Robert Bradford Duckrow, MD

My early contributions to science were in the field of cerebral blood flow and metabolism. At that time, there was considerable interest in the role of hyperglycemia in the evolution of ischemic stroke in humans. Specifically, that it made stroke worse. My initial work found that cerebral blood flow decreased during hyperglycemia and appeared to exclude a causal role of serum osmolality. My subsequent studies eliminated other factors that could explain the finding, including metabolic rate, insulin release, and blood viscosity. Eventually, my application of a continuous laser Doppler blood flow method showed that increased serum osmolality was likely causal and explained the disparity of earlier findings. This work added to the existing body of work on the control of the cerebral circulation. I designed, executed, and reported this work.

Duckrow RB, Beard DC, Brennan RW. (1985) Regional cerebral blood flow decreases during hyperglycemia. Ann. Neurol. 17:267-272

Duckrow RB, Bryan RM. (1987) Regional cerebral glucose utilization during hyperglycemia. J. Neurochem. 48:989-993

Duckrow RB. (1988) Glucose transfer into rat brain during acute and chronic hyperglycemia. Metabolic Brain Disease 3:201-209

Duckrow RB. (1995) Decreased cerebral blood flow during acute hyperglycemia. Brain Res. 703:145-150,

While attempting to develop an acute stroke model, I found an opportunity to study cerebral vascular responses to cortical spreading depression in awake rats. At the time, reports of the blood flow response were variable with the concern that the variation was related to anesthesia. I found that the cerebral blood flow change during spreading depression was related to the baseline flow. This supported the position that eventually became widely accepted. More importantly, by subsequently developing an early form of three-dimensional image reconstruction, I demonstrated the role of nitric oxide synthesis in the modulation of cerebral blood flow during the initial phases of spreading depression. I was the first to report this mechanistic relationship, which was then used by larger groups to address pathophysiological process during acute stroke and migraine headache. I designed, executed, and reported this work.

Duckrow RB. (1991) Regional cerebral blood flow during spreading cortical depression in conscious rats. J. Cereb. Blood Flow Metab. 11:150-154

Duckrow RB. (1993) A brief hypoperfusion precedes spreading depression if nitric oxide synthesis is inhibited. Brain Res. 618:190-195

Analytic methods to measure coincidence and synchronization have been broadly applied to probe brain mechanisms such as synaptic potentiation and feature binding. Accordingly, they have also been applied to questions of seizure onset and propagation in animals and humans. Although correlational and coherence analysis of brain signals began in the 1950s, my work in the field represents an early application coherence analysis to the intracranial EEG of persons with epilepsy in the modern computer era. The central findings supported the concept of information transfer during seizure propagation in mesial temporal lobe structures. I also reported that this transfer did not need to be continuous and separate regions could independently maintain epileptic discharges; a controversial issue at that time. I designed, executed, and reported this work. Continuing collaborative work has included position statements on technical details to provoke a dialog to improve available methods.

Duckrow RB, Spencer SS. (1992) Regional coherence and the transfer of ictal activity during seizure onset in the medial temporal lobe. Electroenceph. clin. Neurophysiol. 82:415-422

Zaveri HP, Duckrow RB, Spencer SS. (2006) On the use of bipolar montages for time-series analysis of intracranial electroencephalograms. Clin. Neurophysiol. 117:2102-2108

Zaveri HP, Duckrow RB, Spencer SS. (2009) Concerning the observation of an electrical potential at a distance from an intracranial electrode contact. Clinical Neurophysiology 120(10):1873-1875

Diagnostic methods to locate and surgical approaches to resect brain tissue responsible for medically intractable epilepsy advanced during the 1980s and 90s. However, surgical failures and a hesitance to resect seizure onset zones that overlapped with areas of critical function spurred the development of implantable neurostimulator systems. Advances in compact signal processors allowed the detection of seizure onset and abortive electrical stimulation of the same region using electrodes on or in the brain. Our group participated in the initial testing of the safety and efficacy of such a device. It was clear from the start that it would provide a novel picture of brain activity by allowing long-term recording of the intracranial EEG in freely moving patients. I was the first to show the potential of this approach by using the device to characterize the daily (circadian) variation in an intracranial EEG feature that correlated with seizure occurrence. This general approach is now the focus of a funding initiative of the Epilepsy Foundation. I was the PI of our site’s participation in the multi-center study of the device, now approved by the FDA, and designed, executed, and reported the work on daily variation.

Duckrow RB, Tcheng TK. (2007) Daily variation in an intracranial EEG feature in humans detected by a responsive neurostimulator system. Epilepsia. 48(8):1614-20

Morrell M, RNS System in Epilepsy Study Group (Duckrow RB, Site Principal Investigator). (2011) Responsive cortical stimulation for the treatment of medically intractable partial epilepsy. Neurology. 77(13):1295-304