While the bilateral common carotid artery (CCA) ligation model is widely used in cerebrovascular disease and dementia studies, it can frequently cause seizures. We examined the validity of seizure as an experimental model of ischemia. Eight-week-old male Wistar and Sprague-Dawley (SD) rats were implanted with electrocorticography (ECoG) electrodes and bilateral CCA ligation was performed and compared to the sham groups. ECoG monitoring was used to confirm the seizure discharge and count the number of spikes in the interictal phase 2 h after ligation, followed by power spectral analysis. Magnetic resonance imaging (MRI) was performed 6 h after bilateral CCA ligation to assess fractional anisotropy (FA), apparent diffusion coefficient (ADC), and cerebral blood flow (CBF) values. Magnetic resonance spectroscopy (MRS) was also performed and the ischemic parameters and electrophysiological changes were compared. The Wistar rat group had significantly higher mortality, frequency of seizures, incidence of non-convulsive seizures, and number of spikes in the interictal period compared to those in the SD rat group. Power spectral analysis showed increased power in the delta band in both Wistar and SD rat groups. MRI, after CCA ligation, showed significantly lower ADC values, lower glutamine and glutamate levels, and higher lactate values in Wistar rats, although there was no difference in FA values. Metabolic and electrophysiological changes after CCA ligation differed according to the rat strain. Wistar rats were prone to increased lactate and decreased glutamine and glutamate levels and the development of status epilepticus. Seizures can affect the results of ischemic experiments.
Transcranial electrical motor evoked potential (TCeMEP) is used to monitor the integrity of intraoperative motor function. Total intravenous anesthesia (TIVA) is the preferred method because its effect on MEP is relatively smaller than volatile anesthetics. However, maintaining the balanced anesthesia in long-time surgery using TIVA is challenging and may sometime cause problems including body movement during microsurgery. Such problems can be avoided by intraoperative anesthesia management using a mixture of propofol and a low concentration of sevoflurane. We recorded TCeMEP under a mixture of propofol and low concentration of sevoflurane anesthesia in three cases of neurosurgery. Anesthesia was induced with a 5.0 µg/mL target-controlled infusion of propofol and 0.6 mg/kg rocuronium. General anesthesia was maintained by propofol and 0.1-0.25 µg/kg/min remifentanil infusion. After the recording of control TCeMEP, sequential inhalation of 0.2 minimum alveolar concentration (MAC) and 0.5 MAC of sevoflurane was performed. The duration of each sevoflurane inhalation was 10 minutes, and the MACs were adjusted by the patient's age. In our cases, the combination of propofol and 0.2 MAC sevoflurane suppressed the amplitude of TCeMEP to 38.0±21.7% (379.8±212.0 µV), but the amplitude was high enough for evaluation of motor function monitoring. On the other hand, the combination of 0.5 MAC sevoflurane greatly decreased the amplitude of TCeMEP to 6.3±6.0% (71.9±66.9 µV) resulting in less than 150 µV, and it was difficult to record the change in TCeMEP amplitude over time. The combination of 0.2 MAC sevoflurane with TIVA might enable TCeMEP monitoring with TIVA.
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