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Pathophysiology of Status Epilepticus: Experimental Data

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Atlas of Epilepsies
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Introduction and Definitions

Some 150 years ago, Armand Trousseau from Paris recognized that during “status epilepticus, something happens [in the brain] that requires an explanation” (Trousseau 1868). In spite of recent progress, treatment success is still limited, since more than 30% of patients develop refractory status epilepticus (SE) that is often associated with severe neuronal and clinical sequelae. There is a long-lasting debate on how long seizure activity should last to define SE (Chen and Wasterlain 2006). While in epidemiological studies, the definition of SE is commonly based on a minimal seizure duration of 30 min (Wasterlain and Chen 2006), in clinical practice, anticonvulsant treatment should be initiated in both generalized convulsive and non-convulsive forms of SE 5 min after onset of seizure activity (Chen and Wasterlain 2006; Meierkord and Holtkamp 2007). However, in some conditions, even shorter periods of seizure activity can result in neuronal damage. To better...

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Abbreviations

AED:

Antiepileptic drug

AMPA:

α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid

BBB:

Blood brain barrier

GABA:

γ-Amino-butyric acid

NMDA:

N-methyl-d-aspartate

ROS:

Radical oxygen species

ROS:

Reactive oxygen species

SE:

Status epilepticus

SSSE:

Self-sustaining status epilepticus

TGF-βR:

Transforming growth factor β receptor

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Heinemann, U., Holtkamp, M. (2010). Pathophysiology of Status Epilepticus: Experimental Data. In: Panayiotopoulos, C.P. (eds) Atlas of Epilepsies. Springer, London. https://doi.org/10.1007/978-1-84882-128-6_36

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  • DOI: https://doi.org/10.1007/978-1-84882-128-6_36

  • Publisher Name: Springer, London

  • Print ISBN: 978-1-84882-127-9

  • Online ISBN: 978-1-84882-128-6

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