• Corpus ID: 4824491

27 Pathophysiology of Neocortical Epileptic Seizures

@inproceedings{Timofeev201027PO,
  title={27 Pathophysiology of Neocortical Epileptic Seizures},
  author={Igor Timofeev},
  year={2010}
}
Introduction and Definitions Neocortical seizures are seizures that are primarily generated within neocortex. Seizures for which primary foci are located in other brain structures and secondarily project to neocortex are not considered to be neocortical. The origin of epileptic seizures accompanying various types of epileptic fits is hotly debated. Neocortical seizures are primarily focal and often become secondarily generalized tonic-clonic seizures (Crunelli and Leresche 2002… 

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Thalamocortical oscillations: local control of EEG slow waves.

TLDR
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Neural Mass Activity, Bifurcations, and Epilepsy

TLDR
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References

SHOWING 1-10 OF 19 REFERENCES

Neocortical seizures: initiation, development and cessation

Relations between cortical and thalamic cellular events during transition from sleep patterns to paroxysmal activity

  • M. SteriadeD. Contreras
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1995
TLDR
It is proposed that the inhibitory processes found in a significant number of TC cells during cortical SW seizures may contribute to the loss of consciousness, due to obliteration of synaptic transmission through the thalamus.

On the cellular and network bases of epileptic seizures.

TLDR
Although epileptic syndromes and their causes are diverse, the cellular mechanisms of seizure generation appear to fall into only two categories: rhythmic or tonic "runaway" excitation or the synchronized and rhythmic interplay between excitatory and inhibitory neurons and membrane conductances.

High‐frequency oscillations: What is normal and what is not?

TLDR
Investigation into the fundamental neuronal processes responsible for pHFOs could provide insights into basic mechanisms of epilepsy, and the potential for pH FOs to act as biomarkers for epileptogenesis and epileptogenicity is also discussed.

How do seizures stop?

TLDR
Known physiological mechanisms contributing to seizure termination are reviewed and additional mechanisms that are likely to be relevant even though specific data are not yet available are discussed.

Nonsynaptic modulation of neuronal activity in the brain: electric currents and extracellular ions.

TLDR
Field effects and ion fluctuations probably have modest effects during physiological activity but have a significant impact on epileptic seizures, and can sustain them in the absence of synaptic transmission.

Posttraumatic Epilepsy: The Roles of Synaptic Plasticity

TLDR
Recent morphological, electrophysiological, and computational studies demonstrating that partial cortical isolation increases the number and duration of silent states in the cortical network, boosting neuronal connectivity and network excitability are summarized.

Cortical dysplasia and epilepsy: animal models.

TLDR
Animal models of cortical dysplasia provide a means by which investigators can not only study the developmental mechanisms that give rise to these brain lesions, but also examine the cause-effect relationships between structural abnormalities and epileptogenesis.

Giant synaptic potential hypothesis for epileptiform activity.

According to one hypothesis, the paroxysmal depolarizing shift observed in the penicillin model of epilepsy results from a giant excitatory postsynaptic potential. This hypothesis has recently been