The crescent shaped aura pattern, as shown in , is often reported 
but the phenomenology of migraine aura is much richer as documented by the variety of illustrations and descriptions collected on the Migraine Aura Foundation website (www.migraine-aura.org
). In a single migraine aura attack, migraineurs can also experience diverse visual, as well as sensory, motor and language disturbances 
. This variety clearly indicates that other areas beside early visual cortex can be affected, even cortical areas outside the occipital lobes, and it therefore seemingly supports the idea that the process causing the aura can engulf all of posterior cortex on its course, like a cortical SD wave observed in animal experiments.
Schematic drawings similar to illustrate engulfing spatio-temporal wave patterns. Such illustrations are found in modern textbooks of headache 
and appeared first in Lauritzen's seminal paper spearheading the SD theory of migraine aura 
. They became paradigmatic for migraine with aura. However, they might need to be revised, as we show. First it must be noted that the hypothesis of such a spatio-temporal development of a migraine attack was likely motivated by the SD pattern on the cortex of animals with cortices much smaller than the human cortex . If the SD wave occupies similar areas in different species, then the SD wave that covers most of the hemisphere in small animals would occupy only a small part of the human V1 area. This probably is the case, because the propagation velocity of SD is similar in all cortices. As a consequence, the SD pattern cannot simply be scaled with the cortex size.
The activity pattern causing crescent shaped aura is remarkably similar to a particle-like wave segment on the cortical surface, a pattern that exists only in cortex being weakly susceptible to SD. For example, the open end of the wave segment shown in slightly grow within the observed 10 minutes interval without curling in to form a reentrant pattern. This indicates a susceptibility value very close to one. In contrast, reentrant SD pattern observed in retina rotate with a period of 2.5 minutes 
which would correspond to the passage of four waves within 10 minutes.
Other factors also support the concept that human cortex is only weakly susceptible to SD, maybe foremost that susceptibility becomes the lower the higher up the species is in the phylogenetic tree. Another clear indication is that SD propagation is modulated by cortical morphology, as can be seen in . Similar pattern were also observed for the gyrencephalic feline brain 
, but there the primary SD wave engulfed the hemisphere and only succeeding secondary waves remained within the originating gyrus and were more fragmented. Since secondary waves run into partly refractory tissue, susceptibility to SD is decreased.
The engulfing wave pattern was originally attributed to the smooth architecture of the cortex of rats and rabbits. It has been debated whether SD can occur in the highly convoluted cortex of humans, until spatial and temporal events were followed using high-field functional MRI 
demonstrating that at least eight characteristics of SD are present and the events are time-locked to percept onset of the aura in human cortex. However, the precise spatio-temporal course of the events is still ambiguous. Much of posterior cortex, including several retinotopically organized visual areas, showed simultaneous activation during much of the period of the aura, while the percept in the visual hemifields is reported to be more spatially confined.
As already noted by Wilkinson 
this mismatch in fMRI data and aura percept can be explained by at least two alternatives: (i) either SD engulfs all of posterior cortex. Then only a subset of this activation results in sensory awareness. Or (ii), the spread of the SD wave is, in contrast to the fMRI data, more limited in extent. Then the rest of the observed activation in adjacent cortical areas represents synaptic activation through feed-forward and feedback circuitry. While (i) is in agreement with observed cortical SD wave patterns in animals, it opens up questions about the nature of the often reported limitation to spatially confined crescent-shaped visual field defects. In (ii) spatially confined SD waves causing corresponding field defects are simply postulated 
If SD in human is more limited in extent, the mismatch with animal data needs to be addressed. To reconcile this, we provide a theoretical framework, which is, moreover, of practical use to both experimental neuroscientists and clinicians. We propose a susceptibility scale σ based on nonlinear bifurcation analysis. Not unlike the Celsius temperature scale, the term susceptibility to SD
is made a precise scale by a two-point definition, i. e., two macroscopically observable cortical states at which a phase transition in SD pattern formation occurs. Before we describe the relevance and applicability of this scale in the following, we end this paragraph briefly discussing other possible definitions of tissue excitability. Using detection or discrimination measures or stimuli reported to trigger migraine (striped patterns or flickering lights) one finds differences between people with and without migraine, which is attributed to abnormal cortical processing in migraine, described by hyper- or hypoexcitability, heightened responsiveness, a lack of habituation and/or a lack of intra-cortical inhibition 
. Such statements on cortical excitability in migraine are based on psychophysical measurements of visual function, in particular early aspects of visual processing. It remains to be investigated how abnormal cortical processing changes susceptibility to SD. Although it seems tempting to suggest that cortical hyperexcitability increases susceptibility to SD or even that neurons prone to hyperexcitabilty trigger SD, such a simple relation cannot be expected.
The weakly susceptible state (1>σ>0) of human cortex to SD can be achieved in experimental migraine models if the tissue is treated reducing excitability towards the gray marked regime in . The procedure to find this regime experimentally is described in the Methods
section for retinal SD. Retinal SD is accompanied with an intrinsic optical signal that makes precise spatio-temporal recordings of the evolutionary SD pattern possible. Similar precise spatio-temporal recordings have been made in cortex using a fluorescent, voltage-sensitive dye 
We predict that effects of antimigraine drugs depend on the susceptibility range they are tested in, because the dynamical behavior of a nonlinear system changes drastically when crossing a bifurcation point. Antimigraine drugs tests and tests to unravel the mechanism of SD in retina 
have been performed far away from the regime (1>σ>0). This can be shown by precisely measuring in this system the complex meandering pattern of spiral SD 
. On the σ scale, obtained from the generic FitzHugh-Nagumo model, these pattern occur above σ>2 and are separated by two further bifurcations 
. In general, SD experiments are performed in the most prone tissue regions where SD can more easily be observed. This might remind of Watzlawick's man searching for his keys under the streetlight rather than where he lost them 
Furthermore, our results supports the idea that SD could activate the trigeminovascular system that generates and maintains migraine pain 
even in diagnosed forms of migraine without aura
. For susceptibility values below the weakly susceptible regime, the model predicts spatio-temporal SD pattern that do not break away from an initially restricted focus. We can draw a direct analogy to clinically silent epilepsy caused by interictal activity that does not break away from a focus. Likewise, previously proposed silent aura, in which “some migraineurs exhibit blood flow ‘fingerprints’ of CSD [cortical SD] and aura but are subjectively unaware that the phenomenon is propagating” 
, may be explained by localized SD patterns occurring at the one end of the increased dynamical repertoire that emerges if being close to a bifurcation.