Use of antiepileptics for seizure prophylaxis after traumatic brain injury

Torbic, Heather; Forni, Allison; Anger, Kevin E.; DeGrado, Jeremy; Greenwood, Bonnie C.

doi:10.2146/ajhp120203

Cited by 79 publications

(65 citation statements)

References 23 publications

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“…Classical ASDs, such as phenytoin, carbamazepine, valproate benzodiazepines, are ineffective in reducing or preventing PTE [34–36]. While early post-injury prophylaxis with ASDs may reduce or prevent early post-injury seizures [37], there is little evidence to indicate that these treatments can be disease-modifying and prevent the development of PTE or spontaneous unprovoked seizures long-term [38]. Once a patient has developed seizures, polypharmacy is often employed in an attempt to control the seizures, yet a significant proportion of TBI patients who develop epilepsy will develop drug-resistance, defined as a failure to achieve seizure cessation after trialling more than two tolerated and appropriate ASD treatments [33, 34].…”

Section: Traumatic Brain Injury and Epilepsymentioning

confidence: 99%

Inflammation in epileptogenesis after traumatic brain injury

Webster

Sun

Crack

et al. 2017

J Neuroinflammation

224

185

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BackgroundEpilepsy is a common and debilitating consequence of traumatic brain injury (TBI). Seizures contribute to progressive neurodegeneration and poor functional and psychosocial outcomes for TBI survivors, and epilepsy after TBI is often resistant to existing anti-epileptic drugs. The development of post-traumatic epilepsy (PTE) occurs in a complex neurobiological environment characterized by ongoing TBI-induced secondary injury processes. Neuroinflammation is an important secondary injury process, though how it contributes to epileptogenesis, and the development of chronic, spontaneous seizure activity, remains poorly understood. A mechanistic understanding of how inflammation contributes to the development of epilepsy (epileptogenesis) after TBI is important to facilitate the identification of novel therapeutic strategies to reduce or prevent seizures.BodyWe reviewed previous clinical and pre-clinical data to evaluate the hypothesis that inflammation contributes to seizures and epilepsy after TBI. Increasing evidence indicates that neuroinflammation is a common consequence of epileptic seizure activity, and also contributes to epileptogenesis as well as seizure initiation (ictogenesis) and perpetuation. Three key signaling factors implicated in both seizure activity and TBI-induced secondary pathogenesis are highlighted in this review: high-mobility group box protein-1 interacting with toll-like receptors, interleukin-1β interacting with its receptors, and transforming growth factor-β signaling from extravascular albumin. Lastly, we consider age-dependent differences in seizure susceptibility and neuroinflammation as mechanisms which may contribute to a heightened vulnerability to epileptogenesis in young brain-injured patients.ConclusionSeveral inflammatory mediators exhibit epileptogenic and ictogenic properties, acting on glia and neurons both directly and indirectly influence neuronal excitability. Further research is required to establish causality between inflammatory signaling cascades and the development of epilepsy post-TBI, and to evaluate the therapeutic potential of pharmaceuticals targeting inflammatory pathways to prevent or mitigate the development of PTE.

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Section: Traumatic Brain Injury and Epilepsymentioning

confidence: 99%

Inflammation in epileptogenesis after traumatic brain injury

Webster

Sun

Crack

et al. 2017

J Neuroinflammation

224

185

View full text Add to dashboard Cite

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“…Levetiracetam may also be used as an alternative since it has demonstrated comparable efficacy to phenytoin for early PTS prophylaxis. 4 The American Academy of Neurology recommends prophylaxis with phenytoin for adult patients with early PTS (typically with prolonged loss of consciousness or amnesia, intracranial hematoma or brain contusion on CT scan, and/or depressed skull fracture), beginning with an early intravenous loading dose (Level A). Prophylaxis with phenytoin, carbamazepine, or valproate is not advised beyond the first 7 days after injury as (Level B).…”

Section: Discussionmentioning

confidence: 99%

Can idiosyncratic drug reactions occur in quick succession? a case of cross sensitivity between levetiracetam and phenytoin

Nayak¹,

Kakode²,

Rataboli³

2017

Int J Basic Clin Pharmacol

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The occurrence of adverse drug reactions (ADRs) to more than one drug in quick succession can cause diagnostic dilemma to the doctor and increased burden of suffering to the patient. We present a single case report of a 23 year old female who developed rash and agranulocytosis in quick succession as ADRs to phenytoin and levetiracetam respectively. These antiepileptic drugs (AEDs) were prescribed as prophylaxis against post traumatic seizures (PTS). Hence a proper rationale for the prophylactic treatment of PTS and pharmacovigilance for early detection of adverse drug reactions is the need of the hour.

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“…Seizures can be controlled by sedation and paralysing agents (eg, atracurium) in the short term,13 or indeed antiepileptics such as phenytoin have been shown to be effective in the prophylaxis of PTS 14. Surgical management can include evacuating any significant haematoma, inserting an extraventricular drain to drain the CSF, or in the case of uncontrollable intracranial hypertension, a decompressive craniectomy to allow more space for the swollen brain tissue 9…”

Section: Central Nervous Systemmentioning

confidence: 99%

Timing of fracture fixation from an Intensive Care Unit perspective: the obstacles to early fracture fixation

Thomson

Fry²,

Jackson

2016

Postgraduate Medical Journal

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Trauma is one of the leading causes of death worldwide, with road traffic accidents being the leading cause of death in the age group of 15-29 years However, with modern advances in management and the introduction of specialised trauma centres, more and more are surviving severe and life-threatening trauma. The ideal timing of fracture fixation has been the subject of debate for a number of decades. There is evidence to suggest that fracture fixation in the patient with polytrauma is best achieved early on to reduce the incidence of morbidity and mortality, with damage control surgery in the more appropriate option in those patients who are haemodynamically unstable. However, early fracture fixation is not always possible, and the focus of this article is to review the common contributing factors resulting in delayed fixation. For the purpose of this discussion, we will consider all trauma as a single entity, taking into account that each type of fixation has its own complications, which are outside the scope of this article.

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Use of antiepileptics for seizure prophylaxis after traumatic brain injury

Cited by 79 publications

References 23 publications

Inflammation in epileptogenesis after traumatic brain injury

Inflammation in epileptogenesis after traumatic brain injury

Can idiosyncratic drug reactions occur in quick succession? a case of cross sensitivity between levetiracetam and phenytoin

Timing of fracture fixation from an Intensive Care Unit perspective: the obstacles to early fracture fixation

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