Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip

Bowyer, Susan M.; Okada, Yoshio; Papuashvili, Nicholas; Moran, John; Barkley, Gregory L.; Welch, K. M. A.; Tepley, N.

doi:10.1016/s0006-8993(99)01892-2

Cited by 55 publications

(43 citation statements)

References 28 publications

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“…Taking into account these observations and timely estimations of the cortical conductivity (e.g., rabbits: 2.73-3.62 mS/cm, Ranck 1963; cats: 1.66 -1.96 mS/cm, Li et al 1968), it was possible through the use of the methodology proposed by Humphrey (1968) to obtain ranges (100 -250 nA/mm 2 ) for the typical transcortical current densities (Freeman 1975;Pollen 1969), which remain valid to this day (Baillet et al 2001). The strengths and spatial extensions of cortical dipoles were in agreement with estimations obtained from EEG and MEG data (10 -100 nA·m: Bowyer et al 1999;Cohen and Cuffin 1983;Chapman et al 1984;Jones et al 2007Jones et al , 2009). In addition, these values were compatible with later predictions of the transcortical current density from anatomophysiological considerations (Hämäläinen and Ilmoniemi 1984;Hämäläinen et al 1993;Hari and Ilmoniemi 1986).…”

supporting

confidence: 69%

Pitfalls in the dipolar model for the neocortical EEG sources

Riera

Ogawa

Goto

et al. 2012

Journal of Neurophysiology

111

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For about six decades, primary current sources of the electroencephalogram (EEG) have been assumed dipolar in nature. In this study, we used electrophysiological recordings from anesthetized Wistar rats undergoing repeated whisker deflections to revise the biophysical foundations of the EEG dipolar model. In a first experiment, we performed threedimensional recordings of extracellular potentials from a large portion of the barrel field to estimate intracortical multipolar moments generated either by single spiking neurons (i.e., pyramidal cells, PC; spiny stellate cells, SS) or by populations of them while experiencing synchronized postsynaptic potentials. As expected, backpropagating spikes along PC dendrites caused dipolar field components larger in the direction perpendicular to the cortical surface (49.7 Ϯ 22.0 nA·mm). In agreement with the fact that SS cells have "close-field" configurations, their dipolar moment at any direction was negligible. Surprisingly, monopolar field components were detectable both at the level of single units (i.e., Ϫ11.7 Ϯ 3.4 nA for PC) and at the mesoscopic level of mixed neuronal populations receiving extended synaptic inputs within either a cortical column (Ϫ0.44 Ϯ 0.20 A) or a 2.5-m 3 -voxel volume (Ϫ3.32 Ϯ 1.20 A). To evaluate the relationship between the macroscopically defined EEG equivalent dipole and the mesoscopic intracortical multipolar moments, we performed concurrent recordings of high-resolution skull EEG and laminar local field potentials. From this second experiment, we estimated the time-varying EEG equivalent dipole for the entire barrel field using either a multiple dipole fitting or a distributed type of EEG inverse solution. We demonstrated that mesoscopic multipolar components are altogether absorbed by any equivalent dipole in both types of inverse solutions. We conclude that the primary current sources of the EEG in the neocortex of rodents are not precisely represented by a single equivalent dipole and that the existence of monopolar components must be also considered at the mesoscopic level.electroencephalogram; neocortex; multipolar current sources; inverse problem THE DIPOLAR MODEL, used by generations of neuroscientists to represent the current sources of the electroencephalogram (EEG) in humans (Niedermeyer and Lopes da Silva 1987; Nunez and Srinivansan 2006;Plonsey 1969;Walter and Walter 1949), has roots in early interpretations by Adrian and Matthews (1934) about the origin of the Berger rhythm (i.e., the alpha rhythm). These authors suggested that the cortical electric potentials formerly observed by Berger (1929) were caused by electrical sources close to the brain surface with a polarity inversion in the axis perpendicular to it. The existence of dipole-like field distributions with axes parallel to the cortical surface was later suggested by Beevers (1944), with confirmations for the kappa rhythm (Kennedy et al. 1948) and the epileptic focal seizures (Gumnit and Takahashi 1965). This model, which eventually gained popularity in many other eme...

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supporting

confidence: 69%

Pitfalls in the dipolar model for the neocortical EEG sources

Riera

Ogawa

Goto

et al. 2012

Journal of Neurophysiology

111

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“…This demonstrates the occurrence of a stereotyped process, spreading at a constant speed. These 2 electrodes straddled the superior temporal sulcus, which may account for the low speed of propagation calculated for ECoG events at these electrodes (in cats 13 [gyrencephalic] PIDs invariably spread around the full depth of a sulcus rather than bridging it, and propagation in sulci is slower than over gyri 14 ).…”

Section: Resultsmentioning

confidence: 99%

Spreading and Synchronous Depressions of Cortical Activity in Acutely Injured Human Brain

Strong

Fabricius

Boutelle

et al. 2002

Stroke

395

284

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Background and Purpose-Cortical spreading depression (CSD) has been much studied experimentally but never demonstrated unequivocally in human neocortex by direct electrophysiological recording. A similar phenomenon, peri-infarct depolarization, occurs in experimental models of stroke and causes the infarct to enlarge. Our current understanding of the mechanisms of deterioration in the days after major traumatic or ischemic brain injury in humans has not yielded any effective, novel drug treatment. This study sought clear evidence for the occurrence and propagation of CSD in the injured human brain. Methods-In 14 patients undergoing neurosurgery after head injury or intracranial hemorrhage, we placed electrocorticographic (ECoG) electrodes near foci of damaged cortical tissue. Results-Transient episodes of depressed ECoG activity that propagated across the cortex at rates in the range of 0.6 to 5.0 mm/min were observed in 5 patients; this rate of propagation is characteristic of CSD. We also observed, in 8 of the 14 patients, transient depressions of ECoG amplitude that appeared essentially simultaneous in all recording channels, without clear evidence of spread. Conclusions-These results indicate that CSD or similar events occur in the injured human brain and are more frequent than previously suggested. On the basis of these observations, we suggest that the related phenomenon, peri-infarct depolarization, is indeed likely to occur in boundary zones in the ischemic human cerebral cortex.

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“…Both the migraine aura and CSD propagate along the cortical surface (Hadjikhani et al, 2001) (Figure 1). For the human aspects, it is important that CSD tends to become extinct when propagating into a sulcus (Bowyer et al, 1999). The rate of spread of the migraine aura corresponds to a propagating velocity of the CSD of 2 to 6 mm/min, that is the rate of spread of CSD is variable, especially in gyrencephalic animals.…”

Section: Migrainementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

682

582

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Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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Analysis of MEG signals of spreading cortical depression with propagation constrained to a rectangular cortical strip

Cited by 55 publications

References 28 publications

Pitfalls in the dipolar model for the neocortical EEG sources

Pitfalls in the dipolar model for the neocortical EEG sources

Spreading and Synchronous Depressions of Cortical Activity in Acutely Injured Human Brain

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

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