Status epilepticus: a modern approach to management

Abstract

Status epilepticus (SE) is a common medical emergency. Two problems continue to militate against improved outcome in SE, namely, failure to recognize the wide spectrum of clinical presentation and failure to treat in an appropriately aggressive and timely manner. In this study, we aim to provide a clear understanding of the clinical presentation of SE, as well as providing an evidence-based review of the pathophysiological consequences of prolonged seizures, enabling the reader to adopt a rational approach to its management. We discuss current best practice for the management of SE as well as discussing alternative strategies, and briefly explore possible future therapeutic interventions.

Lacosamide as adjunctive therapy in refractory epilepsy in adults: A systematic review

“…especially those available in intravenous form, are being investigated in the treatment of RSE. 6 Lacosamide is a new AED believed to exert its anticonvulsant effects through two novel mechanisms of action. The first is through its enhancement of slow inactivation of voltage gated sodium channels (VGSC).…”

The use of vasopressors in Takotsubo cardiomyopathy: Impact on neurological practice

“…The involvement of multiple specialties in the care of the patient is increasingly important. In the case of neurological practice, sedative agents used in the control of seizures and status epilepticus commonly have negative hemodynamic effects [6]. Inotropic support is often instituted based on the assumption of iatrogenic hypotension though it is now evident that the choice of inotrope needs careful consideration if concomitant Takotsubo is suspected.…”

Seizure prevention by the naturally occurring phenols, carvacrol and thymol in a partial seizure-psychomotor model

“…Propofol is emerging as a preferred therapy in aborting seizures in human status epilepticus. 9 It is believed to primarily depress CNS activity by acting as a positive allosteric modulator of GABA A receptors. 10 Other mechanisms may include inhibition of sodium channels 11,12 and NMDA receptors.…”