Reappraisal of the role of motor and somatosensory evoked potentials during open distal aortic repair

ObjectiveIntraoperative motor and somatosensory evoked potentials have been applied to monitor spinal cord ischemia during repair. However, their predictive values remain controversial. The purpose of this study was to evaluate the impact of motor evoked potentials and somatosensory evoked potentials on spinal cord ischemia during open distal aortic repair.MethodsOur group began routine use of both somatosensory evoked potentials and motor evoked potentials at the end of 2004. This study used a historical cohort design, using risk factor and outcome data from our department's prospective registry. Univariate and multivariable statistics for risk-adjusted effects of motor evoked potentials and somatosensory evoked potentials on neurologic outcome and model discrimination were assessed with receiver operating characteristic curves.ResultsBoth somatosensory evoked potentials and motor evoked potentials were measured in 822 patients undergoing open distal aortic repair between December 2004 and December 2019. Both motor evoked potentials and somatosensory evoked potentials were intact for the duration of surgery in 348 patients (42%). Isolated motor evoked potential loss was observed in 283 patients (34%), isolated somatosensory evoked potential loss was observed in 18 patients (3%), and both motor evoked potential and somatosensory evoked potential loss were observed in 173 patients (21%). No spinal cord ischemia occurred in the 18 cases with isolated somatosensory evoked potential loss. When both signals were lost, signal loss happened in the order of motor evoked potentials and then somatosensory evoked potentials. Immediate spinal cord ischemia occurred in none of those without signal loss, 4 of 283 (1%) with isolated motor evoked potential loss, and 15 of 173 (9%) with motor evoked potential plus somatosensory evoked potential loss. Delayed spinal cord ischemia occurred in 12 of 348 patients (3%) with intact evoked potentials, 24 of 283 patients (8%) with isolated motor evoked potentials loss, and 27 of 173 patients (15%) with motor evoked potentials + somatosensory evoked potentials loss (P < .001). Motor evoked potentials and somatosensory evoked potentials loss were each independently associated with spinal cord ischemia. For immediate spinal cord ischemia, no return of motor evoked potential signals at the conclusion of the surgery had the highest odds ratio of 15.87, with a receiver operating characteristic area under the curve of 0.936, whereas motor evoked potential loss had the highest odds ratio of 3.72 with an area under the curve of 0.638 for delayed spinal cord ischemia.ConclusionsSomatosensory evoked potentials and motor evoked potentials are both important monitoring measures to predict and prevent spinal cord ischemia during and after open distal aortic repairs. Intraoperative motor evoked potential loss is a risk for immediate and delayed spinal cord ischemia after open distal aortic repair, and somatosensory evoked potential loss further adds predictive value to the motor evoked potential.     

Spinal cord injury in experimental thoracic aortic occlusion: investigation of combined methods of protection.

