Complex detection, complex decisions: more detail on subclinical seizures in the acutely sick brain.

Commentary Nonconvulsive seizures and nonconvulsive status epilepticus occurring in sick hospitalized patients represent a major challenge. Neurologists are frequently asked to see and advise on the management of patients who are unwell and encephalo-pathic, usually in an intensive care setting. These patients may or may not have a history of established epilepsy, may have a number of pre-existing comorbidities, may be on multiple medications, and are acutely unwell due to either systemic, neurological, or surgical disease. The immediate clinical questions that arise in such patients are the following: 1. What is the cause, or causes, of the encephalopathy? 2. Are convulsive or nonconvulsive seizures clinically appar-ent? 3. Is it possible that subtle or subclinical nonconvulsive seizures are contributing to the clinical picture? 4. What immediate appropriate neurological investigations are indicated (and available) at the particular center? 5. Are suspected or proven nonconvulsive seizures causing homeostatic and neurological harm, thus contributing to secondary brain injury? 6. How aggressive should anti-epileptic drug therapy be in suppressing nonconvulsive seizures, and what difference does this make to long-term outcomes? Translational clinical research attempting to answer some of these highly relevant and common clinical dilemmas is welcomed. The ongoing work of the Critical Care Neurology and Epilepsy Divisions at Columbia University in New York is at the vanguard of this research. In the current paper, the authors attempt to measure aberrant cerebral physiology associated with non-convulsive seizures in 48 comatose (Glasgow Coma Scale </= 8) patients following subarachnoid hemorrhage. Patients with clinically obvious seizures were excluded from this study. As part of their " routine clinical care, " patients were monitored with intracortical electroencephalography using mini-depth electrodes, and multimodal physiological recordings. The latter included measurement of intracranial pressure, interstitial cerebral microdialysis (assaying lactate, pyruvate, and glucose), partial brain tissue oxygenation, and brain temperature. All patients were on prophylactic phenytoin for 1 week after subarachnoid hemorrhage, which was then discon-OBJECTIVE: Seizures have been implicated as a cause of secondary brain injury, but the systemic and cerebral physi-ologic effects of seizures after acute brain injury are poorly understood. METHODS: We analyzed intracortical electroen-cephalographic (EEG) and multimodality physiological recordings in 48 comatose subarachnoid hemorrhage patients to better characterize the physiological response to seizures after acute brain injury. RESULTS: Intracortical seizures were seen in 38% of patients, and 8% had surface seizures. Intracortical seizures were accompanied by elevated heart rate (p = 0.001), blood pressure (p < 0.001), and …