Donald R. Humprhey, PhD

Office: 615 Whitehead Building

Phone: 404-727-7419

Fax: 404-727-2648

Email: dhumphr@emory.edu

Additional Contact Information

Mailing Address:

Department of Physiology

615 Whitehead Building
605m, Whitehead Building

Atlanta, GA 30322

Biography

 Education: From PhD/MD to current position. 

1966 Ph.D. Experimental Psychology, University of Washington

1966 Ph.D. Physiology and Biophysics, University of Washington School of Medicine,

1966-1971  USPHS (US Public Health Service) Fellow and Staff Scientist, NINDS (National Institute of Neurological Diseases and Stroke), NIH (National Institutes of Health).                                                                             

1971-1976  Assistant Professor to Professor, Dept. of Physiology, Emory School of Medicine

1987-1989  Founding Director, Graduate Division of Biological and Biomedical Research

1989-1996  Executive Associate Dean for Research, Emory School of Medicine.

2008-2013  Deputy Chair, Department of Physiology, Emory School of Medicine

2013-          Professor Emeritus, Department of Physiology, Emory School of Medicine

 

Research

Past Research Areas and Significant Achievements:

1. Brain stem areas mediating carotid sinus baroceptor reflexes. First to trace secondary pathways from the nucleus solitarius to major pressor and depressor zones of the medullary reticular formation.  (Humphrey, D.R. Neuronal activity in the medulla oblongata of the cat evoked by stimulation of the carotid sinus nerve. In: Baroceptors and Hypertension,     edited by P.Kezdi, Oxford: Pergamon Press (1967) pp. 131-168)

2. Cellular origins of the EEG. First to show with both experimental data and computer modeling that the major waveforms of the electroencephalogram originate principally from small post-synaptic potentials (PSPs), with much larger action potentials contributing little to the EEG. Received Hans Berger Award from the International EEG and Clinical Neurophysiolgy Society for this work (1968). (Humphrey, DR. Re-analysis of the antidromic cortical response. II. On the contribution of cell discharge and PSPs to the evoked potentials. Electroenceph. Clin. Neurophysiol. (1968) 25:421-442).

3. Cortical neuron discharge can predict parameters of voluntary limb movement in real- time. (Humphrey, DR; Schmidt, EM; Thompson, WD. Predicting measures of motor         performance from multiple cortical spike trains.  Science (1970) 170:758-762.) First paper to show that action potentials recorded simultaneously from groups of 5-10 neurons in the arm    area of the precentral motor cortex could be mathematically processed to predict in real-time the limb position, movement speed, and muscle force generated by the animal during    voluntary movements about a single joint, and that such signals could lead to prostheses by brain potentials could be used for direct control of external devices, This possibility is now       under widespread investigation under the title of “brain-computer interface research”.  The     original patent for this research is held by DRH and Emory University.

 4.  Properties of efferent cell systems in primate motor cortex. Several papers from this PI’s laboratory have outlined the major organizational features and voluntary movement control      functions of corticospinal and corticorubral cell systems in primate motor cortex.  This  collective research was recognized by  awarding one of the first prestigious Jacob Javits        excellence in neuroscience awards given by the NINDS, NIH  to DRH.  This research established, among other things, that cell columns in the precentral motor cortex are         organized for the control of simple movements and not of single muscles (e.g., Humphrey,    DR.      Representation of movements and muscles within the primate precentral motor cortex:        historical and current perspectives. Federation Proceedings (1986) 45:637-649).  In addition, the research suggested different cell systems in the motor cortex may contribute        differently to particular parameters of limb movement (Humphrey, DR  and Reed, DJ.         Separate cortical systems for the control of joint movement and of joint stiffness: Reciprocal         activation and co-activation of antagonist muscles.  Advances in Neurology (1983) 39: 347- 372).

Current Research Interest:   Long-term Changes in Brain Function in Paraplegics

 

     In the year 2000, we published the first brief report indicating that humans with complete to near-complete functional spinal cord transections retained the capacity to voluntarily activate neural tissue in areas of the brain that normally produce voluntary leg and foot movement.  In other words, long-term paralysis of leg and foot muscles did not cause the brain to follow the widely believed “use it or lose it” dogma about non-active neural circuitry.  Since that time, we have collected data from 42 carefully chose paraplegic subjects, controlled for age, completeness of spinal injury, and time since injury.  We are analyzing this 16 year span of data now, and can conclude (1) that there are significant changes over time since injury in the exact locations, sizes and activation levels of brain area leg control regions, but in general – even 40 year after injury, voluntary activation of these areas is retained. (2) The levels of appropriate and restricted brain activation – as in the uninjured subject – are slightly reduced, while activation of motor planning areas is greatly enhanced – as if the brain is “searching’ for the right pathways to activate the leg, but cannot isolate them. Many other findings of neurological interest are emerging, but the good news the remaining capacity for even limited activation of appropriate

brain raises hope that the brain may “re-connect” to the spinal cord in useful ways if the puzzle of how to avoid molecular changes which prevent growth of surviving axons across the injury site can be soived.

Publications