A new direction for spreading depolarization: Investigation in the fly brain

Spong, Kristin E.; Dreier, Jens P.; Robertson, R. Meldrum

doi:10.1080/19336950.2016.1239898

Cited by 16 publications

(17 citation statements)

References 8 publications

(8 reference statements)

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“…70,71 Indeed, multiple studies have shown beneficial properties of SD, including preconditioning, upregulation of growth factors, and neurogenesisis. [72][73][74][75][76][77] In addition, previous studies in insects [78][79][80][81] and rodents 72,73,82,83 suggest that SD may play a neuroprotective role during ischemia. 1,84 It is possible that this protection is enabled by a "neuronal silencing" mechanism associated with SD 85 wherein metabolism is quickly shut down, possibly to conserve residual energy and minimize production of reactive oxygen species, potentially leading to an improved survival and outcome in reversible processes.…”

Section: Discussionmentioning

confidence: 99%

Spreading depolarization and repolarization during cardiac arrest as an ultra-early marker of neurological recovery in a preclinical model

Wilson¹,

Crouzet²,

Lee

et al. 2019

Preprint

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Spreading depolarization (SD) accompanies numerous neurological conditions, including migraine, stroke, and traumatic brain injury. There is significant interest in understanding the relationship between SD and neuronal injury. However, characteristics underlying SD and repolarization (RP) induced by global cerebral ischemia (e.g., cardiac arrest (CA)) and reperfusion are not well understood. Quantifying features of SD and RP during CA and cardiopulmonary resuscitation (CPR) may provide important metrics for diagnosis and prognosis of neurological injury from hypoxia-ischemia. We characterized SD and RP in a rodent model of asphyxial CA+CPR using a multimodal platform including electrocorticography (ECoG) and optical imaging. We detected SD and RP by (1) alternating current (AC), (2) direct current (DC), and (3) optical imaging of spreading ischemia, spreading edema, and vasoconstriction. Earlier SD (r=-0.80; p<0.001) and earlier RP (r=-0.71, p<0.001) were associated with better neurological recovery after 24hrs. SD+RP onset times predicted good vs poor neurological recovery with 82% sensitivity and 91% specificity. To our knowledge, this is the first preclinical study to link SD and RP characteristics with neurological recovery post-CA. These data suggest that SD and RP may be ultra-early, real-time prognostic markers of post-CA outcome, meriting further investigation into translational implications during global cerebral ischemia.

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Section: Discussionmentioning

confidence: 99%

Spreading depolarization and repolarization during cardiac arrest as an ultra-early marker of neurological recovery in a preclinical model

Wilson¹,

Crouzet²,

Lee

et al. 2019

Preprint

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“…Patient 1 (A-E). Spreading depolarization (SD) is observed as a large negative direct current (DC) shift propagating between different electrodes (A) (subdural full-band DC/alternate current (AC)-electrocorticography (ECoG) between 0 and 45 Hz, electrode separation: 1 cm) (Dreier et al, 2017). This short-lasting SD was recorded in a patient with aneurysmal subarachnoid hemorrhage (aSAH) in a metabolically largely intact and sufficiently perfused neocortex region.…”

Section: Discussionmentioning

confidence: 99%

Peer Review #1 of "Migraine aura, a predictor of near-death experiences in a crowdsourced study (v0.2)"

2019

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Background: Near-death experiences (NDE) occur with imminent death and in situations of stress and danger but are poorly understood. Evidence suggests that NDE are associated with rapid eye movement (REM) sleep intrusion, a feature of narcolepsy. Previous studies further found REM abnormalities and an increased frequency of dream-enacting behavior in migraine patients, as well as an association between migraine with aura and narcolepsy. We therefore investigated if NDE are more common in people with migraine aura. Methods: We recruited 1037 laypeople from 35 countries and 5 continents, without any filters except for English language and age ≥18 years, via a crowdsourcing platform. Reports were validated using the Greyson NDE Scale. Results: Eighty-one of 1037 participants had NDE (7.8%; CI 6.3-9.7%). There were no significant associations between NDE and age (p>0.6, t-test independent samples) or gender (p>0.9, chi-square test). The only significant association was between NDE and migraine aura: Forty-eight (6.1%) of 783 subjects without migraine aura and 33 (13.0%) of 254 subjects with migraine aura had NDE (p<0.001, chi-square test, odds ratio (OR) = 2.29). In multiple logistic regression analysis, migraine aura remained significant after adjustment for age (p<0.001, OR 2.31), gender (p<0.001, OR 2.33), or both (p<0.001, OR 2.33). Conclusions: In our sample, migraine aura was a predictor of NDE. This indirectly supports the association between NDE and REM intrusion and might have implications for the understanding of NDE, because a variant of spreading depolarization (SD), terminal SD, occurs in humans at the end of life, while a short-lasting variant of SD is considered the pathophysiological correlate of migraine aura.

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“…Also the large negative DC shift characteristic of spreading depolarization had been recorded in many species (Marshall 1959). Today, we know that spreading depolarization is not only the characteristic injury potential of the gray matter of mammals but also occurs in analogous neural structures of fish, insects, reptiles, and birds (Kraig and Nicholson 1978;Lauritzen et al 1988;Martins-Ferreira et al 1974;Robertson et al 2017;Spong et al 2017). The fact that this large negative DC shift is also found in brain slices that lack an intact blood-brain barrier (BBB) is one of the many arguments that it is not generated at the BBB (Kang et al 2013;Somjen 2001).…”

Section: Spreading Depolarization Is the Injury Potential Of The Braimentioning

confidence: 97%

Direct electrophysiological evidence that spreading depolarization-induced spreading depression is the pathophysiological correlate of the migraine aura and a review of the spreading depolarization continuum of acute neuronal mass injury

et al. 2019

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Spreading depolarization is observed as a large negative shift of the direct current potential, swelling of neuronal somas, and dendritic beading in the brain's gray matter and represents a state of a potentially reversible mass injury. Its hallmark is the abrupt, massive ion translocation between intraneuronal and extracellular compartment that causes water uptake (= cytotoxic edema) and massive glutamate release. Dependent on the tissue's energy status, spreading depolarization can co-occur with different depression or silencing patterns of spontaneous activity. In adequately supplied tissue, spreading depolarization induces spreading depression of activity. In severely ischemic tissue, nonspreading depression of activity precedes spreading depolarization. The depression pattern determines the neurological deficit which is either spreading such as in migraine aura or migraine stroke or nonspreading such as in transient ischemic attack or typical stroke. Although a clinical distinction between spreading and nonspreading focal neurological deficits is useful because they are associated with different probabilities of permanent damage, it is important to note that spreading depolarization, the neuronal injury potential, occurs in all of these conditions. Here, we first review the scientific basis of the continuum of spreading depolarizations. Second, we highlight the transition zone of the continuum from reversibility to irreversibility using clinical

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A new direction for spreading depolarization: Investigation in the fly brain

Cited by 16 publications

References 8 publications

Spreading depolarization and repolarization during cardiac arrest as an ultra-early marker of neurological recovery in a preclinical model

Spreading depolarization and repolarization during cardiac arrest as an ultra-early marker of neurological recovery in a preclinical model

Peer Review #1 of "Migraine aura, a predictor of near-death experiences in a crowdsourced study (v0.2)"

Direct electrophysiological evidence that spreading depolarization-induced spreading depression is the pathophysiological correlate of the migraine aura and a review of the spreading depolarization continuum of acute neuronal mass injury

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