Skip to main content

Neuropathology of Generalized Convulsive Status Epilepticus

  • Chapter
  • First Online:
Status Epilepticus

Part of the book series: Current Clinical Neurology ((CCNEU))

Abstract

Generalized convulsive status epilepticus is a life-threatening condition with high mortality; it also causes cellular damage. Systemic physiologic changes in blood pressure, oxygenation, and temperature can cause widespread neuronal injury, but even when systemic physiologic parameters are controlled, status epilepticus can cause focal cell loss in the hippocampus. There is progressive loss of GABAergic inhibitory neurotransmission and sustained glutamatergic excitatory neurotransmission during the course of status epilepticus. Glutamate-mediated excitotoxicity is the most likely cause of focal neuronal injury. If status epilepticus continues for more than an hour, these changes can eventually result in hippocampal cell death, probably because N-methyl-d-aspartate (NMDA) glutamate receptors are concentrated in this region. The pattern of cell loss is similar to hypoxic cell damage but is also distinct and identical to the pattern of cell loss found in medial temporal lobe epilepsy due to hippocampal sclerosis. Early treatment of status epilepticus is necessary to prevent irreversible neuronal injury and cell death.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

eBook
USD 16.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 159.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Similar content being viewed by others

References

  1. Dodrill CB, Wilensky AJ. Intellectual impairment as an outcome of status epilepticus. Neurology. 1990;40(Suppl 2):23–7.

    CAS  PubMed  Google Scholar 

  2. Aicardi J, Chevrie JJ. Convulsive status epilepticus in infants and children. A study of 239 cases. Epilepsia. 1970;11(2):187–97.

    Article  CAS  PubMed  Google Scholar 

  3. Lothman EW, Bertram EH. Epileptogenic effects of status epilepticus. Epilepsia. 1993;34(Suppl 1):S59–70.

    Article  PubMed  Google Scholar 

  4. Kapur J. Status epilepticus in epileptogenesis. Curr Opin Neurol. 1999;12(2):191–5.

    Article  CAS  PubMed  Google Scholar 

  5. Hesdorffer DC, Logroscino G, Cascino G, Annegers JF, Hauser WA. Incidence of status epilepticus in Rochester, Minnesota, 1965–1984. Neurology. 1998;50(3):735–41.

    Article  CAS  PubMed  Google Scholar 

  6. Eriksson KJ, Koivikko MJ. Status epilepticus in children: aetiology, treatment, and outcome. Dev Med Child Neurol. 1997;39(10):652–8.

    Article  CAS  PubMed  Google Scholar 

  7. Gaspard N, Foreman BP, Alvarez V, Cabrera Kang C, Probasco JC, Jongeling AC, et al. Critical Care EEG Monitoring Research Consortium (CCEMRC). New-onset refractory status epilepticus: Etiology, clinical features, and outcome. Neurology. 2015;85(18):1604–13.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Hesdorffer DC, Logroscino G, Cascino G, Annegers JF, Hauser WA. Risk of unprovoked seizure after acute symptomatic seizure: effect of status epilepticus. Ann Neurol. 1998;44(6):908–12.

    Article  CAS  PubMed  Google Scholar 

  9. Kramer RE, Luders H, Lesser RP, Weinstein MR, Dinner DS, Morris HH, Wyllie E. Transient focal abnormalities of neuroimaging studies during focal status epilepticus. Epilepsia. 1987;28(5):528–32.

    Article  CAS  PubMed  Google Scholar 

  10. Nohria V, Lee N, Tien RD, Heinz ER, Smith JS, DeLong G, et al. Magnetic resonance imaging evidence of hippocampal sclerosis in progression: a case report. Epilepsia. 1994;35(6):1332–6.

    Article  CAS  PubMed  Google Scholar 

  11. Tien RD, Felsberg GJ. The hippocampus in status epilepticus: demonstration of signal intensity and morphologic changes with sequential fast spin-echo MR imaging. Radiology. 1995;194(1):249–56.

    Article  CAS  PubMed  Google Scholar 

  12. Wieshmann UC, Woermann FG, Lemieux L, Free SL, Bartlett PA, Smith SJ, et al. Development of hippocampal atrophy: a serial magnetic resonance imaging study in a patient who developed epilepsy after generalized status epilepticus. Epilepsia. 1997;38(11):1238–41.

