2018
DOI: 10.1093/brain/awy102
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The negative ultraslow potential, electrophysiological correlate of infarction in the human cortex

Abstract: Experimental studies indicate that, following focal or global ischaemia, progressive recruitment of neocortical neurons into death begins when spreading depolarization gives way to a negative ultraslow potential. By monitoring patients with subarachnoid haemorrhage, Lückl et al. identify this process as the electrophysiological correlate of infarction and a neuromonitoring-detected medical emergency.

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Cited by 94 publications
(163 citation statements)
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References 96 publications
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“…In the most common scenario, arrest of systemic circulation, respiration and ECoG activity develops more or less simultaneously, while terminal SD follows the complete arrest of ECoG activity with a latency of 13 to 266 seconds (Dreier et al, 2018). Along this sequence, the invasively recorded direct current (DC)/alternate (AC)-ECoG activity can be roughly divided into four different phases which are illustrated with an original recording from a previous study (Dreier et al, 2018) in Figure 1B : In phase 1, spontaneous ECoG activity is still measurable; phase 2 is characterized by a complete loss of ECoG activity starting simultaneously in different cortical regions and layers, which is referred to as non-spreading depression of spontaneous activity (Dreier, 2011); in phase 3, the terminal SD starts but, from a phenomenologically point of view, is initially similar to SD spreading in healthy grey brain matter ( Figure 1A ) (Dreier & Reiffurth, 2015; Hartings et al, 2017a); and finally, in phase 4 a negative ultraslow potential signals the second phase of terminal SD (Oliveira-Ferreira et al, 2010; Hartings et al, 2017b; Dreier et al, 2018, 2019; Lückl et al, 2018; Carlson et al, 2018).…”
Section: Discussionmentioning
confidence: 99%
“…In the most common scenario, arrest of systemic circulation, respiration and ECoG activity develops more or less simultaneously, while terminal SD follows the complete arrest of ECoG activity with a latency of 13 to 266 seconds (Dreier et al, 2018). Along this sequence, the invasively recorded direct current (DC)/alternate (AC)-ECoG activity can be roughly divided into four different phases which are illustrated with an original recording from a previous study (Dreier et al, 2018) in Figure 1B : In phase 1, spontaneous ECoG activity is still measurable; phase 2 is characterized by a complete loss of ECoG activity starting simultaneously in different cortical regions and layers, which is referred to as non-spreading depression of spontaneous activity (Dreier, 2011); in phase 3, the terminal SD starts but, from a phenomenologically point of view, is initially similar to SD spreading in healthy grey brain matter ( Figure 1A ) (Dreier & Reiffurth, 2015; Hartings et al, 2017a); and finally, in phase 4 a negative ultraslow potential signals the second phase of terminal SD (Oliveira-Ferreira et al, 2010; Hartings et al, 2017b; Dreier et al, 2018, 2019; Lückl et al, 2018; Carlson et al, 2018).…”
Section: Discussionmentioning
confidence: 99%
“…Since the depolarization period is commonly believed to be injurious, 63,64 we examined the total combined duration of depolarization pre-and post-CPR. There was no association between combined depolarization duration and NDS, likely due to earlier depolarizing rats also repolarizing earlier (Fig.…”
Section: Total Depolarization Duration From Sd Onset To Rp Onset Is Nmentioning
confidence: 99%
“…In the most common scenario, arrest of systemic circulation, respiration and ECoG activity develops more or less simultaneously, while terminal SD follows the complete arrest of ECoG activity with a latency of 13 to 266 seconds (Dreier et al, 2018). Along this sequence, the Manuscript to be reviewed invasively recorded direct current (DC)/alternate (AC)-ECoG activity can be roughly divided into four different phases which are illustrated with an original recording from a previous study (Dreier et al, 2018) in Figure 1B: In phase 1, spontaneous ECoG activity is still measurable; phase 2 is characterized by a complete loss of ECoG activity starting simultaneously in different cortical regions and layers, which is referred to as non-spreading depression of spontaneous activity (Dreier, 2011); in phase 3, the terminal SD starts but, from a phenomenologically point of view, is initially similar to SD spreading in healthy grey brain matter ( Figure 1A) (Dreier & Reiffurth, 2015;Hartings et al, 2017a); and finally, in phase 4 a negative ultraslow potential signals the second phase of terminal SD (Oliveira-Ferreira et al, 2010;Hartings et al, 2017b;Dreier et al, 2018Dreier et al, , 2019Lückl et al, 2018;Carlson et al, 2018).…”
Section: Nde and The Neurobiology Of Dyingmentioning
confidence: 99%
“…It is important to understand that this terminal SD marks the onset of the toxic cellular changes that ultimately lead to death, but it is not a marker of death per se, since the SD is reversible -to a certain point -with restoration of the circulation (Hossmann & Sato, 1970;Heiss & Rosner, 1983;Memezawa, Smith & Siesjö, 1992;Ayad, Verity & Rubinstein, 1994;Shen et al, 2005;Pignataro, Simon & Boison, 2007;Nozari et al, 2010;Lückl et al, 2018). Thus, in contrast to what happens during coma or sedation, when the brain dies, it undergoes a massive and unstoppable depolarization process (and hence, a very last state of "activation") (Dreier, 2011).…”
Section: Nde and The Neurobiology Of Dyingmentioning
confidence: 99%