The efficacy of combined methods of spinal cord protection during thoracoabdominal aortic reconstruction was evaluated because a recent clinical study failed to substantiate the value of cerebrospinal fluid drainage when used alone in the prevention of paraplegia. The effect of cerebrospinal fluid drainage and aortofemoral shunting were analyzed with regard to neurologic outcome and spinal cord blood flow in a model of thoracic aortic occlusion. In addition, we studied the use of motor-evoked potentials as compared with somatosensory-evoked potentials in monitoring cord perfusion. Thirty-two dogs underwent proximal and distal thoracic aortic occlusion for 60 minutes. The control group (n = 8) underwent thoracic aortic cross-clamping only. Spinal cord protection was used in three groups: cerebrospinal fluid drainage alone (n = 8), aortofemoral shunting alone (n = 8), and cerebrospinal fluid drainage and aortofemoral shunting (n = 8). Neurologic outcome improved in all treatment groups as compared with controls (p less than 0.001). The addition of cerebrospinal fluid drainage to aortofemoral shunting did not further improve neurologic outcome. Spinal cord blood flow measured with microspheres in the lumbar gray matter was significantly higher in the dogs with aortofemoral shunting (+/- cerebrospinal fluid drainage) as compared with those with cerebrospinal fluid drainage alone (p less than 0.05) or the controls (p less than 0.001). Aortofemoral shunting also prevented the development of acidosis and hyperglycemia. Loss or changes in amplitude and latency of motor-evoked potentials did not distinguish between the groups. Loss of somatosensory-evoked potentials had a high sensitivity (92%) but lower specificity (68%) in predicting neurologic injury, whereas loss of motor-evoked potentials had a high specificity (100%) but a very low sensitivity (16%). We conclude that cerebrospinal fluid drainage or aortofemoral shunting significantly improve spinal cord blood flow and neurologic outcome. The greatest increase in spinal cord blood flow was seen with aortofemoral shunting, which also prevented metabolic disturbances of reperfusion. Although the addition of cerebrospinal fluid drainage to aortofemoral shunting was the only group in which no neurologic injury occurred, this group did not have a significant improvement in outcome when compared with aortofemoral shunting alone. Spinal cord ischemia was more accurately detected with somatosensory-evoked potentials when aortofemoral shunting was used, whereas motor-evoked potentials recorded from the spinal cord were not sensitive enough to predict neurologic injury.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. I. Relationship of aortic cross-clamp duration, changes in somatosensory evoked potentials, and incidence of neurologic dysfunction

To determine if intraoperative monitoring of somatosensory evoked potentials detects spinal cord ischemia, we subjected 21 dogs to aortic cross-clamping distal to the left subclavian artery. Group I animals (short-term studies, n = 6) demonstrated decay and loss of somatosensory evoked potentials at 8.5 +/- 1.1 minutes after aortic cross-clamping. During loss of somatosensory evoked potentials, significant decreases in spinal cord blood flow occurred in cord segments below T6. Significant reactive hyperemia occurred without normalization of somatosensory evoked potentials after reperfusion. Fifteen Group II animals (long-term studies) were studied to determine the relationship between duration of spinal cord ischemia (evoked potential loss) and subsequent incidence of paraplegia. Extension of aortic cross-clamping for 5 minutes after loss of somatosensory evoked potentials in six dogs resulted in no paraplegia (mean cross-clamp time 12.7 +/- 0.6 minutes). Prolongation of aortic cross-clamping for 10 minutes after evoked potential loss in nine dogs (mean cross-clamp time 17.6 +/- 0.6 minutes) resulted in a 67% (6/9) incidence of paraplegia 7 days postoperatively (p = 0.02 versus 10 minutes of aortic cross-clamping). These findings demonstrate that simple aortic cross-clamping uniformly results in spinal cord ischemia and that such ischemia is detectable by monitoring of somatosensory evoked potentials. Duration of ischemia, as measured by the time of evoked potential loss during the cross-clamp interval, is related to the incidence of postoperative neurologic injury.     

Sustained spinal cord compression: part II: effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials

BACKGROUND: The efficacy of methylprednisolone in the treatment of traumatic spinal cord injury is controversial. We examined the effect of methylprednisolone on regional spinal cord blood flow and attempted to determine whether recovery of electrophysiological function is dependent on reperfusion, either during sustained spinal cord compression or after decompression. METHODS: The effects of methylprednisolone therapy on recovery of somatosensory evoked potentials and on spinal cord blood flow were examined in a canine model of dynamic spinal cord compression. Methylprednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered to thirty-six beagles (eighteen in each group) five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. Somatosensory evoked potentials and spinal cord blood flow were evaluated throughout the period of sustained compression and for three hours after decompression. RESULTS: Seven dogs treated with methylprednisolone and none treated with saline solution recovered measurable somatosensory evoked potentials during sustained compression. After decompression, three more dogs treated with methylprednisolone and seven dogs treated with saline solution recovered somatosensory evoked potentials. Four dogs treated with methylprednisolone lost their previously measurable somatosensory evoked potentials. In the methylprednisolone group, spinal cord blood flow was significantly higher (p < 0.05) in the dogs that had recovered somatosensory evoked potentials than it was in the dogs that had not. Reperfusion blood flow was significantly higher (p < 0.05) in the saline-solution group than it was in the methylprednisolone group. Spinal cord blood flow in the saline-solution group returned to baseline levels within five minutes after decompression. It did not return to baseline levels in the dogs treated with methylprednisolone. CONCLUSIONS: The methylprednisolone administered in this study did not provide a large or significant lasting benefit with regard to neurological preservation or restoration. Methylprednisolone may reduce regional spinal cord blood flow through mechanisms affecting normal autoregulatory blood-flow function.     

Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome

We studied the effect of thoracic aortic occlusion and cerebrospinal fluid (CSF) drainage on regional spinal cord blood flow and its correlation with neurologic outcome. Using isotope-tagged microspheres, we determined blood flow to the gray and white matter of five regions of the spinal cord in dogs: group I (control), group II (cross-clamp only), group III (cross-clamp plus CSF drainage). At 60 minutes after thoracic aortic occlusion in group II, median gray matter blood flow (GMBF) in the lower thoracic and lumbar cord decreased from 23.1 and 27.0 ml/100 gm/min at baseline to 4.0 and 2.5 ml/100 gm/min, respectively. The addition of CSF drainage improved GMBF during aortic cross-clamping in the lower thoracic and lumbar cord to 11.3 (p less than 0.05) and 15.1 ml/100 gm/min (p less than 0.03), respectively. After removal of the aortic cross-clamp, median blood flow more than tripled from baseline blood flow in group II, whereas CSF drainage prevented significant reperfusion hyperemia. Both low GMBF during cross-clamping and reperfusion hyperemia were associated with a worse neurologic outcome. In group II, no dog was neurologically normal, and more than 60% of the dogs had spastic paraplegia. In contrast, almost 60% of dogs in group III were normal, and none had spastic paraplegia (p less than 0.001). We conclude that CSF drainage in dogs during thoracic aortic occlusion maintained spinal cord perfusion above critical levels, diminished reperfusion hyperemia, and improved neurologic outcome.     

Successful monitoring of neurogenic mixed evoked potentials elicited by anterior spinal cord stimulation through thoracoscopy during spine surgery.

STUDY DESIGN: Neurogenic mixed evoked potentials were recorded after thoracoscopic spinal cord stimulation in patients undergoing video-assisted spine surgery. OBJECTIVE: To demonstrate the feasibility and value of thoracoscopic spinal cord monitoring. SUMMARY OF BACKGROUND DATA: Video-assisted thoracic surgery recently has been proposed as a new technique for thoracic spine surgery. It can be used for anterior spinal release of patients with severe spinal deformities and for thoracic hernia removal. METHODS: Five patients undergoing video-assisted thoracic surgery for spinal fusion were studied. Neurogenic mixed evoked potentials were elicited by electrodes seated into intervertebral discs through thoracoscopy and recorded from peripheral nerves of the lower limbs. Moreover, the study included the case of a patient with a thoracic hernia who underwent video-assisted thoracic surgery with combined thoracoscopic neurogenic mixed evoked potential and standard somatosensory evoked potential monitoring. RESULTS: Neurogenic mixed evoked potentials were recorded consistently after spinal cord stimulation in all patients. For the patient with a thoracic hernia, neurogenic mixed evoked potentials suddenly disappeared, whereas somatosensory evoked potentials were not significantly modified, leading to surgery interruption. Neurogenic mixed evoked potentials progressively reappeared after a 30-minute delay. Postoperation examination revealed a Brown-Sequard's syndrome with incomplete right motor deficit. CONCLUSIONS: Neurogenic mixed evoked potentials evoked by anterior stimulation through thoracoscopy are of interest for spinal cord monitoring when posterior electrical stimulation is impossible, and they provide reliable information regarding spinal motor pathways.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. III. Intraoperative identification of vessels critical to spinal cord blood supply

