The Wedding at Cana (John 2:1-11)

Collage by Alexey Kondakov

In 1983, David Copperfield made the Statue of Liberty disappear and reappear on live TV. The illusion was impressive, perhaps astounding, and I think most of us who saw it gazed on in amazement.

In contrast, consider the spectacle of Jesus turning water into wine at the wedding of Cana. At the wedding, Jesus’ mother told him, “They have no wine.” Jesus replied, “Oh Woman, what has this to do with me? My hour has not yet come.” His mother then said to the servants, “Do whatever he tells you” (John 2:3-5). Jesus ordered the servants to fill containers with water and to draw out some and take it to the chief steward (waiter). After tasting it, without knowing where it came from, the steward remarked to the bridegroom that he had departed from the custom of serving the best wine first by serving it last (John 2:6-10). John adds that: “Jesus did this, the first of his signs, in Cana of Galilee, and it revealed his glory; and his disciples believed in him” (John 2:11).

What makes the Marriage at Cana a miraculous event and not a magical act, like a Copperfield illusion?

One difference must be that some people who witnessed the water change into wine immediately saw it as the expresssion of the Holy Spirit embodied in Jesus. Without noticing this aspect, the event would be astonishing, perhaps strange, but not a religious miracle. Like Copperfield’s Statue of Liberty illusion, people would respond out of incredulity or astonishment, but no more.

The significance of the person who commits the act is the meaning of the event as a relgious miracle, not the event itself islolated from this context, and is what witnesses are supposed to see, from a religious perspective. Without this understanding, the Wedding at Cana is simply an impressive illusion.

Eben Alexander: ‘Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife’ (2012) – is consciousness cortical?

Proof of Heaven: A Neurosurgeon’s Journey into the Afterlife‘ (2012), by neurosurgeon Eben Alexander, presents a narration and interpretation of the near-death 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 near-death 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 coma-induced 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; Charland-Verville 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 ‘event-related desynchronization’. There is a vast and well-established 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 subcortical-cortical 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 non-mammalian 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 subcortical-cortical 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 near-death 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.

Charland-Verville, V., Habbal, D., Laureys, S., & Gosseries, O. (2012). Coma and related disorders. Swiss archives of neurology and psychiatry, 163(8): 265-72.

Churchland, P. M. (2007). Neurophilosophy at work. Cambridge, UK: Cambridge University Press.

Churchland, P. S. (1989). Neurophilosophy: Toward a unified science of the mind-brain. Cambridge, Mass.: The MIT Press.

Churchland, P. S. (2002). Brain-wise: 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: 1809-1821.

Laureys, S., Owen, A. M., & Schiff, N. D. (2004a). Brain function in coma, vegetative state, and related disorders. The Lancet Neurology, 3(9), 537-546.

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), 916-918.

Llinas, R. R. (2001). I of the Vortex: From Neurons to Self. Cambridge, Mass.: MIT Press.

Pfurtscheller, G., & Aranibar, A. (1979). Evaluation of event-related desynchronization (ERD) preceding and following voluntary self-paced movement. Electroencephalography and clinical neurophysiology, 46(2), 138-146.

Pfurtscheller, G. (1992). Event-related synchronization (ERS): an electrophysiological correlate of cortical areas at rest. Electroencephalography and clinical neurophysiology, 83(1), 62-69.

Pfurtscheller, G., & Lopes da Silva, F. H. (1999). Event-related EEG/MEG synchronization and desynchronization: basic principles. Clinical neurophysiology, 110(11), 1842-1857.

van Rysewyk, S. (2013). Pain is Mechanism. Unpublished PhD Thesis. University of Tasmania.