Cortical spreading depression and spreading depolarization (CSD) are waves of neuronal depolarization that spread across the cortex, leading to a temporary saturation of brain activity. They are associated with various brain disorders such as migraine and ischemia. We consider a reduced version of a biophysical model of a neuron-astrocyte network for the initiation and propagation of CSD waves [Huguet et al., Biophys. J. 111(2), 452-462, 2016], consisting of reaction-diffusion equations. The reduced model considers only the dynamics of the neuronal and astrocytic membrane potentials and the extracellular potassium concentration, capturing the instigation process implicated in such waves. We present a computational and mathematical framework based on the parameterization method and singular perturbation theory to provide semi-analytical results on the existence of a wave solution and to compute it jointly with its velocity of propagation. The traveling wave solution can be seen as a heteroclinic connection of an associated system of ordinary differential equations with a slow-fast dynamics. The presence of distinct time scales within the system introduces numerical instabilities, which we successfully address through the identification of significant invariant manifolds and the implementation of the parameterization method. Our results provide a methodology that allows to identify efficiently and accurately the mechanisms responsible for the initiation of these waves and the wave propagation velocity.
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http://dx.doi.org/10.1063/5.0160509 | DOI Listing |
Exp Neurol
December 2024
Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45267, USA; Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, OH 45267, USA. Electronic address:
Cortical spreading depolarizations (CSDs) are the most common electrophysiological dysfunction following a traumatic brain injury (TBI), and clustered CSDs (≥3 CSDs in 2 h) are associated with poor outcomes 6 months after TBI. While many experimental studies have investigated a single CSD after injury, no known studies have investigated how time after injury affects the characteristics and impact of a CSD cluster. This study sought to determine the characteristics of a cluster of repetitive CSDs when induced at three different time points after moderate experimental TBI.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Laboratory of Neuropathology, Department of Imaging and Pathology, Leuven Brain Institute, KU Leuven, Leuven, Belgium.
The accumulation of abnormal phosphorylated Tau protein (pTau) in neurons of the brain is a pathological hallmark of Alzheimer's disease (AD). PTau pathology also occurs in the retina of AD cases. Accordingly, questions arise whether retinal pTau can act as a potential seed for inducing cerebral pTau pathology and whether retinal pTau pathology causes degeneration of retinal neurons.
View Article and Find Full Text PDFJ Headache Pain
December 2024
Translational Research Center and Danish Headache Center, Rigshospitalet, University of Copenhagen, Nordstjernevej 42, Glostrup, Copenhagen, 2600, Denmark.
Introduction: It is largely accepted that migraine with aura (MA) is caused by cortical spreading depression (CSD) and that migraine without aura (MO) is not. This is mostly based on old studies of regional cerebral blood flow (rCBF) and studies of vascular responses. These studies are partly forgotten today and may, therefore, be worthwhile reviewing.
View Article and Find Full Text PDFGigascience
January 2024
Technical University of Munich, School of Medicine, rechts der Isar Hospital, Clinical Department of Neurology, Munich 81675, Germany.
Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease, which still lacks effective disease-modifying therapies. Similar to other neurodegenerative disorders, such as Alzheimer and Parkinson disease, ALS pathology is presumed to propagate over time, originating from the motor cortex and spreading to other cortical regions. Exploring early disease stages is crucial to understand the causative molecular changes underlying the pathology.
View Article and Find Full Text PDFFront Neurosci
December 2024
Department of Paediatrics, University Hospital Brno, Faculty of Medicine, Masaryk University Brno, Brno, Czechia.
Background: The research on possible cerebral involvement in Crohn's disease (CD) has been largely marginalized and failed to capitalize on recent developments in magnetic resonance imaging (MRI).
Objective: This cross-sectional pilot study searches for eventual macrostructural and microstructural brain affection in CD in remission and early after the disease onset.
Methods: 14 paediatric CD patients and 14 healthy controls underwent structural, diffusion weighted imaging and quantitative relaxation metrics acquisition, both conventional free precession and adiabatic rotating frame transverse and longitudinal relaxation time constants as markers of myelination, iron content and cellular loss.
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