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Cortical spreading depression

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https://www.readbyqxmd.com/read/29756530/the-occurrence-of-spontaneous-cortical-spreading-depression-is-increased-by-blood-constituents-and-impairs-neurological-recovery-after-subdural-hematoma-in-rats
#1
Harald Krenzlin, Daniel Jussen, Michaela Maria Plath, Stephan Tretzel, Tobias Kraemer, Oliver Kempski, Beat Alessandri
Acute subdural haemorrhage (ASDH) is common and associated with severe morbidity and mortality. To date, the role of spontaneous cortical spreading depression (sCSD) in exaggerating secondary injury after ASDH, is poorly understood. The present study contains two experimental groups: First, we investigated and characterized the occurrence of sCSD after subdural blood infusion (300 µl) via tissue impedance (IMP) measurement in a rat model. Second, we compared the occurrence and influence of sCSD on lesion growth and neurological deficit in the presence and absence of whole blood constituents...
May 14, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29740328/emerging-role-of-endo-cannabinoids-in-migraine
#2
REVIEW
Pinja Leimuranta, Leonard Khiroug, Rashid Giniatullin
In this mini-review, we summarize recent discoveries and present new hypotheses on the role of cannabinoids in controlling trigeminal nociceptive system underlying migraine pain. Individual sections of this review cover key aspects of this topic, such as: (i) the current knowledge on the endocannabinoid system (ECS) with emphasis on expression of its components in migraine related structures; (ii) distinguishing peripheral from central site of action of cannabinoids, (iii) proposed mechanisms of migraine pain and control of nociceptive traffic by cannabinoids at the level of meninges and in brainstem, (iv) therapeutic targeting in migraine of monoacylglycerol lipase and fatty acid amide hydrolase, enzymes which control the level of endocannabinoids; (v) dual (possibly opposing) actions of cannabinoids via anti-nociceptive CB1 and CB2 and pro-nociceptive TRPV1 receptors...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29722303/harnessing-migraines-for-neural-regeneration
#3
REVIEW
Jonathan M Borkum
The success of naturalistic or therapeutic neuroregeneration likely depends on an internal milieu that facilitates the survival, proliferation, migration, and differentiation of stem cells and their assimilation into neural networks. Migraine attacks are an integrated sequence of physiological processes that may protect the brain from oxidative stress by releasing growth factors, suppressing apoptosis, stimulating neurogenesis, encouraging mitochondrial biogenesis, reducing the production of oxidants, and upregulating antioxidant defenses...
April 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29719223/the-transient-receptor-potential-ankyrin-type-1-plays-a-critical-role-in-cortical-spreading-depression
#4
Liwen Jiang, Yan Wang, Yuewei Xu, Dongqing Ma, Minyan Wang
The transient receptor potential ankyrin type-1 (TRPA1) channels have been proposed as a potential target for migraine therapy. Yet the role of cortical TRPA1 channels in migraine mechanism has not been fully understood. Cortical spreading depression (CSD) is known as an underlying cause of migraine aura. The aim of this study is to investigate if cortical TRPA1 activity is required for CSD genesis and propagation. A mouse brain slice CSD model with intrinsic optical imaging was applied for TRPA1 signaling pharmacology...
April 29, 2018: Neuroscience
https://www.readbyqxmd.com/read/29703787/dissociation-between-csd-evoked-metabolic-perturbations-and-meningeal-afferent-activation-and-sensitization-implications-for-mechanisms-of-migraine-headache-onset
#5
Jun Zhao, Dan Levy
The onset of the headache phase during attacks of migraine with aura, which occur in about 30% of migraineurs, is believed to involve cortical spreading depression (CSD) and the ensuing activation and sensitization of primary afferent neurons that innervate the intracranial meninges, and their related large vessels. The mechanism by which CSD enhances the activity and mechanosensitivity of meningeal afferents remains poorly understood, but may involve cortical metabolic perturbations. We employed extracellular single-unit recording of meningeal afferent activity and monitored changes in cortical blood flow and tissue partial pressure of oxygen (tpO2 ) in anesthetized male rats to test whether the prolonged cortical hypoperfusion and reduction in tissue oxygenation that occur in the wake of CSD contribute to meningeal nociception...
