Cerebral ischemia is a major cause of morbidity and mortality in the neurosurgical patient population, yet the ability to accurately identify and treat ischemia before irreversible tissue damage occurs remains poor. Many functional imaging techniques such as PET and fMRI are based upon the tight linkage between neuronal activation and cerebral blood flow (CBF), termed activation flow coupling (AFC), which is known to exist under physiologic conditions. There is evidence that pathological states such as cerebral ischemia alter the AFC response. It is hypothesized that the AFC response may well be the most sensitive indicator of subclinical cerebral ischemia. The proposed research will examine the alterations of AFC during graded CBF reduction in a rat model of forepaw somatosensory stimulation. Ischemia will be induced by modifying a previously described model of cortical compression and tissue pathology will be completed to make morphological calculations of infarct volume. Laser Doppler flowmetry will be used to monitor the CBF response to somatosensory stimulation. Recordings of somatosensory evoked potential are also planned as a measure of neuronal activity. Advances in functional imaging and optical imaging promise to make basic research efforts such as this readily transferable to the neurologic and neurosurgical patient care setting.
| Burnett, Mark G; Shimazu, Tomokazu; Szabados, Tamas et al. (2006) Electrical forepaw stimulation during reversible forebrain ischemia decreases infarct volume. Stroke 37:1327-31 |
| Burnett, Mark G; Detre, John A; Greenberg, Joel H (2005) Activation-flow coupling during graded cerebral ischemia. Brain Res 1047:112-8 |
| Durduran, Turgut; Burnett, Mark G; Yu, Guoqiang et al. (2004) Spatiotemporal quantification of cerebral blood flow during functional activation in rat somatosensory cortex using laser-speckle flowmetry. J Cereb Blood Flow Metab 24:518-25 |
| Durduran, Turgut; Yu, Guoqiang; Burnett, Mark G et al. (2004) Diffuse optical measurement of blood flow, blood oxygenation, and metabolism in a human brain during sensorimotor cortex activation. Opt Lett 29:1766-8 |
