Abstracts

Rationale: Burst-suppression (BS) is an electroencephalogram (EEG) pattern with periods of bursts cerebral electrical activity consisting of waves with a variable frequency, voltage and morphology alternated with a low or almost completely attenuated activity1. It can be physiological in early development, or pathological, most commonly seen in severe epileptic encephalopathy, in comatose patients with acute brain injuries or with central nervous system (CNS) depressant drugs2. BS asynchronous has been associated with a defective or agenesis of the corpus callosum (CC). CC is one of the largest structures that promote synchrony between the two hemispheres, which leads us to conclude that asynchronous BS (ABS) is unexpected. In sedated patients, with no previous history of CNS lesion2,3. Our aim was to evaluate BS induced by sedative drugs for identification of ABS prevalence and its correlation to etiologies and to final follow-up. Methods: The digital database of Neurology Departments Electroencephalography Laboratory of Clinical Hospital - University of Sao Paulo (Brazil) was retrospectively analyzed, searching for EEG with BS pattern during the period of 3 years (2013-2015). Exclusion criteria included previous epileptic encephalopathy, no sedation at the time of exam and missing data. All included EEGs were reviewed by an experienced neurophysiologist. Every recording was classified as asynchronous BS or synchronous BS (SBS). It was analyzed the percentage of brain injury, stroke, tumor/abscess and other conditions, according to charts reviewed. Results: Out of 15184 analyzed exams, 174 with BS were included, which were recorded in 107 patients, 67 male (63,21%), with the average age of 45.9 yrs., ranging from 5 to 113 yrs. ABS was found in 88 (51%) recordings. Among causes for induced sedation, traumatic brain injury was the most prevalent in both groups, with 50 (58.82%) in SBS and 58 (65.91%) in ABS (graphic 1). Follow-up showed that 68 patients died, 38 (55,88%) of them with at least 1 EEG showing ABS. Conclusions: ABS was a relatively common finding in comatose patients and it is not known its significance in neurologic acute diseases. We demonstrated that almost half of patients had ABS. The high prevalence in cases of acute traumatic brain injuries could have a meaningful, although many other variables are present in comatose patients. One possible explanation is that patients who had greater involvement of sagittal structures or bilaterally lesions could have the asynchronous pattern. A future study in order to expand the number of cases, and to improve these data, is currently being drawn. References: 1. Hirsch, LJ ET AL. American Clinical Neurophysiology Society's Standardized Critical Care EEG Terminology: 2012 version. 2. Lazar, LM et al. Asynchronous pentobarbital-induced burst suppression with corpus callosum hemorrhage. Clin Neurophysiol 1999;110:1036-40. 3. An DS, Straumann D, Wieser HG. One-way asynchrony of burst-suppression activity Clin Neurophysiol 1996;26:329-34. Funding: No funding.