Early EEG correlates of neuronal injury after brain anoxia
CarleneStanko, Clinical Research Intern Scholar (CRISP)-Mayo Clinic, University of North Florida and Mayo CRISP studentcarlene1313@gmail.com
WDFreeman, MD Jacksonville, FL
Submitted April 10, 2012
We read with great interest the article by Rosetti et al. [1] on the early EEG correlates of neuronal injury after brain anoxia in which they studied
61 cardiac arrest patients treated with therapeutic hypothermia (TH) with continuous (24-48hr) or 20-30min EEG. We reviewed our hypothermia database from 2006 to 2012, in which 91 patients received TH for cardiac arrest. Nine patients received EEG similar to the methods Rosetti et al. described [1], 8 of which (89%) occurred within the last 3 years. Three patients had suppression burst (SB) activity on EEG, all of which died (CPC =5). The remaining 6 patients did not have SB pattern on EEG, two of which had CPC 1-2 (good) outcome and at least 7Hz background on EEG. Of these, 4 patients had a CPC outcome of 5 and EEGs with either delta, theta or alpha background cerebral activity, except one patient with GPEDs. Therefore, SB pattern and GPED's on EEG had a 100% specificity for poor prognosis whereas other EEG rhythms had poor specificity and sensitivity for eventual outcome. Rosetti's data support the need for 'multimodal'
prognostic research trials for TH-treated cardiac arrest patients similar to other forms of brain injury [2].
1. Rossetti AO, Carrera E, Oddo M. Early EEG correlates of neuronal injury
after brain anoxia. Neurology 2012;78:796-802. Epub 2012 Feb
8.
2. Ko SB, Choi HA, Parikh G, Helbok R, et al. Multimodality monitoring for
cerebral perfusion pressure optimization in comatose patients with
intracerebral hemorrhage. Stroke 2011;42:3087-92. Epub 2011 Aug
18.
For disclosures, contact the editorial office at journal@neurology.org.
We read with great interest the article by Rosetti et al. [1] on the early EEG correlates of neuronal injury after brain anoxia in which they studied 61 cardiac arrest patients treated with therapeutic hypothermia (TH) with continuous (24-48hr) or 20-30min EEG. We reviewed our hypothermia database from 2006 to 2012, in which 91 patients received TH for cardiac arrest. Nine patients received EEG similar to the methods Rosetti et al. described [1], 8 of which (89%) occurred within the last 3 years. Three patients had suppression burst (SB) activity on EEG, all of which died (CPC =5). The remaining 6 patients did not have SB pattern on EEG, two of which had CPC 1-2 (good) outcome and at least 7Hz background on EEG. Of these, 4 patients had a CPC outcome of 5 and EEGs with either delta, theta or alpha background cerebral activity, except one patient with GPEDs. Therefore, SB pattern and GPED's on EEG had a 100% specificity for poor prognosis whereas other EEG rhythms had poor specificity and sensitivity for eventual outcome. Rosetti's data support the need for 'multimodal' prognostic research trials for TH-treated cardiac arrest patients similar to other forms of brain injury [2].
1. Rossetti AO, Carrera E, Oddo M. Early EEG correlates of neuronal injury after brain anoxia. Neurology 2012;78:796-802. Epub 2012 Feb 8.
2. Ko SB, Choi HA, Parikh G, Helbok R, et al. Multimodality monitoring for cerebral perfusion pressure optimization in comatose patients with intracerebral hemorrhage. Stroke 2011;42:3087-92. Epub 2011 Aug 18.
For disclosures, contact the editorial office at journal@neurology.org.