Spreading depression can be restricted to distinct depths of the rat cerebral cortex

Richter, Frank; Lehmenkühler, A.

doi:10.1016/0304-3940(93)90484-3

Cited by 50 publications

(32 citation statements)

References 15 publications

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“…It might be added that whether or not SD will trigger migraine headache may also depend, for example, on cortical layers and regions been invaded (Karatas et al, 2013;Richter and Lehmenkü hler, 1993) and on levels of SD-released noxious substances that discharge primary afferents.…”

Section: Sd and Headachementioning

confidence: 99%

The Stroke-Migraine Depolarization Continuum

Dreier

Reiffurth

2015

Neuron

285

359

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The term spreading depolarization (SD) refers to waves of abrupt, sustained mass depolarization in gray matter of the CNS. SD, which spreads from neuron to neuron in affected tissue, is characterized by a rapid near-breakdown of the neuronal transmembrane ion gradients. SD can be induced by hypoxic conditions--such as from ischemia--and facilitates neuronal death in energy-compromised tissue. SD has also been implicated in migraine aura, where SD is assumed to ascend in well-nourished tissue and is typically benign. In addition to these two ends of the "SD continuum," an SD wave can propagate from an energy-depleted tissue into surrounding, well-nourished tissue, as is often the case in stroke and brain trauma. This review presents the neurobiology of SD--its triggers and propagation mechanisms--as well as clinical manifestations of SD, including overlaps and differences between migraine aura and stroke, and recent developments in neuromonitoring aimed at better diagnosis and more targeted treatments.

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Section: Sd and Headachementioning

confidence: 99%

The Stroke-Migraine Depolarization Continuum

Dreier

Reiffurth

2015

Neuron

285

359

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“…However, several issues of concern have been addressed regarding this technique. Richter and Lenmenkuhler have shown that the CSD elicited by KCl may be confined only in the upper cortical layers [4]. Although this observation may be of significance in term of cortical activation, it has less effect on the process of nociception since the pain sensitive structures, especially pial vessels, reside adjacent to cortical surface.…”

Section: Discussionmentioning

confidence: 98%

Cortical spreading depression, meningeal inflammation and trigeminal nociception

et al. 2004

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This study investigated whether perivascular inflammation is necessary in the process of cortical spreading depression (CSD)-induced trigeminovascular nociception. CSD was induced by application of potassium chloride on rat parietal surface. Cortical microcirculation was studied using intravital fluorescent videomicroscopy, laser Doppler flowmetry and electron microscopy. Trigeminal nociception was determined using Fos immunoreactivity as the indicator. We found that KCl application caused cyclic cortical hyperaemia and pial microvascular dilation. Neither increased leukocyte-endothelial adhesion nor extravasation of macromolecule was demonstrated. Ultrastructural study revealed increased endothelial pinocytosis but tight junction remained intact. Despite no intense perivascular inflammation, we observed significantly increased Fos-immunoreactivity in trigeminal nucleus caudalis. These results suggest that perivascular inflammation is not necessary in the process of CSD-evoked trigeminovascular nociception.

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“…Electrical activity associated with CSD has been shown to occur only on the cortical surface and does not penetrate to deeper brain layers [7]. This led to the concept of this phenomenon being a local cortical event, although more recent studies have shown that marked changes can occur in subcortical nuclei, perhaps for a prolonged period of time.…”

Section: Introductionmentioning

confidence: 98%

Cortical spreading depression: Its role in migraine pathogenesis and possible therapeutic intervention strategies

Parsons¹

2004

Current Science Inc

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Cortical spreading depression (CSD) is a well-characterized phenomenon in experimental animals. Recent data show that CSD actually can occur in the injured human brain and compelling evidence is accumulating to support the concept that CSD is responsible for migraine aura. The aim of this review is to highlight recent key advances regarding our understanding of CSD in animal and human studies and its relevance to the pathophysiology of migraine and its potential treatment options.

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Spreading depression can be restricted to distinct depths of the rat cerebral cortex

Cited by 50 publications

References 15 publications

The Stroke-Migraine Depolarization Continuum

The Stroke-Migraine Depolarization Continuum

Cortical spreading depression, meningeal inflammation and trigeminal nociception

Cortical spreading depression: Its role in migraine pathogenesis and possible therapeutic intervention strategies

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