Somatosensory evoked potentials were used to locate intercostal arteries critical to spinal cord blood flow in nine dogs. To mimic a clinical situation, the proximal descending thoracic aorta (left subclavian artery to T7) was excluded with cross-clamps, and partial pulsatile left atrial-femoral artery bypass was instituted to maintain distal aortic pressure at 100 mm Hg. Progressively lower aortic segments were excluded (T7-10, T10-L1, L1-3, L3-6, L6-7) until loss of somatosensory evolved potentials occurred. Spinal cord blood flow measurements at the time of evoked potential loss revealed significant ischemia (p less than 0.02 versus baseline) in the excluded segment in seven animals but normal spinal cord blood flow in the remainder of the cord. Upon reperfusion, significant reactive hyperemia (p less than 0.02) was noted only in previously ischemic cord segments. Two animals exhibited no change in somatosensory evoked potentials or spinal cord blood flow despite exclusion of the entire thoracoabdominal aorta, presumably as a result of spinal collaterals. Loss of somatosensory evoked potentials despite adequate distal perfusion indicates that critical intercostal vessels have been excluded from systemic and bypass circulations. Use of evoked potential measurements in both experimental and clinical situations provides a means for assessing adequacy of spinal cord blood flow during cross-clamping and can alert the surgeon to the need for reimplantation of critical intercostal arteries during surgical resection of the thoracoabdominal aorta.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. IV. Clinical observations and results

Thirty-three patients undergoing operations on the descending thoracic or thoracoabdominal aorta were monitored to evaluate causes and effects of spinal cord ischemia as manifested by changes in somatosensory evoked potentials. Maintenance of distal aortic perfusion pressure (greater than 60 mm Hg) by either shunt or bypass techniques in 17 patients resulted in preservation of somatosensory evoked potentials and a normal postoperative neurologic status, irrespective of the interval of thoracic cross-clamping (range 23 to 105 minutes). In 16 other patients in whom cross-clamp time ranged from 16 to 124 minutes, evoked potential loss was observed because of failure to provide distal perfusion (n = 8), inadequate maintenance of distal perfusion pressure (less than 60 mm Hg) despite shunt/bypass (n = 6), or interruption of critical intercostal arteries (n = 2). Incidence of paraplegia in the entire group was 15.1% (5/33) and was limited to only those patients in whom evoked potential loss occurred (5/16, 31.2%) (p = 0.02). Loss of somatosensory evoked potentials for more than 30 minutes resulted in a 71.2% (5/7) incidence of paraplegia, whereas no neurologic deficit was noted in patients (0/26) in whom evoked potential loss was either prevented or limited in duration to 30 minutes (p less than 0.001 versus loss for more than 30 minutes). Intraoperative monitoring of somatosensory evoked potentials is a sensitive indicator of spinal cord ischemia. Simple aortic cross-clamping, failure to maintain distal perfusion pressure above 60 mm Hg, and inability to reimplant critical intercostals in a timely fashion result in a high rate of paraplegia if duration of spinal cord ischemia as measured by somatosensory evoked potentials exceeds 30 minutes. Routine evoked potential monitoring during thoracoabdominal procedures appears useful in assessing the adequacy of spinal cord perfusion. Furthermore, it can alert the surgeon to the necessity for critical intercostal artery reimplantation as well as the need for adjustment or regulation of distal aortic perfusion.     

