Toshinori Horiuchi

Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients.

Sevoflurane and propofol have been widely used as anesthetic agents for neurosurgery. Recent evidence has suggested that the influence of these anesthetics on cerebral oxygenation may differ. In the present study, the authors investigated jugular bulb oxygen saturation (SjO2) during propofol and sevoflurane/nitrous oxide anesthesia under mildly hypothermic conditions. After institutional approval and informed consent, 20 patients undergoing elective craniotomy were studied. Patients were randomly divided to the group S/N2O (sevoflurane/nitrous oxide/fentanyl anesthesia) or the group P (propofol/fentanyl anesthesia). After induction of anesthesia, the catheter was inserted retrograde into the jugular bulb and SjO2 was analyzed. During the operation, patients were cooled and tympanic membrane temperature was maintained at 34.5°C. SjO2 was measured at normocapnia during mild hypothermia and at hypocapnia during mild hypothermia. There were no statistically significant differences in demographic variables between the groups. During mild hypothermia, SjO2 values were significantly lower in group P than in group S/N2O. The incidence of SjO2 less than 50% under mild hypothermic-hypocapnic conditions was significantly higher in group P than in group S/N2O. These results suggest that hyperventilation should be more cautiously applied during mild hypothermia in patients anesthetized with propofol and fentanyl versus sevoflurane/nitrous oxide/fentanyl.

Tetanic stimulation of the peripheral nerve before transcranial electrical stimulation can enlarge amplitudes of myogenic motor evoked potentials during general anesthesia with neuromuscular blockade

Background: Neuromuscular blockade can suppress myogenic motor evoked potentials (MEPs). The authors hypothesized that tetanic stimulation (TS) of the peripheral nerve before transcranial stimulation may enhance myogenic MEPs during neuromuscular blockade. In the current study, the authors evaluated MEP augmentations by TS at different levels of duration, posttetanic interval, neuromuscular blockade, and stimulus intensity. Methods: Thirty-two patients undergoing propofol–fentanyl–nitrous oxide anesthesia were examined. Train-of-five stimulation was delivered to C3–C4, and MEPs were recorded from the abductor hallucis muscle. In study 1, TS with a duration of 1, 3, or 5 s was delivered at 50 Hz to the tibial nerve 1, 3, or 5 s (interval) before transcranial stimulation, and the effects of TS on MEP amplitude were evaluated. In study 2, TS-induced MEP augmentations were evaluated at the neuromuscular blockade level (%T1) of 50% or 5%. In study 3, MEP augmentations by TS at stimulus intensities of 0, 5, 25, and 50 mA were evaluated. Results: The application of TS significantly enlarged the amplitudes of MEPs at the combinations of duration (3, 5 s) and interval (1, 3, 5 s) compared with those without TS. TS-induced MEP augmentations were similarly observed at %T1 of both 50% and 5%. TS-induced MEP augmentations were observed at stimulus intensities of 25 and 50 mA. Conclusions: The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.

Effects of minocycline on hind-limb motor function and gray and white matter injury after spinal cord ischemia in rats.

Study Design. A prospective, randomized laboratory investigation. Objective. To investigate whether administration of minocycline attenuates hind-limb motor dysfunction and gray and white matter injury after spinal cord ischemia. Summary of Background Data. Minocycline, a semisynthetic tetracycline antibiotic, has been shown to have neuroprotective effects in models of focal and global cerebral ischemia. However, there have been no data available regarding the effects of minocycline in a model of spinal cord ischemia. Methods. Thirty-six rats were randomly allocated to one of three groups; control (C) group (n = 11), minocycline (M) group (n = 13), or sham group (n = 12). Minocycline or saline was intraperitoneally administered for 3 days beginning at 12 hours before 10 minutes of spinal cord ischemia or sham operation. Spinal cord ischemia was induced with intraaortic balloon catheter and blood withdrawal. Seventy-two hours after reperfusion, hind-limb motor functions were assessed using Basso, Beattie, Bresnahan (BBB) Scale (0 = paraplegia, 21 = normal). For histologic assessments, the gray and white matter injury was evaluated using the number of normal neurons and the extents of vacuolations in the white matter, respectively. Activated microglia was also evaluated using Iba-1 immunohistochemistry. Results. BBB scores and the numbers of normal neurons in the M group were significantly higher than those in the C group. The percentage areas of vacuolations in the white matter and the number of Iba-1 positive cells were significantly lower in the M group compared with those in the C group. Conclusion. The results indicated that minocycline administration improved hind-limb motor function and attenuated gray and white matter injury and microglial activation after spinal cord ischemia in rats.

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.

