dc.contributor.author
Lemale, Coline L.
dc.contributor.author
Lückl, Janos
dc.contributor.author
Horst, Viktor
dc.contributor.author
Reiffurth, Clemens
dc.contributor.author
Major, Sebastian
dc.contributor.author
Hecht, Nils
dc.contributor.author
Woitzik, Johannes
dc.contributor.author
Dreier, Jens P.
dc.date.accessioned
2022-08-30T08:52:53Z
dc.date.available
2022-08-30T08:52:53Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/36066
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-35782
dc.description.abstract
Neuronal cytotoxic edema is the morphological correlate of the near-complete neuronal battery breakdown called spreading depolarization, or conversely, spreading depolarization is the electrophysiological correlate of the initial, still reversible phase of neuronal cytotoxic edema. Cytotoxic edema and spreading depolarization are thus different modalities of the same process, which represents a metastable universal reference state in the gray matter of the brain close to Gibbs-Donnan equilibrium. Different but merging sections of the spreading-depolarization continuum from short duration waves to intermediate duration waves to terminal waves occur in a plethora of clinical conditions, including migraine aura, ischemic stroke, traumatic brain injury, aneurysmal subarachnoid hemorrhage (aSAH) and delayed cerebral ischemia (DCI), spontaneous intracerebral hemorrhage, subdural hematoma, development of brain death, and the dying process during cardio circulatory arrest. Thus, spreading depolarization represents a prime and simultaneously the most neglected pathophysiological process in acute neurology. Aristides Leao postulated as early as the 1940s that the pathophysiological process in neurons underlying migraine aura is of the same nature as the pathophysiological process in neurons that occurs in response to cerebral circulatory arrest, because he assumed that spreading depolarization occurs in both conditions. With this in mind, it is not surprising that patients with migraine with aura have about a twofold increased risk of stroke, as some spreading depolarizations leading to the patient percept of migraine aura could be caused by cerebral ischemia. However, it is in the nature of spreading depolarization that it can have different etiologies and not all spreading depolarizations arise because of ischemia. Spreading depolarization is observed as a negative direct current (DC) shift and associated with different changes in spontaneous brain activity in the alternating current (AC) band of the electrocorticogram. These are non-spreading depression and spreading activity depression and epileptiform activity. The same spreading depolarization wave may be associated with different activity changes in adjacent brain regions. Here, we review the basal mechanism underlying spreading depolarization and the associated activity changes. Using original recordings in animals and patients, we illustrate that the associated changes in spontaneous activity are by no means trivial, but pose unsolved mechanistic puzzles and require proper scientific analysis.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
migraine aura
en
dc.subject
traumatic brain injury
en
dc.subject
circulatory arrest
en
dc.subject
subarachnoid hemorrhage
en
dc.subject
spreading depolarization
en
dc.subject
spreading depression
en
dc.subject
brain ischemia
en
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Migraine Aura, Transient Ischemic Attacks, Stroke, and Dying of the Brain Share the Same Key Pathophysiological Process in Neurons Driven by Gibbs–Donnan Forces, Namely Spreading Depolarization
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
837650
dcterms.bibliographicCitation.doi
10.3389/fncel.2022.837650
dcterms.bibliographicCitation.journaltitle
Frontiers in Cellular Neuroscience
dcterms.bibliographicCitation.originalpublishername
Frontiers Media SA
dcterms.bibliographicCitation.volume
16
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
35237133
dcterms.isPartOf.eissn
1662-5102