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Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
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Epilepsy is primarily characterized by unpredictable seizures, either provoked by an identifiable factor, such as injury or illness, or unprovoked, occurring spontaneously without apparent cause.
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Rodent and human seizures demonstrate a dynamic interplay with spreading depolarizations.

Jacob H Norby1, Daniel Hummel1, Noah Ricks2

  • 1Department of Cell Biology and Physiology, Brigham Young University, Provo, UT, USA; Neuroscience Center, Brigham Young University, Provo, UT, USA.

Neurobiology of Disease
|May 10, 2025
PubMed
Summary

Spreading depolarizations (SDs) prominently follow seizures in humans and rodents, shortening seizure duration. Increased low gamma activity, not potassium levels, predicts SD induction, suggesting SDs as a target for seizure termination.

Keywords:
EpilepsyIctal dischargeInfraslow oscillationsSpreading depression

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Area of Science:

  • Neuroscience
  • Epilepsy Research
  • Clinical Neurophysiology

Background:

  • Spreading depolarizations (SDs) are implicated in seizure termination in experimental epilepsy models.
  • The precise mechanisms and occurrence of SDs during human seizures remain debated.
  • Understanding SDs' role is crucial for developing novel seizure control strategies.

Purpose of the Study:

  • To investigate the co-occurrence and characteristics of SDs during human and rodent seizures.
  • To elucidate the mechanisms underlying SD induction during ictal events.
  • To explore the potential of SDs for premature seizure termination.

Main Methods:

  • Analysis of human clinical electroencephalography (EEG) recordings during seizures.
  • Electrophysiological recordings in a rodent model of ictogenesis.
  • Correlation analysis of SD occurrence with seizure duration, low gamma activity, and extracellular potassium ([K+]o) levels.

Main Results:

  • SDs were prominent features following ictal events in both human and rodent data.
  • SDs were associated with shorter seizure-like events (SLEs) and delayed subsequent SLEs in rodents.
  • Increased low gamma activity during SLEs predicted SD induction more strongly than [K+]o levels.

Conclusions:

  • SDs are a hallmark of ictal activity and are strongly associated with seizure termination.
  • Neuronal dynamics, particularly increased low gamma activity, play a key role in SD induction during seizures.
  • These findings support further investigation of SDs as a therapeutic target for premature seizure termination.