    Article  CAS  PubMed  Google Scholar 

  13. Riela AR, Sires BP, Penry JK. Transient magnetic resonance imaging abnormalities during partial status epilepticus. J Child Neurol. 1991;6(2):143–5.

    Article  CAS  PubMed  Google Scholar 

  14. Salmenperä T, Kälviäinen R, Partanen K, Mervaala E, Pitkänen A. MRI volumetry of the hippocampus, amygdala, entorhinal cortex, and perirhinal cortex after status epilepticus. Epilepsy Res. 2000;40(2–3):155–70.

    Article  PubMed  Google Scholar 

  15. Henry TR, Drury I, Brunberg JA, Pennell PB, McKeever PE, Beydoun A. Focal cerebral magnetic resonance changes associated with partial status epilepticus. Epilepsia. 1994;35(1):35–41.

    Article  CAS  PubMed  Google Scholar 

  16. DeGiorgio CM, Gott PS, Rabinowicz AL, Heck CN, Smith T, Correale J. Neuron-specific enolase, a marker of acute neuronal injury, is increased in complex partial status epilepticus. Epilepsia. 1996;37(7):606–9.

    Article  CAS  PubMed  Google Scholar 

  17. DeGiorgio CM, Heck CN, Rabinowicz AL, Gott PS, Smith T, Correale J. Serum neuron-specific enolase in the major subtypes of status epilepticus. Neurology. 1999;52(4):746–9.

    Article  CAS  PubMed  Google Scholar 

  18. Correale J, Rabinowicz AL, Heck CN, Smith TD, Loskota WJ, DeGiorgio CM. Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier. Neurology. 1998;50(5):1388–91.

    Article  CAS  PubMed  Google Scholar 

  19. Rabinowicz AL, Correale J, Bracht KA, Smith TD, DeGiorgio CM. Neuron-specific enolase is increased after nonconvulsive status epilepticus. Epilepsia. 1995;36(5):475–9.

    Article  CAS  PubMed  Google Scholar 

  20. Meyer Z, Beck E, Shepherd M. Unusually severe lesions in the brain following status epilepticus. J Neurol Neurosurg Psychiatry. 1955;18(1):24–33.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Norman RM. The neuropathology of status epilepticus. Med Sci Law. 1964;4:46–51.

    Article  CAS  PubMed  Google Scholar 

  22. Corsellis JAN, Bruton CJ. Neuropathology of status epilepticus in humans. In: Delgado-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, editors. Status epilepticus. Advances in Neurology, vol. 34. New York: Raven Press; 1983. p. 129–140.

    Google Scholar 

  23. Nixon J, Bateman D, Moss T. An MRI and neuropathological study of a case of fatal status epilepticus. Seizure. 2001;10(8):588–91.

    Article  CAS  PubMed  Google Scholar 

  24. Albala BJ, Moshé SL, Okada R. Kainic-acid-induced seizures: a developmental study. Brain Res. 1984;315(1):139–48.

    Article  CAS  PubMed  Google Scholar 

  25. Stafstrom CE, Thompson JL, Holmes GL. Kainic acid in the developing brain: status epilepticus and spontaneous recurrent seizures. Brain Res Dev Brain Res. 1992;65(2):227–36.

    Article  CAS  PubMed  Google Scholar 

  26. Cilio MR, Sogawa Y, Cha BH, Liu X, Huang LT, Holmes GL. Long-term effects of status epilepticus in the immature brain are specific for age and model. Epilepsia. 2003;44(4):518–28.

    Article  PubMed  Google Scholar 

  27. Fujikawa DG, Itabashi HH, Wu A, Shinmei SS. Status epilepticus-induced neuronal loss in humans without systemic complications or epilepsy. Epilepsia. 2000;41(8):981–91.

    Article  CAS  PubMed  Google Scholar 

  28. DeGiorgio CM, Tomiyasu U, Gott PS, Treiman DM. Hippocampal pyramidal cell loss in human status epilepticus. Epilepsia. 1992;33(1):23–7.

