Effect of spinal cord ischemia on compound muscle action potentials and spinal evoked potentials following spinal cord stimulation in the dog

We recorded the compound muscle action potentials (CMAP) from the soleus muscle and spinal evoked potentials (SpEP) from the caudal spinal cord after stimulation of the rostral spinal cord via epidural electrodes in 18 dogs. We examined the changes of CMAP and SpEP after the cord was made ischemic by clamping the aorta at different levels. Clamping the abdominal aorta below the artery of Adamkiewicz (five dogs) did not change either CMAP or SpEP significantly. When the thoracic aorta was clamped above the radicular and Adamkiewicz arteries (10 dogs), CMAP disappeared entirely within 5-10 min of occlusion, but SpEP showed only minimal latency prolongation limited to the late peaks in seven of 10 dogs. In the remaining three dogs, both CMAP and SpEP disappeared within 30 min of occlusion but with the more rapid deterioration of CMAP than of SpEP. Progressive ligation of lumbar arteries (three dogs) from caudal to rostral levels did not change CMAP until ligation of Adamkiewicz artery. Then CMAP disappeared, but SpEP remained unchanged. These findings suggest that CMAP and SpEP are mediated through different pathways and that CMAP reflect anterior cord function. The described electrophysiologic technique would be useful to monitor spinal cord motor function during surgery of the spine, spinal cord, or thoracoabdominal aorta.     

急性脊髓损伤后磁刺激运动诱发电位及体感诱发电位的诊断意义

目的 研究磁刺激运动诱发电位（ｍｏｔｏｒ ｅｖｏｋｅｄ ｐｏｔｅｎｔｉａｌｓ,ＭＥＰ）对脊髓损伤（ｓｐｉｎａｌ ｃｏｒｄ ｉｎｊｕｒｉｅｓ,ＳＣＩ）后运动传导功能的诊断价值。方法 采用Ｍａｇ－２型磁刺激仪对３２例ＳＣＩ患者进行经颅磁刺激ＭＥＰ检查,分别在双侧外展拇短肌（ａｂｄｕｃｔｏｒ ｐｏｌｌｉｃｉｓ ｂｒｅｖｉｓ,ＡＰＢ）和胫前肌（ａｎｔｅｒｉｏｒ ｔｉｂｉａｌｉｓ,ＡＴ）进行记录。同时检测Ｆ     

Monitoring of motor action potentials after stimulation of the spinal cord

We recorded motor action potentials in cats, using surface electrodes placed over the soleus muscle. The action potentials were generated by stimulating the spinal cord with electrodes in the epidural space at the level of the fifth or sixth thoracic vertebra. This also was done in humans, using the same methods of stimulating and recording, but the intensity of the stimulus was adjusted to produce little or no twitch of the paraspinal muscles. In the animal experiment, the motor action potential was abolished after transection of the pyramidal tract and was progressively attenuated with effective doses of a curare-like agent. We also tested the effect of distraction, using the same technique as is used in Harrington instrumentation, and found that the amount of distraction that caused reduction of the amplitude of the motor action potential of more than 50 per cent, when sustained for longer than seven minutes, caused permanent paraplegia in two cats. The evaluation of spinal evoked potentials that were obtained from epidural electrodes placed caudad to the level of distraction, and of motor action potentials that were recorded over the soleus muscle, following the same stimulus, showed a similar pattern of reduction after distraction in five of seven cats. The other two cats had irreversible reduction of motor action potential associated with unchanged spinal evoked potential, and both cats became paraplegic.(ABSTRACT TRUNCATED AT 250 WORDS)     

An experimental study on conductive spinal cord action potentials evoked by direct stimulation of the spinal cord--pathway and source of conductive action potentials in the spinal cord

