0.125% 8 ml/h v.s. 0.25% 8 ml/h of levobupivacaine in continuous paravertebral block for postoperative analgesia in video-assisted thoracoscopic surgery: a randomized, controlled, double-blind study.

PURPOSE: Research has shown that a higher dose of bupivacaine administered in continuous paravertebral block (CPVB) provides a greater analgesic effect after video-assisted thoracoscopic surgery (VATS). In this randomized, controlled, double-blind study, we hypothesized that 0.25% 8 ml/h of levobupivacaine administered in CPVB after VATS provides a greater analgesic effect than 0.125% 8 ml/h. METHODS: Fifty patients who underwent unilateral VATS were randomized to receive a postoperative continuous infusion of 0.125% (low group, n = 25) or 0.25% (high group, n = 25) levobupivacaine at 8 mL/h for CPVB. The primary outcome was the visual analog scale (VAS) score during coughing on the morning of postoperative day (POD) 1. The secondary outcomes were the VAS scores at rest and during coughing on POD 2, the number of anesthetized dermatomes, the frequency of rescue analgesics, postoperative nausea and vomiting, patient satisfaction, and adverse events and complications. RESULTS: There was no significant difference in the VAS score during coughing on the morning of POD 1 between the low and high groups [median, 37.5 (interquartile range 21-50) vs. 40.0 (interquartile range 21-50), respectively; p = 0.79]. Similarly, there were no significant differences in any secondary outcomes between the two groups. CONCLUSIONS: Levobupivacaine at 0.25% 8 ml/h in CPVB did not provide better analgesia after VATS over 0.125% 8 ml/h. CLINICAL TRIAL REGISTRATION NUMBER: UMIN000037930.

Use of Ultrasound-Guided Selective Sensory Nerve Blocks to Provide Satisfactory Postoperative Analgesia Without Motor Paralysis in Bilateral Distal Radius Fracture Fixation: A Case Report.

Peripheral nerve blocks for postoperative pain management in distal radius fracture fixation with volar locking plates can cause undesirable motor paralysis. We performed bilateral ultrasound-guided selective sensory nerve blocks to the lateral cutaneous nerve of the forearm, superficial branch of the radial nerve, and anterior interosseous nerve for a patient undergoing bilateral distal radius fracture fixation with volar locking plates. This case report describes the first successful use of this ultrasound-guided selective sensory nerve block, which provided satisfactory postoperative analgesia and preserved the patient's motor function following distal radius fracture fixation with volar locking plates.

A novel technique for ultrasound-guided central venous catheterization under short-axis out-of-plane approach: "stepwise flashing with triangulation".

In ultrasound-guided central venous catheterization, there is no standard technique either for the needle tip visualization or for the adequate needle angle and entry to the skin with short-axis view under out-of-plane technique. In the present study, we propose a novel technique named "stepwise flashing with triangulation", and the efficacy of this technique is assessed. Before and after a didactic session in which the technique was explained, 12 novice residents were asked to position the needle tip on or into the imitation vessels and to avoid deeper penetration by using an agar tissue phantom with ultrasound guidance. "Stepwise flashing" technique was for stepwise visualization of the needle tip, and "triangulation" technique was for adequate needle angle and entry to the skin. After the session, the success rate was increased and a deeper penetration rate was decreased. This technique will help us to facilitate vascular access and to avoid complications in clinical settings.

[Ischemic Changes in the Electrocardiogram and Circulatory Collapse Accompanied by Severe Anemia Owing to the Delay of Red Blood Cell Concentrate Transfusion in Two Patients with Intraoperative Massive Bleeding].

We present two patients developing intraoperative massive bleeding and showed ischemic changes in the electrocardiogram and circulatory collapse accompanied by severe anemia owing to the delay of red blood cell concentrate transfusion. One patient underwent hepatectomy and the other pancreaticoduodenectomy. Their lowest hemoglobin concentration was around 2 g x dl(-1), and they showed ischemic changes in the electrocardiogram and severe decreases in blood pressure. The former received compatible red blood cell concentrate and the latter received uncrossmatched same blood group red blood cell concentrate immediately, and their electrocardiogram and blood pressure quickly improved. To avoid life-threatening anemia, emergency red blood cell concentrate transfusion including compatible different blood group transfusion should be applied for intraoperative massive bleeding.

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.

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

PURPOSE: Monitoring 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. METHODS: The 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. RESULTS: Three 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. CONCLUSION: Monitoring 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.