April 27, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29697154/a-phase-by-phase-review-of-migraine-pathophysiology
#6
David W Dodick
Migraine is a common, disabling neurological disorder characterized by multiple phases: premonitory, aura, headache, postdrome, and interictal. Our understanding of the pathophysiology of each phase of migraine has evolved over recent years. The premonitory phase begins as early as 3 days before the headache phase, and involves a complex interplay between various cortical and subcortical brain regions, including the hypothalamus and brainstem nuclei that modulate nociceptive signaling. The headache phase involves activation of the trigeminovascular system, a pathway that is well characterized...
May 2018: Headache
https://www.readbyqxmd.com/read/29695168/cortical-spreading-depression-as-a-site-of-origin-for-migraine-role-of-cgrp
#7
Liesl N Close, Sajedeh Eftekhari, Minyan Wang, Andrew C Charles, Andrew F Russo
Premise Migraine is a complex neurologic disorder that leads to significant disability, yet remains poorly understood. Problem One potential triggering mechanism in migraine with aura is cortical spreading depression, which can activate the trigeminal nociceptive system both peripherally and centrally in animal models. A primary neuropeptide of the trigeminal system is calcitonin gene-related peptide, which is a potent vasodilatory peptide and is currently a major therapeutic target for migraine treatment. Despite the importance of both cortical spreading depression and calcitonin gene-related peptide in migraine, the relationship between these two players has been relatively unexplored...
January 1, 2018: Cephalalgia: An International Journal of Headache
https://www.readbyqxmd.com/read/29671241/current-prophylactic-medications-for-migraine-and-their-potential-mechanisms-of-action
#8
REVIEW
Till Sprenger, M Viana, C Tassorelli
A relatively high number of different medications is currently used for migraine prevention in clinical practice. Although these compounds were initially developed for other indications and differ in their mechanisms of action, some general themes can be identified from the mechanisms at play. Efficacious preventive drugs seem to either suppress excitatory nervous signaling via sodium and/or calcium receptors, facilitate GABAergic inhibition, reduce neuronal sensitization, block cortical spreading depression and/or reduce circulating levels of CGRP...
April 18, 2018: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/29668855/the-negative-ultraslow-potential-electrophysiological-correlate-of-infarction-in-the-human-cortex
#9
Janos Lückl, Coline L Lemale, Vasilis Kola, Viktor Horst, Uldus Khojasteh, Ana I Oliveira-Ferreira, Sebastian Major, Maren K L Winkler, Eun-Jeung Kang, Karl Schoknecht, Peter Martus, Jed A Hartings, Johannes Woitzik, Jens P Dreier
Spreading depolarizations are characterized by abrupt, near-complete breakdown of the transmembrane ion gradients, neuronal oedema, mitochondrial depolarization, glutamate excitotoxicity and activity loss (depression). Spreading depolarization induces either transient hyperperfusion in normal tissue; or hypoperfusion (inverse coupling = spreading ischaemia) in tissue at risk for progressive injury. The concept of the spreading depolarization continuum is critical since many spreading depolarizations have intermediate characteristics, as opposed to the two extremes of spreading depolarization in either severely ischaemic or normal tissue...
April 16, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29595109/levosimendan-reduces-prostaglandin-f2a-dependent-vasoconstriction-in-physiological-vessels-and-after-experimentally-induced-subarachnoid-hemorrhage
#10
Stefan Wanderer, Jan Mrosek, Florian Gessler, Volker Seifert, Juergen Konczalla
Background Delayed cerebral vasospasm (dCVS) following aneurysmal subarachnoid hemorrhage (aSAH) is (next to possible aneurysm rebleeding, cortical spreading depression and early brain injury) one of the main factors contributing to poor overall patient outcome. Since decades intensive research has been ongoing with the goal of improving our understanding of the pathophysiological principles underlying dCVS. Endothelin-1 (ET-1) and prostaglandin F2 alpha (PGF2a) seem to play a major role during dCVS. The synthesis of ET-1 is enhanced after subarachnoid hemorrhage (SAH) to mediate a long-lasting vasoconstriction, and PGF2a contributes to cerebral inflammation and vasoconstriction...