The following experiments were carried out in adult cats to clarify the pathway and origin of the conductive spinal cord action potential evoked by dorsal epidural stimulation. (1) Comparison with the potential by surface stimulation of the spinal cord: Since waveforms, conduction velocity, and the relationships between the stimulation site and the change in threshold level were equal to those of surface stimulation, epidural stimulation and direct surface stimulation apparently induced the potential deriving from the same origin. (2) Recording of single fiber action potential: The mean conduction velocity of the dorsal column fiber was approximately 50 m/sec and that of the dorsolateral funiculus fiber was about 80 m/sec. 15-20% of potential N1 and 80-85% of potentials N2 and N3 were composed by the dorsal column fibers, whereas 80-85% of N1 and 15-20% of N2 and N3 were composed by the dorsolateral funiculus fibers.     

Change of muscle motor-evoked potentials after motor cortex stimulation caused by acute spinal cord injury in cats

The validity of the evoked compound muscle action potential (ECMAP) as an index of spinal cord injury has not been established in neurophysiologic monitoring of motor function, although evoked spinal cord potential (ESCP) has been. In the current study, nine cats were used. After craniotomy, electric stimuli were applied to the motor area. Four cats were given stimulation of various numbers and frequencies, and the other five cats underwent graded compression of the spinal cord, and then ECMAPs and ESCPs were recorded. Three cats were awakened and their motor functions were assessed 3 weeks later. The amplitude of the ESCP never decreased to 60% or less of the control value, even when ECMAPs disappeared. No motor dysfunction was present 3 weeks after the experiment. ECMAP is clinically useful, providing information on impairments of the spinal cord that otherwise would remain undetected.     

Dissociation of muscle action potentials and spinal somatosensory evoked potentials after ischemic damage of spinal cord

In patients undergoing spinal fusion and Cotrel-Dubousset instrumentation we recorded compound muscle action potentials (CMAP) from the lower limb and spinal somatosensory evoked potentials (SSEP) from the caudal epidural space after direct stimulation of rostral spinal cord via epidural electrodes. In three of 30 patients tested, the derotation maneuver altered CMAP but not SSEP. In ten dogs, we observed similar dissociation with decrease or disappearance of CMAP amplitude and unchanged SSEP after ligation of the thoracoabdominal aorta or intercostal arteries at each level. In contrast, both CMAP and SSEP were unchanged by clamping the artery at the lumbar level. This is likely due to the lack of collateral vascular flow at the thoracic cord level, the anterior cord in particular, which is mainly supplied by a single large radicular artery (Adamkiewicz artery). These findings support that the CMAP and SSEP are mediated through two independent pathways located in the anterior and posterior spinal cord, respectively. We postulate that the dissociate alteration of CMAP and SSEP by derotation maneuver is due to greater vulnerability of the anterior cord or motor tract to ischemia caused by the displacement of anterior spinal or radiculomedullary artery. Therefore, the patients requiring major derotation procedure would benefit from CMAP monitoring, which provides more sensitive measure of anterior cord function that the conventional SSEP monitoring.     

Studies on motor action potentials following transcranial stimulation and somatosensory evoked potentials including absolute refractory time in experimental spinal cord injury

The motor action potential (MAP) following transcranial stimulation and absolute refractory time (ART) in somatosensory evoked potential (SSEP) were investigated after experimental spinal cord injuries in rabbits. The thoracic cords were injured at the level of the 11th vertebrae by Allen's method. The paralysis after the trauma was classified into 4 groups depend on its severity; severe, mild, transient and non palsy group. A single transcranial stimulation evoked the double MAPs (MAP1 and MAP2) which were characteristic for the palsy groups. The amplitude of the MAP1 was greater than MAP2 in the transient palsy group, while that of the MAP1 was lower than MAP2 in both severe and mild palsy groups. The amplitude of the MAP was significantly reduced in all injured animals. There was no correlation between the amplitude or latency of the SSEP and the severity of the palsy. However, the ART of the SSEP was considerably prolonged in all injured animals regardless of the severity of the palsy.     

