|We Die to Remember: Exodus of Tubulins||Memory|
Life review is a near-death experience, in which a person rapidly sees much of his or her life history within a few seconds. It occurs mostly during cardiac arrest or drowning (Noyes and Kletti, 1977; Stevenson and Cook, 1995; van Lommel et al., 2001; van Lommel, 2011; 2006 PDF file). This chapter will discuss the underlying mechanism.
The End-of-Life EEG Surge
In 2009, Chawla and colleagues discovered the end-of-life surges in electroencephalography (EEG) activity from the studies on patients who were neurologically intact but critically ill, requiring life support. The EEG activity was converted to the bispectral index (BIS) which can vary between 0 and 100. Higher scores correlate to higher levels of consciousness. Smaller values indicate reduced brain activity. A value between 40 and 60 is an appropriate level for general anesthesia. After the life support was withdrawn, the BIS score gradually decreased. Surprisingly, a brief surge emerged before death (Figure 13-1).
The EEG surge can be ascribed to the failure of the enzyme Na+/K+-ATPase (also known as the Na+/K+ pump). This enzyme is essential for the maintenance of the resting membrane potential (about -70 mV). If the enzyme fails, the membrane potential will increase (depolarize). As soon as the membrane potential reaches the threshold (about -55 mV), the nerve impulse will be generated. The function of the Na+/K+ pump requires adenosine triphosphate (ATP), which is produced from oxygen. The major role of blood circulation is to deliver oxygen to various types of cells for the production of ATP. When the heart stops beating, the oxygen supply will be cut off and the enzyme will fail. This may lead to membrane depolarization, thereby resulting in neuronal firing.
It has been speculated that the EEG surge could be the origin of near-death experiences such as life review and out-of-body experiences (Chawla et al., 2009). However, the life review requires neuronal firing that involves activation of a specific set of synapses at a given moment, but the Na+/K+ pump does not target any particular synapse. The synapse-specificity can be explained by the exodus of tubulins from the postsynaptic density (PSD) when ATP is exhausted.
Synaptic Reactivation by the Exodus of Tubulins
The underlying mechanism for the life review could be essentially the same as the synaptic reactivation that leads to spontaneous thoughts (see Chapter 8). Both may result from the exit of tubulins from PSD, owing to the inactivation of CaMKII. Their major difference lies in the cause of CaMKII inactivation. In a healthy brain, CaMKII is inactivated by its inhibitor, CaMKIIN. At near-death, CaMKII could be inactivated by the lack of ATP because its activation is known to require ATP (Pradeep et al., 2009; Yilmaz et al., 2013). The CaMKIIN could be tightly regulated so that the mind may wander slowly from one thought to another. By contrast, the depletion of ATP at near-death may cause large-scale exodus of tubulins from PSD, resulting in fast replay of life history.
The EEG surge lasts only 30 -180 seconds. However, the conscious near-death experiences may persist for several hours while the brain activity is completely silent, suggesting that consciousness can continue even without the brain (van Lommel et al., 2001; van Lommel, 2011; 2006 PDF file). As discussed in Chapter 11, consciousness arises from the activation of the resting state networks, which may produce a geon that can exist on its own for a finite period of time. The next chapter will present evidence that the EEG surge may include the activation of the resting state networks.
Author: Frank Lee