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‘Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife‘ (2012), by neurosurgeon Eben Alexander,
presents a narration and interpretation of the neardeath experience (NDE) of its author. Alexander developed
bacterial meningitis, and was hospitalized. During hospitalization, he became deeply comatose, a condition
which lasted seven days. Alexander was fortunate to come out of his coma state and retain full wakeful
consciousness. Following wakefulness, Alexander reported remarkably clear visions, sensations and thoughts he
claims to have had during his neardeath coma. In his book, Alexander interprets this NDE as proof that life
follows death, death is not the end, there exists an extremely pleasant and serene afterlife, and that
consciousness is independent of the cortical brain. It is the last claim of Alexander’s that I will consider in this
post. Specifically, is consciousness independent of cortex?
According to Alexander, his comainduced NDE occured when his cerebral cortex was ‘completely shut down’,
‘inactivated’, and ‘totally offline’. In the article he wrote for Newsweek, Alexander writes that the absence of
cortical activity in his brain was ‘clear from the severity and duration of my meningitis, and from the global
cortical involvement documented by CT scans and neurological examinations.’ The problem with Alexander’s
view of coma is that it is not supported by evidence. First, ‘global’ (complete) cortical ‘shut down’ does not
result in coma, as Alexander believes. Complete cortical ‘shut down’ is fatal, and results in brain death (e.g.,
Cavanna et al. 2010; CharlandVerville et al. 2012; Laureys et al. 2004a; Laureys et al. 2004b). Second, ‘flat’
EEG recordings concurrent with high alpha cortical brain activity are frequently observed in comatose patients;
this event is termed ‘eventrelated desynchronization’. There is a vast and wellestablished scientific literature
on this topic (e.g., Pfurtscheller & Aranibar, 1979; Pfurtscheller, 1992; Pfurtscheller et al. 1999). Thus, coma
does not require complete cortical deactivation.
Alexdander’s claim that NDEs require complete cortical shut down carries the implication that fully (wakeful)
sensory consciousness must involve only cortex. Alexander’s argument is in line with a trend in consciousness
studies research to investigate cortical regions, pathways, and activity guided by the slogan ‘seeking the neural
correlates of consciousness.’ Clinical studies of cortical lesions have motivated this approach, largely due to
robust correlations such as fusiform lesions leading to prosopagnosia, or ventral stream lesions leading to the
visual inability to percieve shapes. The convenience of neuroimaging cortical activity with MEG, EEG, PET
and fMRI has likely also played a part in the focus on cortex.
However, viewing (wakeful) sensory consciousness as purely cortical neglects essential subcorticalcortical
behavioural aspects (e.g., Churchland, 2002; Damasio, 1999; Guillery & Sherman, 2002; Llinas, 2001; van
Rysewyk, 2013). Put very simply (and briefly), a basic function of mammalian and nonmammalian nervous
systems is to enable and regulate movements necessary to evolutionary goals such as feeding and reproducing.
Peripheral axons that carry sensory information have collateral branches that project both to subcortical motor
structures (primarily, thalamus) and cortical motor structures (primary motor cortex, M1). According to
Guillery and Sherman (2002), all peripheral sensory input communicates information about ongoing
instructions to such subcorticalcortical motor stuctures, which implies that a sensory signal can become a
prediction about what movement will happen next. Thus, as an organism learns the effects of a specific
movement, it learns about what in the world will likely occur next (planning), and thus what it might do
following that event (deciding, acting). Temporality emerges as central to the nature of consciousness. In order
to keep the body alive, nervous systems face numerous complex challenges in learning, continuous effective
prediction, attention to different sensorimotor events, and calling up stored (timing) information.
Neuroanatomical loops between thalamocortico structures are a plausible physical substrate involved in
(identical to?) the temporal and causal aspects of the world, and of one’s own body (e.g., Damasio, 1999;
Guillery & Sherman, 2002; Llinas, 2001). This leads to the empirical prediction that in a neardeath event,
normal functioning of thalamocortico loops is compromised.
References
Cavanna, A. E., Cavanna, S. L., Servo, S., & Monaco, F. (2010). The neural correlates of impaired
consciousness in coma and unresponsive states. Discovery medicine, 9(48), 431.
CharlandVerville, V., Habbal, D., Laureys, S., & Gosseries, O. (2012). Coma and related disorders. Swiss
archives of neurology and psychiatry, 163(8): 26572.
Churchland, P. S. (1989). Neurophilosophy: Toward a unified science of the mindbrain. Cambridge, Mass.:
The MIT Press.
Churchland, P. S. (2002). Brainwise: Studies in neurophilosophy. Cambridge, Mass.: The MIT Press.
Churchland, P. S. (2011). Braintrust: What neuroscience tells us about morality. Princeton: Princeton
University Press.
Damasio, A. R. (1999). The Feeling of What Happens. New York: Harcourt Brace.
Guillery, R. W., & Sherman, S. M. (2002). The thalamus as a monitor of motor outputs. Philos. Trans. R Soc.
Lond. B Biol. Sci., 357: 18091821.
Laureys, S., Owen, A. M., & Schiff, N. D. (2004a). Brain function in coma, vegetative state, and related
disorders. The Lancet Neurology, 3(9), 537546.
Laureys, S., Perrin, F., Faymonville, M. E., Schnakers, C., Boly, M., Bartsch, V., Majerus, S., Moonen, G., &
Maquet, P. (2004b). Cerebral processing in the minimally conscious state. Neurology, 63(5), 916918.
Llinas, R. R. (2001). I of the Vortex: From Neurons to Self. Cambridge, Mass.: MIT Press.
Pfurtscheller, G., & Aranibar, A. (1979). Evaluation of eventrelated desynchronization (ERD) preceding and
following voluntary selfpaced movement. Electroencephalography and clinical neurophysiology, 46(2), 138
146.
Pfurtscheller, G., & Lopes da Silva, F. H. (1999). Eventrelated EEG/MEG synchronization and
desynchronization: basic principles. Clinical neurophysiology, 110(11), 18421857.
van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.
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