The brain is the most complex structure known in the universe. 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. Here, we review the basal mechanism underlying spreading depolarization and the associated activity changes. The same spreading depolarization wave may be associated with different activity changes in adjacent brain regions. These are non-spreading depression and spreading activity depression and epileptiform activity. 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. However, it is in the nature of spreading depolarization that it can have different etiologies and not all spreading depolarizations arise because of ischemia. 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. Aristides Leão 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. Thus, spreading depolarization represents a prime and simultaneously the most neglected pathophysiological process in acute neurology. 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. 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. 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. 9Einstein Center for Neurosciences Berlin, Berlin, Germany.8Bernstein Center for Computational Neuroscience Berlin, Berlin, Germany.
7Department of Neurosurgery, Evangelisches Krankenhaus Oldenburg, University of Oldenburg, Oldenburg, Germany.6Department of Neurosurgery, Berlin Institute of Health, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.5Department of Neurology, Berlin Institute of Health, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.4Department of Neurology, University of Szeged, Szeged, Hungary.3Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary.2Department of Experimental Neurology, Berlin Institute of Health, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.1Center for Stroke Research Berlin, Berlin Institute of Health, Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.Lemale 1,2, Janos Lückl 1,3,4, Viktor Horst 1, Clemens Reiffurth 1,2, Sebastian Major 1,2,5, Nils Hecht 6, Johannes Woitzik 7 and Jens P.
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