March 28, 2018: Current Neurovascular Research
https://www.readbyqxmd.com/read/29568973/neurogenic-inflammation-and-its-role-in-migraine
#11
REVIEW
Roshni Ramachandran
The etiology of migraine pain involves sensitized meningeal afferents that densely innervate the dural vasculature. These afferents, with their cell bodies located in the trigeminal ganglion, project to the nucleus caudalis, which in turn transmits signals to higher brain centers. Factors such as chronic stress, diet, hormonal fluctuations, or events like cortical spreading depression can generate a state of "sterile inflammation" in the intracranial meninges resulting in the sensitization and activation of trigeminal meningeal nociceptors...
March 22, 2018: Seminars in Immunopathology
https://www.readbyqxmd.com/read/29549622/targeted-acid-sensing-ion-channel-therapies-for-migraine
#12
REVIEW
Nazia Karsan, Eric B Gonzales, Gregory Dussor
Acid-sensing ion channels (ASICs) are a family of ion channels, consisting of four members; ASIC1 to 4. These channels are sensitive to changes in pH and are expressed throughout the central and peripheral nervous systems-including brain, spinal cord, and sensory ganglia. They have been implicated in a number of neurological conditions such as stroke and cerebral ischemia, traumatic brain injury, and epilepsy, and more recently in migraine. Their expression within areas of interest in the brain in migraine, such as the hypothalamus and PAG, their demonstrated involvement in preclinical models of meningeal afferent signaling, and their role in cortical spreading depression (the electrophysiological correlate of migraine aura), has enhanced research interest into these channels as potential therapeutic targets in migraine...
March 16, 2018: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/29541495/rgb-camera-based-imaging-of-cerebral-tissue-oxygen-saturation-hemoglobin-concentration-and-hemodynamic-spontaneous-low-frequency-oscillations-in-rat-brain-following-induction-of-cortical-spreading-depression
#13
Afrina Mustari, Naoki Nakamura, Satoko Kawauchi, Shunichi Sato, Manabu Sato, Izumi Nishidate
To evaluate cerebral hemodynamics and spontaneous low-frequency oscillations (SLFOs) of cerebral blood flow in rat brain, we investigated an imaging method using a digital RGB camera. In this method, the RGB values were converted into tristimulus values in the CIE (Commission Internationale de l'Eclairage) XYZ color space, which is compatible with the common RGB working spaces. Monte Carlo simulation for light transport in tissue was then used to specify the relationship among the tristimulus XYZ values and the concentrations of oxygenated hemoglobin ( C HbO ), deoxygenated hemoglobin ( C HbR ), and total hemoglobin ( C HbT ) and cerebral tissue oxygen saturation ( StO 2 )...
March 1, 2018: Biomedical Optics Express
https://www.readbyqxmd.com/read/29538620/camkii-dependent-endoplasmic-reticulum-fission-by-whisker-stimulation-and-during-cortical-spreading-depolarization
#14
Krzysztof Kucharz, Martin Lauritzen
Cortical spreading depolarization waves, the cause underlying migraine aura, are also the markers and mechanism of pathology in the acutely injured human brain. Propagation of spreading depolarization wave uniquely depends on the interaction between presynaptic and postsynaptic glutamate N-methyl-d-aspartate receptors (NMDARs). In the normally perfused brain, even a single wave causes a massive depolarization of neurons and glia, which results in transient loss of neuronal function and depression of the ongoing electrocorticographic activity...
