Naoko Kurita

The Effects of Sevoflurane and Hyperventilation on Electrocorticogram Spike Activity in Patients with Refractory Epilepsy

We investigated the effects of sevoflurane and hyperventilation on intraoperative electrocorticogram (ECoG) spike activity in 13 patients with intractable epilepsy. Grid electrodes were placed on the brain surface and ECoG was recorded under the following conditions: 1) 0.5 minimal alveolar anesthetic concentration (MAC) sevoflurane, 2) 1.5 MAC sevoflurane, and 3) 1.5 MAC sevoflurane with hyperventilation. The number of spikes per 5 min and the percentage of leads with spikes were assessed in each condition. In 4 patients with chronically implanted-subdural electrodes, the leads with seizure onset and with spikes during the interictal periods in the awake state were compared with those during sevoflurane anesthesia at 0.5 MAC and 1.5 MAC. The number of spikes and the percentage of leads with spikes were significantly more under 1.5 MAC sevoflurane anesthesia compared with those under 0.5 MAC sevoflurane (P < 0.05). The induction of hyperventilation significantly increased the number of spikes and percentage of leads with spikes (P < 0.05). With 0.5 MAC sevoflurane, the leads with spikes were similar to those at seizure onset in the awake state, whereas with 1.5 MAC sevoflurane, spikes were similar to those occurring during interictal periods in the awake state. These results indicate that sevoflurane and hyperventilation can affect the frequency and extent of ECoG spike activity in patients with intractable epilepsy. Careful attention should be paid to the concentration of sevoflurane used and ventilatory status when intraoperative EcoG is used to localize epileptic lesions.

Delta opioid receptors stimulation with [D-Ala2, D-Leu5] enkephalin does not provide neuroprotection in the hippocampus in rats subjected to forebrain ischemia.

It has been reported that delta opioid agonists can have neuroprotective efficacy in the central nervous system. This study was conducted to test the hypothesis that a delta opioid receptor (DOR) agonist, [D-Ala2, D-Leu5] enkephalin (DADLE), can improve neuron survival against experimental forebrain ischemia in rats. Using male rats (n=125), intraperitoneal injection of DADLE (0, 0.25, 1, 4, 16 mg kg-1) was performed 30 min before ischemia. Ten minutes interval forebrain ischemia was provided by the bilateral carotid occlusion combined with hypotension (35 mm Hg) under isoflurane (1.5%) anesthesia. All animals were neurologically and histologically evaluated after a recovery period of 1 week. As histological evaluation, percentages of ischemic neurons in the CA1, CA3, dentate gyrus (DG) were measured. During the recovery period, 27 rats died because of apparent upper airway obstruction, seizure, or unidentified causes. There were no differences in the motor activity score among the groups. Ten minutes forebrain ischemia induced approximately 75, 20, and 10% neuronal death in the CA1, CA3, and DG, respectively. Any doses of DADLE did not attenuate neuronal injury in the hippocampus after ischemia. Pre-ischemic treatment of DORs agonism with DADLE did not provide any neuroprotection to the hippocampus in rats subjected to forebrain ischemia.

Reevaluation of gray and white matter injury after spinal cord ischemia in rabbits.

Background:Although gray matter injury has been well characterized, the available data on white matter injury after spinal cord ischemia (SCI) in rabbits are limited. The current study was conducted to investigate the evolution of ischemia induced injury to gray and white matter and to correlate this damage to hind-limb motor function in rabbits subjected to SCI. Methods:Thirty-eight rabbits were randomly assigned to 24-h, 4-day, or 14-day reperfusion groups or a sham group (n = 9 or 10 per group). SCI was induced by occlusion of the infrarenal aorta for 16 min. Hind-limb motor function was assessed using the Tarlov scale (0 = paraplegia, 4 = normal). The gray matter damage was assessed on the basis of the number of normal neurons in the anterior spinal cord. White matter damage was assessed on the basis of the extent of vacuolation and accumulation of amyloid precursor protein immunoreactivity. Results:Tarlov scores gradually decreased and reached a nadir 14 days after reperfusion. There were no significant differences in the number of normal neurons among the 24-h, 4-day, and 14-day groups. The extent of vacuolation, expressed as a percent of total white matter area, was significantly greater in the 4-day and 14-day groups in comparison with the sham group. By contrast, there was no difference in vacuolation between the sham and 24-h groups. Amyloid precursor protein immunoreactivity was greater in the 4-day and 14-day groups. Conclusion:The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.

