Abstracts

RATIONALE: Our previous study showed that imaging of intrinsic optical signals (IOS) can be used to map spatial and temporal patterns of epileptiform activity in human cortex (Nature, 1992). Interpretation of these earlier data is difficult because the IOS is generated by at least three components: i) changes in blood volume, ii) changes in blood oxygenation, and iii) blood-independent changes due to activity-induced cell swelling. In order for IOS to become a practical modality for localizing seizure foci in humans, it is necessary to better understand the physiological mechanisms that generate the optical signals. Here we show that our improved IOS technique allows us to [ssquote]dissect[ssquote] the various components contributing to the generation of IOS during epileptiform activity.
METHODS: Optical recordings were acquired from the cortices of anesthetized Macaque monkeys. A [ssquote]cranial window[ssquote] constructed over visual cortex allowed for the acquisition of optical and electrophysiological recordings. Acute epileptic foci were created by placing a bicuculline-soaked pledget briefly on the surface of the cortex. Single unit and field recordings were acquired during some experiments. Optical imaging data was acquired with narrow bandpass filters at selected wavelengths that were specifically sensitive to changes in either blood oxygenation or blood volume. Image analysis was performed to quantify the blood oxygenation and volume changes within the various vascular and non-vascular anatomical compartments.
RESULTS: Our modified IOS method allowed us to acquire series of images with high spatial and temporal resolutions of cortical changes in blood oxygenation and volume during epileptiform activity. Blood volume changes were limited to those pial arterioles which dilated during changes in activity. Blood oxygen changes were greatest in the cortical venules that were draining active tissue. During seizure activity, we found distinctly different hemodynamic patterns between those cortical areas involved in burst generation, the non-bursting regions immediately surrounding these foci, and non-involved tissue regions at further distances from the bursting foci. Single unit recordings acquired from these regions surrounding the foci indicated that neuronal activity was actually supressed from baseline.
CONCLUSIONS: Imaging of activity-evoked IOS allowed us to independently monitor changes in blood oxygenation and blood volume during epileptiform activity. By using wavelengths specific to changes in either blood oxygenation or blood volume, we were able to map patterns of hemodynamic changes in the cortex during epileptiform activity. These initial studies suggest that epileptiform-evoked changes in cortical blood volume and oxygenation may play a direct role in controlling the spread of seizure activity in cortex.
Support: NIH Clinical Investigator Development Award to MMH