    Article  CAS  PubMed  Google Scholar 

  29. Knopman D, Margolis G, Reeves AG. Prolonged focal epilepsy and hypoxemia as a cause of focal brain damage: a case study. Ann Neurol. 1977;1(2):195–8.

    Article  CAS  PubMed  Google Scholar 

  30. Soffer D, Melamed E, Assaf Y, Cotev S. Hemispheric brain damage in unilateral status epilepticus. Ann Neurol. 1986;20(6):737–40.

    Article  CAS  PubMed  Google Scholar 

  31. Kaplan PW. Nonconvulsive status epilepticus: to lump or to split? (abstract). Epilepsia. 1994;35(Suppl 8):9.

    Google Scholar 

  32. Fountain NB, Lothman EW. Pathophysiology of status epilepticus. J Clin Neurophysiol. 1995;12(4):326–42 Review.

    Article  CAS  PubMed  Google Scholar 

  33. Shneker B, Fountain NB. Epilepsy as chronic sequelae following nonconvulsive status epilepticus (abstract). Epilepsia. 2001;42(Suppl 7):147.

    Google Scholar 

  34. Scholtes FB, Reiner WO, Meinardi H. Non-convulsive status epilepticus: causes, treatment and outcome in 65 patients. J Neurol Neurosurg Psychiatry. 1996;61(1):93–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Shneker BF, Fountain NB. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus. Neurology. 2003;61(8):1066–73.

    Article  PubMed  Google Scholar 

  36. Jope RS, Morrisett RA, Snead OC. Characterization of lithium potentiation of pilocarpine-induced status epilepticus in rats. Exp Neurol. 1986;91(3):471–80.

    Article  CAS  PubMed  Google Scholar 

  37. Turski WA, Cavalheiro EA, Schwarz M, Czuczwar SJ, Kleinrok Z, Turski L. Limbic seizures produced by pilocarpine in rats: behavioural, electroencephalographic and neuropathological study. Behav Brain Res. 1983;9(3):315–35.

    Article  CAS  PubMed  Google Scholar 

  38. Lothman EW, Collins RC. Kainic acid induced limbic seizures: metabolic, behavioral, electroencephalographic and neuropathological correlates. Brain Res. 1981;218(1–2):299–318.

    Article  CAS  PubMed  Google Scholar 

  39. Lothman EW, Collins RC, Ferrendelli JA. Kainic acid-induced limbic seizures: electrophysiologic studies. Neurology. 1981;31(7):806–12.

    Article  CAS  PubMed  Google Scholar 

  40. Walton NY, Treiman DM. Experimental secondarily generalized convulsive status epilepticus induced by D, L-homocysteine thiolactone. Epilepsy Res. 1988;2(2):79–86.

    Article  CAS  PubMed  Google Scholar 

  41. Todorovic MS, Cowan ML, Balint CA, Sun C, Kapur J. Characterization of status epilepticus induced by two organophosphates in rats. Epilepsy Res. 2012;101(3):268–76.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Deshpande LS, Carter DS, Blair RE, DeLorenzo RJ. Development of a prolonged calcium plateau in hippocampal neurons in rats surviving status epilepticus induced by the organophosphate diisopropylfluorophosphate. Toxicol Sci. 2010;116(2):623–31.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. McDonough JH Jr, Dochterman LW, Smith CD, Shih TM. Protection against nerve agent-induced neuropathology, but not cardiac pathology, is associated with the anticonvulsant action of drug treatment. Neurotoxicology. 1995;16(1):123–32.

    CAS  PubMed  Google Scholar 

  44. Ben Ari Y, Lagowska J, Tremblay E, Gal La Salle G. A new model of focal status epilepticus: intra-amygdaloid application of kainic acid elicits repetitive secondarily generalized convulsive seizures. Brain Res. 1979;163(1):176–179.

    Google Scholar 

  45. Furtado MA, Castro OW, Del Vecchio F, de Oliveira JAC, Garcia-Cairasco N. Study of spontaneous recurrent seizures and morphological alterations after status epilepticus induced by intrahippocampal injection of pilocarpine. Epilepsy Behav. 2011;20(2):257–66.

    Article  CAS  PubMed  Google Scholar 

  46. Tanaka T, Kaijima M, Daita G, Ohgami S, Yonemasu Y, Riche D. Electroclinical features of kainic acid-induced status epilepticus in freely moving cats. Microinjection into the dorsal hippocampus. Electroencephalogr Clin Neurophysiol. 1982;54(3):288–300.