大剂量维生素C联合小剂量甲基强的松龙对脊髓损伤后脊髓病理生理变化的影响

[目的]探讨脊髓受压及减压后,大剂量维生素C(vitaminC)联合小剂量甲基强的松龙(MP)对脊髓灰质血流量,体感诱发电位(SEP),组织学变化,运动功能的影响.[方法]36只犬随机分为3组,每组12只.A组于SEP消失后5min静脉注射MP 30 mg/kg,以5.4 mg (kg·h)输液泵静脉注射;B组于SEP消失后5min以同样方式注射vitaminC 200 mg/kg+ MP 10 mg/kg,减压后12 h,24h各注射vitaminC 200 mg/kg;C组于SEP消失后5min静脉注射0.9％氯化钠,同样以5.4 mg(kg·h)输液泵静脉注射.均持续90 min后减压,期间检测SEP及脊髓灰质血流量,减压后3h重复检测,并进行改良Tarlov评分.减压后28 d通过病理组织学分析确定损伤的范围.[结果]在持续压迫期间A组4只犬出现了SEP,B组5只犬出现了SEP,C组无一出现.减压后A组有2只犬出现SEP,B组有2只犬出现SEP,C组有1只犬出现SEP.三组犬中出现SEP的脊髓灰质血流量明显高于没有出现SEP的犬(P＜0.05).A、B组脊髓灰质血流量明显高于C组(P＜0.05).A、B组动物后肢的运动功能可以较快恢复,C组不能恢复.A、B组脊髓损伤范围与C组具有显著性差异,病理改变与SEP及脊髓血流量具有相关性,与运动功能的恢复具有相关性.[结论]大剂量维生素C与小剂量甲基强的松龙联合应用在神经功能保护及恢复方面提供了显著持续的作用,可能增加了脊髓局部的血流量.维生素C可以部分替代甲基强的松龙对于脊髓损伤的作用.     

Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology

BACKGROUND: The objective of this study is to determine whether there is a relationship between the duration of sustained spinal cord compression and the extent of spinal cord injury and the capacity for functional recovery after decompression. METHODS: Sixteen dogs underwent sustained spinal cord compression for thirty or 180 minutes. The cords were compressed with use of a loading device with a hydraulic piston. A pressure transducer was attached to the surface of the piston, which transmitted real-time spinal cord interface pressures to a data-acquisition system. Somatosensory evoked potentials were monitored during a sixty-minute recovery period as well as at twenty-eight days after the injury. Functional motor recovery was judged throughout a twenty-six-day period after the injury with use of a battery of motor tasks. The volume of the lesion and damage to the tissue were assessed with both magnetic resonance imaging and histological analysis. RESULTS: Sustained spinal cord compression was associated with a gradual decline in interface pressure. Despite this, there was continuous decline in the amplitude of the somatosensory evoked potentials, which did not return until the cord was decompressed. Within one hour after the decompression, the dogs in the thirty-minute-compression group had recovery of somatosensory evoked potentials, but no animal had such recovery in the 180-minute group. Recovery of the somatosensory evoked potentials in the thirty-minute group was sustained over the twenty-eight days after the injury. Motor tests demonstrated rapid recovery of hindlimb motor function in the thirty-minute group, but there was considerable impairment in the 180-minute group. Within two weeks after the injury, balance, cadence, stair-climbing, and the ability to walk up an inclined plane were significantly better in the thirty-minute group than in the 180-minute group. The longer duration of compression produced lesions of significantly greater volume, which corresponded to the long-term functional outcome. CONCLUSIONS: The relatively rapid viscoelastic relaxation of the spinal cord during the early phase of sustained cord compression suggests that there are mechanisms of secondary injury that are linked to tissue displacement. Longer periods of displacement allow propagation of the secondary injury process, resulting in a lack of recovery of somatosensory evoked potentials, limited functional recovery, and more extensive tissue damage.     

脊髓损伤后早期减压对诱发电位影响的实验研究

[目的]观察脊髓损伤后早期减压对体感诱发电位及经颅磁刺激运动诱发电位的影响，以探讨诱发电位在判断手术时机及预后中的应用价值。[方法]日本大耳兔32只随机分4组。A组为对照组，不造成脊髓损伤。B、C、D组为脊髓损伤组。对每组动物于不同时间分别检测SEP、MEP。分析波形的潜伏期、峰问波幅。用后肢的Tarlov分级法作伤后运动功能评分。取脊髓标本，行组织学观察。[结果]随着脊髓压迫时间的延长，SEP、MEP的潜伏期逐渐延长，波幅逐渐减小．波幅变化较潜伏期更为敏感。在恢复过程中，脊髓受压时间越短，诱发电位恢复越早。潜伏期恢复早于波幅，而且SEP恢复早于MEP，MEP的恢复早于功能评分。[结论]SEP与TMS-MEP对脊髓损伤十分敏感，能较早反映脊髓损伤程度，可用于指导临床手术治疗和判断预后。     

