Delayed recovery of cortical auditory evoked potentials and blood flow precede cortical neuronal death after transient cerebral ischemia in gerbils.
Hiroto Ichiki, Toshihiko Kuroiwa, I Taniguchi, Riki Okeda
Abstract
Hiroto Ichiki, Toshihiko Kuroiwa, I Taniguchi, Riki Okeda
Abstract
Cortical neurons develop into neuronal death four days after transient cerebral ischemia. The aim of this study is to detect early post-ischemic changes in the cortex that will develop into cortical neuronal death later. The detection is important for starting adequate treatment within the therapeutic window. We have examined changes in middle-latency auditory evoked potentials (MAEPs) and cortical blood flow (CBF) in relation to the histological changes in the auditory cortex of Mongolian gerbils subjected to transient cerebral ischemia. At 2 min after bilateral carotid occlusion, the amplitude of MAEPs and CBF were reduced to 22.2 to 23.4% and 24.3 to 27.4% of the pre-ischemic level, respectively. In the 4-min ischemia group, the amplitude of each parameter recovered rapidly to the pre-ischemic level. In the 12-min ischemia group, the recovery of MAEPs and CBF was delayed by, from 20 to 30 min, and about 10 min, respectively. Also, scattered eosinophilic neurons were observed in the auditory cortex, and a mild but significant decrease in the number of surviving neurons was also detectable. The recovery of MAEPs in both groups was characterized by the appearance of a transient high amplitude (2.67 +/- 0.6 microV) low frequency (62.2 +/- 3.4Hz) wave. The present findings show that cortical neuronal death in the auditory cortex, which results from transient cerebral ischemia in the gerbil, is predictable by detecting the delay in the recovery of MAEPs amplitude and CBF during the very early post-ischemic phase. Clinical data is mandatory for the application of the presented method in clinical cases to save many patients with acute cerebrovascular diseases in the future.
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Cortical neurons develop into neuronal death four days after transient cerebral ischemia. The aim of this study is to detect early post-ischemic changes in the cortex that will develop into cortical neuronal death later. The detection is important for starting adequate treatment within the therapeutic window. We have examined changes in middle-latency auditory evoked potentials (MAEPs) and cortical blood flow (CBF) in relation to the histological changes in the auditory cortex of Mongolian gerbils subjected to transient cerebral ischemia. At 2 min after bilateral carotid occlusion, the amplitude of MAEPs and CBF were reduced to 22.2 to 23.4% and 24.3 to 27.4% of the pre-ischemic level, respectively. In the 4-min ischemia group, the amplitude of each parameter recovered rapidly to the pre-ischemic level. In the 12-min ischemia group, the recovery of MAEPs and CBF was delayed by, from 20 to 30 min, and about 10 min, respectively. Also, scattered eosinophilic neurons were observed in the auditory cortex, and a mild but significant decrease in the number of surviving neurons was also detectable. The recovery of MAEPs in both groups was characterized by the appearance of a transient high amplitude (2.67 +/- 0.6 microV) low frequency (62.2 +/- 3.4Hz) wave. The present findings show that cortical neuronal death in the auditory cortex, which results from transient cerebral ischemia in the gerbil, is predictable by detecting the delay in the recovery of MAEPs amplitude and CBF during the very early post-ischemic phase. Clinical data is mandatory for the application of the presented method in clinical cases to save many patients with acute cerebrovascular diseases in the future.
Key concepts: Gerbil, Ischemia, Cerebral cortex, Auditory cortex, Cerebral blood flow, Medicine, Cortex (anatomy), Anesthesia