Guys do you believe Howard Storm's NDE?

[Angrboda]

Misplaced confidence in EEG measurements

Within Near Death Experience research, a number of investigators have argued that a flat electroencephalogram (EEG) reading can be taken as evidence of total brain inactivity (and van Lommel et al. recruit this argument into their interpretation; Fenwick & Fenwick, 1995; Parnia & Fenwick, 2001; Parnia et al., 2001; Sabom, 1998). This claim is totally incorrect. It is certainly the case that a flat cortical EEG would be indicative of a brain that is in some trouble. Assuming no technical error or problems with electrode contact, a flat EEG is far from desirable. However, the assumption that a flat EEG can be taken as strong evidence of global and total brain inactivity is unfounded. (It is also noteworthy that the studies making large claims about flat EEGs provide no information regarding the level of gain employed on the EEG device, assuming they were digital-QEEG devices. This would seem important as any EEG can become almost flat with the gain turned to a minimum. A flat EEG at maximum gain would be more indicative of neocortical inactivity, though again, not full-brain inactivity).

Unless surgically implanted into the brain directly, the EEG principally measures surface cortical activity. The waveforms seen in cortical EEG are largely regarded to come from the synchronistic firing of cortical pyramidal neurons. As such, it is entirely conceivable that deep sub-cortical brain structures could be firing, and even in seizure, in the absence of any cortical signs of this activity (for evidence based on electrical stimulation and seizure propagation, see Gloor, 1986; Gloor, Olivier, Quesney, Andermann, & Horowitz, 1982). Indeed, evidence reviewed by Gloor (1986) argued that inter-ictal discharges in the hippocampus or amygdala alone were more than sufficient to produce complex meaningful hallucinations – no involvement from the cortex was necessary!

A related idea is that seizure-based hallucinatory EEG patterns have been absent from the background EEG in some instances of NDE, even when the EEG itself was not flat (Fenwick & Fenwick, 1995). By this account, if the NDE was a hallucinatory process based in disinhibition, then the logic is that such disinhibition should be clearly visible in the EEG at that time.

However, the emerging evidence is somewhat unhelpful for the survivalist. Tao, Ray, Hawes-Ebersole, and Ebersole (2005) compared EEG activity from surgically implanted electrodes placed in or around deep sub-cortical regions of epileptic patients with cortical EEG electrodes placed on the scalp of the same patients. The results were quite surprising. Tao et al. showed that for 90% of cases, large amplitude paroxysmal firing needed to recruit 10 cm2 of brain tissue in order to show up against background cortical EEG traces. In other words, large seizure-based activity was being recorded by the surgically implanted electrodes (indexing clear and widespread brain-seizure activity) which was completely absent from scalp-based EEG traces until it propagated through and excited 10 cm2 of brain volume. This is a considerable amount of brain tissue.

Furthermore, a recent study that employed both EEG and brain-imaging (fMRI) techniques to explore seizure processes found significant increases in localised cortical neural activity (indicative of a seizure) in the fMRI BOLD (blood-oxygen-level dependant) response, which was completely absent from the EEG data (Kobayashi, Hawco, Grova, Dubeau, & Gotman, 2006). This is particularly striking in that this occurred despite the fact that the intense seizure activity occurred in a region where EEG electrodes were closely spaced. Kobayashi et al. note that this is striking as the EEG completely missed the most intensely discharging region despite the fact that this region was also located at the cortical level.

... differing brain regions have differing numbers of neurons, with diverse connections and characteristics – all of which have differing oxygen demands

The implication for NDE research is, of course, that the EEG does not provide a highly reliable measure of complete neural activity. Even high-amplitude seizure activity can fail to manifest itself in the background EEG if it does not recruit enough neural landscape. To summarise: confidence in previous claims that flat EEG represents total neural inactivity appears severely misplaced. These cases may represent instances of ‘false positives’ (positive from the perspective of the survivalist wanting to recruit such instances as evidence of a dead brain). In addition, even in the presence of a background EEG, seizure-based activity (which is sufficient to support hallucinatory imagery and aura) could be considerable and yet may not become manifest in the cortical scalp-based EEG. Note also that the above empirical estimates were based on epileptic brains which produce large-amplitude brain activity. These estimates themselves may need to be increased even further for the normal non-epileptic brain which does not typically produce such high-amplitude synchronistic characteristics.

http://www.critical-thinking.org.uk/para...-brain.php

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What the dying brain hypothesis really says: The importance of neural disinhibition

When one considers the dying-brain account in its full context it is clear to see that the emphasis placed on cerebral anoxia misses the true essence of the account. As a consequence, many of the criticisms against the dying-brain hypothesis border on the irrelevant. For the dying-brain account, the central assumption does not revolve around the presence or absence of anoxia per se, but of neural disinhibition. So the dying-brain hypothesis is perhaps more accurately characterised as one that models NDEs as an experiential consequence of a disinhibited brain (Blackmore, 1996, 1993, 1992, 1990; Braithwaite, 1998; Carr, 1982, 1981; Jansen, 1996, 1990; Saavedra-Aguilar & Gomez-Jeria, 1989; Woerlee, 2003). Of course, such neural disinhibition can be induced by anoxia, and it is likely that under more prolonged near-death situations it is likely to be present; but as a process, disinhibition can actually be triggered by many psychological and neurological factors such as: confusion, trauma, sensory deprivation, illness, pathology, epilepsy, migraine, drug use and brain stimulation (for comprehensive reviews see: Appleby, 1989; Baldwin, 1970; Blackmore, 1993; Sacks, 1995; Siegal, 1980). Without exception, all these instances that induce neural disinhibition and seizure-type activity can all be associated with aura and hallucination.

In principle then, anoxia does not need to be present at all to produce hallucinatory imagery. However, under cases where people are ‘near death’ or suffer cardiac insufficiency for any prolonged period of time, it is likely (i.e. reasonable to assume) a degree of anoxia would be present. Therefore, while anoxia is one route via which disinhibition can occur, it is by no means the only route. In addition, the dying-brain hypothesis predicts that more vivid, profound, and meaningful NDEs are likely to be associated with greater degrees of disinhibition. Thus, NDEs reported when people truly are nearer to death (and hence the level of disinhibition would conceivably be greater), should be more vivid, profound, detailed and meaningful, relative to those reported when people only believed themselves to be so. This is exactly what has been found (Drab, 1981; Gabbard & Twemlow, 1984; Gabbard, Twemlow, & Jones, 1981; Owens, Cook, & Stevenson, 1990).

http://www.critical-thinking.org.uk/para...-brain.php