| Office Location: | 125 Bell Bldg |
| Office Phone: | +1 919 668 0477 |
| Email Address: | ![]() ![]() |
| Web Page: | http://faculty.duke.edu/faculty/info?pid=1132 |
| M.D. | University of Minnesota Medical School - Minneapolis | 1969 |
Current Research Efforts:
A) Basic Science:
1) Mechanism of NMDA receptor antagomist neuroneurotoxicity: Although NMDA receptor antagonists are useful in protecting against excitotoxicity and ischemic injury, they also can cause neuronal apoptosis in the cingulate gyrus and clinically abused NMDA receptor antagomists such as angels dust can produce a schizoprenic like syndrome. We are studying the disinhibitory effects of NMDA receptor antagonists on the cortical puramidal cells of the posterior cingulate region to determine how these agents produce neuronal injury (Li, Q, Clark, S, Lewis, DV, and Wilson, WA. NMDA receptor antagonists disinhibit rat posterior cingulate and retrosplenial cortices: A potential mechanism of neurotoxicity. J Neurosci, In Press, 2001).
2) Mechanism of development of tolerance and dependence to GHB (gammahydroxybutyric acid), a commonly abused sedative agent. We are studying the effect of GHB on the inhibitory circuitry of the neocortex in rats to determine the changes in GABA receptor expression and sensitivity that may underlie the development of tolerance, dependence and withdrawal phenomena associated with GHB abuse.
B) Clinical Research
1) Relationship between complex febrile convulsions and hippocampal sclerosis; The hypothesis that complex febrile convulsions (CFCs) cause hippocampal injury that evolves to sclerosis and then to temporal love epilepsy has been promulgated for decades since the advent of surgical treatment of temporal love epilepsy. However, this concept has never been addressed with a prospective clinical study. With the availability of magnetic resonance imaging techniques capable of discerning hippocampal edema and measuring hippocampal volume, patients suffering CFCs can now be studied acutely and chronically to determine if hippocampal injury does occur using CFCs and under what clinical circumstances. We are planning a multicenter study of this phenomenon based on the publication describing our initial findings ina small group of infants with CFCs (VanLandingham et al., Annals of Neurology, 43:413-426, 1998; Lewis DV. Febrile convulsions and mesial temporal sclerosis. Current Opinion in Neurology, 12:197-201, 1999; Lewis, DV et al. Do Prolonged Febrile Seizures Produce Mesial Temporal Sclerosis? Hypotheses, MRI Evidence and Unanswered Questions, Prog. Brain Res. In Press, 2001; Mitchell, TV and Lewis, DV. Do prolonged febrile seizures injure the hippocampus: Human MRI studies. In, Febrile Seizures, Eds. TZ Baram and S Shinnar, In Press, 2001.