    Article  CAS  PubMed  Google Scholar 

  47. Lothman EW, Bertram EH, Bekenstein JW, Perlin JB. Self-sustaining limbic status epilepticus induced by ‘continuous’ hippocampal stimulation: electrographic and behavioral characteristics. Epilepsy Res. 1989;3(2):107–19.

    Article  CAS  PubMed  Google Scholar 

  48. McIntyre DC, Nathanson D, Edson N. A new model of partial status epilepticus based on kindling. Brain Res. 1982;250(1):53–63.

    Article  CAS  PubMed  Google Scholar 

  49. Mazarati AM, Wasterlain CG, Sankar R, Shin D. Self-sustaining status epilepticus after brief electrical stimulation of the perforant path. Brain Res. 1998;801(1–2):251–3.

    Article  CAS  PubMed  Google Scholar 

  50. Kapur J, MacDonald RL. Rapid seizure-induced reduction of benzodiazepine and Zn2+ sensitivity of hippocampal dentate granule cell GABAA receptors. J Neurosci. 1997;17(19):7532–40.

    CAS  PubMed  PubMed Central  Google Scholar 

  51. Goodkin HP, Joshi S, Mtchedlishvili Z, Brar J, Kapur J. Subunit-specific trafficking of GABA(A) receptors during status epilepticus. J Neurosci. 2008;28(10):2527–38.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Naylor DE, Liu H, Wasterlain CG. Trafficking of GABAA receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus. J Neurosci. 2005;25(34):7724–33.

    Article  CAS  PubMed  Google Scholar 

  53. Kapur J, Lothman EW, DeLorenzo RJ. Loss of GABAA receptors during partial status epilepticus. Neurology. 1994;44(12):2407–8.

    Article  CAS  PubMed  Google Scholar 

  54. Kapur J, Coulter DA. Experimental status epilepticus alters gamma-aminobutyric acid type A receptor function in CA1 pyramidal neurons. Ann Neurol. 1995;38(6):893–900.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Terunuma M, Xu J, Vithlani M, Sieghart W, Kittler J, Pangalos M, et al. Deficits in phosphorylation of GABA(A) receptors by intimately associated protein kinase C activity underlie compromised synaptic inhibition during status epilepticus. J Neurosci. 2008;28(2):376–84.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  56. Joshi S, Rajasekaran K, Hawk KM, Brar J, Ross BM, Tran CA, et al. Phosphatase inhibition prevents the activity-dependent trafficking of GABAA receptors during status epilepticus in the young animal. Epilepsia. 2015;56(9):1355–65.

    Article  CAS  PubMed  Google Scholar 

  57. Walton NY, Treiman DM. Response of status epilepticus induced by lithium and pilocarpine to treatment with diazepam. Exp Neurol. 1988;101(2):267–75.

    Article  CAS  PubMed  Google Scholar 

  58. Jones DM, Esmaeil N, Maren S, MacDonald RL. Characterization of pharmacoresistance to benzodiazepines in the rat Li-pilocarpine model of status epilepticus. Epilepsy Res. 2002;50(3):301–12.

    Article  CAS  PubMed  Google Scholar 

  59. Goodkin HP, Yeh JL, Kapur J. Status epilepticus increases the intracellular accumulation of GABAA receptors. J Neurosci. 2005;25(23):5511–20.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Naylor DE, Liu H, Niquet J, Wasterlain CG. Rapid surface accumulation of NMDA receptors increases glutamatergic excitation during status epilepticus. Neurobio Dis. 2013;54:225–38.

    Article  CAS  Google Scholar 

  61. Borris DJ, Bertram EH, Kapur J. Ketamine controls prolonged status epilepticus. Epilepsy Res. 2000;42(2–3):117–22.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Yen W, Williamson J, Bertram EH, Kapur J. A comparison of three NMDA receptor antagonists in the treatment of prolonged status epilepticus. Epilepsy Res. 2004;59(1):43–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Martin BS, Kapur J. A combination of ketamine and diazepam synergistically controls refractory status epilepticus induced by cholinergic stimulation. Epilepsia. 2008;49(2):248–55.

