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| Format: | Recurso digital |
| Language: | English |
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Zenodo
2026
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| Online Access: | https://doi.org/10.5281/zenodo.19410235 |
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Table of Contents:
- <p>During a migraine aura, patients experience a scintillating scotoma: sparkling, brilliant<br>white light with vivid spectral colours that expands across the visual field. This luminous<br>experience is often described as beautiful and awe-inspiring. Yet two independent lines of<br>neurophysiological evidence reveal that this light coincides not with increased neural<br>activity, but with its profound suppression. Magnetoencephalography (MEG) shows that<br>alpha-band power collapses to zero for the duration of the scintillations, while gammaband<br>power likewise decreases. Simultaneously, visually evoked potentials (VEPs) -- the<br>cortex's measurable electrical response to external light -- are suppressed or completely<br>abolished, as demonstrated by MacLean et al. (1975) and confirmed by Nyrke et al. (1990).<br>The cortex does not respond to light from the outside world, yet the patient perceives<br>brilliant inner light.<br>Key findings include:<br>• MEG Evidence: During scintillating scotoma, alpha-band power drops to zero and<br>gamma-band power decreases, ruling out compensatory excitation. The brain is<br>demonstrably silent.<br>• VEP Evidence: Flash-VEPs show that the early components (P1, N1, P2) are suppressed<br>or completely abolished in the hemisphere contralateral to the visual disturbance. The<br>cortex is functionally offline for visual processing.<br>• Disinhibition Fails: The disinhibition hypothesis is refuted by decreased VEPs and<br>gamma power. The phenomenological quality of the aura (prolonged, structured,<br>beautiful) does not match chaotic cortical firing.<br>• Temporal Match: Scintillations correlate precisely with the prolonged depression<br>phase (5-30 minutes) of cortical spreading depolarisation, not the brief depolarisation<br>burst (seconds), indicating sustained cortical silence.<br>• Terminal Spreading Depolarisation (TSD): The irreversible wave of cortical silencing<br>at death (TSD) is the intense, permanent version of the reversible cortical spreading<br>depression (CSD) seen in migraine. If the mild scintillating light of migraine corresponds<br>to reversible cortical depression, the profound light of near-death experiences plausibly<br>corresponds to the permanent cortical depression of TSD. The natural extrapolation<br>along this continuum is that more cortical silence corresponds to more luminous<br>experience, not less. The burden of proof falls on the production model to explain why<br>this empirically established inverse correlation would suddenly reverse at the severe<br>end.<br>• Clinical Confirmation: Ischemic scintillations in patients with carotid stenosis, where<br>brilliant light arises directly from cortical ischemia, further support this pattern.<br>• Double Dissociation: Retinal ischemia (eye fails, cortex intact) leads to darkness, while<br>cortical ischemia (cortex fails, eye intact) leads to brilliant light. The production model<br>predicts darkness in both cases. Only the filter theory correctly predicts both outcomes.<br>If this brilliant light correlates with the absence of neural activity rather than its presence, it<br>has no neural correlate. It is not produced by the brain. It is revealed by the brain's silence.<br>Ultimately, a profound contrast emerges: physical, external light that is blocked (as in<br>retinal ischemia) results in darkness, whereas inner, non-physical light increases when<br>cortical depression sets in. These two phenomena appear to be mutually exclusive: the<br>perception of physical light precludes the experience of non-physical light, and the<br>emergence of non-physical light requires the exclusion of physical light.<br>Keywords<br>filter theory; consciousness; scintillating scotoma; migraine aura; MEG; alpha<br>desynchronization; visually evoked potentials; double dissociation; cortical ischemia;<br>spreading depolarization; terminal spreading depolarization; near-death experience<br>Resource Type<br>Preprint<br>License<br>Creative Commons Attribution 4.0 International (CC BY 4.0</p>