests that inhalational anaesthetic agents have a hydrophobic
site of action. Inhalational agents may bind to both membrane lipids and
proteins. It is not clear which of the different theories are most likely to be
the main mechanism of action of inhalational anaesthetic agents.The Meyer-
Overton theory describes the correlation between lipid solubility of inhaled
anaesthetics and MAC and suggests that anaesthesia occurs when a
sufficient number of inhalational anaesthetic molecules dissolve in the lipid
cell membrane. The Meyer-Overton theory postulates that it is the number of
molecules dissolved in the lipid cell membrane, and not the type of
inhalational agent, that causes anaesthesia. Combinations of different
inhaled anesthetics may have additive effects at the level of the cell
membrane.

The protein receptor hypothesis postulates that protein receptors in the

central nervous system are responsible for the mechanism of action of
inhaled anaesthetics. This theory is supported by the steep dose-response
curve for inhaled anaesthetics. However, it remains unclear if inhaled agents
disrupt ion flow through membrane channels by an indirect action on the
lipid membrane, via a second messenger or by direct and specific binding to
channel proteins.Another theory describes the activation of gamma-
aminobutyric acid (GABA) receptors by the inhalational anaesthetics. Volatile
agents may activate GABA channels and hyperpolarise cell membranes. In
addition, they may inhibit certain calcium channels and therefore prevent the
release of neurotransmitters and inhibit glutamate channels. Volatile
anaesthetics therefore may share common cellular actions with other
sedative, hypnotic and analgesic drugs.

We have already discussed the hypothesis that the current content of consiousness is
the equivalent of that part of short term memory which would appear on the video
display unit in computer terms. All material must be brought into consciousness to be
processd, ie. thought about. There are varying degrees of consciousness ranging from
wide awake and alert to coma.

Thought is the content of consciousness

Short term memory is the capacity of consciousness
Attention maintains the current content of consciousness
Distraction clears current content.

It is lesser degrees of loss of cortical arousal which are important to the teacher and
learning. The teacher may know if a child is sleepy and lethargic but there are
obviously different degrees of arousal which are not always easy to define.
If a child is on certain anticonvulsant medication , is bored, was watching television
till late at night then he may be drowsy with impaired speed and accuracy of thought
processes. The same applies to the taking of drugs, alcohol or solvent sniffing.
Sleep

Anaesthesia

Coma Scores
ATTENTION.
Attention is the willed or voluntary selection of a topic to hold within consciousness
utilising short term memory in order to allow mental processing (thinking). Attention
is the focusing of conscious awareness upon
i) a particular motor activity - especially whilst it is being learned.
ii) a specific sensory input or perception.
iii) memories and concepts retrieved from long term memory stores into
short term memory.
Sustained attention requires a high level of arousal and the drowsy child or bored
child will have a short attention span. Distractability is the opposite to “paying
attention” the child loses attention, short term memory is cleared and one loses the
train of thought. Attention is accompanied by the rejection of simultaneous unwanted
sensory stimuli which are said to be "gated" out eg. enviornmental noise as distinct
from speech sounds, sensation from muscles, skin eg seating and clothing and other
visual stimuli other than those relevant to the task in hand. If these irrelevant stimuli
are not gated out they enter conscious awareness and interfere with thought processes
so that one may " lose the stream of thought " ie one is distracted and this clears short
term memory so one has to start again. Attention is also lost, a secondary attention
deficit, when the material is boring, irrelevant, or provokes anxiety and equally is
sustained when it is interesting and excites curiosity.
It is though that the intralaminar thalamic nuclei and the pre-frontal lobes are
important anatomically in the maintenance of attention. It is a well documented
clinical observation that certain drugs such as phenobarbitone and benzodiazipines will
disrupt attention causing the child to be more distractible. Frontal lobe damage
following head injury can often be demonstarted by SPECT scans and is associated
with a major attention deficit. True Lead poisoning with clinical signs can cause severe
overactive behaviour but the evidence that normal low levels are responsible for any
behavioural abnormality is not proven. The evidence that colouring agents, salicylates
and E numbers in foods cause a true toxic encephalopathy with selective damage to the
prefrontal lobes and intralaminar thalamic nuclei is not convincing. Children with
Coeliac disease certainly are overactive in the true sense with a measurable increase in
motor activity and restlessness are also very irritable children possibly due to a true
toxic encephalopathy from absorbtion of larger peptides which improves with
institution of gluten free diet.

If Attention loss is situational eg when trying to read, and yet the child will perform
the most boring tasks when succeeding, such as watch T.V. for long periods, sustain
play or games and may sit patiently for several hours during assessment or computer
psychometrics then a primary attention deficit is unlikely. Anxiety is certainly a cause
of disrupted attention, the child will concentrate if succeeding but as soon as his area
of difficulty arises and failure is iminent then concentration goes and the child figits
and becomes restless. In very many children with learning disorder the attention
defect is a secondary situational disorder from induced anxiety and not a primary
biological defect.
A primary disorder of attention has been postulated for many years as a major cause of
learning disorder. A.D.D. or attention deficit disorder, this is considered in more detail
in another chapter of this book ( see page - ). This is in some cases a more acceptable
excuse for P.D.D. - parent discipline disorder. This is not to deny the existence of a
hyperkinetic syndrome with learning disorder, poor concentration and distractibility
which shows concordance in twin studies and suggests a true genetic basis. For a
sustainable diagnosis the condition must be diagnosed before 7 years with at least 6
symptoms attributable to attention deficit and 6 to hyperactivity or poor impulse
control ie “rages”. The condition must also not be situational and so occur at school
and at home. Anxiety with parental marriage breakdown and inconsistent discipline
particularly during the “terrible twos” stage may cause hyperactivity at home and
anxiety from an undiagnosed learning disorder mainly at school. True cases may show
impaired frontal lobe perfusion which is reversed with sympathomimetic amine
therapy such as Methylphenidate. This is thought to be a dopamine reuptake inhibitor.
Search for an abnormality of Dopamine receptors particularly DRD4 have bees
suggestive but not conclusive. Poor impulse control with bias of the fight and flight
reaction in favour of fight shows as a low frustration tolerance and rage reactions.
Sleep disturbance is also a major component and often an early sign present from
infancy. The place for ADD as the causation of the vast majority of children with
learning disorder is questioned by the authors. The attention disorder is in most cases
due to anxiety from chronic failure and the answer is a good remedial teacher who
makes the child feel secure and not a failure and motivates him rather than prescribing
large doses of sympathomimetic amines.

Children with epilepsy especially complex partial seizure arising in the temporal lobe
or children brain damaged from asphyxia at birth, encephalopathy of low birth weight,
hydrocephalus and after head injury may certainly show attention deficit and learning
disorder. Most children with learning disorders are not brain damaged.

In the case of the mentally handicapped child his deficit in cognitive learning means
that he cannot sustain thought on a particular subject as for example how to sustain
play through imagination and "saying to himself" in order to know what to do with a
toy car or aeroplane. The child cannnot sustain play and flits from toy to toy or activity
to activity this makes him appear to have attention defect which is again a secondary
phenomn due to his cognitive difficulty.