An experimental study on spinal cord ischemia during cross-clamping of the thoracic aorta: The monitoring of spinal cord ischemia with motor evoked potential by transcranial stimulation of the cerebral cortex in dogs

The usefulness of spinal motor evoked potential by transcranial stimulation of the motor cortex (MEPt) in detecting spinal ischemia and predicting postoperative neurological dysfunction was evaluated using a model of spinal ischemia. Group 1 was comprised of 11 dogs used for measuring the basic wave form of spinal MEPt. The normal spinal MEPt response curve consists of two major peaks: peak I and peak II. The latency of peak I and peak II at T13–L1 was 6.0±0.6 and 7.1±0.6 msec, and the amplitude, 3.3±1.6 and 6.1±2.6 V, respectively. Group 2 was comprised of six animals subjected to spinal ischemia, in which a time-related deterioration of the MEPt as well as evoked spinal cord potential (ESP) was demonstrated. The time taken until the loss of peak I and peak II was 19.2±5.3 and 21.7±6.2 min, respectively, while the time taken until the loss of ESP was 36.7±14.0 min. In group 3, comprised of seven animals, the aorta was unclamped and the animals were allowed to recover when the spinal MEPt had disappeared. Four had paraparesis immediately after the operation, two had a normal gait, one died, and one developed spastic paraplegia after 24h. We concluded that the change in spinal MEPt during spinal ischemia occurred earlier than the change in ESP, and that the loss of MEPt suggested irreversible spinal cord damage.     

Comparison of spinal cord evoked potentials and peripheral nerve evoked potentials by electric stimulation of the spinal cord under acute spinal cord compression in cats

STUDY DESIGN: Spinal cord evoked potentials and peripheral nerve evoked potentials after spinal cord stimulation were recorded under acute spinal cord compression in 19 cats. OBJECTIVES: To investigate the effects of acute compression upon grey matter and white matter by comparing both potentials. METHODS: We compared peripheral nerve evoked potentials, recorded at the biceps brachii branch of the musculocutaneous nerve, with descending spinal cord evoked potentials, recorded from the lumbar spinal cord, by stimulation to the C2 level, under compression of the C6 segment. RESULTS: The amplitude of both potentials decreased with increased compression. The second wave of peripheral nerve evoked potentials, which are motor fibre action potentials, decreased sooner than those of the spinal cord evoked potentials. CONCLUSION: These findings indicate that peripheral nerve evoked potentials are sensitive to acute damage of the segmented compression. This suggests that grey matter is more vulnerable to compression than white matter.     

Motor evoked potentials elicited from pyramidal stimulation and recorded from the spinal cord in the rat

This study investigated the spinal evoked response to focal electrical stimulation of the sensorimotor cortex in 32 rats. The results demonstrate a long-latency response (beginning at 8 milliseconds) elicited by electrical stimulation, which is distinct from the short-latency motor evoked potential previously reported. The conduction velocity of this later response is similar to that reported for the pyramidal tract in the rat. Experiments confirm that the longer latency response depends upon the integrity of the pyramidal system. Focal stimulation outside the sensorimotor cortex failed to elicit a response. Experimental lesions of the pyramidal tract or ablating the sensorimotor cortex eliminated the spinal cord evoked response. The results demonstrate that focal stimulation of the sensorimotor cortex results in a spinal cord evoked response that represents activity within the pyramidal system. The utility of this response in the rat model for assessing experimental cord injury is discussed.     

