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Seizures

  • Elisabeth Ronne-Engström
Chapter

Abstract

There are no randomised, controlled, double-blind studies regarding treatment of early seizures after TBI, but from observational studies in the literature, there are good reasons to believe that seizures should be treated as soon as they occur. The basic idea with neurointensive care of TBI is to identify and treat conditions that compromise the brain’s supply and use of oxygen and glucose. Seizure activity in the acute phase impairs this in a number of ways and can therefore worsen the brain trauma. Neuronal firing causes a massive release of the potentially neurotoxic transmitter glutamate (GLU). In order to clear the synaptic space from GLU, there is an efficient glial uptake. However, this is highly energy dependent. Seizure activity can thus cause a significant increase in the energy demand, which can turn the brain into a manifest ischemia due to energy failure. Seizure activity can also cause significant changes in cerebral blood flow, with both increases and decreases observed.

Keywords

Traumatic Brain Injury Status Epilepticus Seizure Activity Traumatic Brain Injury Patient Energy Failure 
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.

References

  1. Adelson PD, Bratton SL, Carney NA, Chesnut RM, Du Coudray HEM, Goldstein B, Kochanek PM, Miller HC, Partington MD, Selden NR, Warden CR, Wright DW (2003) Guidelines for the acute medical treatment of severe traumatic brain injury in infants, children and adolescents. Chapter 19; The role of anti-seizure prophylaxis following severe traumatic brain injury. Pediatr Crit Care Med 31(6 Suppl):S488–S491Google Scholar
  2. Annegers JF, Coan SP (2000) The risks of epilepsy after traumatic brain injury. Seizure 9(7):453–457PubMedCrossRefGoogle Scholar
  3. Bratton SL et al (2007) Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. J Neurotrauma 24 Suppl 1:S83–S86PubMedGoogle Scholar
  4. During MJ, Spencer DD (1993) Extracellular hippocampal glutamate and spontaneous seizure in the conscious human brain. Lancet 341(8861):1607–1610PubMedCrossRefGoogle Scholar
  5. Emanuelson I, Uvebrant P (2009) Occurrence of epilepsy during the first 10 years after traumatic brain injury acquired in childhood up to the age of 18 years in the south western Swedish population-based series. Brain Inj 23(7):612–616PubMedCrossRefGoogle Scholar
  6. Liesemer K et al (2011) Early post-traumatic seizures in moderate to severe pediatric traumatic brain injury: rates, risk factors, and clinical features. J Neurotrauma 28(5):755–762PubMedCrossRefGoogle Scholar
  7. Lowenstein DH (2009) Epilepsy after head injury: an overview. Epilepsia 50(Suppl 2):4–9PubMedCrossRefGoogle Scholar
  8. Magistretti PJ, Pellerin L (1999) Astrocytes couple synaptic activity to glucose utilization in the brain. News Physiol Sci 14:177–182PubMedGoogle Scholar
  9. Olivecrona M et al (2009) Absence of electroencephalographic seizure activity in patients treated for head injury with an intracranial pressure-targeted therapy. J Neurosurg 110(2):300–305PubMedCrossRefGoogle Scholar
  10. Pohlmann-Eden B, Bruckmeir J (1997) Predictors and dynamics of posttraumatic epilepsy. Acta Neurol Scand 95(5):257–262PubMedCrossRefGoogle Scholar
  11. Ronne-Engstrom E, Winkler T (2006) Continuous EEG monitoring in patients with traumatic brain injury reveals a high incidence of epileptiform activity. Acta Neurol Scand 114(1):47–53PubMedCrossRefGoogle Scholar
  12. Ronne-Engstrom E et al (1992) Intracerebral microdialysis of extracellular amino acids in the human epileptic focus. J Cereb Blood Flow Metab 12(5):873–876PubMedCrossRefGoogle Scholar
  13. Ronne-Engstrom E, Carlson H, Blom S, Flink R, Gazelius B, Spännare B, Hillered L (1993) Monitoring of cortical blood flow in human epileptic foci using laser doppler flowmetry. J Epilepsy 6:145–151CrossRefGoogle Scholar
  14. Samuelsson C et al (2007) Cerebral glutamine and glutamate levels in relation to compromised energy metabolism: a microdialysis study in subarachnoid hemorrhage patients. J Cereb Blood Flow Metab 27(7):1309–1317PubMedCrossRefGoogle Scholar
  15. Vespa P (2005) Continuous EEG monitoring for the detection of seizures in traumatic brain injury, infarction, and intracerebral hemorrhage: “to detect and protect”. J Clin Neurophysiol 22(2):99–106PubMedCrossRefGoogle Scholar
  16. Vespa P et al (1998) Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study. J Neurosurg 89(6):971–982PubMedCrossRefGoogle Scholar
  17. Vespa PM et al (1999) Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring. J Neurosurg 91(5):750–760PubMedCrossRefGoogle Scholar
  18. Vespa PM et al (2007) Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis. Crit Care Med 35(12):2830–2836PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  1. 1.Department of NeurosurgeryUppsala University HospitalUppsalaSweden

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