Status Epilepticus

Manno, Edward M.

doi:10.1177/1941875210383176

Cited by 25 publications

(13 citation statements)

References 66 publications

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“…The definition of SE has been constantly changing. It is also suggested that it depends on the context of SE, in humans or experimental models ( 11 , 12 ). There has been a consensus that the duration or length of convulsive seizures (CS) during SE should be sufficient to cause long-term brain injury, enabling the brain to generate spontaneous seizures i.e., “an enduring epilepticus” ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

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Status Epilepticus: Behavioral and Electroencephalography Seizure Correlates in Kainate Experimental Models

et al. 2018

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Various etiological factors, such as head injury, chemical intoxication, tumors, and gene mutation, can induce epileptogenesis. In animal models, status epilepticus (SE) triggers epileptogenesis. In humans, convulsive SE for >30 min can be a life-threatening medical emergency. The duration and severity of convulsive SE are highly variable in chemoconvulsant animal models. A continuous video-electroencephalography (EEG) recording, and/or diligent direct observation, facilitates quantification of exact duration of different stages of convulsive seizures (Racine stages 3–5) to determine the severity of SE. A continuous convulsive SE for >30 min usually causes high mortality in some rodents and results in widespread brain damage in the surviving animals, in spite of treating with antiepileptic drugs (AEDs). AEDs control behavioral seizures but not EEG seizures. The severity of initial SE impacts epileptogenesis and cognitive function; therefore, quantitative assessment of behavioral SE and EEG in animal models will help to understand the impact of SE severity on epileptogenesis. There are several excellent reviews on experimental models of seizure/SE/epilepsy. This review focusses on the comparison of induction and characterization of behavioral SE and EEG correlates in mice and rats induced by kainate. We also discuss the advantages of repeated low dose of kainate (i.p. route), which minimizes variability in the initial SE severity between animals and reduces mortality rate. A refined approach to induce SE with kainate also addresses the two of the 3Rs (i.e., refinement and reduction), the guiding principles for ethical and scientific standpoint of animal research.

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Section: Introductionmentioning

confidence: 99%

“…Seizures are normally self-terminated by activating inhibitory mechanisms. Failure of these mechanisms can result in prolonged seizures (SE), which may require interventional drugs ( 12 ). However, according to the clinical trial guidelines, the treatment should be initiated only if the CS last for ~5 min ( 11 , 14 – 16 ).…”

Section: Introductionmentioning

confidence: 99%

Status Epilepticus: Behavioral and Electroencephalography Seizure Correlates in Kainate Experimental Models

et al. 2018

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“…Current treatment of SE in patients and animals is focused on the prompt delivery of benzodiazepines such as diazepam or midazolam [7]. Additionally, in animal models of SE induced by chemoconvulsants, organophosphate toxicity, or nerve agent exposure, anticholinergics such as scopolamine or atropine are often employed [8].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Contributes to Status Epilepticus Associated Mortality

et al. 2017

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Status epilepticus is a common manifestation of nerve agent toxicity and represents a serious medical emergency with high rates of mortality and neurologic injury in those that survive. The aim of the current study was to determine if targeting oxidative stress with the catalytic antioxidant, AEOL10150, would reduce pilocarpine-induced mortality and attenuate neuronal death and neuroinflammation. We found that treatment with AEOL10150 in conjunction with scopolamine and diazepam following pilocarpine-induced SE was able to significantly reduce mortality compared to treatment with just scopolamine and diazepam. Mortality was further reduced when AEOL10150 was used in conjunction with atropine and diazepam which is considered the standard of care for nerve agent exposures. Both treatment paradigms offered significant protection against SE-induced oxidative stress. Additionally, treatment with scopolamine, AEOL10150 and diazepam attenuated SE-induced neuronal loss and neuroinflammation. Taken together, the data suggest that pharmacological targeting of oxidative stress can improve survival and attenuate secondary neurological damage following SE induced by the nerve agent surrogate pilocarpine.

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“…The duration and severity of SE determines the outcome of epileptogenesis. The definition of SE depends on the context, and has been constantly changing (Manno, 2011; Seinfeld, 2016). According to the recommendation of the Commission on Classification and Terminology and the Commission on Epidemiology of the International League Against Epilepsy (ILAE), the SE is defined as “ a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures (after time point t1).…”

Section: Severity Of Status Epilepticus Determines Epileptogenesismentioning

confidence: 99%

“…This duration is now widely accepted for studies that investigate the long-term consequences of SE i.e., epileptogenesis and epilepsy (Commission on Epidemiology and Prognosis, 1993; Dodson et al, 1993). Seizures normally self-terminate by activating the inhibitory mechanism, however, if this mechanism fails it can lead to prolonged seizures (SE), which may then require administration of intervention drugs to terminate SE (Manno, 2011). Interestingly, the clinical trial guidelines recommend ~5 min to intervene in the case of continuous convulsive seizures (Dodson et al, 1993; Lowenstein et al, 1999; Shinnar et al, 2001; Seinfeld et al, 2016).…”

Section: Severity Of Status Epilepticus Determines Epileptogenesismentioning

confidence: 99%

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

Sharma

Puttachary

Thippeswamy

2017

J of Neuroscience Research

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Epileptogenesis is the process of developing an epileptic condition and/or its progression once it is established. The molecules that initiate, promote, and propagate remarkable changes in the brain during epileptogenesis are emerging as targets for prevention/treatment of epilepsy. Epileptogenesis is a continuous process that follows immediately after status epilepticus (SE) in animal models of acquired temporal lobe epilepsy (TLE). Both SE and epileptogenesis are potential therapeutic targets for the discovery of anticonvulsants and antiepileptogenic or disease-modifying agents. For translational studies, SE targets are appropriate for screening anticonvulsive drugs prior to their advancement as therapeutic agents, while targets of epileptogenesis are relevant for identification and development of therapeutic agents that can either prevent or modify the disease or its onset. The acute seizure models do not reveal antiepileptogenic properties of anticonvulsive drugs. This review highlights the important components of epileptogenesis and the long-term impact of intervening one of these components, nitric oxide (NO), in rat and mouse kainate models of TLE. NO is a putative pleotropic gaseous neurotransmitter and an important contributor of nitro-oxidative stress that coexists with neuroinflammation and epileptogenesis. The long-term impact of inhibiting the glial source of NO during early epileptogenesis in the rat model of TLE is reviewed. The importance of sex as a biological variable in disease modification strategies in epilepsy is also briefly discussed.

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Status Epilepticus

Cited by 25 publications

References 66 publications

Status Epilepticus: Behavioral and Electroencephalography Seizure Correlates in Kainate Experimental Models

Status Epilepticus: Behavioral and Electroencephalography Seizure Correlates in Kainate Experimental Models

Oxidative Stress Contributes to Status Epilepticus Associated Mortality

Glial source of nitric oxide in epileptogenesis: A target for disease modification in epilepsy

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