Cortical spreading depression: culprits and mechanisms

Mathew, Aparna Ann; Panonnummal, Rajitha

doi:10.1007/s00221-022-06307-9

Cited by 14 publications

(5 citation statements)

References 114 publications

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“…Increased MO of the inferior fronto-occipital fasciculus implies an abnormal information flow from the occipital lobe to other cortical regions due to a loss of crossing fibers, and thus may lead to the hyper-excitability of the visual cortex. It is thought that the increased excitability of the visual cortex predisposes the brain to develop spontaneous neuronal depolarization, which may lead to cortical spreading depression (CSD), triggering headaches [ 47 ]. The CSD is a wave of slowly propagating depolarization followed by sustained suppression of neural activity, and has been thought to be the underlying mechanism of migraine [ 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Causal relationships between migraine and microstructural white matter: a Mendelian randomization study

Zhao

Zhao²,

Anttila³

et al. 2023

J Headache Pain

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Background Migraine is a disabling neurological disorder with the pathophysiology yet to be understood. The microstructural alteration in brain white matter (WM) has been suggested to be related to migraine in recent studies, but these evidence are observational essentially and cannot infer a causal relationship. The present study aims to reveal the causal relationship between migraine and microstructural WM using genetic data and Mendelian randomization (MR). Methods We collected the Genome-wide association study (GWAS) summary statistics of migraine (48,975 cases / 550,381 controls) and 360 WM imaging-derived phenotypes (IDPs) (31,356 samples) that were used to measure microstructural WM. Based on instrumental variables (IVs) selected from the GWAS summary statistics, we conducted bidirectional two-sample MR analyses to infer bidirectional causal associations between migraine and microstructural WM. In forward MR analysis, we inferred the causal effect of microstructural WM on migraine by reporting the odds ratio (OR) that quantified the risk change of migraine for per 1 standard deviation (SD) increase of IDPs. In reverse MR analysis, we inferred the causal effect of migraine on microstructural WM by reporting the β value that represented SDs of changes in IDPs were caused by migraine. Results Three WM IDPs showed significant causal associations (p < 3.29 × 10− 4, Bonferroni correction) with migraine and were proved to be reliable via sensitivity analysis. The mode of anisotropy (MO) of left inferior fronto-occipital fasciculus (OR = 1.76, p = 6.46 × 10− 5) and orientation dispersion index (OD) of right posterior thalamic radiation (OR = 0.78, p = 1.86 × 10− 4) exerted significant causal effects on migraine. Migraine exerted a significant causal effect on the OD of left superior cerebellar peduncle (β = − 0.09, p = 2.78 × 10− 4). Conclusions Our findings provided genetic evidence for the causal relationships between migraine and microstructural WM, bringing new insights into brain structure for the development and experience of migraine.

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Section: Discussionmentioning

confidence: 99%

Causal relationships between migraine and microstructural white matter: a Mendelian randomization study

Zhao

Zhao²,

Anttila³

et al. 2023

J Headache Pain

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“…Also unclear is whether similar metabolic processes may play a role in cortical spreading depression (CSD), an electrophysiological phenomenon involving a local depression of neuronal activity which can spread to adjacent areas and can be observed in association with numerous neurological disorders, including epileptic seizures, ischemic stroke, traumatic brain injury and migraine with aura [44,45]. CSD is characterized by a brief neuronal excitation followed by a long-lasting depression of cortical activity.…”

Section: Metabolic Constraints Induced By Epileptic Seizures and Isch...mentioning

confidence: 99%

Cellular Stress, Energy Constraints and the Energy Allocation Hypothesis of Sleep

Schmidt,

Schindler

2024

CTN

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A growing body of literature demonstrates a critical role for sleep in upregulating diverse biological processes related to protein synthesis, immune function, and cellular housekeeping such as intracellular transport and membrane repair. The energy allocation (EA) hypothesis places sleep in a broader context of resource optimization where sleep–wake partitioning of metabolic operations optimizes resource utilization. The EA hypothesis of sleep carries important implications in health, disease, and homeostatic mechanisms. Specifically, conditions that lead to cellular stress, energy constraints or depression of neuronal activity, such as epilepsy, ischemic stroke or cortical spreading depression, are here proposed to follow similar conserved processes that favor sleep. This review examines the role of local mechanisms, including cytokine release or the accumulation of adenosine, in downregulating wakefulness to favoring sleep, loss of functional connectivity and the upregulation sleep-coupled processes that promote survival.

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“…In order to explain how the electrical phenomenon is triggered, several hypotheses have been made: Harreveld [ 56 ] and Grafstein [ 57 ], supposed a role of various conditions such as hypoxia, ischemia, and hypoglycemic activity [ 55 ]. A recent review collates most of the triggering factors that make one prone to the CSD condition, listed below [ 58 ]: Inadequate tissue oxygenation; Fluctuations in ionic concentration (potassium, calcium, sodium, chloride); Change in direct current potential; Cytotoxic edema, mediated by higher osmolality (more significant influx of sodium and calcium); Dendritic beading with spine loss; Alteration in glucose metabolism; Lactic acid accumulation; Decreases in pH and ATP with increased cAMP and ADP levels; Disregulation of release and diffusion of serotonin, neurokinin, calcitonin gene-related peptide, and brain-derived neurotrophic factor. …”

Section: Pathophysiology: Neocortical Dysexcitabilitymentioning

confidence: 99%

A Narrative Review of Visual Hallucinations in Migraine and Epilepsy: Similarities and Differences in Children and Adolescents

D’Agnano

Cascio

Correnti³

et al. 2023

Brain Sciences

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Since the earliest descriptions of the simple visual hallucinations in migraine patients and in subjects suffering from occipital lobe epilepsy, several important issues have arisen in recognizing epileptic seizures of the occipital lobe, which often present with symptoms mimicking migraine. A detailed quantitative and qualitative clinical scrutiny of timing and characteristics of visual impairment can contribute to avoiding mistakes. Differential diagnosis, in children, might be challenging because of the partial clinical, therapeutic, and pathophysiological overlaps between the two diseases that often coexist. Ictal elementary visual hallucinations are defined by color, shape, size, location, movement, speed of appearance and duration, frequency, and associated symptoms and their progression. The evaluation of the distinctive clinical features of visual aura in migraine and visual hallucinations in occipital epilepsy could contribute to understanding the pathogenetic mechanisms of these two conditions. This paper aims to critically review the available scientific evidence on the main clinical criteria that address diagnosis, as well as similarities and differences in the pathophysiological mechanisms underlying the visual impairment in epilepsy and migraine.

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Cortical spreading depression: culprits and mechanisms

Cited by 14 publications

References 114 publications

Causal relationships between migraine and microstructural white matter: a Mendelian randomization study

Causal relationships between migraine and microstructural white matter: a Mendelian randomization study

Cellular Stress, Energy Constraints and the Energy Allocation Hypothesis of Sleep

A Narrative Review of Visual Hallucinations in Migraine and Epilepsy: Similarities and Differences in Children and Adolescents

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