Experimental and clinical assessment of the adequacy of partial bypass in maintenance of spinal cord blood flow during operations on the thoracic aorta

We studied both experimentally and clinically the efficacy of partial bypass techniques in maintaining spinal cord blood flow and physiological function during surgical procedures on the thoracoabdominal aorta. We attempted to define the level of distal aortic pressure required to safely ensure normal neurological function in the absence of critical intercostal occlusion. Six dogs underwent left thoracotomy with baseline measurements of spinal cord blood flow and spinal cord impulse conduction (somatosensory evoked potentials). Following exclusion of the entire descending thoracic aorta from the left subclavian artery to the T-13 level, partial left atrium-femoral artery bypass was instituted, and baseline levels of proximal and distal aortic pressure were maintained during a 30-minute stabilization period. Mean distal aortic pressure then was progressively altered at 30-minute intervals to 100, 70, and 40 mm Hg. Measurements of spinal cord blood flow and somatosensory evoked potential were repeated at the end of each interval for comparison with baseline. No significant changes in spinal cord blood flow or somatosensory evoked potential were observed in any animal with a distal aortic pressure greater than or equal to 70 mm Hg. With a pressure of 40 mm Hg, normal flow and somatosensory evoked potentials were maintained in 5 of the 6 dogs. Loss of somatosensory evoked potential, with simultaneous loss of spinal cord blood flow at the T-6 level, occurred in 1 dog. Restoration of distal aortic pressure to 70 mm Hg in all animals resulted in immediate return of somatosensory evoked potential. Loss of somatosensory evoked potential routinely occurred in animals with a distal aortic pressure less than 40 mm Hg. Clinically, 9 patients have undergone operation for lesions of the thoracoabdominal aorta using shunt or bypass techniques. Normal somatosensory evoked potentials were preserved in 7 patients with maintenance of adequate distal aortic pressure (greater than or equal to 60 mm Hg) without evidence of postoperative neurological deficit. Two patients showed hypotensive somatosensory evoked potential loss (distal aortic pressure less than 40 mm Hg). Prolonged distal hypotension (85 minutes of aortic cross-clamping) in the latter resulted in paraplegia. We conclude that maintenance of a distal aortic pressure greater than 60 to 70 mm Hg will uniformly preserve spinal cord blood flow in the absence of critical intercostal exclusion. Should distal aortic pressure be inadequate, early reversible changes in the somatosensory evoked potential will alert the surgeon. Failure to institute measures to reverse these changes may result in paraplegia.     

Intraoperative neurophysiological monitoring of the spinal cord

It is more than 60 years since averaged somatosensory evoked potentials (SEPs) were devised. During this period, other evoked potentials including spinal cord evoked potentials and motor evoked potentials (MEPs) were developed. In cases needing identification of the pathologic level of myelopathy and monitoring the function of the spinal cord, these evoked potentials are now indispensable. The combination of these evoked potentials (multimodality monitoring) has been demonstrated to be sensitive and specific for detecting intraoperative neurologic injury during spine surgery. Although there is still a low level of evidence that intraoperative evoked potentials reduce the rate of new or worsened perioperative neurologic deficits, it is recommended to monitor MEP for thoracoabdominal aortic surgery and multimodal evoked potentials including at least spinal cord evoked potentials and MEP for spine surgery, when the spinal cord is considered to be at risk.     

Response of spinal cord blood flow and motor and sensory evoked potentials to aortic ligation

To produce spinal cord ischemia in the lamb, ligation of the thoracic aorta was performed for 15, 30, and 45 minutes in three animals each. Spinal cord blood flow and motor and sensory evoked potentials were measured before, during, and after aortic ligation. Ischemia with a blood flow of zero during ligation was encountered in the thoracic and lumbar cords, followed by hyperemia upon release of the ligature. Both somatosensory and motor evoked potentials were obliterated during aortic ligation and gradually recovered following resumption of flow. Motor and sensory evoked potentials behaved similarly to high aortic ligation.     

