Cortical spreading depression recorded from the human brain using a multiparametric monitoring system

Mayevsky, Avraham; Doron, Amihood; Manor, Tamar; Meilin, Sigal; Zarchin, N.; Ouaknine, George E.

doi:10.1016/s0006-8993(96)00874-8

Cited by 263 publications

(151 citation statements)

References 27 publications

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“…The issue of a possible dependence of PID frequency on plasma glucose concentration has taken on new importance for clinical management of acute brain injury, since there is widespread support in general intensive care units for a policy of tight control of plasma glucose with insulin (Van den Berghe et al, 2001). Furthermore, studies of microdialysate glucose concentration in patients with acute brain injury have indicated that depletion of the brain glucose pool carries a poor prognosis (Langemann et al, 1995;Vespa et al, 2003), and there is now good evidence for the occurrence of depolarisation events in the injured brain in many patients (Mayevsky et al, 1996;Strong et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Hopwood

Parkin

Bezzina

et al. 2005

J Cereb Blood Flow Metab

114

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Peri-infarct depolarisations (PIDs) contribute to infarct expansion in experimental focal ischaemia; furthermore, depolarisations propagate in the injured human brain. Glucose utilisation is increased under both conditions, and depletion of brain glucose carries a poor prognosis. We studied dynamics of cerebral glucose and lactate in relation to PID patterns in experimental stroke. The middle cerebral artery was occluded for 3 h in 23 cats under terminal chloralose anaesthesia. We used fluorescence imaging to detect occurrence of PIDs, and rapid-sampling online microdialysis (rsMD), coupled to a flow-injection assay, to examine changes in cerebral cortical extracellular glucose and lactate at intervals of 30 sec each. After 30 min' ischaemia, lactate had increased by 43.67s.d. 45.9 lmol/L, and stabilised in that range for 3 h. In contrast, glucose fell only slightly initially (11.979.7 lmol/L), but progressively decreased to a reduction of 56.7747.2 lmol/L at 3 h, with no evidence of stabilisation. There was a highly significant inverse relationship of frequency of PIDs with plasma glucose (Po0.001). The results also characterise a metabolic signature for PIDs for possible application in clinical work, and emphasise potential risks in the use of insulin to control plasma glucose in patients with brain injury.

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Section: Introductionmentioning

confidence: 99%

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Hopwood

Parkin

Bezzina

et al. 2005

J Cereb Blood Flow Metab

114

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“…Spontaneous cordisturbances associated with the development of a migraine tical SD's were also reported in patients with severe head inheadache) (Lauritzen, 1994). Recurrent SD may also conjury (Mayevsky et al, 1995). tribute to neuronal damage, subsequent to experimental focal The potential clinical relevance of SD has triggered much interest in its pharmacology, and it is now established that both its elicitation and propagation require activation of the N-methyl-D-aspartate (NMDA)-receptor ionophore complex 'Author for correspondence at: Department of Neurochemistry, 801) potently block SD, but their undesirable psychotomimetic and pathomorphologic effects preclude their use in clinical practice (Willetts et al, 1990;Fix et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of cortical spreading depression by L‐701,324, a novel antagonist at the glycine site of the N‐methyl‐D‐aspartate receptor complex

Obrenovitch¹,

Zilkha²

1996

British J Pharmacology

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1 Spreading depression (SD) is a propagating transient suppression of electrical activity, associated with cellular depolarization, which probably underlies the migraine aura and may contribute to neuronal damage in focal ischaemia. The purpose of this study was to examine whether L-701,324 (7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-2-(lH)-quinolone), a high affinity antagonist at the glycine site of the Nmethyl-D-aspartate (NMDA) 6 Taken together, these data demonstrate that L-701,324 has an inhibitory effect on both SD initiation and propagation. This action may be beneficial in focal ischaemia, and possibly also against migraine, especially as this drug was shown to be active when administered orally.

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“…Primate retina and brain are capable of supporting SD (34,35). Cortical SD waves are believed to be involved in certain clinical neurological disorders (7), including migraine aura (8), which can be accompanied by a temporary partial or complete loss of vision over a portion of or the entire visual field (36).…”

Section: Discussionmentioning

confidence: 99%

Reentrant spiral waves of spreading depression cause macular degeneration in hypoglycemic chicken retina

Yu¹,

Santos²,

Mattiace³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Spreading depression (SD), a slow diffusion-mediated self-sustained wave of depolarization that severely disrupts neuronal function, has been implicated as a cause of cellular injury in a number of central nervous system pathologies, including blind spots in the retina. Here we show that in the hypoglycemic chicken retina, spontaneous episodes of SD can occur, resulting in irreversible punctate lesions in the macula, the region of highest visual acuity in the central region of the retina. These lesions in turn can act as sites of origin for secondary self-sustained reentrant spiral waves of SD that progressively enlarge the lesions. Furthermore, we show that the degeneration of the macula under hypoglycemic conditions can be prevented by blocking reentrant spiral SDs or by blocking caspases. The observation that spontaneous formation of reentrant spiral SD waves leads to the development of progressive retinal lesions under conditions of hypoglycemia establishes a potential role of SD in initiation and progression of macular degeneration, one of the leading causes of visual disability worldwide.diabetes | retinal migraine | scotomas C urrent research has revealed a number of molecular mechanisms underlying the pathophysiology of macular degeneration (1), a disease that involves damage to the central retina, where the higher density of photoreceptors results in maximal visual acuity (2). Macular degeneration is a leading cause of visual disability (1, 2). However, the reasons for the particular sensitivity of the macula remain speculative. A number of patients report the presence of monocular scotomas that gradually enlarge and move across the retinal field, and this phenomenon, which can lead to loss of vision, has been ascribed to retinal migraine (3, 4). Although the occurrence of retinal migraine has been disputed (5), the likely cause is spreading depression (SD), a phenomenon initially described in the central nervous system by Leão (6). SD is a slow diffusion-mediated self-sustained wave of generalized depolarization of gray matter or retina that does not respect synaptic connectivity (7) and severely disrupts neuronal function. SD results in a temporary collapse of transmembrane ionic gradients and membrane potential (8, 9), and is characterized by a negative field potential 10-20 mV in amplitude and 1-2 min in duration, propagating at a velocity of a few millimeters per minute (6-10). The advancing wave front is accompanied by a burst of action potentials and K + efflux into the interstitial space, followed by electrical silence, which is associated with the negative field potential (11, 12). Na + and Cl − enter the cells, causing an influx of water, swelling, and reduction in the volume of the extracellular space. In addition, proinflammatory compounds are released, often accompanied by edema and extravasation of blood proteins (13). Recovery can occur in minutes, but repeated episodes of SD increase neuronal loss surrounding traumatic brain lesions, and have been implicated in other central nervous syst...

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Cortical spreading depression recorded from the human brain using a multiparametric monitoring system

Cited by 263 publications

References 27 publications

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Inhibition of cortical spreading depression by L‐701,324, a novel antagonist at the glycine site of the N‐methyl‐D‐aspartate receptor complex

Reentrant spiral waves of spreading depression cause macular degeneration in hypoglycemic chicken retina

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