Presentation, Evaluation, and Treatment of Nonconvulsive Status Epilepticus

Drislane, Frank W.

doi:10.1006/ebeh.2000.0100

Cited by 152 publications

(125 citation statements)

References 75 publications

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“…Twelve percent to 30% of adult patients with a new diagnosis of epilepsy first present in SE. SE can be convulsive or nonconvulsive, and SE can cause neuronal damage under both situations (Fountain & Lothman, 1995;Drislane, 2000).…”

Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

260

286

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Epilepsy is one of the most common neurological disorders. Although epilepsy can be idiopathic, it is estimated that up to 50% of all epilepsy cases are initiated by neurological insults and are called acquired epilepsy (AE). AE develops in 3 phases: (1) the injury (central nervous system [CNS] insult), (2) epileptogenesis (latency), and (3) the chronic epileptic (spontaneous recurrent seizure) phases. Status epilepticus (SE), stroke, and traumatic brain injury (TBI) are 3 major examples of common brain injuries that can lead to the development of AE. It is especially important to understand the molecular mechanisms that cause AE because it may lead to innovative strategies to prevent or cure this common condition. Recent studies have offered new insights into the cause of AE and indicate that injury-induced alterations in intracellular calcium concentration levels [Ca 2+ ] i and calcium homeostatic mechanisms play a role in the development and maintenance of AE. The injuries that cause AE are different, but they share a common molecular mechanism for producing brain damage -an increase in extracellular glutamate concentration that causes increased intracellular neuronal calcium, leading to neuronal injury and/or death. Neurons that survive the injury induced by glutamate and are exposed to increased [Ca 2+ ] i are the cellular substrates to develop epilepsy because dead cells do not seize. The neurons that survive injury sustain permanent long-term plasticity changes in [Ca 2+ ] i and calcium homeostatic mechanisms that are permanent and are a prominent feature of the epileptic phenotype. In the last several years, evidence has accumulated indicating that the prolonged alteration in neuronal calcium dynamics plays an important role in the induction and maintenance of the prolonged neuroplasticity changes underlying the epileptic phenotype. Understanding the role of calcium as a second messenger in the induction and maintenance of epilepsy may provide novel insights into therapeutic advances that will prevent and even cure AE.

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Section: Status Epilepticus: Causes Neuronal Injury and Increased Glumentioning

confidence: 99%

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

DeLorenzo

Sun

Deshpande

2005

Pharmacology & Therapeutics

260

286

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“…SE is a major neurological emergency associated with considerable morbidity and mortality . SE is known to cause extensive neuronal damage resulting in further brain abnormalities such as memory deficits and the development of acquired epilepsy (Drislane, 2000). Neuronal injury secondary to SE is a consequence of excessive neuronal excitability and the underlying etiology of SE (Lowenstein and Alldredge, 1998).…”

Section: Discussionmentioning

confidence: 99%

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

et al. 2007

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SummaryIt is established that the majority but not all of the seizure-induced cell death is associated with status epilepticus while spontaneous recurrent seizures associated with epilepsy do not cause neuronal death. Extracellular effects and compensatory changes in brain physiology complicate assessment of neuronal death in vivo as the result of seizures. In this study we utilized a well-characterized in vitro hippocampal neuronal culture model of both continuous high-frequency epileptiform discharges (status epilepticus) and spontaneous recurrent epileptiform discharges (acquired epilepsy) to investigate the direct effects of continuous and episodic electrographic epileptiform discharges on cell death in a carefully controlled extracellular environment. The results from this study indicate that continuous high-frequency epileptiform discharges can cause neuronal death in a time-dependent manner. Episodic epileptiform seizure activity occurring for the life of the neurons in culture was not associated with increased neuronal cell death. Our data confirm observations from clinical and some animal studies that spontaneous recurrent seizures do not initiate cell death. The hippocampal neuronal culture model provides a powerful in vitro tool for carefully evaluating the effects of seizure activity alone on neuronal viability in the absence of various confounding factors and may provide new insights into the development of novel therapeutic agents to prevent neuronal injury during status epilepticus.

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“…7) The clinical characteristics of NCSE are also ambiguous and nonspecific, making the diagnosis difficult and uncertain. 1,4,6,7,11) In the absence of continuous EEG monitoring, the diagnosis is likely to be missed or delayed. Because the morbidity and mortality of NCSE are largely determined by duration and delay to diagnosis, improving its outcome will require the availability and timely use of EEG testing.…”

Section: Discussionmentioning

confidence: 99%

“…If these medications are not effective, induction of burst suppression could be done with pentobarbital or propofol. 4,7,11) …”

Section: Discussionmentioning

confidence: 99%

Nonconvulsive Seizures of Traumatic Brain Injury Patients

Lee

Hur

Moon

et al. 2013

Korean J Neurotrauma

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Objective: Seizures are common consequence of traumatic brain injury and have been reported in clinical series as an incidence of 15% to 22%. Among them, nonconvulsive seizures (NCS) are often unrecognized during the early period of neurosurgical hospitalization because their clinical presentations can be misunderstood as consequent symptoms of clinical course, and the diagnosis can be confirmed only by the electroencephalographic (EEG) recording. Methods: We retrospectively reviewed our clinical database of traumatic brain injury (TBI) patients admitted between March 2008 and September 2012. Twenty one patients with suspicious symptoms of NCS, such as decrease of consciousness, aphasia or irritability, were included. Routine wake and sleep EEG or bedside continuous EEG monitoring were done in all patients. Results: Ten out of twenty-one patients showed abnormal activities on EEG. Ictal discharges were documented on four patients. Based on clinical symptoms and EEG findings, these four patients were diagnosed as NCS. Two out of four NCS patients showed EEG findings of nonconvulsive status epilepticus (NCSE). Another six patients with abnormal EEG activities were considered as 'suspicious NCS' because only interictal activities were recorded on EEG but increasing dose or adding on antiepileptics relieved their symptoms. All NCS/NCSE were successfully controlled by appropriate antiepileptic therapy. Conclusion: Our result showed that NCS was diagnosed in about 20% of patients with suspicious symptoms. There's a possibility that actual NCS might have happened more. Because untreated NCS/NCSE might cause worse clinical outcome, careful observation and urgent EEG recordings should be considered in a patient with suspicious NCS symptoms. (Korean J Neurotrauma 2013;9:64-68) KEY WORDS: Traumatic brain injury ㆍNonconvulsive seizure ㆍStatus epilepticus ㆍElectroencephalography.

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Presentation, Evaluation, and Treatment of Nonconvulsive Status Epilepticus

Cited by 152 publications

References 75 publications

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

Cellular mechanisms underlying acquired epilepsy: The calcium hypothesis of the induction and maintainance of epilepsy

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

Nonconvulsive Seizures of Traumatic Brain Injury Patients

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