大鼠分级脊髓损伤对经颅电刺激运动诱发电位的影响

目的 了解不同程度脊髓损伤（ＳＣＩ）对运动诱发电位（ＭＥＰ）的影响以及ＭＥＰ对ＳＣＩ运动功能预后的价值。方法 采用改良Ａｌｌｅｎ′ｓ法,分别以３０ｇｃｆ、５０ｇｃｆ、８０ｇｃｆ和１００ｇｃｆ冲量打击４０只ＳＤ大鼠Ｔ８￣９脊髓,造成不同程度ＳＣＩ,于伤前及伤后１个月连续记录Ｌ１￣２脊髓硬膜外ＭＥＰ（ｓｃＭＥＰ）和双侧腓肠肌ＭＥＰ（ｍＭＥＰ）,并采用斜板试验和Ｔａｒｌｏｖ评分评估运动神经功能。结果（１     

Effects of anesthetic agents and physiologic changes on intraoperative motor evoked potentials

Motor evoked potentials (MEPs) have shown promise as a valuable tool for monitoring intraoperative motor tract function and reducing postoperative plegia. MEP monitoring has been reported to contribute to deficit prevention during resection of tumors adjacent to motor structures in the cerebral cortex and spine, and in detecting spinal ischemia during thoracic aortic reconstruction. Many commonly used anesthetic agents have long been known to depress MEP responses and reduce MEP specificity for motor injury detection. Although new stimulation techniques have broadened the spectrum of anesthetics that can be used during MEP monitoring, certain agents continue to have dose-dependent effects on MEP reliability. Understanding the effects of anesthetic agents and physiologic alterations on MEPs is imperative to increasing the acceptance and application of this technique in the prevention of intraoperative motor tract injury. This review is intended as an overview of the effects of anesthetics and physiology on the reproducibility of intraoperative myogenic MEP responses, rather than an analysis of the sensitivity and specificity of this monitoring method in the prevention of motor injury.     

The effect of an anesthetic induction dose of midazolam on motor potentials evoked by transcranial magnetic stimulation in the monkey

The effect of a hypnotic dose (0.5 mg/kg) of midazolam (MDZ) on motor evoked potentials (MEPs) was examined in 12 monkeys. MEPs were elicited by transcranial magnetic stimulation (TMS) and the resultant potentials recorded from abductor pollicis brevis (APB) and anterior tibialis (AT) muscles contralateral to the stimulation site. After administration of MDZ, sequential MEP recordings were obtained at postinduction, hypnosis, awakening, emergence, and recovery periods. The results were compared with control values using one-way analysis of variance and Tukey's post-hoc test. Under hypnosis, MEP reproducibility was problematic as the potentials were occasionally ill identified and questionable. MDZ resulted in marked MEP scalp field reduction, coil demography alteration, stimulation threshold elevation, and amplitude suppression (p <0.01). Latency response was unaltered. During hypnosis, awakening, and recovery periods, the mean APB and AT thresholds were elevated by 39, 23, and 0% and by 60, 34, and 4% respectively; while APB and AT amplitudes were depressed by 95, 86, and 53% and by 99, 91, and 60%, respectively. We conclude that an induction dose of MDZ can produce profound and prolonged attenuation of TMS MEPs. The drug inhibitory effect on MEPs may persist after recovery. Anesthetic doses of MDZ should cautiously be used in the settings of MEP monitoring.     

Comparison of evoked spinal potentials by stimulation of the sciatic nerve and the spinal cord

Spinal cord monitoring during surgery using evoked spinal potentials (ESP) is now popular. In cats, ESPs due to both sciatic nerve (SN-ESP) and spinal cord stimulation (SC-AESP and SC-DESP) were recorded from the epidural space. Both SN-ESP and SC-AESP were compared by parameter studies. Stimulus frequencies up to 100 Hz did not significantly alter the SC-AESP, whereas the later components of the SN-ESP decreased greatly in amplitude. The SN-ESP was more sensitive to asphyxia than the SC-AESP. Augmentation of the ESP occurred approximately 5 minutes after the asphyxia was introduced, which was interpreted as an impending sign of anoxia of the spinal cord. The SN-ESP had more potentials arising from synaptic and postsynaptic activities, while the SC-AESP was mainly derived from the spinal tracts. To monitor the function of the spinal cord, both methods should be used.     

