Phenytoin, levetiracetam, and pregabalin in the acute management of refractory status epilepticus in patients with brain tumors.

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BACKGROUND: There were nearly 700,000 patients in the United States in 2010 living with brain tumor diagnoses. The incidence of seizures in this population is as high as 70% and is historically difficult to control. Approximately 30-40% of brain tumors patients who present with status epilepticus (SE) will not respond to typical therapy consisting of benzodiazepines and phenytoin (PHT), resulting in patients with refractory status epilepticus (RSE). RSE is usually treated with anesthetic doses of propofol or midazolam infusions. This therapy can have significant risk, particularly in patients with cancer. METHODS: A retrospective chart review was performed on 23 patients with primary or metastatic brain tumors whose SE was treated with intravenous PHT, levetiracetam (LEV), and oral pregabalin (PGB). RESULTS: In all the patients under study, PHT or LEV was used as first-line therapy. PGB was typically used as third-line treatment. The median daily dose of PGB was 375 mg (usually divided BID or TID), and the median daily dose of LEV 3000 mg (usually divided BID). Cessation of SE was seen in 16/23 (70%) after administration of PHT, LEV, and PGB. SE was aborted, on average, 24 h after addition of the third antiepileptic drug. Only one patient in the responder group required intubation. Mortality rate was zero in the responder group. No adverse reactions to this medication regimen were observed. CONCLUSION: Our study suggests that the administration of PHT, LEV, and PGB in brain tumor patients with RSE is safe and highly effective.





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Swisher, Christa B, Meghana Doreswamy, Krista J Gingrich, James J Vredenburgh and Brad J Kolls (2012). Phenytoin, levetiracetam, and pregabalin in the acute management of refractory status epilepticus in patients with brain tumors. Neurocrit Care, 16(1). pp. 109–113. 10.1007/s12028-011-9626-4 Retrieved from

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Bradley Jason Kolls

Associate Professor of Neurology

As a neurointensivist, I am interested in improving our ability to monitor brain function and impact of therapy on our patients in the critical care setting. To this end I am developing new approaches to patient monitoring that will integrate patient physiologic monitoring with brain activity recorded by electroencephalography (EEG). On the basic science side I am interested in the central nervous system's response to injury. Although much attention has been focused on closed head injury as of late, stroke and brain hemorrhage are just as common in the civilian population and pose many of the same clinical challenges as traumatic brain injury. Using mouse models of clinically relevant brain injury, including models of stroke, subarachnoid hemorrhage, lobar hemorrhage, closed head injury and penetrating brain injury, we can explore the key molecular events that lead to edema, secondary brain injury, hyperexcitability and epilepsy, and other sequelae which contribute to poor patient recovery, and significant morbidity following brain injury. By investigating the underlying mechanisms that contribute to these adaptive changes using electrophysiology and molecular biology approaches we can then find ways to prevent them from becoming maladaptive and develop new therapies for our patients with head injuries.

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