Hypothermic retrograde venous perfusion with adenosine cools the spinal cord and reduces the risk of paraplegia after thoracic aortic clamping

OBJECTIVE: We evaluated the utility of retrograde venous perfusion to cool the spinal cord and protect neurologic function during aortic clamping. We hypothesized that hypothermic adenosine would preserve the spinal cord during ischemia. METHODS: Six swine (group I) underwent thoracic aortic occlusion for 30 minutes at normothermia. Group II animals underwent spinal cooling by retrograde perfusion of the paravertebral veins with hypothermic (4 degrees C) saline solution during aortic occlusion. The spinal cords of group III animals were cooled with a hypothermic adenosine solution in a similar fashion. Intrathecal temperature was monitored and somatosensory evoked potentials assessed the functional status of spinal pathways. RESULTS: Spinal cooling without systemic hypothermia significantly improved neurologic Tarlov scores in group III (4.8 +/- 0.2) and group II (3.8 +/- 0.4) when compared with group I scores (1.3 +/- 0.6) (P <.001). Furthermore, 5 of the 6 animals in group III displayed completely normal neurologic function, whereas only one animal in group II and no animals in group I did (P =.005). Somatosensory evoked potentials were lost 10.6 +/- 1.4 minutes after ischemia in group I. In contrast, spinal cooling caused rapid cessation of neural transmission with loss of somatosensory evoked potentials at 6.9 +/- 1.2 minutes in group II and 7.0 +/- 0.8 minutes in group III (P =.06). Somatosensory evoked potential amplitudes returned to 85% of baseline in group III and 90% of baseline in group II compared with only 10% of baseline in group I (P =.01). CONCLUSIONS: We conclude that retrograde cooling of the spinal cord is possible and protects against ischemic injury and that adenosine enhances this effect. The efficacy of this method may be at least partly attributed to a more rapid reduction in metabolic and electrical activity of the spinal cord during ischemia.     

脊髓缺血再灌注损伤中运动诱发电位的监测作用

目的　探讨运动诱发电位（ＭＥＰ）对脊髓缺血再灌注损伤中神经功能的监测作用。　方法　对２６ 只大鼠腰骶段脊髓缺血前、缺血１５、２５ 、４０ 分钟及再灌注后５、１５、３０ 分钟、１、２ 和２４ 小时ＭＥＰ变化进行监测。　结果　在缺血１５ 分钟时ＭＥＰ潜伏期明显延长（Ｐ＜ ０．０１） ,波幅在缺血２５ 分钟时明显减小（ Ｐ＜ ０－０１） ,缺血４０ 分钟时波形消失;再灌注后５ 分钟时波形恢复,但潜伏期大于正常（Ｐ＜０－０１） ,波幅小于正常（Ｐ＜０－０１）;再灌注后１５ 分钟至２ 小时波幅恢复正常（Ｐ＞ ０－０５）,潜伏期无恢复;再灌注后２４ 小时潜伏期虽然呈恢复趋势,但与再灌注早期相比,差异无显著性意义,此时波幅又明显下降低于正常（Ｐ＜０－０１） ,再灌注后２４ 小时双下肢运动功能比再灌注早明显降低（ Ｐ＜ ０－０５） 。　结论ＭＥＰ能够准确监测脊髓神经功能在缺血再灌注损伤中的变化     

The influence of long-term nifedipine or indomethacin therapy on neurologic recovery from experimental spinal cord injury.

Inhibition of prostaglandin pathways and calcium channel conduction has been shown to improve neurological outcome after spinal cord injury. Functional recovery from such intervention has been routinely evaluated by a simple motor examination or somatosensory evoked potentials (SSEPs) after short-term drug administration. We comprehensively evaluated the influence of continuously administered indomethacin and nifedipine on functional outcome after impact spinal cord injury. SSEP and cortico-motor evoked potential records and neurologic examinations were obtained over 6 weeks after injury. Terminal histopathologic changes within the spinal cord were also examined. Only indomethacin significantly improved neurological function and reduced the severity of histopathologic change. Evoked potential analysis was not found to be of prognostic value. Modulation of prostaglandin pathways may enhance neurological recovery after spinal cord injury.     