    Article  CAS  PubMed  Google Scholar 

  64. Rice AC, DeLorenzo RJ. N-Methyl-aspartate receptor activation regulates refractoriness of status epilepticus to diazepam. Neuroscience. 1999;93(1):117–23.

    Article  CAS  PubMed  Google Scholar 

  65. Fujikawa DG. The temporal evolution of neuronal damage from pilocarpine-induced status epilepticus. Brain Res. 1996;725(1):11–22.

    Article  CAS  PubMed  Google Scholar 

  66. Honchar MP, Olney JW, Sherman WR. Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats. Science. 1983;220(4594):323–5.

    Article  CAS  PubMed  Google Scholar 

  67. Clifford DB, Olney JW, Maniotis A, Collins RC, Zorumski CF. The functional anatomy and pathology of lithium-pilocarpine and high-dose pilocarpine seizures. Neuroscience. 1987;23(3):953–68.

    Article  CAS  PubMed  Google Scholar 

  68. Dingledine R, Varvel NH, Dudek FE. When and how do seizures kill neurons, and is cell death relevant to epileptogenesis? Adv Exp Med Biol. 2014;813:109–22.

    Article  PubMed  PubMed Central  Google Scholar 

  69. Turski WA, Cavalheiro EA, Bortolotto ZA, Mello LM, Schwarz M, Turski L. Seizures produced by pilocarpine in mice: a behavioral, electroencephalographic and morphological analysis. Brain Res. 1984;321(2):237–53.

    Article  CAS  PubMed  Google Scholar 

  70. Schwob JE, Fuller T, Price JL, Olney JW. Widespread patterns of neuronal damage following systemic or intracerebral injections of kainic acid: a histological study. Neuroscience. 1980;5(6):991–1014.

    Article  CAS  PubMed  Google Scholar 

  71. Buckmaster PS, Dudek FE. Neuron loss, granule cell axon reorganization, and functional changes in the dentate gyrus of epileptic kainate-treated rats. J Comp Neurol. 1997;385(3):385–404.

    Article  CAS  PubMed  Google Scholar 

  72. Fujikawa DG, Daniels AH, Kim JS. The competitive NMDA receptor antagonist CGP 40116 protects against status epilepticus-induced neuronal damage. Epilepsy Res. 1994;17(3):207–19.

    Article  CAS  PubMed  Google Scholar 

  73. Bertram EH, Lothman EW, Lenn NJ. The hippocampus in experimental chronic epilepsy: a morphometric analysis. Ann Neurol. 1990;27(1):43–8.

    Article  CAS  PubMed  Google Scholar 

  74. Du F, Eid T, Lothman EW, Kohler C, Schwarcz R. Preferential neuronal loss in layer III of the medial entorhinal cortex in rat models of temporal lobe epilepsy. J Neurosci. 1995;15(10):6301–13.

    CAS  PubMed  Google Scholar 

  75. Kobayashi M, Buckmaster PS. Reduced inhibition of dentate granule cells in a model of temporal lobe epilepsy. J Neurosci. 2003;23(6):2440–52.

    CAS  PubMed  Google Scholar 

  76. Sun C, Mtchedlishvili Z, Bertram EH, Erisir A, Kapur J. Selective loss of dentate hilar interneurons contributes to reduced synaptic inhibition of granule cells in an electrical stimulation-based animal model of temporal lobe epilepsy. J Comp Neurol. 2007;500(5):876–93.

    Article  PubMed  PubMed Central  Google Scholar 

  77. Mathern GW, Bertram EH 3rd, Babb TL, Pretorius JK, Kuhlman PA, Spradlin S, Mendoza D. In contrast to kindled seizures, the frequency of spontaneous epilepsy in the limbic status model correlates with greater aberrant fascia dentata excitatory and inhibitory axon sprouting, and increased staining for N-methyl-d-aspartate, AMPA and GABA(A) receptors. Neuroscience. 1997;77(4):1003–19.

    Article  CAS  PubMed  Google Scholar 

  78. Obenaus A, Esclapez M, Houser CR. Loss of glutamate decarboxylase mRNA-containing neurons in the rat dentate gyrus following pilocarpine-induced seizures. J Neurosci. 1993;13(10):4470–85.

