OPTICAL IMAGING OF INTRINSIC SIGNAL DURING EPILEPTIFORM AFTERDISCHARGES IN HUMAN CORTEX
Abstract number :
1.128
Submission category :
Year :
2005
Submission ID :
5180
Source :
www.aesnet.org
Presentation date :
12/3/2005 12:00:00 AM
Published date :
Dec 2, 2005, 06:00 AM
Authors :
1Minah Suh, 2Sonya Bahar, 1Ashesh D. Mehta, 1Hongtao Ma, 1Mingrui Zhao, 3Saadat Shariff, 1Koonho Wong, and 1Theodore H. Schwartz
Epileptiform events are characterized by synchronous activity in a large population of neurons. Whether cerebral blood flow is adequate to meet the increased metabolic demand is not well understood. We have recently demonstrated a decrease in hemoglobin oxygenation during interictal and ictal events in an animal model. Whether human epileptiform events are similarly associated with transient tissue hypoxia is unclear. We measured cerebral blood volume (CBV) and deoxygenated hemoglobin (Hbr) during stimulus-induced afterdischarges in the human neocortex using optical recording of intrinsic signal (ORIS) and spontaneous electrocorticography (EEG). In a separate experiment, an FDA-approved oxygen sensor (LICOX) was used to confirm the optical data. Afterdischarges were induced with bipolar cortical stimulation (1 msec pulses at 60 Hz for 2-5 seconds, current amplitude at 3-15 mA) into the cortex of 3 patients undergoing craniotomy for resection of medically intractable epilepsy. For optical imaging, a sterile glass footplate was placed on the brain surface to reduce cortical pulsation. Changes in light reflectance, imaged with a sterilely-draped CCD camera, were calculated by dividing each image by an image prior to stimulation. EEG was recorded through a strip electrode that was placed on the surface of the cortex and was amplified and digitized at 2000 Hz. Afterdischarges (n=6 in 3 patients) lasted 18 [plusmn]6 msec. ORIS revealed a 2.5 [plusmn]1 (%) increase in Hbr and a 2.0 [plusmn]0.7 (%) increase in CBV. Direct measurement of tissue oxygenation confirmed our result and demonstrated a decrease in tissue oxygenation by 2.0 [plusmn]0.8 (%). These findings confirm that the increase in metabolic demand associated with epileptiform events is not adequately met by cerebrovascular perfusion causing a transient tissue ischemia in human cortex. (Supported by NIH.)