Risk of seizure recurrence after the first late posttraumatic seizure

Haltiner, Alan M.; Temkin, Nancy; Dikmen, Sureyya

doi:10.1016/s0003-9993(97)90196-9

Cited by 186 publications

(131 citation statements)

References 15 publications

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“…Recognizing the high risk of seizure recurrence in severely injured TBI populations, 5 our PTE operationalization is also consistent with the most recent ILAE report. 6 Acknowledged study design limitations precluded data capture about seizure recurrence, frequency, and treatment response.…”

Section: Connor Wathensupporting

confidence: 86%

In response to comments on IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

et al. 2014

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Section: Connor Wathensupporting

confidence: 86%

In response to comments on IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

et al. 2014

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“…Prolonged unconsciousness and skull fractures also increase the risk for posttraumatic epilepsy (Herman, 2002). Interestingly, the occurrence of seizures during the first week after a head injury increases the probability of spontaneous recurrent seizures later on in life (Haltiner et al, 1997). Of special clinical importance, posttraumatic epilepsy is often refractory to current anticonvulsant therapeutics (Semah et al, 1998).…”

Section: Traumatic Brain Injury: Causes Neuronal Injury and Increasedmentioning

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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“…To the extent the new drug is effective, this practice will diminish the observed difference between placebo and active study drugs after the study drugs were, by protocol, to be stopped. In reality, the power to detect a truly antiepileptogenic drug may not be too badly compromised by this factor, because remote symptomatic seizures have been the most difficult to get into remission (81) and >80% of patients in a study of PHT after traumatic brain injury had additional seizures despite being treated with therapeutic levels of PHT after the first unprovoked seizure and as clinically indicated after the second (82).…”

Section: Discussionmentioning

confidence: 99%

Antiepileptogenesis and Seizure Prevention Trials with Antiepileptic Drugs: Meta‐Analysis of Controlled Trials

2001

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Summary:Purpose: To synthesize evidence concerning the effect of antiepileptic drugs (AEDs) for seizure prevention and to contrast their effectiveness for provoked versus unprovoked seizures.Methods: Medline, Embase, and The Cochrane Clinical Trials Register were the primary sources of trials, but all trials found were included. Minimal requirements: seizureprevention outcome given as fraction of cases; AED or control assigned by random or quasi-random mechanism. Single abstracter. Aggregate relative risk and heterogeneity evaluated using Mantel-Haenszel analyses; random effects model used if heterogeneity was significant.Results: Forty-seven trials evaluated seven drugs or combinations for preventing seizures associated with fever, alcohol, malaria, perinatal asphyxia, contrast media, tumors, craniotomy, and traumatic brain injury. Conclusions: Effective or promising results predominate for provoked (acute, symptomatic) seizures. For unprovoked (epileptic) seizures, no drug has been shown to be effective, and some have had a clinically important effect ruled out.

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Risk of seizure recurrence after the first late posttraumatic seizure

Cited by 186 publications

References 15 publications

In response to comments on IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

In response to comments on IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

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

Antiepileptogenesis and Seizure Prevention Trials with Antiepileptic Drugs: Meta‐Analysis of Controlled Trials

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