Assessment of intraoperative motor evoked potentials for predicting postoperative paraplegia in thoracic and thoracoabdominal aortic aneurysm repair

PurposeMonitoring motor evoked potentials (MEPs) has been recognized as a highly reliable method to detect intraoperative spinal cord ischemia (SCI) in aortic repair. However, the data regarding the sensitivity and specificity of MEPs for predicting postoperative paraplegia are limited. We retrospectively assessed the value of intraoperative MEP amplitudes for predicting postoperative paraplegia.MethodsThe medical records of 44 patients were reviewed. A train-of-five stimulation was delivered to C3–C4, and MEPs were recorded from the abductor pollicis brevis and the tibialis anterior muscles. The cutoff point for detecting SCI was set at 75% decrease of the baseline MEP. Receiver operating characteristic curves were applied at various cutoff points.ResultsThree patients (6.8%) had postoperative paraplegia. The minimum MEP during surgery had 100% sensitivity and 64.9% specificity in predicting paraplegia, and the MEP at the end of surgery had 66.7% sensitivity and 78.0% specificity in predicting paraplegia: only 1 patient, who had borderline paraplegia (right monoparesis), showed a false-negative result. Receiver operating characteristic curves indicated that adequate cutoff points for the minimum MEP during surgery and for the MEP amplitude at the end of surgery were a 75–90% decrease and a 64–75% decrease of the baseline MEP, respectively.ConclusionMonitoring MEPs had relatively high sensitivity and acceptable specificity, with the cutoff point set at 75% decrease of the baseline MEP, for predicting paraplegia and paraparesis. Because of the small sample in our study, further investigations would be necessary to investigate an adequate cutoff point that could predict postoperative paraplegia.

Effects of Increasing Concentrations of Propofol on Jugular Venous Bulb Oxygen Saturation in Neurosurgical Patients under Normothermic and Mildly Hypothermic Conditions

Background:Recent evidence suggested that propofol can deteriorate the cerebral oxygen balance compared with inhalational anesthetics. However, dose-related influences of propofol on cerebral oxygen balances were not clearly investigated. In the current study, the authors investigated the effects of increasing concentrations of propofol on jugular venous bulb oxygen saturation (Sjo2) in neurosurgical patients under normothermic and mildly hypothermic conditions. Methods:After institutional approval and informed consent were obtained, 30 adult patients undergoing elective craniotomy were studied. Patients were randomly allocated to either normothermic or hypothermic group (n = 15 in each group). In the normothermic and hypothermic groups, tympanic membrane temperature was maintained at 36.5° and 34.5°C, respectively. Sjo2 was measured at predicted propofol concentrations of 3, 5, and 7 &mgr;g/ml using a target-controlled infusion system in both groups. Results:At a predicted propofol concentration of 3 &mgr;g/ml, there were no significant differences in Sjo2 values between the normothermic and hypothermic groups, although the incidence of desaturation (Sjo2 < 50%) was significantly higher in the normothermic group than in the hypothermic group (30% vs. 13%; P < 0.05). Sjo2 values and the incidence of desaturation remained unchanged during the changes in predicted propofol concentration from 3 to 7 &mgr;g/ml both in the normothermic and hypothermic groups. Conclusion:The results indicated that the increasing concentrations of propofol did not affect Sjo2 values in neurosurgical patients under normothermic and mildly hypothermic conditions.

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.

The Effects of the Neuromuscular Blockade Levels on Amplitudes of Posttetanic Motor-Evoked Potentials and Movement in Response to Transcranial Stimulation in Patients Receiving Propofol and Fentanyl Anesthesia

BACKGROUND: Patient movement in response to transcranial stimulation during monitoring of myogenic motor-evoked potentials (MEPs) may interfere with surgery. We recently reported a new technique to augment the amplitudes of myogenic MEPs, called “post-tetanic MEPs (p-MEPs),” in which tetanic stimulation of a peripheral nerve was applied prior to transcranial stimulation. We conducted the present study to determine an appropriate level of neuromuscular blockade during the monitoring of p-MEPs with a focus on patient movement. METHODS: In 15 patients under propofol/fentanyl anesthesia, conventional MEPs (c-MEPs) and p-MEPs in response to transcranial electrical stimulation were recorded from the abductor hallucis muscle. For p-MEP recording, tetanic stimulation to the posterior tibial nerve at an intensity of 50 mA for 5 s was started 6 s prior to transcranial stimulation. The level of neuromuscular blockade was assessed by recording the amplitude of compound muscle action potentials (T1) from the abductor hallucis brevis muscle in response to supramaximal electrical stimulation of the median nerve at the wrist. After the baseline recordings of c-MEP and p-MEP at a T1 of 50% of control, 0.1 mg/kg of vecuronium was injected and the amplitudes of c-MEPs and p-MEPs were recorded. Patient movement was also assessed with the movement score ranging from 1 to 4 (1 = no movement, 4 = severe movement). RESULTS: T1, %T1, the amplitudes of c-MEPs and p-MEPs, and the movement score changed in parallel after the administration of vecuronium. The amplitudes of p-MEPs before and 15–45 min after the administration of vecuronium were significantly higher than those of c-MEPs. When T1 and %T1 were less than and equal to 1 mV and 10%, respectively, the movement score was 1 or 2 in all patients, indicating that microscopic surgery was possible without the interruption of surgical procedures. When T1 was around 1 mV (0.8–1.2 mV), the success rates of recording of c-MEPs and p-MEPs were 73% (11 of 15) and 100% (15 of 15), respectively. CONCLUSIONS: Under propofol/fentanyl anesthesia, p-MEP could be recorded at a T1 of 1 mV, in which patient movement in response to transcranial stimulation did not interfere with surgery. This technique may be used in patients without preoperative motor deficits, in which patient movement during surgical procedures is not preferable.

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 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.