scintillating scotoma: when the visual cortex fails, brilliant inner white light appears

During a migraine aura, patients experience sparkling, brilliant white light with vivid spectral colours — often described as shimmering, kaleidoscopic, and intrinsically beautiful. The conventional production model claims that Cortical Spreading Depression (CSD) generates this light through spontaneous excitation in the visual cortex. However, this explanation suffers from a profound internal inconsistency. Extensive clinical evidence demonstrates that CSD consistently produces functional deficits wherever it travels: hemiparesis in the motor cortex, paresthesia in the somatosensory cortex, and aphasia in language areas. It is illogical to posit that CSD produces functional loss everywhere except in the visual cortex, where it supposedly produces a gain of function — brilliant light. The logically consistent interpretation is that CSD causes functional failure in the visual cortex as well, and that this sparkling, brilliant inner light appears as a result of cortical silence. Before presenting the evidence, a crucial methodological distinction must be made. The landmark fMRI study by Hadjikhani et al. (2001) beautifully localized the spatial propagation of CSD across the visual cortex, but it measured an indirect hemodynamic proxy (the BOLD signal) – a vascular response, not direct neural activity. By contrast, the MEG study by Hall et al. (2004) directly measured the magnetic fields generated by neural currents. That direct measurement revealed that the visual cortex is not hyperactive but profoundly silent for the full duration of the scintillations. Three independent and converging lines of neurophysiological evidence confirm this interpretation. First, MEG data show that alpha- and gamma-band rhythms collapse for the duration of the scintillations and return abruptly the moment they cease (Hall et al., 2004). Second, VEP studies show that the cortex no longer responds to external light during the aura (MacLean et al., 1975; Nyrke et al., 1989). Third, novel SEEG evidence (McLeod et al., 2025) offers the most direct confirmation to date: intracranial recording reveals a low-voltage suppression — a near-silent cortical signal — that correlates precisely with the scintillating scotoma. *The temporal alignment is definitive: the scintillations last as long as the depression phase of CSD (minutes), not the brief depolarisation wavefront (seconds). The strongest refutation of the wavefront hypothesis comes from clinical cases of chronic cortical ischemia. Klingebiel et al. (2008) documented a patient with high-grade carotid stenosis who experienced three weeks of continuous scintillations – without any propagating CSD wavefront, only sustained cortical depression. The scintillations ceased abruptly when blood flow was restored by endarterectomy. This proves that cortical silence alone is sufficient for brilliant light; a wavefront is not necessary.* The paper extends this reasoning along the CSD–TSD continuum, where Terminal Spreading Depolarization represents the permanent, irreversible form of CSD that occurs at death. A clarifying double dissociation is presented: retinal ischaemia (failure of the eye) leads to darkness, whereas cortical ischaemia (failure of the brain) leads to brilliant light. The production model predicts darkness in both cases – and is therefore falsified by the cortical ischaemia cases. Only the filter theory correctly predicts both outcomes. This pattern is consistent with the filter theory of consciousness (Bergson, 1896; Huxley, 1954; Kastrup, 2019), which holds that when the brain's filtering function fails, a broader, intrinsic dimension of experience is revealed — not produced, but uncovered.