The slow voltage variation of cortical spreading depression of activity
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Cited by (83)
Acute and chronic cardiorespiratory consequences of focal intrahippocampal administration of seizure-inducing agents. Implications for SUDEP
2021, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Spreading depolarization has been reported in the brainstem of several genetically altered strains of mice expressing epilepsy-related mutations. The prototype for this phenomenon is spreading depression in the cerebral cortex (Leao, 1951), which essentially is a slowly propagating process where neurons depolarize so much that their sodium channels inactivate and membranes become highly permeable. Using hippocampal slices exposed to low calcium solutions in vitro, we found a similar, but less disruptive, process we termed field bursts; they lasted tens of seconds rather than many minutes, and could recur much more frequently than spreading depression (Bikson et al., 2003; Jefferys and Haas, 1982; Jiruska et al., 2010).
Resuscitating the Globally Ischemic Brain: TTM and Beyond
2020, NeurotherapeuticsEvidence for distinct clusters of diverse anomalous experiences and their selective association with signs of elevated cortical hyperexcitability
2019, Consciousness and CognitionCitation Excerpt :Aberrant excitation in the cerebral cortex has long been associated with the formation of both elementary and complex hallucinations (Elliott, Joyce, & Shorvon, 2009; ffytche et al., 1998; Manford & Andermann, 1998; McGuire, Murray, & Shah, 1993; Panayiotopoulos, 1994; Sass & Parnas, 2003). For example, patients who have been diagnosed with complex partial seizures of the temporal lobe, migraine with aura, and schizophrenia will commonly report a host of auric hallucinatory experiences – and all these conditions/disorders are associated with increased and excessive neural activity (see Abraham & Duffy, 2001; Dahlem & Müller, 2003; Dahlem, Engelmann, Löwel, & Müller, 2000; Hadjikhani et al., 2001; Lauritzen, 2001; Leão, 1951; Merabet, Kobayashi, Barton, & Pascual-Leone, 2003; Salanova, Andermann, Oliver, Rasmussen, & Quesney, 1992; van den Maagdenberg et al., 2004; Weiss & Heckers, 1999). Neurological studies have supported the association between the underlying degree of visual cortical hyperexcitability and resultant aberrant experience (Abraham & Duffy, 2001; Dahlem & Müller, 2003; Salanova et al., 1992; Weiss & Heckers, 1999).
Epilepsy and migraine—Are they comorbidity?
2018, Genes and DiseasesCitation Excerpt :He observed in animal experiments with cortical EEG when the cortex encountered adverse stimulus, it would appear after occipital EEG activity decreased to about 2–6 mm/min speed slow forward and expand accompanied by a large number of ions transfer called CSD. Animal studies have shown that at the beginning of CSD, neurons and glial cells are depolarized with a sudden occurrence of a few seconds of high spike wave activity (representing a potential local epileptic discharge event), followed by a resting state of nerve cells for several minutes.76 These high spike waves are different from epileptic seizures, but they have potential properties that prompt synchronization of the neural network and promote seizures and spread under certain conditions.