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ARTICLES: Andrea O. Rossetti, Mauro Oddo, Lucas Liaudet, and Peter W. Kaplan Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia Neurology 2009; 72: 744-749 [Abstract] [Full text] [PDF]

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Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia

William D. Freeman, Kevin M Barrett, Michelle L Freeman, Margaret Johnson, Gavin Divertie   (1 April 2009)

Reply from the authors

Andrea O. Rossetti, Peter W. Kaplan, Baltimore (MD)   (1 April 2009)

Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia 1 April 2009
William D. Freeman, Mayo Clinic 4500 San Pablo Rd, Cannaday 2E, Jacksonville, Florida 32224, Kevin M Barrett, Michelle L Freeman, Margaret Johnson, Gavin Divertie Send Correspondence to journal: Re: Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia freeman.william1{at}mayo.edu William D. Freeman, et al.	We read with great interest the article by Rossetti et al. who studied six cardiac arrest (CA) cases with post-anoxic status epilepticus (PSE) treated with therapeutic hypothermia. [1] The authors highlight important observations about EEG in the age of therapeutic hypothermia. The study raises the question: If specific EEG patterns emerge after CA, would these patterns now represent a treatable CA with potential for better outcomes? However, the authors apparently did not perform EEG during the hypothermic period in which vecuronium was used. Nonetheless, the authors’ data showed half of their cases with clinically evident seizures at the bedside confirmed by EEG while the other half had PSE detected only on EEG in coma. The authors’ observations demonstrate that not all clinically evident post CA myoclonic jerking represents myoclonus status epilepticus, which is a poor prognostic sign. Recently published AAN guidelines emphasized the utility of EEG after CA. [2] It has been our observation in two years of using hypothermia after CA that myoclonic jerks after CA are an ominous sign especially in concert with absent or partially absent brainstem reflexes. We find the authors’ study important for clinicians, since all myoclonic jerking seen at the bedside after CA should not be interpreted as indicative of myoclonus status epilepticus without EEG confirmation. To do so could lead to a self-fulfilling prophecy of poor outcome and untreated status epilepticus. Additionally, the majority of the authors’ cases with PSE on EEG had background reactivity, intact brainstem reflex testing, and intact N20 responses on somatosensory evoked potential testing. This group of patients might be expected to do better than most. For example, we treated 26 patients with hypothermia after cardiac arrest over two year (mixed in and out of hospital arrest, ventricular fibrillation, pulseless electrical activity and asystole) and observed three cases (11%) with severe myoclonic jerking after hypothermia, sedation, and muscle relaxation was lifted. In these patients, there was typically partial loss of brainstem reflexes pre- and post-hypothermia, and in one case absent N20 potentials. In two of our cases, the EEG indicated a myoclonus status epilepticus pattern, in which the background is typically suppressed, unreactive, and alternating bursts of activity correlated with myoclonic jerks. [3] Whether the hypothermia improves the EEG patterns relative to clinical outcomes during the period of therapeutic hypothermia is still unclear. References 1. Rossetti AO, Oddo M, Liaudet L, Kaplan PW. Predictors of awakening from postanoxic status epilepticus after therapeutic hypothermia Neurology 2009;72:744–749. 2. Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2006;67:203–210. 3. Wijdicks EF, Parisi JE, Sharbrough FW. Prognostic value of myoclonus status in comatose survivors of cardiac arrest. Ann Neurol 1994;35:239–243. Disclosure: The authors report no disclosures.
Reply from the authors 1 April 2009
Andrea O. Rossetti, CHUV Service de Neurologie BH 07; CHUV; CH-1011-Lausanne (Switzerland), Peter W. Kaplan, Baltimore (MD) Send Correspondence to journal: Re: Reply from the authors andrea.rossetti{at}chuv.ch Andrea O. Rossetti, et al.	We thank Dr. Freeman and colleagues for their valuable comments on our article. As they correctly point out, we did not perform EEG recordings during hypothermia for three reasons: low temperature may affect cerebral electrogenesis [4]; administered medications likely exert a further influence on EEG [1]; and EEG tracings obtained within 12-24 hours after cardiac arrest may overestimate the extension of brain damage. [2] This is especially important considering EEG reactivity. It will be important in the future to conduct prospective observations on EEG during hypothermia to determine whether this may further our understanding of postanoxic patients’ prognoses. In our cohort, a minority of subjects (4/33) showed subclinical status epilepticus, the majority (24/33) had electroclinical SE, and 5/33 presented with “reticular myoclonus”. All patients in the last category died. We agree that a multi-modal approach is paramount in the evaluation of postanoxic patients, including somatosensory evoked potentials and repeated clinical evaluation. As in the patients described by Freeman et al., loss of brainstem reflexes and, even more reliably N20 responses are solid markers of a dismal outcome. [2] In our opinion, a component of “self fulfilling prophecy” will unfortunately always bias, at least to some extent, observational studies on postanoxic patients. [1,2,5] A careful design and honesty in the interpretation of the results are critical when evaluating this severe condition. References 4. Stecker MM, Cheung AT, Pochettino A, et al. Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials. Ann Thorac Surg 2001;71:14-21. 5. Rossetti AO, Logroscino G, Liaudet L, et al. Status epilepticus: an independent outcome predictor after cerebral anoxia. Neurology 2007;69:255-260. Disclosure: Dr. Kaplan served on the scientific advisory board for GSK, was on the speaker's bureau for GSK, UCB and Ortho-McNeil, reviewed EEGs under a contract to Schering-Plough, was funded by grants under Ortho-McNeil and Schwarz Pharma, and is funded by NIH grants #100665;100666, and 101549.