A machine generated summary based on the work of Skorobogatykh, Kirill; van Hoogstraten, Willem Sebastiaan; Degan, Diana; Prischepa, Anastasia; Savitskaya, Anastasya; Ileen, Biondo Michela; Bentivegna, Enrico; Skiba, Iaroslav; D’Acunto, Laura; Ferri, Livia; Sacco, Simona; Hansen, Jakob Møller; Amin, Faisal Mohammad; 2019 in The Journal of Headache and Pain.

3.4 Neuroimaging

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Neuroimaging clues of migraine aura

DOI: https://doi.org/10.1186/s10194- 019- 0983- 2

Abstract-Summary There are however interictal imaging studies that can shed light on the pathophysi- ology of the migraine with aura (MWA) cascade.

Whether asymptomatic CSD also happens in some migraine without aura is still

under debate.

New evidence points to glial activation in MWA, indicating the involvement of astrocytes in the neuroinflammatory cascade that follows CSD, as well as dural macrophages, supporting the involvement of the trigeminovascular system in migraine pain.

Background Symptomatic aura is obviously not obligatory prior to the migraine pain, otherwise neither MWoA nor MWA patients having aura symptoms starting after the headache phase would be possible.

There is evidence to suggest that cortical dysfunction, possibly involving CSD-

like phenomena, is also present in migraine without aura [349–353].

Woods and others [351] reported in 1994 spreading cerebral hypoperfusion in a patient suffering from migraine without aura, providing the first evidence that CSD may also underlie MWoA—although one should mention that the patient in the report by Woods actually experienced transient visual symptoms (hazy vision).

Admitting that CSD is the substrate of aura and possibly occurs in migraine with atypical, subtle, or no aura symptom, the possibility exists that some MWoA patients have the headache associated—or even induced - by relatively silent CSD.

Conclusion Neuroimaging data indicate that: (1) migraine aura is related to a CSD-like phe- noma in MWA patients; (2) spreading phenomena similar to CSD may occur in MWoA, suggesting that either CSD can be asymptomatic, that symptomatic aura depends on other factors than just CSD, or that CSD in MWA differs fundamentally from the spreading oligoemia found in MWoA; (3) visual aura most probably starts at visual cortical areas such as V3A and MT; (4) glial activation is present following migraine attacks at areas previously shown to be involved with aura generation and/ or pain processing, increasing in accordance to the headache frequency; (5) activa- tion of meningeal macrophages in MWA further support the activation of the tri- geminovascular system by CSD.

It remains to be explained how the aura phenotype varies vastly even when the same cortical areas are involved; to which extent CSD happens in MWoA and what makes it phenotypically apparent, and how a CSD-like phenomenon as demon- strated by neuroimaging couples mechanistically with the other phases of the migraine attack.

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3 Diagnosis

Acknowledgement A machine generated summary based on the work of Hadjikhani, Nouchine; Vincent, Maurice. 2019 in The Journal of Headache and Pain.

Understanding migraine as a cycling brain syndrome: reviewing the evidence from functional imaging