Further Observations on the Spreading Depression of Activity in the Cerebral Cortex

Leo, Aristides A. P.

doi:10.1152/jn.1947.10.6.409

Cited by 559 publications

(310 citation statements)

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“…Thus, the term nonspreading depression accurately describes this phenomenon. Nonspreading depression typically preceded the terminal SD by several tens of seconds, similar to previous observations in animals 7. It has been proposed that the underlying mechanism of nonspreading depression is related to a neuronal or glial oxygen sensor that shuts down neuronal activity once it senses a steep decline in p ti O 2 4.…”

Section: Discussionsupporting

confidence: 82%

“…Note the similarity between the patterns of the terminal SD in the rodent experiment and in the patient ( red arrows in A and C). In both cases, the terminal SD propagated from one electrode to the next corresponding with previous evidence from experiments in animals in vivo and in brain slices 7, 12, 13, 14. In contrast to the spread of the terminal SD, the nonspreading depression (cf asterisks) is seen in the rodent recordings as a silencing of the spontaneous electrical activity (alternating current [AC]–electrocorticography [ECoG]: 0.5–45Hz) that develops simultaneously across the array of the regional 2 electrodes (cf Figs 3B, 4B, 5A, 5C, and 6 for nonspreading depression in patients).…”

Section: Methodssupporting

confidence: 78%

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Terminal spreading depolarization and electrical silence in death of human cerebral cortex

Dreier

Major

Foreman

et al. 2018

Annals of Neurology

116

138

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ObjectiveRestoring the circulation is the primary goal in emergency treatment of cerebral ischemia. However, better understanding of how the brain responds to energy depletion could help predict the time available for resuscitation until irreversible damage and advance development of interventions that prolong this span. Experimentally, injury to central neurons begins only with anoxic depolarization. This potentially reversible, spreading wave typically starts 2 to 5 minutes after the onset of severe ischemia, marking the onset of a toxic intraneuronal change that eventually results in irreversible injury.MethodsTo investigate this in the human brain, we performed recordings with either subdural electrode strips (n = 4) or intraparenchymal electrode arrays (n = 5) in patients with devastating brain injury that resulted in activation of a Do Not Resuscitate–Comfort Care order followed by terminal extubation.ResultsWithdrawal of life‐sustaining therapies produced a decline in brain tissue partial pressure of oxygen (ptiO2) and circulatory arrest. Silencing of spontaneous electrical activity developed simultaneously across regional electrode arrays in 8 patients. This silencing, termed “nonspreading depression,” developed during the steep falling phase of ptiO2 (intraparenchymal sensor, n = 6) at 11 (interquartile range [IQR] = 7–14) mmHg. Terminal spreading depolarizations started to propagate between electrodes 3.9 (IQR = 2.6–6.3) minutes after onset of the final drop in perfusion and 13 to 266 seconds after nonspreading depression. In 1 patient, terminal spreading depolarization induced the initial electrocerebral silence in a spreading depression pattern; circulatory arrest developed thereafter.InterpretationThese results provide fundamental insight into the neurobiology of dying and have important implications for survivable cerebral ischemic insults. Ann Neurol 2018;83:295–310

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Section: Discussionsupporting

confidence: 82%

Section: Methodssupporting

confidence: 78%

Terminal spreading depolarization and electrical silence in death of human cerebral cortex

Dreier

Major

Foreman

et al. 2018

Annals of Neurology

116

138

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“…Leão also showed a change in cortical direct current (DC) potential, evidence of depolarization (Leao, 1947), now known to represent a mass neuronal and astrocytic depolarization.…”

Section: Introductionmentioning

confidence: 99%

Persisting Depletion of Brain Glucose following Cortical Spreading Depression, despite Apparent Hyperaemia: Evidence for Risk of an Adverse Effect of Leão's Spreading Depression

Hashemi

Bhatia

Nakamura

et al. 2008

J Cereb Blood Flow Metab

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Rapid sampling microdialysis (rsMD) directed towards the cerebral cortex has allowed identification of a combined time-series signature for glucose and lactate that characterizes peri-infarct depolarization in experimental focal ischaemia, but no comparable data exist for 'classical' cortical spreading depression (CSD) associated with hyperaemia in the normally perfused brain. Here, we examined the rsMD responses of dialysate glucose and lactate to five hyperaemic spreading depressions induced with intracortical microinjections, typically of 1 mol/L KCl, in open-skull preparations in five cats under chloralose anaesthesia. Depolarization was verified with microelectrodes, and laser speckle flowmetry was used to examine propagation of the events and perfusion responses near the MD probe. Ten minutes after depolarization, dialysate glucose fell and lactate rose by 28% and 58% respectively. There was no recovery of dialysate glucose 30 mins after depolarization. Mean baseline indicative cerebral blood flow was 25.5±4.1 mL/100 g/min and mean maximum hyperaemic increase was by 29.6 ± 6 mL/100 g/min; hyperaemia remained present 30 mins after CSD. As CSD events are repetitive, frequent, and often clustered temporally in human acute brain injury, these results indicate a high risk of depletion of extracellular glucose in association with depolarization events of a pattern previously thought to be largely benign.

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“…Spreading depression (SD) of Leao (1944Leao ( , 19471951) represents a stereotyped response of the cen tral gray matter, elicitable by a number of chemical, mechanical, and electrical stimuli. Several lines of evidence suggest that SD or SD-like spontaneous depolarization occurs in cortical regions surround ing an acute ischemic lesion (Gill et aI., 1992;Iijima et aI., 1992;Nedergaard and Hansen, 1993 ;Bak et aI., 1994;Dietrich et aI., 1994) and may contribute to progression of the ischemic process (Gill et aI., 1992;Iijima et aI., 1992;Chen et aI., 1993).…”

mentioning

confidence: 99%

Spreading Waves of a Reduced Diffusion Coefficient of Water in Normal and Ischemic Rat Brain

Hasegawa

Latour

Formato

et al. 1995

J Cereb Blood Flow Metab

111

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Summary: Using echo planar diffusion-weighted mag netic resonance imaging, we measured three-dimensional changes in the apparent diffusion coefficient (ADC) of water in eight contiguous coronal slices, encompassing the entire rat brain, before and after local cortical stimu lation. We applied chemical (potassium chloride applica tion; n = 6) and mechanical (needle stab; n = 4) stimu lations to the right posterior parietal rat cortex. In all animals in which potassium chloride or the needle stab was applied, a region of decreased ADC values to a mean of 0.45 ± 0.03 x 1O-5cm2/s occurred. These reduced ADC levels appeared in the posterior parietal cortex within 1 min after cortical stimulation and the change recovered within 1 min. Then a ripple-like movement of

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Further Observations on the Spreading Depression of Activity in the Cerebral Cortex

Cited by 559 publications

References 0 publications

Terminal spreading depolarization and electrical silence in death of human cerebral cortex

Terminal spreading depolarization and electrical silence in death of human cerebral cortex

Persisting Depletion of Brain Glucose following Cortical Spreading Depression, despite Apparent Hyperaemia: Evidence for Risk of an Adverse Effect of Leão's Spreading Depression

Spreading Waves of a Reduced Diffusion Coefficient of Water in Normal and Ischemic Rat Brain

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