Spreading Cortical Depression of Leão

Marshall, Wade H.

doi:10.1152/physrev.1959.39.2.239

Cited by 343 publications

(142 citation statements)

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“…The response was localized to the cortex and the prop agation speed was -3.4 mm/min. These observa tions agree with electrophysiological studies dem onstrating that SD is restricted to the depth of the cortex (Monakhov et aI., 1962) and propagates at 2-5 mm/min (Marshall, 1959;Hansen and Zeuthen, 1981;Somjen et aI., 1992) and strongly imply that the ADC decline represents SD. In this study, echo planar diffusion-weighted imaging was utilized to obtain multislice ADC maps with 30-s time resolu tion.…”

Section: Discussionsupporting

confidence: 87%

“…Glutamate or agonists of the glutamate receptor elicit SD (Van Harreveld, 1959;Lauritzen et al, 1988), and glutamate recep tor antagonists effectively inhibit SD (Goroleva et al, 1987;Lauritzen and Hansen, 1992;Nellgard and Wielock, 1992). Brain temperature is one of the fac tors influencing the occurrence of SD (Marshall, 1959). Recently, evidence has accumulated that the number of DC deflections correlates with ultimate infarct volume and that suppression of DC deflec tion by a glutamate antagonist of brain temperature modulation decreases infarct volume (Gill et al, 1992;Iijima et al, 1992;Chen et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…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). A car dinal sign of SD is a spontaneously reversible fail ure of brain ion homeostasis accompanied by a de polarization of neurons and glial cells, which spreads across the cortical surface from its initia tion site as a wave with a speed of 2-5 mm/min (Marshall, 1959;Hansen and Zeuthen, 1981;Som jen et aI., 1992). During SD, redistribution of ions and water occurs in the intra-and extracellular space.…”

mentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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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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“…Cortical SD can be evoked by tetanic electrical stimuli, mechanical stimuli such as pressure on or puncture of the cortex, alkaline pH, low osmolarity, and chemical stimuli such as potassium ions or glutamate [36][37][38] . Recently, we demonstrated that transient tissue oxidation in a restricted local area of the rat cerebral cortex also induces cortical SD [3] .…”

Section: Leao's Cortical Spreading Depressionmentioning

confidence: 99%

“…This phenomenon was then extensively studied around the world [33][34][35][36] , and has been characterized as a self-propagating wave of depolarization associated with a transient negative shift of the DC potential [2] and temporal elevation of the CBF [3,4] . These changes in DC potential and CBF spread throughout the cortical gray matter at a rate of ~3 mm/min [1, 5,6] .Cortical SD can be evoked by tetanic electrical stimuli, mechanical stimuli such as pressure on or puncture of the cortex, alkaline pH, low osmolarity, and chemical stimuli such as potassium ions or glutamate [36][37][38] . Recently, we demonstrated that transient tissue oxidation in a restricted local area of the rat cerebral cortex also induces cortical SD [3] .…”

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confidence: 99%

Role of cortical spreading depression in the pathophysiology of migraine

2014

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A migraine is a recurring neurological disorder characterized by unilateral, intense, and pulsatile headaches. In one-third of migraine patients, the attacks are preceded by a visual aura, such as a slowly-propagating scintillating scotoma. Migraine aura is thought to be a result of the neurovascular phenomenon of cortical spreading depression (SD), a self-propagating wave of depolarization that spreads across the cerebral cortex. Several animal experiments have demonstrated that cortical SD causes intracranial neurogenic infl ammation around the meningeal blood vessels, such as plasma protein extravasation and pro-inflammatory peptide release. Cortical SD has also been reported to activate both peripheral and central trigeminal nociceptive pathways. Although several issues remain to be resolved, recent evidence suggests that cortical SD could be the initial trigger of intracranial neurogenic inflammation, which then contributes to migraine headaches via subsequent activation of trigeminal afferents.Keywords: cortical spreading depression; migraine; neurogenic inflammation; PET; trigeminal nociceptive pathway ·Review· IntroductionCortical spreading depression (SD), described first by Leao [1] , is a self-propagating wave of transient neuronal/ glial membrane depolarization that is accompanied by a transient negative shift of the direct current (DC) potential [2] and temporal elevation of cerebral blood flow (CBF) [3,4] throughout the cerebral hemisphere at a rate of 2-5 mm/ min [1, 5,6] . The rate of spreading correlates with the observed spread of the aura of a classical migraine [7] , which is characterized by a spot of fl ickering light that appears near the center of the visual field and then gradually expands outward [8][9][10] . Recently, cortical SD has been hypothesized to be the initial event involved in migraine headaches.Moskowitz et al. [11,12] proposed that pro-inflammatory peptides, such as substance P and calcitonin generelated peptide (CGRP), released from trigeminocervical nerve terminals in response to some unknown stimulation, probably cortical SD, induces vasodilation and plasma protein extravasation. Such neurogenic inflammation is thought to trigger a headache via stimulation of trigeminal afferents. Consistent with this hypothesis, cortical SD induced intracranial neurogenic inflammation around the meningeal blood vessels [13][14][15] , and subsequent activation of both peripheral [16] and central [17] trigeminal nociceptive pathways has been described. Here, we review the experimental evidence mainly from neurophysiological studies that has advanced the understanding of whether and how the neurovascular phenomenon of cortical SD causes intracranial neurogenic inflammation, and subsequently participates in triggering a migraine headache. Migraine PathophysiologyA migraine is a recurring neurological disorder characterized Yilong Cui, et al . Role of cortical spreading depression in the pathophysiology of migraine 813 by unilateral, intense, and pulsatile headaches lasting 4-72 h [18] , a...

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Measuring Cation Activity of Living Brain

Portnoy¹,

Thomas²,

Gurdjian³

1963

Archives of Neurology

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DETROITRecent development of special glasses capable of discriminating sodium and potassium ions has made possible a method for recording the concentration of these ions in vivo. [4][5][6]8,9 Electrodes made from these glasses function exactly like the common pH (hydrogen ion) electrode. In fact, in an acid solution, the sodium and potassium electrodes may be used to measure pH. However, in a sodium or potassium salt solution above pH 6, the response to hydrogen ion activity is negligible and the electrodes respond essentially only to changes in sodium or potassium ion activity. In the same manner a pH electrode will respond to changes in sodium and potassium ions above pH 11.

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Spreading Cortical Depression of Leão

Cited by 343 publications

References 0 publications

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

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

Role of cortical spreading depression in the pathophysiology of migraine

Measuring Cation Activity of Living Brain

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