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Advances in the pathophysiology of status epilepticus.

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Title: Advances in the pathophysiology of status epilepticus.
Authors: Chen, J. W. Y., Naylor, D. E., Wasterlain, C. G.
Source: Acta Neurologica Scandinavica: Supplementum. Mar2007 Supplement 186, Vol. 115, p7-15. 9p.
Subjects: Epilepsy, Spasms, Seizures (Medicine), Pathological physiology, GABA, Benzodiazepines
Abstract: Status epilepticus (SE) describes an enduring epileptic state during which seizures are unremitting and tend to be self-perpetuating. We describe the clinical phases of generalized convulsive SE, impending SE, established SE, and subtle SE. We discuss the physiological and biochemical cascades which characterize self-sustaining SE (SSSE) in animal models. At the transition from single seizures to SSSE, GABAA (gamma-aminobutyric acid) receptors move from the synaptic membrane to the cytoplasm, where they are functionally inactive. This reduces the number of GABAA receptors available for binding GABA or GABAergic drugs, and may in part explain the development of time-dependent pharmacoresistance to benzodiazepines and the tendency of seizures to become self-sustaining. At the same time, ‘spare’ subunits of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and NMDA (N-methyl-D-aspartic acid) receptors move from subsynaptic sites to the synaptic membrane, causing further hyperexcitability and possibly explaining the preserved sensitivity to NMDA blockers late in the course of SE. Maladaptive changes in neuropeptide expression occur on a slower time course, with depletion of the inhibitory peptides dynorphin, galanin, somatostatin and neuropeptide Y, and with an increased expression of the proconvulsant tachykinins, substance P and neurokinin B. Finally, SE-induced neuronal injury and epileptogenesis are briefly discussed. [ABSTRACT FROM AUTHOR]
Copyright of Acta Neurologica Scandinavica: Supplementum is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Advances in the pathophysiology of status epilepticus.
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  Data: <searchLink fieldCode="AR" term="%22Chen%2C+J%2E+W%2E+Y%2E%22">Chen, J. W. Y.</searchLink><br /><searchLink fieldCode="AR" term="%22Naylor%2C+D%2E+E%2E%22">Naylor, D. E.</searchLink><br /><searchLink fieldCode="AR" term="%22Wasterlain%2C+C%2E+G%2E%22">Wasterlain, C. G.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Acta+Neurologica+Scandinavica%3A+Supplementum%22">Acta Neurologica Scandinavica: Supplementum</searchLink>. Mar2007 Supplement 186, Vol. 115, p7-15. 9p.
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  Data: <searchLink fieldCode="DE" term="%22Epilepsy%22">Epilepsy</searchLink><br /><searchLink fieldCode="DE" term="%22Spasms%22">Spasms</searchLink><br /><searchLink fieldCode="DE" term="%22Seizures+%28Medicine%29%22">Seizures (Medicine)</searchLink><br /><searchLink fieldCode="DE" term="%22Pathological+physiology%22">Pathological physiology</searchLink><br /><searchLink fieldCode="DE" term="%22GABA%22">GABA</searchLink><br /><searchLink fieldCode="DE" term="%22Benzodiazepines%22">Benzodiazepines</searchLink>
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  Data: Status epilepticus (SE) describes an enduring epileptic state during which seizures are unremitting and tend to be self-perpetuating. We describe the clinical phases of generalized convulsive SE, impending SE, established SE, and subtle SE. We discuss the physiological and biochemical cascades which characterize self-sustaining SE (SSSE) in animal models. At the transition from single seizures to SSSE, GABAA (gamma-aminobutyric acid) receptors move from the synaptic membrane to the cytoplasm, where they are functionally inactive. This reduces the number of GABAA receptors available for binding GABA or GABAergic drugs, and may in part explain the development of time-dependent pharmacoresistance to benzodiazepines and the tendency of seizures to become self-sustaining. At the same time, ‘spare’ subunits of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and NMDA (N-methyl-D-aspartic acid) receptors move from subsynaptic sites to the synaptic membrane, causing further hyperexcitability and possibly explaining the preserved sensitivity to NMDA blockers late in the course of SE. Maladaptive changes in neuropeptide expression occur on a slower time course, with depletion of the inhibitory peptides dynorphin, galanin, somatostatin and neuropeptide Y, and with an increased expression of the proconvulsant tachykinins, substance P and neurokinin B. Finally, SE-induced neuronal injury and epileptogenesis are briefly discussed. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Acta Neurologica Scandinavica: Supplementum is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=24259483
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              Text: Mar2007 Supplement 186
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