Clinical Neurophysiology Lab
The Clinical Neurophysiology Lab team studies the neurophysiology of acute brain trauma and stroke.
While immediate damage caused by brain injury is irreversible, secondary events that occur in the hours and days after injury can cause further damage and be life-threatening. Understanding of this secondary pathology and methods to continuously monitor critical parameters of the brain are limited.
The premise of our research is that improvements in patient outcomes can be achieved through better means to monitor patients by allowing for early detection of secondary deterioration and delivery of therapies tailored to specific brain pathologies.
Neurophysiology is an attractive target for brain monitoring since it provides real-time, dynamic information reflecting brain metabolism, blood flow, structural integrity, and secondary injury processes.
The major focus of othe team's work is elucidating the role of cortical spreading depolarizations (CSD: Leão's spreading depression and peri-infarct depolarizations) in clinical brain trauma and stroke.
In the seminal electrophysiology experiments of the 1970s that led to discovery of the “penumbra” concept, it was found that waves of elevated [K+]e spontaneously propagated through the border zone of focal ischemia (J Neurol Sci 32:305-21, 1977; Stroke 8:51-7, 1977). These events, confirmed as CSD, were later proven to cause progressive infarct growth through time (i.e. "time is brain").
Since the study of Strong and colleagues (Stroke 33:2738-43, 2002), it is now known that CSD also occurs in a majority of patients suffering severe stroke and brain trauma.
Working with clinicians, neuroscientists, bioengineers and colleagues from the COSBID consortium, the lab's purpose is to develop the clinical science for monitoring CSD and determine its utility in understanding, diagnosing, and treating secondary injury.
Results to date suggest that CSD events are associated with critical parameters targeted in the management of head injury (see Figure), and may be associated with progressive brain lesion development. This suggests that monitoring CSD may aid in evaluation of therapeutic efficacy and that CSD may be a target for future therapeutic interventions to improve outcomes.
We are coordinating a multi-center study of CSD in brain trauma funded by the Department of Defense through the U.S. Army Psychological Health/Traumatic Brain Injury Research Program.
Learn more about this study.
Figure 1. Repetitive cycles of CSD during sustained elevated intracranial pressure in a brain trauma patient with delayed deterioration. Arrows point to the spreading waves of CSD in the low-frequency electrocorticogram (ECoG, 0.01-0.5 Hz), which correspond to progressive deterioration of the high frequency (0.5-50 Hz) activity. Fourteen CSDs in this eight-hour period result in a prolonged isoelectric state.
Personnel & Collaborations
University of Cincinnati
Jed A. Hartings, PhD, Research Associate Professor
J. Adam Wilson, PhD, Post-Doctoral Fellow
Jason Hinzman, PhD, Post-Doctoral Fellow
Eric Mahoney, MS, Senior Research Assistant
Sebastien Pollandt, PhD, Post-Doctoral Fellow
Ope Adeoye, MD, Neurocritical Care Division
Norberto Andaluz, MD, Director, Neurotrauma
Pooja Khatri, MD, Neurology
Achala Vagal, MD, Neuroradiology
Co-Operative Study on Brain Injury Depolarizations (www.cosbid.org):
Ross Bullock, MD, PhD, University of Miami
Jens Dreier, MD, PhD, Charité University Medicine (Berlin)
Martin Fabricius, MD, DMSc, Glostrup Hospital (Copenhagen)
Bruce Mathern, MD, Virginia Commonwealth University
David Okonkwo, MD, PhD, University of Pittsburgh
Clemens Pahl, DM, King's College Hospital (London)
Oliver Sakowitz, DM, University of Cincinnati Medical Center Heidelberg (Germany)
Anthony Strong, DM, King's College Hospital (London)
Tomas Watanabe, MD, PhD, Naval Medical Research Center
Frank Tortella, PhD, Walter Reed Army Institute of Research