Factors predictive of outcome in patients with de novo status epilepticus

Tsai, Meng-Han; Chuang, Yao-Chung; Chang, Hsueh‐Wen; Chang, Wen-Cheng; Lai, Shung-Lon; Huang, Chin-Wei; Tsai, Nai‐Wen; Wang, H.-C.; Lin, Yujun; Lu, Chen-Hsien

doi:10.1093/qjmed/hcn149

Cited by 50 publications

(49 citation statements)

References 27 publications

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“…Indeed SE alone is sufficient to induce TLE in models of both developing and adult rodents (Dunleavy et al, 2010;Loscher, 2002). Circumstantial evidence supports the idea that SE contributes to the pathogenesis of TLE in humans (Annegers et al, 1979;Tsai et al, 2009;VanLandingham et al, 1998).…”

Section: Introductionmentioning

confidence: 77%

The cellular and synaptic location of activated TrkB in mouse hippocampus during limbic epileptogenesis

Helgager

Liu

McNamara

2012

J of Comparative Neurology

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Understanding the mechanisms of limbic epileptogenesis in cellular and molecular terms may provide novel therapeutic targets for its prevention. The neurotrophin receptor, tropomyosinrelated kinase B (TrkB), is thought to be critical for limbic epileptogenesis. Enhanced activation of TrkB, revealed by immunodetection of enhanced phosphorylated TrkB (pTrkB), a surrogate measure of its activation, has been identified within hippocampus in multiple animal models. Knowledge of the cellular locale of activated TrkB is necessary to elucidate its functional consequences. Using an antibody selective to pTrkB in conjunction with confocal microscopy and cellular markers, we determined the cellular and subcellular locale of enhanced pTrkB induced by status epilepticus (SE) evoked by infusion of kainic acid into the amygdala of adult mice. SE induced enhanced pTrkB immunoreactivity in two distinct populations of principal neurons within hippocampus, the dentate granule cells and CA1 pyramidal cells. Enhanced immunoreactivity within granule cells was found within mossy fiber axons and giant synaptic boutons. By contrast, enhanced immunoreactivity was found within apical dendritic shafts and spines of CA1 pyramidal cells. A common feature of this enhanced pTrkB at these cellular locales is its localization to excitatory synapses between excitatory neurons, presynaptically in the granule cells and postsynaptically in CA1 pyramidal cells. Long term potentiation (LTP) is one cellular consequence of TrkB activation at these excitatory synapses that may promote epileptogenesis.

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Section: Introductionmentioning

confidence: 77%

The cellular and synaptic location of activated TrkB in mouse hippocampus during limbic epileptogenesis

Helgager

Liu

McNamara

2012

J of Comparative Neurology

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“…Several authors show that the likelihood of death and poor outcomes increases with age after adjusting for other covariates, including age, sex, possible etiology and potential medical complications, especially for those older than 80 years [32,33]. However, most agree that the main determinant of adverse outcomes is etiology, which varies considerably depending on the age group (Table 1).…”

Section: Resultsmentioning

confidence: 99%

Status Epilepticus: Epidemiology and Public Health Needs

Sánchez

Rincón

2016

JCM

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Status epilepticus (SE) is defined as a continuous clinical and/or electrographic seizure activity lasting five minutes or more or recurrent seizure activity without return to baseline. There is a paucity of epidemiological studies of SE, as most research is derived from small population studies. The overall incidence of SE is 9.9 to 41 per 100,000/year, with peaks in children and the elderly and with febrile seizures and strokes as its main etiologies. The etiology is the major determinant of mortality. Governments and the academic community should predominantly focus on the primary prevention of etiologies linked to SE, as these are the most important risk factors for its development. This review describes the incidence, prevalence, etiology, risk factors, outcomes and costs of SE and aims to identify future research and public health needs.

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“…About 38% with "overt" SE and 82% with "subtle" SE continued to have seizures after receiving 2 AEDs, and only 2% and 5%, respectively, stopped having seizures after receiving a third agent [12,11]. Studies addressing the long-term seizure outcome in convulsive RSE are very few [12,13].…”

Section: Introductionmentioning

confidence: 99%