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Pathophysiology of Termination of Seizures

  • Stephen Fried
  • Fred A. Lado
Reference work entry

Introduction and Definitions

The pathophysiology of seizure termination is often overshadowed by the factors contributing to seizure initiation and propagation. Nevertheless, seizure termination is a critical factor in the return to the interictal or postictal state. The mechanisms involved in this process range in scale from the regulation of transmembrane potentials, to local neuronal network interactions, to mediation from relatively remote structures such as the brain stem and basal ganglia. This chapter discusses the roles of mechanisms that are involved in seizure termination in successively increasing “size scales,” subdivided into (1) those acting at the level of single neurons, (2) those acting on a local network of neurons, and (3) those acting remotely to limit excitation and seizure spread.

Structural and Functional Correlates

Mechanisms Acting at the Level of Single Neurons

Several mechanisms are involved in seizure termination at the neuronal level ( Fig. 37-1). The first...

Keywords

Status Epilepticus Silent Period Seizure Termination Seizure Discharge Seizure Onset Zone 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

List of Abbreviations

ATP

Adenosine triphosphate

EPSC

Excitatory post-synaptic current

EEG

Electroencephalography

NPY

Neuropeptide-Y

STN

Subthalamic nucleus

SNR

Substantia nigra pars reticulata

References

  1. Bikson M, Hahn PJ, Fox JE, Jeffreys JG (2003) Depolarization block of neurons during maintenance of electrographic seizures. J Neurophysiol 90:2402–2408CrossRefPubMedGoogle Scholar
  2. Chen JW, Naylor DE, Wasterlain CG (2007) Advances in the pathophysiology of status epilepticus. Acta Neurol Scand 115(Suppl 186):7–15CrossRefPubMedGoogle Scholar
  3. de Curtis M, Manfridi A, Biella G (1998) Activity-dependent pH shifts and periodic recurrence of spontaneous interictal spikes in a model of focal epileptogenesis. J Neurosci 18:7543–7551PubMedGoogle Scholar
  4. Groves DA, Brown VJ (2005) Vagal nerve stimulation: a review of its applications and potential mechanisms that mediate its clinical effects. Neurosci Biobehav Rev 29:493–500CrossRefPubMedGoogle Scholar
  5. Heinemann U, Lux HD, Gutnick MJ (1977) Extracellular free calcium and potassium during paroxsmal activity in the cerebral cortex of the cat. Exp Brain Res 27:237–243CrossRefPubMedGoogle Scholar
  6. Jenssen S, Gracely EJ, Sperling MR (2006) How long do most seizures last? A systematic comparison of seizures recorded in the epilepsy monitoring unit. Epilepsia 47:1499–1503CrossRefPubMedGoogle Scholar
  7. Kirchner A, Veliskova J, Velisek L (2006) Differential effects of low glucose concentrations on seizures and epileptiform activity in vivo and in vitro. Eur J Neurosci 23:1512–1522CrossRefPubMedGoogle Scholar
  8. Koo B (2001) EEG changes with vagus nerve stimulation. J Clin Neurophysiol 18:434–441CrossRefPubMedGoogle Scholar
  9. Mancilla JG, Lewis TJ, Pinto DJ, Rinzel J, Connors BW (2007) Synchronization of electrically coupled pairs of inhibitory interneurons in neocortex. J Neurosci 27:2058–2073CrossRefPubMedGoogle Scholar
  10. NeuroPace (2008) Responsive Neurostimulator (RNSTM) System Long-Term Treatment Clinical Investigation. In: ClinicalTrials.gov [Internet]. National Library of Medicine (US), Bethesda, p 2000Google Scholar
  11. Ochoa JG (2006) Oral electrolyte therapy for refractory epilepsy. American Epilepsy Society Annual Meeting, San DiegoGoogle Scholar
  12. Schweitzer JS, Wang H, Xiong ZQ, Stringer JL (2000) pH Sensitivity of non-synaptic field bursts in the dentate gyrus. J Neurophysiol 84:927–933PubMedGoogle Scholar
  13. Shinnar S, Berg AT, Moshe SL, Shinnar R (2001) How long do new-onset seizures in children last? Ann Neurol 49:659–664CrossRefPubMedGoogle Scholar
  14. Spray DC, Harris AL, Bennett MV (1981) Gap junctional conductance is a simple and sensitive function of intracellular pH. Science 211:712–715CrossRefPubMedGoogle Scholar
  15. Staley KJ, Longacher M, Bains JS, Yee A (1998) Presynaptic modulation of CA3 network activity. Nat Neurosci 1:201–209CrossRefPubMedGoogle Scholar
  16. Stell BM, Brickley SG, Tang CY, Farrant M, Mody I (2003) Neuroactive steroids reduce neuronal excitability by selectively enhancing tonic inhibition mediated by delta subunit-containing GABAA receptors. Proc Natl Acad Sci USA 100:14439–14444CrossRefPubMedGoogle Scholar
  17. Young D, Dragunow M (1994) Status epilepticus may be caused by loss of adenosine anticonvulsant mechanisms. Neuroscience 58:245–261CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag London Limited 2010

Authors and Affiliations

  • Stephen Fried
    • 1
  • Fred A. Lado
    • 1
  1. 1.Department of NeurologyMontefiore Medical Center/Albert Einstein College of MedicineBronxUSA

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