The gamma-band activity model of the near-death experience: a critique and a reinterpretation. [version 1; peer review: 1 approved, 2 approved with reservations]

Near-death experiences (NDEs) are profound mental events occurring near biological death, often interpreted as hallucinations by materialist theories. Recent animal and clinical studies report a paradoxical surge of high-frequency gamma-band activity (GBA) in the electroencephalogram around the time of death, when cortical activity is otherwise low. This perimortem GBA burst has been proposed as the neural basis of NDE. The study examines three issues: whether standard GBA is contaminated by muscle artifacts; whether NDE-mimicking agents also involve GBA; and the origin of the perimortem GBA surge, which may arise subcortically in the amygdala and be recorded at the cortex via volume conduction. Although intriguing, there is little evidence this GBA surge could serve as a neurobiological foundation for NDE.

Study at a glance

Abstract

Near-death experience (NDE) is a transcendent mental event of uncertain etiology that arises on the cusp of biological death. Since the discovery of NDE in the mid-1970s, multiple neuroscientific theories have been developed in an attempt to account for it in strictly materialistic or reductionistic terms. Therefore, in this conception, NDE is at most an extraordinary hallucination without any otherworldly, spiritual, or supernatural denotations. During the last decade or so, a number of animal and clinical studies have emerged which reported that about the time of death, there may be a surge of high frequency electroencephalogram (EEG) at a time when cortical electrical activity is otherwise at a very low ebb. This oscillatory rhythm falls within the range of the enigmatic brain wave-labelled gamma-band activity (GBA). Therefore, it has been proposed that this brief, paradoxical, and perimortem burst of the GBA may represent the neural foundation of the NDE. This study examines three separate but related questions concerning this phenomenon. The first problem pertains to the electrogenesis of standard GBA and the extent to which authentic cerebral activity has been contaminated by myogenic artifacts. The second problem involves the question of whether agents that can mimic NDE are also underlain by GBA. The third question concerns the electrogenesis of the surge in GBA itself. It has been contended that this is neither cortical nor myogenic in origin. Rather, it arises in a subcortical (amygdaloid) location but is recorded at the cortex via volume conduction, thereby mimicking standard GBA. Although this surge of GBA contains genuine electrophysiological activity and is an intriguing and provocative finding, there is little evidence to suggest that it could act as a kind of neurobiological skeleton for a phenomenon such as NDE.