The hemodynamic responses to 4-aminopyridine (4-AP) induced focal epileptic spikes and electrical stimulations are compared in a rat model. Nonlinearities are quantified with biophysical models. Supranormal oxygen consumption from epileptic spikes is inferred. In one recording, interictal spikes followed an almost periodic pattern. Such rhythmic spiking is a well-documented phenomenon in electrophysiological studies, but the hemodynamics correlates have been less studied. Spikes occurred every 12.5 ± 1.0 s. Peaks in total hemoglobin (HbT), a proxy for regional cerebral blood volume, followed spikes by 2.6 ± 0.3 s. Troughs in HbT preceded spikes by 1.68 ± 1.2 s. The narrowness of this distribution is surprising. From it, one may derive a significant but paradoxical fall in HbT several seconds before the spikes, but which this decrease in HbT is better interpreted as being due to the interictal spike that occurred before.
In this study, we explore the hemodynamic response in the lesioned rat spinal cord following peripheral nerve
stimulation. Oxy and deoxy hemoglobin were measured (using a four color LED multispectral intrinsic optical imaging
system) simultaneously with blood flow (laser speckle measurement). Both optical and electrophysiological data are
compared spatially and against stimulation strength. When compared with non-lesioned animals, the hemodynamic
response is seen to display significant differences exhibiting increased initial dip and decreased blood drain following
stimulation. The origin of the difference is observed to be due to the vascular nature of the injury. The distinct
hemodynamic responses may have a strong impact on General Linear Model based fMRI studies of spinal cord lesions
due to the difficulty in separating vascular effects from neuronal plasticity following injury.