To assess the potential biologic significance of variations in burst-suppression patterns (BSPs) after cardiac arrest in relation to recovery of consciousness. In the context of recent theoretical models of BSP, bursting frequency may be representative of underlying network dynamics; discontinuous activation of membrane potential during impaired cellular energetics may promote neuronal rescue.
We reviewed a database of 73 comatose post-cardiac arrest patients who underwent therapeutic hypothermia to assess for the presence of BSP and clinical outcomes. In a subsample of patients with BSP (n = 14), spectral content of burst and suppression periods were quantified using multitaper method.
Burst-suppression pattern was seen in 45/73 (61%) patients. Comparable numbers of patients with (31.1%) and without (35.7%) BSP regained consciousness by the time of hospital discharge. In addition, in two unique cases, BSP initially resolved and then spontaneously reemerged after completion of therapeutic hypothermia and cessation of sedative medications. Both patients recovered consciousness. Spectral analysis of bursts in all patients regaining consciousness (n = 6) showed a prominent theta frequency (5–7 Hz) feature, but not in age-matched patients with induced BSP who did not recover consciousness (n = 8).
The prognostic implications of BSP after hypoxic brain injury may vary based on the intrinsic properties of the underlying brain state itself. The presence of theta activity within bursts may index potential viability of neuronal networks underlying recovery of consciousness; emergence of spontaneous BSP in some cases may indicate an innate neuroprotective mechanism. This study highlights the need for better characterization of various BSP patterns after cardiac arrest.
*Department of Neurology, Columbia University Medical Center, New York, New York, U.S.A.;
‡Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York, U.S.A.;
†Division of Clinical Neurophysiology, Department of Neurology, Weill Cornell Medical College, New York, New York, U.S.A.; and
§Center for Clinical and Translational Science, The Rockefeller University, New York, New York, U.S.A.
Address correspondence and reprint requests to Peter B. Forgacs, MD, Department of Neurology, Feil Family Brain and Mind Research Institute, 525 East 68th St, New York, NY 10065, U.S.A.; e-mail: firstname.lastname@example.org.
The authors have no funding or conflicts of interest to disclose.
Supported by the NIH NINDS K23 NS096222; Leon Levy Neuroscience Fellowship Award; NIH UL1 TR000043 NCATS Rockefeller CTSA Program and The Stavros Niarchos Foundation; NIH NINDS RO1 HD051912; The James S. McDonnell Foundation.
The content of this paper was presented in a poster format in December 3, 2017 at the American Epilepsy Society (AES) Annual Meeting, Washington, DC.