April 1, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29527186/basilar-artery-lateral-displacement-may-be-associated-with-migraine-with-aura
#15
Cen Zhang, John A Detre, Scott E Kasner, Brett Cucchiara
Objective: The objective of this study is to determine whether structural features of the vertebrobasilar arterial system are related to migraine. Background: Alterations in cerebral vascular structure and function have been associated with migraine, possibly mediated by hypoperfusion and/or endothelial dysfunction triggering cortical spreading depression. Vessel tortuosity, in particular, has been associated with both altered hemodynamics and endothelial function...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29526745/integrated-models-of-neurovascular-coupling-and-bold-signals-responses-for-varying-neural-activations
#16
Elshin J Mathias, Allanah Kenny, Michael J Plank, Tim David
A state-of-the-art integrated model of neurovascular coupling (NVC) (Dormanns et al., 2015b; Dormanns et al., 2016; Kenny et al., 2018) and the BOLD response (Mathias et al., 2017a; Mathias et al., 2017b) is presented with the ability to simulate the fMRI BOLD responses due to continuous neuronal spiking, bursting and cortical spreading depression (CSD) along with the underlying complex vascular coupling. Simulated BOLD responses are compared to experimental BOLD signals observed in the rat barrel cortex and in the hippocampus under seizure conditions showing good agreement...
July 1, 2018: NeuroImage
https://www.readbyqxmd.com/read/29512922/bilateral-sensory-disturbance-after-cortical-spreading-depression-revealed-by-fluorescence-imaging-of-voltage-sensitive-dye
#17
Qin Huang, Rui Liu, Shen Gui, Jinling Lu, Pengcheng Li
Cortical spreading depression (CSD), a propagation wave of transient neuronal and glial depolarization followed by suppression of spontaneous brain activity, has been hypothesized to be the underlying mechanism of migraine aura and triggers the headache attack. Evidence from various animal models accumulates since its first discovery in 1944 and provides support for this hypothesis. In this paper, alterations of bilateral cortical responses are investigated in a mice migrainous model of CSD using voltage-sensitive dye imaging under hindlimb and cortical stimulation...
March 7, 2018: Journal of Biophotonics
https://www.readbyqxmd.com/read/29508147/glutamate-and-its-receptors-as-therapeutic-targets-for-migraine
#18
REVIEW
Jan Hoffmann, Andrew Charles
There is substantial evidence indicating a role for glutamate in migraine. Levels of glutamate are higher in the brain and possibly also in the peripheral circulation in migraine patients, particularly during attacks. Altered blood levels of kynurenines, endogenous modulators of glutamate receptors, have been reported in migraine patients. Population genetic studies implicate genes that are involved with glutamate signaling in migraine, and gene mutations responsible for familial hemiplegic migraine and other familial migraine syndromes may influence glutamate signaling...
April 2018: Neurotherapeutics: the Journal of the American Society for Experimental NeuroTherapeutics
https://www.readbyqxmd.com/read/29502713/cortical-spreading-depression-and-ischemia-in-neurocritical-patients
#19
REVIEW
Néstor Wainsztein, Federico Rodríguez Lucci
Spreading depolarization in cerebral cortex is associated with swelling of neurons, distortion of dendritic spines, massive ion translocation with a large change of the slow electrical potential, and silencing of brain electrical activity. The term spreading depression represents a wave of spontaneous activity of the electrocorticogram that propagates through contiguous cerebral gray matter at a characteristic velocity. Spreading depression is a consequence of cortical spreading depolarization. Therefore, spreading depolarization is not always accompanied by spreading depression and the terms are not synonymous...
April 2018: Neurosurgery Clinics of North America
https://www.readbyqxmd.com/read/29430561/the-cgrp-receptor-antagonist-bibn4096-inhibits-prolonged-meningeal-afferent-activation-evoked-by-brief-local-k-stimulation-but-not-cortical-spreading-depression-induced-afferent-sensitization
#20
Jun Zhao, Dan Levy
Introduction: Cortical spreading depression (CSD) is believed to promote migraine headache by enhancing the activity and mechanosensitivity of trigeminal intracranial meningeal afferents. One putative mechanism underlying this afferent response involves an acute excitation of meningeal afferents by cortical efflux of K+ and the ensuing antidromic release of proinflammatory sensory neuropeptides, such as calcitonin gene-related peptide (CGRP). Objectives: We sought to investigate whether (1) a brief meningeal K+ stimulus leads to CGRP-dependent enhancement of meningeal afferent responses and (2) CSD-induced meningeal afferent activation and sensitization involve CGRP receptor signaling...
January 2018: Pain Reports (Baltimore, Md.)
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