Age-dependent mortality in the pilocarpine model of status epilepticus
Status epilepticus (SE) is an acute neurological emergency associated with significant morbidity and mortality. Age has been shown to be a critical factor in determining outcome after SE. Understanding the causes of this increased mortality with aging by developing an animal model to study this cond...
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Published in | Neuroscience letters Vol. 453; no. 3; pp. 233 - 237 |
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Format | Journal Article |
Language | English |
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10.04.2009
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Abstract | Status epilepticus (SE) is an acute neurological emergency associated with significant morbidity and mortality. Age has been shown to be a critical factor in determining outcome after SE. Understanding the causes of this increased mortality with aging by developing an animal model to study this condition would play a major role in studying mechanisms to limit the mortality due to SE. Here we employed pilocarpine to induce SE in rats aged between 5 and 28 weeks. Similar to clinical studies in man, we observed that age was a significant predictor of mortality following SE. While no deaths were observed in 5-week-old animals, mortality due to SE increased progressively with age and reached 90% in 28-week-old animals. There was no correlation between the age of animals and severity of SE. With increasing age mortality occurred earlier after the onset of SE. These results indicate that pilocarpine-induced SE in the rat provides a useful model to study age-dependent SE-induced mortality and indicates the importance of using animal models to elucidate the mechanisms contributing to SE-induced mortality and the development of novel therapeutic interventions to prevent SE-induced death. |
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AbstractList | Status epilepticus (SE) is an acute neurological emergency associated with significant morbidity and mortality. Age has been shown to be a critical factor in determining outcome after SE. Understanding the causes of this increased mortality with aging by developing an animal model to study this condition would play a major role in studying mechanisms to limit the mortality due to SE. Here we employed pilocarpine to induce SE in rats aged between 5 and 28 weeks. Similar to clinical studies in man, we observed that age was a significant predictor of mortality following SE. While no deaths were observed in 5-week-old animals, mortality due to SE increased progressively with age and reached 90% in 28-week-old animals. There was no correlation between the age of animals and severity of SE. With increasing age mortality occurred earlier after the onset of SE. These results indicate that pilocarpine-induced SE in the rat provides a useful model to study age-dependent SE-induced mortality and indicates the importance of using animal models to elucidate the mechanisms contributing to SE-induced mortality and the development of novel therapeutic interventions to prevent SE-induced death. Status epilepticus (SE) is an acute neurological emergency associated with significant morbidity and mortality. Age has been shown to be a critical factor in determining outcome after SE. Understanding the causes of this increased mortality with aging by developing an animal model to study this condition would play a major role in studying mechanisms to limit the mortality due to SE. Here we employed pilocarpine to induce SE in rats aged between 5 to 28 weeks. Similar to clinical studies in man, we observed that age was a significant predictor of mortality following SE. While no deaths were observed in 5-week old animals, mortality due to SE increased progressively with age and reached 90% in 28-week old animals. There was no correlation between the age of animals and severity of SE. With increasing age mortality occurred earlier after the onset of SE. These results indicate that pilocarpine-induced SE in the rat provides a useful model to study age-dependent SE-induced mortality and indicates the importance of using animal models to elucidate the mechanisms contributing to SE-induced mortality and the development of novel therapeutic interventions to prevent SE-induced death. |
Author | Blair, Robert E. DeLorenzo, Robert J. Holbert, William H. Deshpande, Laxmikant S. Churn, Severn B. |
Author_xml | – sequence: 1 givenname: Robert E. surname: Blair fullname: Blair, Robert E. organization: Department of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA – sequence: 2 givenname: Laxmikant S. surname: Deshpande fullname: Deshpande, Laxmikant S. organization: Department of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA – sequence: 3 givenname: William H. surname: Holbert fullname: Holbert, William H. organization: Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA – sequence: 4 givenname: Severn B. surname: Churn fullname: Churn, Severn B. organization: Department of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA – sequence: 5 givenname: Robert J. surname: DeLorenzo fullname: DeLorenzo, Robert J. email: rdeloren@hsc.vcu.edu organization: Department of Neurology, Virginia Commonwealth University, Richmond, VA 23298, USA |
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CitedBy_id | crossref_primary_10_1111_epi_14497 crossref_primary_10_3390_brainsci10110856 crossref_primary_10_1016_j_nbd_2019_02_017 crossref_primary_10_1016_j_eplepsyres_2015_11_001 crossref_primary_10_1007_s12640_017_9789_7 crossref_primary_10_1016_j_jneumeth_2015_09_007 crossref_primary_10_1111_nyas_14500 crossref_primary_10_1016_j_nbd_2021_105547 crossref_primary_10_1016_j_clinsp_2022_100159 crossref_primary_10_1371_journal_pone_0018200 crossref_primary_10_1093_toxsci_kfy065 crossref_primary_10_1111_j_1528_1167_2010_02523_x |
Cites_doi | 10.1016/S0074-7742(06)81007-X 10.1016/S0006-8993(10)80015-0 10.1016/S0165-3806(99)00075-9 10.1016/S0920-1211(96)00047-2 10.1016/S1474-4422(04)00881-6 10.1016/j.neuroscience.2007.01.065 10.1016/S0920-1211(99)00119-9 10.1016/S0920-1211(98)00031-X 10.1016/j.devbrainres.2005.02.001 10.1016/0165-3806(87)90227-6 10.1016/j.jneumeth.2008.04.019 10.1016/0166-4328(83)90136-5 10.1542/peds.83.3.323 10.1111/j.0013-9580.2004.66103.x 10.1016/0165-0173(86)90010-X 10.1016/0166-4328(88)90019-8 10.1097/00004691-199512040-00003 10.1016/0014-4886(91)90042-B 10.1016/S0920-1211(02)00072-4 10.1212/WNL.58.4.537 10.1016/0013-4694(72)90177-0 10.1111/j.1528-1157.1994.tb02908.x 10.1038/sj.bjp.0701231 10.1073/pnas.94.24.13311 10.1016/j.physbeh.2007.06.017 10.1016/S0306-4522(02)00979-X |
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Keywords | Senescence Sprague–Dawley rats Mortality Development Pilocarpine Status epilepticus Age Nervous system diseases Rat Epilepsy Rodentia Cerebral disorder Vertebrata Sprague-Dawley rats Mammalia Animal Central nervous system disease Models |
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SubjectTerms | Age Age Factors Animals Biological and medical sciences Convulsants Development Electroencephalography Fundamental and applied biological sciences. Psychology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Male Medical sciences Mortality Nervous system (semeiology, syndromes) Neurology Pilocarpine Rats Rats, Sprague-Dawley Senescence Sprague–Dawley rats Status epilepticus Status Epilepticus - chemically induced Status Epilepticus - mortality Status Epilepticus - physiopathology Vertebrates: nervous system and sense organs |
Title | Age-dependent mortality in the pilocarpine model of status epilepticus |
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