Consciousness

(Tuis.) #1

Chapter


Four


Neuroscience


Alternatively, she might be in a ‘persistent vegetative state’ (PVS), which we
touched on earlier in the chapter. Functional neuroimaging makes possible the
investigation of brain states in global disorders of consciousness (Schiff, 2007).
These states usually occur with damage to higher parts of the brain but not the
brain stem, and patients may progress through to a full recovery or remain in
PVS, coma, or a minimally conscious state. In PVS, there is activity in the early
sensory areas but not in higher association areas, and no apparent sensory
consciousness.


Anaesthesia is a more familiar state to most of us, and research on this provides
further insight into NCCs. By varying the dose of anaesthetics and observing the
effects with neuroimaging, it is possible to explore the transition from conscious-
ness to unconsciousness, and even the loss of specific functions with deepening
anaesthesia. Early experiments with PET scans using the anaesthetics propofol
and isoflurane showed a global suppression of cortical functioning with increas-
ing doses, but no evidence of any specific ‘consciousness circuits’ (Alkire, Haier,
and Fallon, 1998).


Subsequent research suggests that for many different anaesthetics the suppres-
sion may be caused by blocking at the level of the thalamus, or in thalamocortical
and cortico-cortical reverberant loops. This would entail a disconnection some-
thing like that seen in PVS (Alkire and Miller, 2005), and has led to the thalamus
being described as a possible ‘consciousness switch’ (Alkire, Hudetz, and Tononi,
2008, p. 877). Alkire and colleagues (2008) argue that the breakdown of corti-
co-thalamic connectivity prevents the brain from integrating information, and
link this to the Integrated Information Theory of consciousness that we will come
to in Chapters 5 and 6 – a theory which Tononi and Koch have suggested is the
best framework for studying the neural correlates of ‘consciousness and other
brain functions’ (2008, p. 239). On this account, consciousness is not all-or-noth-
ing, but increases and decreases along with the integration of information in the
brain. This means that there can be gradual ‘shrinking or dimming of the field of
consciousness’, though at a critical concentration of anaesthetic ‘the integrated
repertoire of neural states underlying consciousness may collapse nonlinearly’
(2008, p. 880).


But not all anaesthetics work in this way. For example, ketamine is a dissociative
anaesthetic that is also used as a recreational drug, since at low doses it induces
changes in body image, distortions of self, and feelings of dissociation from the
surroundings. Ketamine produces an increase rather than suppression in cere-
bral metabolism, and acts as an antagonist of the N-methyl-D-aspartate (NMDA)
receptor, blocking the normal excitatory effect of the neurotransmitter glutamate.
Other anaesthetics act on other parts of this complex, including nitrous oxide or
laughing gas, which is a much smaller molecule but has somewhat similar effects
to ketamine. This has led to the suggestion that the normal functioning of the
NMDA synapse is necessary for consciousness (Flohr, 2000), which means locat-
ing the NCC at a molecular level rather than a higher functional level. However, it
may be that despite working in a different way these anaesthetics still affect the
thalamus, for example by scrambling rather than blocking signals at the level of
thalamocortical interactions (Alkire and Miller, 2005).


Although in principle we should be able to understand consciousness by study-
ing its absence, neither the science nor the logic is straightforward. The use of


‘anaesthetics seem to
cause unconsciousness
when they block
the brain’s ability to
integrate information’

(Alkire, Hudetz, and Tononi,
2008, p. 876)

‘Consciousness is not a
unitary phenomenon
but a catch-all term that
includes wakefulness
and awareness’

(Shushruth, 2013, p. 1758)
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