Effects of nitrous oxide on spike activity on electrocorticogram under sevoflurane anesthesia in epileptic patients.

We sought to investigate the effects of nitrous oxide on intraoperative electrocorticogram (ECoG) spike activities in 11 patients with intractable epilepsy. Grid electrodes were placed on the brain surface, and ECoG was recorded under the following conditions: 1.5 minimal alveolar anesthetic concentration (MAC) sevoflurane without nitrous oxide and 1.5 MAC sevoflurane with 50% nitrous oxide. The number of spikes for 5 minutes and the percentage of leads with spikes of total leads measured were assessed in each condition. The median numbers (25-75th) of spikes without and with nitrous oxide were 127 (87-368) and 61 (43-247), respectively. The numbers of spikes with nitrous oxide were significantly lower than those without nitrous oxide (P < 0.05). The median percentages of leads with spikes without and with nitrous oxide were 68 (25-81) and 61 (28-70), respectively, and there were no significant differences in percentages of leads with spikes between the conditions. These results indicate that nitrous oxide attenuated the frequency of spikes on ECoG in epileptic patients, although it did not affect the extent of areas with spike activity.

The Long-Term Effects of Mild to Moderate Hypothermia on Gray and White Matter Injury After Spinal Cord Ischemia in Rats

BACKGROUND: The short-term effects of hypothermia on gray matter injury after spinal cord ischemia (SCI) have been established. We sought to investigate the long-term effects of mild to moderate hypothermia on gray and white matter injury after SCI. METHODS: Ninety-five rats were randomly divided into eight groups according to body temperature during SCI (32°C, 35°C, or 38°C) and reperfusion interval (2 or 28 days). SCI was conducted for 15 min using a balloon catheter and blood withdrawal. After assessing the hindlimb motor function, gray and white matter injury was assessed using the number of normal neurons and the extent of vacuolation, respectively. RESULTS: Hindlimb motor function at 2 and 28 days was significantly better in hypothermic groups of 32°C and 35°C than in the normothermic group. The number of normal neurons at 2 and 28 days was significantly higher in the hypothermic group of 32°C than in the normothermic group. The percentage areas of vacuolation at 2 and 28 days were significantly lower in hypothermic groups of 32°C and 35°C than in the normothermic group. CONCLUSIONS: The neuroprotective effects of intraischemic mild to moderate hypothermia on gray and white matter injury are mostly sustained for a long-term period of 28 days after SCI.

Long-term assessment of hind limb motor function and neuronal injury following spinal cord ischemia in rats.

Recent evidence suggests that brain injury caused by ischemia is a dynamic process characterized by ongoing neuronal loss for at least 14 days after ischemia. However, long-term outcome following spinal cord ischemia has not been extensively examined. Therefore, we investigated the changes of hind limb motor function and neuronal injury during a 14-day recovery period after spinal cord ischemia. Male Sprague-Dawley rats received spinal cord ischemia (n = 64) or sham operation (n = 21). Spinal cord ischemia was induced by inflation of a 2F Fogarty catheter placed into the thoracic aorta for 6, 8, or 10 minutes. The rats were killed 2, 7, or 14 days after reperfusion. Hind limb motor function was assessed with the 21-point Basso, Beattie, and Bresnahan (BBB) scale during the recovery period. The number of normal and necrotic neurons was counted in spinal cord sections stained with hematoxylin/eosin. Longer duration of spinal cord ischemia produced severer hind limb motor dysfunction at each time point. However, BBB scores gradually improved during the 14-day recovery period. Neurologic deterioration was not observed between 7 and 14 days after reperfusion. The number of necrotic neurons peaked 2 days after reperfusion and then decreased. A small number of necrotic neurons were still observed 7 and 14 days after reperfusion in some of the animals. These results indicate that, although hind limb motor function may gradually recover, neuronal loss can be ongoing for 14 days after spinal cord ischemia.

