Status epilepticus-related etiology, incidence and mortality: A meta-analysis

Lv, Ruijuan; Wang, Qun; Tao, Cui; Zhu, Fei; Shao, Xiaoqiu

doi:10.1016/j.eplepsyres.2017.07.006

Cited by 84 publications

(61 citation statements)

References 32 publications

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“…One implication of the present study is that adult neurogenesis in the DG normally will benefit adult animals by protecting them from excitotoxic effects of SE. Notably, SE does occur in the normal population, so this is potentially significant (Hesdorffer, Logroscino, Cascino, Annegers, & Hauser, ; Lv, Wang, Cui, Zhu, & Shao, ; Sanchez & Rincon, ). In addition, the pattern of damage in the hippocampus following SE also occurs after traumatic brain injury (TBI), early life infection (ELI), and febrile seizures (FS) in both laboratory animals and humans (Baram & Shinnar, ; England, Liverman, Schultz, & Strawbridge, ; Frankowski, Kim, & Hunt, ; Swartz et al, ).…”

Section: Discussionmentioning

confidence: 99%

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

et al. 2019

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Previous studies suggest that reducing the numbers of adult‐born neurons in the dentate gyrus (DG) of the mouse increases susceptibility to severe continuous seizures (status epilepticus; SE) evoked by systemic injection of the convulsant kainic acid (KA). However, it was not clear if the results would be the same for other ways to induce seizures, or if SE‐induced damage would be affected. Therefore, we used pilocarpine, which induces seizures by a different mechanism than KA. Also, we quantified hippocampal damage after SE. In addition, we used both loss‐of‐function and gain‐of‐function methods in adult mice. We hypothesized that after loss‐of‐function, mice would be more susceptible to pilocarpine‐induced SE and SE‐associated hippocampal damage, and after gain‐of‐function, mice would be more protected from SE and hippocampal damage after SE. For loss‐of‐function, adult neurogenesis was suppressed by pharmacogenetic deletion of dividing radial glial precursors. For gain‐of‐function, adult neurogenesis was increased by conditional deletion of pro‐apoptotic gene Bax in Nestin‐expressing progenitors. Fluoro‐Jade C (FJ‐C) was used to quantify neuronal injury and video‐electroencephalography (video‐EEG) was used to quantify SE. Pilocarpine‐induced SE was longer in mice with reduced adult neurogenesis, SE had more power and neuronal damage was greater. Conversely, mice with increased adult‐born neurons had shorter SE, SE had less power, and there was less neuronal damage. The results suggest that adult‐born neurons exert protective effects against SE and SE‐induced neuronal injury.

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Section: Discussionmentioning

confidence: 99%

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

et al. 2019

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“…It is well known that SE is associated with higher fatality rates and unfavorable clinical outcome. 116 The AHA and ESO guidelines stated against the routine use of antiepileptic drugs in ES and there is also insufficient evidence with regard to the initiation and type of antiepileptics (if required). 117,118 There is no evidence of immediate primary prophylaxis in ES, but based on our results about 40% of these patients were treated.…”

Section: Discussionmentioning

confidence: 99%

Early seizures after ischemic stroke: focus on thrombolysis

et al. 2019

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Introduction.Stroke is a significant underlying cause of epilepsy. Seizures due to ischemic stroke (IS) are generally categorized into early seizures (ESs) and late seizures (LSs). Seizures in thrombolysis situations may raise the possibility of other etiology than IS.Aim.We overtook a systematic review focusing on the pathogenesis, prevalence, risk factors, detection, management, and clinical outcome of ESs in IS and in stroke/thrombolysis situations. We also collected articles focusing on the association of recombinant tissue-type plasminogen activator (rt-PA) treatment and epileptic seizures.Results.We have identified 37 studies with 36,775 participants. ES rate was 3.8% overall in patients with IS with geographical differences. Cortical involvement, severe stroke, hemorrhagic transformation, age (<65 years), large lesion, and atrial fibrillation were the most important risk factors. Sixty-one percent of ESs were partial and 39% were general. Status epilepticus (SE) occurred in 16.3%. 73.6% had an onset within 24 h and 40% may present at the onset of stroke syndrome. Based on EEG findings seizure-like activity could be detected only in approximately 18% of ES patients. MRI diffusion-weighted imaging and multimodal brain imaging may help in the differentiation of ischemia vs. seizure. There are no specific recommendations with regard to the treatment of ES.Conclusion.ESs are rare complications of acute stroke with substantial burden. A significant proportion can be presented at the onset of stroke requiring an extensive diagnostic workup.

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“…Short-term mortality of SE ranges from 0% to 4% 26,48,49 in children and 2%-40% in adults, with higher mortality in RSE. 26,48,[50][51][52] Long-term mortality data after an episode of SE, including in-hospital deaths, is 0%-22% in children 5,6,17,[26][27][28][29][33][34][35]37,38,45,53 and 0%-57% in adults. [10][11][12]17,19,20,43,54 Although long-term mortality rates are high, the underlying etiology and the period of followup are major determinants of outcome.…”

Section: Mortalitymentioning

confidence: 99%

Long‐term outcomes of status epilepticus: A critical assessment

et al. 2018

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SummaryWe reviewed 37 studies reporting long‐term outcomes after a status epilepticus (SE) episode in pediatric and adult populations. Study design, length of follow‐up, outcome measures, domains investigated (mortality, SE recurrence, subsequent epilepsy, cognitive outcome, functional outcome, or quality of life), and predictors of long‐term outcomes are summarized. Despite heterogeneity in the design of prior studies, overall risk of poor long‐term outcome after SE is high in both children and adults. Etiology is the main determinant of outcome, and the effect of age or SE duration is often difficult to distinguish from the underlying cause. The effect of the treatment on long‐term outcome after SE is still unknown.

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Status epilepticus-related etiology, incidence and mortality: A meta-analysis

Cited by 84 publications

References 32 publications

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures

Early seizures after ischemic stroke: focus on thrombolysis

Long‐term outcomes of status epilepticus: A critical assessment

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