    CAS  PubMed  Google Scholar 

  79. Cavalheiro EA, Silva DF, Turski WA, Calderazzo-Filho LS, Bortolotto ZA, Turski L. The susceptibility of rats to pilocarpine-induced seizures is age-dependent. Brain Res. 1987;465(1–2):43–58.

    Article  CAS  PubMed  Google Scholar 

  80. Lynch M, Sayin U, Bownds J, Janumpalli S, Sutula T. Long-term consequences of early postnatal seizures on hippocampal learning and plasticity. Eur J Neurosci. 2000;12(7):2252–64.

    Article  CAS  PubMed  Google Scholar 

  81. Kubová H, Mares P, Suchomelová L, Brozek G, Druga R, Pitkänen A. Status epilepticus in immature rats leads to behavioural and cognitive impairment and epileptogenesis. Eur J Neurosci. 2004;19(12):3255–65.

    Article  PubMed  Google Scholar 

  82. Sankar R, Shin DH, Liu H, Mazarati A. Pereira de Vasconcelos A, Wasterlain CG. Patterns of status epilepticus-induced neuronal injury during development and long-term consequences. J Neurosci. 1998;18(20):8382–93.

    CAS  PubMed  Google Scholar 

  83. Blennow G, Brierley JB, Meldrum BS, Siesjö BK. Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism. Brain. 1978;101(4):687–700.

    Article  CAS  PubMed  Google Scholar 

  84. Fountain NB. Status epilepticus: risk factors and complications. Epilepsia. 2000;41(Suppl 2):S23–30.

    Article  PubMed  Google Scholar 

  85. Teitelbaum JS, Zatorre RJ, Carpenter S, Gendron D, Evans AC, Gjedde A, Cashman NR. Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. N Engl J Med. 1990;322(25):1781–7.

    Article  CAS  PubMed  Google Scholar 

  86. Perl TM, Bedard L, Kosatsky T, Hockin JC, Todd EC, Remis RS. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N Engl J Med. 1990;322(25):1775–80.

    Article  CAS  PubMed  Google Scholar 

  87. Sparenborg S, Brennecke LH, Jaax NK, Braitman DJ. Dizocilpine (MK-801) arrests status epilepticus and prevents brain damage induced by soman. Neuropharmacology. 1992;31(4):357–68.

    Article  CAS  PubMed  Google Scholar 

  88. Brandt C, Potschka H, Loscher W, Ebert U. N-methyl-d-aspartate receptor blockade after status epilepticus protects against limbic brain damage but not against epilepsy in the kainate model of temporal lobe epilepsy. Neuroscience. 2003;118(3):727–40.

    Article  CAS  PubMed  Google Scholar 

  89. Chen J, Zheng G, Guo H, Shi ZN. Role of endoplasmic reticulum stress via the PERK signaling pathway in brain injury from status epilepticus. J Mol Neurosci. 2014;53(4):677–83.

    Article  CAS  PubMed  Google Scholar 

  90. Sokka AL, Putkonen N, Mudo G, Pryazhnikov E, Reijonen S, Khiroug L, et al. Endoplasmic reticulum stress inhibition protects against excitotoxic neuronal injury in the rat brain. J Neurosci. 2007;27(4):901–8.

    Article  CAS  PubMed  Google Scholar 

  91. Vezzani A, Dingledine R, Rossetti AO. Immunity and inflammation in status epilepticus and its sequelae: possibilities for therapeutic application. Expert Rev Neurother. 2015;15(9):1081–92.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Nathan B. Fountain .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2018 Springer Science+Business Media LLC

About this chapter

Check for updates. Verify currency and authenticity via CrossMark

Cite this chapter

Fountain, N.B., Joshi, S. (2018). Neuropathology of Generalized Convulsive Status Epilepticus. In: Drislane, F., Kaplan MBBS, P. (eds) Status Epilepticus. Current Clinical Neurology. Springer, Cham. https://doi.org/10.1007/978-3-319-58200-9_10

Download citation

  • DOI: https://doi.org/10.1007/978-3-319-58200-9_10

  • Published:

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-58198-9

  • Online ISBN: 978-3-319-58200-9

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics