Status epilepticus pathophysiology

Chen, J.W.Y., Wasterlain, C.G. (2006). Status epilepticus pathophysiology and management in adults. Lancet Neurol. 5 246-56. 

Adapted from Phelps SJ, Hovinga CA, Boucher BA. Status epilepticus. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 1054, with permission. 

Wasterlain C. G., Fujikawa D. G., PenixL., and Sankar R. (1993). Pathophysiological mechanisms of brain damage from status epilepticus. Epilepsia 34 S37-S53. 

GCSE is the most common and severe form of status epilepticus and is characterized by repeated primary or secondary generalized seizures that involve both hemispheres of the brain and are associated with a persistent postictal state. This chapter will focus on the epidemiology, pathophysiology, presentation, and management of GCSE. 

Prager, E.M., Aroniadou-Anderjaska, V, Almeida-Suhett, C.P., et al, 2014. The recovery of acetylcholinesterase activity and the progression of neuropatho-logical and pathophysiological alterations in the rat basolateral amygdala after soman-induced status epilepticus relation to anxiety-like behavior. Neuropharmacology 81C, 64-74. 

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