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 degrees C, 35 degrees C, or 38 degrees 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 degrees C and 35 degrees 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 degrees C than in the normothermic group. The percentage areas of vacuolation at 2 and 28 days were significantly lower in hypothermic groups of 32 degrees C and 35 degrees 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.

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

PURPOSE: Although 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. METHODS: Forty rats were randomly allocated to one of following five groups: vehicle or SNC80 with 10 min of SCI at 38 degrees C (V-38-10m or SNC-38-10m, respectively), vehicle or SNC80 with 22 min of SCI at 35 degrees 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. RESULTS: The 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). CONCLUSION: The 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.

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.

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.

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 (Sj(O2)) 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 degrees and 34.5 degrees C, respectively. Sj(O2) was measured at predicted propofol concentrations of 3, 5, and 7 microg/ml using a target-controlled infusion system in both groups. RESULTS: At a predicted propofol concentration of 3 microg/ml, there were no significant differences in Sj(O2) values between the normothermic and hypothermic groups, although the incidence of desaturation (Sj(O2) < 50%) was significantly higher in the normothermic group than in the hypothermic group (30% vs. 13%; P < 0.05). Sj(O2) values and the incidence of desaturation remained unchanged during the changes in predicted propofol concentration from 3 to 7 microg/ml both in the normothermic and hypothermic groups. CONCLUSION: The results indicated that the increasing concentrations of propofol did not affect Sj(O2) values in neurosurgical patients under normothermic and mildly hypothermic conditions.

Evaluation of relatively low dose of oral transmucosal ketamine premedication in children: a comparison with oral midazolam.

BACKGROUND: Oral Transmucosal ketamine (lollipop) has been shown to be an effective, harmless preoperative medication for children. However, its efficacy was not compared with commonly used premedication drugs. We, therefore, compared the efficacy of oral transmucosal ketamine with oral midazolam for premedication in children. METHODS: Fifty-five children (2-6 years of age) were randomized to receive orally either a lollipop containing 50 mg of ketamine (the group K; n = 27) or syrup containing 0.5 mg.kg(-1) of midazolam (the group M; n = 28) before minor surgery. A five points-sedation score (1 = asleep to 5 = agitated; scores 2 and 3 were defined as 'effective') on arrival in the operating room and a three points-acceptance score of separation from the parents and a three points-mask cooperation score at induction of anesthesia (1 = easy to 3 = markedly resistant; score 3 was defined as 'poor') were used. RESULTS: Sedation scores in group K were significantly higher than those in group M (P = 0.012), and the incidence of 'effective' in sedation was significantly lower in group K than in group M (P = 0.036). The incidence of 'poor' at separation from the parents and for mask cooperation was significantly higher in group K than in group M (P = 0.017, P = 0.019, respectively). CONCLUSION: These results indicate that a relatively low dose of oral transmucosal ketamine premedication provides no benefits over oral midazolam in children.

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.

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 effects of the delta-opioid agonist SNC80 on hind-limb motor function and neuronal injury after spinal cord ischemia in rats.

Recent investigation suggested neuroprotective efficacy of a delta-opioid agonist in the brain. We investigated the effects of intrathecal treatment with a delta-opioid agonist (SNC80) on spinal cord ischemia (SCI) in rats. SCI was induced with an intraaortic balloon catheter. The animals were randomly allocated to one of the following five groups: 1) SNC80 before 9 min of SCI (SNC-9; n = 12), 2) vehicle before 9 min of SCI (V-9; n = 12), 3) SNC80 before 11 min of SCI (SNC-11; n = 10), 4) vehicle before 11 min of SCI (V-11; n = 12), or 5) sham (n = 12). SNC80 (400 nmol) or vehicle was administered 15 min before SCI. Forty-eight hours after reperfusion, hind-limb motor function was assessed by using the Basso, Beattie, Bresnahan (BBB) scale (0 = paraplegia; 21 = normal) and histological assessment of the L4 and L5 spinal segments was performed. BBB scores in the SNC-9 group were higher compared with those in the V-9 group (P < 0.05), whereas there were no differences in BBB scores between the SNC-11 and V-11 groups. There were significantly more normal neurons in the SNC-9 and SNC-11 groups than in the V-9 and V-11 groups (P < 0.05). The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate hind-limb motor dysfunction and neuronal injury after SCI in rats.

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 degrees 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.

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.