Somatosensory evoked potentials and spinal cord perfusion pressure are significant predictors of postoperative neurologic dysfunction

Paraplegia after thoracoabdominal aneurysm repair can occur in 3% to 40% of patients. This study investigated the efficacy of cerebrospinal fluid (CSF) drainage to protect the spinal cord during aortic cross-clamping (AXC) and the interrelationship between drainage, spinal cord perfusion pressure (SCPP), and changes in somatosensory evoked potentials (SEP) in a canine model of spinal cord ischemia. SCPP was defined as the mean distal aortic pressure minus the CSF pressure. In the experimental group, CSF was drained before AXC. SEP changes were quantitated as time to latency increase of 10% (L-10) and time to complete SEP loss. Drainage of CSF had no significant effect on the distal aortic pressure but significantly increased SCPP from 9.4 to 21.8 mm Hg and decreased the incidence of postoperative neurologic injury. Ischemic SEP changes were highly significant predictors of postoperative neurologic injury, occurring more than two times earlier in the paralyzed and paraparetic animals. Dogs without neurologic injury had significantly higher SCPP, delayed L-10 time, and delayed SEP loss.     

Strategies for managing decreased motor evoked potential signals while distracting the spine during correction of scoliosis

Surgical correction of kyphoscoliosis may result in spinal cord injury and neurologic deficits. Monitoring somatosensory evoked potentials (SSEPs) and transcranial motor evoked potentials (MEPs) intraoperatively may allow for early detection and reversal of spinal cord injury. Controlled hypotension and isovolemic hemodilution are often used during these cases to reduce blood loss and transfusion. However, these physiologic parameters may affect the quality of SSEP and MEP signals. Acute reduction or loss of MEP or SSEP signals during spinal distraction presents a crisis for the operative team: should distraction be immediately relieved? The authors describe three patients who showed a decrease in evoked potential signals under hypotensive, hemodiluted conditions at the stage of spinal distraction. Each case illustrates a different strategy for successful management of these patients.     

Direct noninvasive monitoring of spinal cord motor function during thoracic aortic occlusion: use of motor evoked potentials

Spinal cord monitoring during thoracic aneurysmectomy by somatosensory evoked potentials has been criticized for its failure to measure anterior (motor) spinal cord function. We have developed a clinically applicable, noninvasive technique for intraoperative monitoring of motor evoked potentials (MEP), which allows direct functional assessment of spinal cord motor tracts during thoracic aortic occlusion. Twelve dogs underwent continuous intraoperative monitoring of MEP before, during, and after thoracic aortic cross-clamping. Motor tract response to noninvasive cord stimulation (5 to 10 mA, 0.02 msec, 4.3 H2) was recorded by subcutaneous electrodes placed along the length of the spine (T-10, L-1, and L-4). Six animals (group I) subjected to aortic cross-clamping alone demonstrated a characteristic time- and level-dependent deterioration and loss of MEP. Ischemic cord dysfunction (as determined by time from clamping to loss of MEP) progressed from the distal to the proximal cord (L-4 = 11.3 +/- 1.5 minutes; L-1 = 14.9 +/- 2.3 minutes; T-10 = 16.9 +/- 2.3 minutes; p less than 0.05 between all levels). Reperfusion of the distal aorta 20 minutes after clamping resulted in MEP return that progressed from the proximal (T-10) to distal (L-1 and L-4) cord. In another six animals (group II), distal perfusion (mean blood pressure = 95 mm Hg) was maintained for 1 hour after cross-clamping by left atrial-femoral artery bypass. Normal configuration and amplitude of MEP was maintained throughout the cross-clamping period. These data suggest that distinctive changes in MEP indicative of reversible ischemia of spinal cord motor tracts occur after aortic cross-clamping. Such ischemia begins in the most distal cord, exhibits upward progression with time, and can be prevented by maintenance of adequate distal aortic perfusion. Clinical use of MEP monitoring during thoracic aneurysmectomy may provide a method for intraoperative assessment of the adequacy of motor tract perfusion.