Functional Ablation by Spreading Depression: Possible Use in Human Stereotactic Neurosurgery

Šramka, M; Brožek, G; Bureš, Jan; Nádvorník, P

doi:10.1159/000102431

Cited by 46 publications

(37 citation statements)

References 12 publications

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“…Sramka and coworkers had in fact elicited spreading depolarizations back in 1977 by microinjection of small amounts of potassium chloride into the caudate nucleus or hippocampus in ten patients treated for focal epilepsy [76]. Large negative slow potential changes were recorded in both structures in a similar fashion to what had been observed in animal experiments earlier.…”

Section: A Brief History Of Spreading Depolarizationsupporting

confidence: 64%

“…Human studies on spreading depolarization started in the late 1970s with Sramka and colleagues' paper on potassium-induced, invasively recorded spreading depolarizations in the human caudate nucleus and hippocampus [76]. At approximately the same time, Symon's group showed spreading depolarizations in the periphery of ischemic regions in the baboon [77].…”

Section: A Brief History Of Spreading Depolarizationmentioning

confidence: 99%

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Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

et al. 2011

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Spreading depolarization is a mechanism of abrupt, massive ion translocation between intraneuronal and extracellular space that entails cytotoxic edema in the brain’s gray matter. It is observed in patients as a large change of the slow electrical potential. Dependent on the energy status of the tissue, spreading depolarization is either preceded by nonspreading silencing due to neuronal hyperpolarization or accompanied by spreading silencing of electrical brain activity due to a depolarization block. Nonspreading silencing seems to translate into the initial clinical symptoms of ischemic stroke and spreading silencing translates into migraine aura. Direct electrophysiological evidence exists that spreading depolarization occurs in abundance in aneurysmal subarachnoid hemorrhage, delayed ischemic stroke after subarachnoid hemorrhage, malignant hemispheric stroke, spontaneous intracerebral hemorrhage and traumatic brain injury. Indirect evidence suggests its occurrence during migraine aura. In animals, spreading depolarizations facilitate neuronal death when they invade metabolically compromised tissue, whereas they are relatively innocuous in healthy tissue. Therapies targeting spreading depolarization may potentially treat these neurological conditions.

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Section: A Brief History Of Spreading Depolarizationsupporting

confidence: 64%

Section: A Brief History Of Spreading Depolarizationmentioning

confidence: 99%

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

et al. 2011

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“…Several published studies [17][18][19][20][21] have sug- showing multiple episodes of ECoG suppression, propagating in either direction with reference to the recording strip. Recordings commenced 19 hours after injury and continued for 47 hours: 10 events occurred, of which 4 met the criteria for definite spread; the others indicated possible spread.…”

Section: Previous Studiesmentioning

confidence: 99%

Spreading and Synchronous Depressions of Cortical Activity in Acutely Injured Human Brain

Strong

Fabricius

Boutelle

et al. 2002

Stroke

389

284

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Background and Purpose-Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. Methods-In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. Results-Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. Conclusions-These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.

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“…It is worth mentioning that, whilst CSD has been experimentally demonstrated in animal models, the strongest evidences for CSD in humans are the migraine aura itself, and the spreading oligemia phenomenon observed in migraine patients, consisting in a decrease of the cerebral blood flow in the posterior part of the brain at the beginning of the attack, followed by the spreading of the low flow region at a speed which is similar to those found for CSD in animals. Some electrophysiological evidences that human grey matter in vivo supports CSD have also been reported (see, e.g., [7]). A deeper understanding of CSD phenomenology would be useful to test current and novel prophylactic drugs, while providing knowledge on mechanisms of action relevant for migraine [8].…”

Section: Introductionmentioning

confidence: 91%

Temporal Excitation Patterns on the Cerebral Cortex as a Result of Migraine Modeling

Kroos

Diez

Cortés

et al. 2017

Emergent Complexity From Nonlinearity, in Physics, Engineering and the Life Sciences

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The complex, highly individual, geometry of the cerebral cortex in humans presents a major challenge in studying the spreading of spontaneous neuronal activity. Recent computational advances [1] allow to simulate the propagation of depolarization waves on the macroscale and for individual geometries, reconstructed from accurate medical imaging as MRI, with high levels of detail. In this paper we take advantage of such technique to study the temporal excitation patterns that follow the passage of a depolarization wave on the cerebral cortex.

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Functional Ablation by Spreading Depression: Possible Use in Human Stereotactic Neurosurgery

Cited by 46 publications

References 12 publications

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

Spreading and Synchronous Depressions of Cortical Activity in Acutely Injured Human Brain

Temporal Excitation Patterns on the Cerebral Cortex as a Result of Migraine Modeling

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