Effects of xenon on ischemic spinal cord injury in rabbits: a comparison with propofol.

Background: Xenon has been shown to reduce cellular injury after cerebral ischemia. However, the neuroprotective effects of xenon on ischemic spinal cord are unknown. The authors compared the effects of xenon and propofol on spinal cord injury following spinal cord ischemia in rabbits.

Effects of delta-opioid agonist SNC80 on white matter injury following spinal cord ischemia in normothermic and mildly hypothermic rats

PurposeAlthough the delta-opioid agonist SNC80 has been shown to attenuate hind-limb motor function and gray matter injury in normothermic rats subjected to spinal cord ischemia (SCI), its effects on white matter injury remain undetermined. In the present study, we investigated whether SNC80 could attenuate white matter injury in normothermic and mildly hypothermic rats.MethodsForty rats were randomly allocated to one of following five groups: vehicle or SNC80 with 10 min of SCI at 38°C (V-38-10m or SNC-38-10m, respectively), vehicle or SNC80 with 22 min of SCI at 35°C (V-35-22m or SNC-35-22m, respectively), or sham. SNC80 or vehicle was intrathecally administered 15 min before SCI. Forty-eight hours after reperfusion, the white matter injury was evaluated by the extent of vacuolation.ResultsThe percent area of vacuolation in the ventral white matter was significantly lower in the SNC-38-10m and SNC-35-22m groups compared with that in the V-38-10m and V-35-22m groups, respectively (P < 0.05).ConclusionThe results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate the ventral white matter injury following SCI in rats under normothermic and mildly hypothermic conditions.

An evaluation of white matter injury after spinal cord ischemia in rats: a comparison with gray matter injury.

We quantitatively assessed both gray and white matter injury after spinal cord ischemia in rats, and the relationship between the magnitude of gray and white matter injury was determined. Twenty-five male rats were anesthetized with isoflurane, and spinal cord ischemia (SCI) was induced by balloon intraaortic occlusion combined with hypotension. The animals were randomly allocated to one of the following three groups: animals with SCI for 12 min (SCI-12; n = 8), 15 min (SCI-15; n = 9), or those with sham operation (n = 8). Twenty-four hours after reperfusion, hindlimb motor function was assessed using the Basso-Beattie-Bresnahan scale scoring. Gray matter damage was assessed on the basis of the number of normal neurons in the ventral horn. White matter damage was assessed on the basis of the extent of vacuolation and amyloid precursor protein immunoreactivity in the ventral and ventrolateral white matter. There were significantly less normal neurons in the SCI-15 group compared with those in the SCI-12 and sham groups (P < 0.05). There was a significant positive correlation between the Basso-Beattie-Bresnahan scores and the number of normal neurons. The percentages of vacuolation areas in the SCI-15 group were significantly larger compared with those in the SCI-12 and sham groups (30% ± 10% versus 9% ± 7%, 0% ± 0%, P < 0.05). Immunohistochemical analysis revealed increased amyloid precursor protein immunoreactivity in the swollen axons, especially in the SCI-15 group. There was a significant negative correlation between the number of normal neurons and percentages of vacuolation areas. These results indicate that both gray and white matter were injured after SCI in rats and the degree of white mater injury was correlated with the severity of gray matter injury after a relatively short recovery period.

The Validity of Bispectral Index Values from a Dislocated Sensor: A Comparison with Values from a Sensor Located in the Commercially Recommended Position

BACKGROUND:The influence of sensor dislocation on bispectral index (BIS) values is not clear. We compared the BIS values obtained from dislocated sensors with those from the commercially recommended positions. METHODS:We used two BIS sensors for each patient receiving propofol-based anesthesia; one in the recommended position and one positioned around the lateral corner of the right eye. RESULTS:Bland and Altman analysis revealed better agreement of two BIS values when the values during induction of and emergence from anesthesia were excluded. CONCLUSIONS:The results indicate that during induction of and emergence from general anesthesia, a dislocated BIS sensor may produce questionable BIS values.