Optical imaging of somatosensory evoked potentials in the rat cerebral cortex after spinal cord injury

Optical imaging techniques have made it possible to monitor neural activity and to determine its spatiotemporal patterns. Traumatic spinal cord injury (SCI) results in both the death of gray matter neurons and the disruption of ascending and descending white matter tracts at the injury site, leading to the loss of motor and sensory functions. In this study, we monitored and compared cortical responses to the stimulation of sensory tracts in normal control and spinal-cord-injured rats using an optical imaging technique based on a voltage-sensitive dye (VSD). The sciatic nerve was stimulated with a platinum bipolar electrode, and the exposed cortical surface was stained with Di-2-ANEPEQ. Optical signals were recorded from the cerebral cortex using the MiCAM02 optical imaging system. Characteristic spatiotemporal patterns were observed in response to electrical stimulation of the sciatic nerve in normal control rats. In spinal-cord-injured rats, the optical signals were dramatically reduced compared to those of normal rats. Four weeks after SCI, however, the activation area increased in the vicinity of the focal sensory area compared to that of the rats 1 week after SCI. These results suggest that optical imaging with VSD may be useful to map functional changes after SCI.     

Isoflurane-induced attenuation of motor evoked potentials caused by electrical motor cortex stimulation during surgery

Dysfunction of spinal motor conduction during surgical procedures may not be reflected by changes in somatosensory evoked potential waveforms. A method of monitoring that allows direct and continuous assessment of motor function within the central nervous system during surgery would be useful. This paper describes one such method utilizing noninvasive electric cortical stimulation to evoke muscle activity (the motor evoked potential, or MEP) during surgery. The effect of isoflurane (superimposed on a baseline of N2O/narcotic anesthesia) on MEP's in response to cortical stimulation is specifically examined. Eight patients undergoing elective neurosurgical operations were included in the study. All patients received a background of general anesthesia and partial nondepolarizing neuromuscular blockade. The motor cortex was stimulated electrically via self-adhesive scalp electrodes. Electromyographic responses from multiple muscles were measured with subdermal electroencephalograph-type needle electrodes. Motor responses to stimulation were continually recorded on magnetic tape for off-line analysis. Once closing of the surgical incision was begun, a series of four to five stimuli of constant magnitude were applied to obtain "baseline" MEP responses. Patients were then ventilated with isoflurane for up to 8 minutes, during which time stimuli were continued every 15 to 20 seconds. Comparison was made of MEP responses for trials before, 1 minute after, and 5 minutes after the addition of isoflurane. All patients demonstrated reproducible motor responses to cortical stimulation during surgery. Addition of isoflurane [isoflurane)exp, less than or equal to 0.5%) to pre-existing anesthesia caused marked attenuation of MEP amplitudes in all patients within 5 minutes of its application, without affecting neuromuscular transmission as judged by direct peripheral nerve stimulation. It is concluded that: 1) monitoring motor system integrity and function with electric transcranial cortical stimulation during surgery is feasible when utilizing an N2O/narcotic anesthetic protocol; and 2) the quality of data obtained will likely suffer with the addition of isoflurane.     

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.     

Post-tetanic transcranial motor evoked potentials augment the amplitude of compound muscle action potentials recorded from innervated and non-innervated muscles

Background Context

Transcranial electrical stimulation used to produce motor evoked potentials (TES-MEPs) and subsequent compound muscle action potential (CMAP) recording is widely used to monitor motor function during surgery when there is risk of damaging the spinal cord. Nonetheless, some muscles do not produce CMAP amplitudes sufficient for intraoperative monitoring.

The effect of graded spinal cord injury on the extrapyramidal and pyramidal motor evoked potentials of the rat.

This study investigated the differential effects of graded spinal cord injury on the rat extrapyramidal motor evoked potential (exp-MEP) and pyramidal motor evoked potential (pyr-MEP) and the prognostic value of these effects in predicting postinjury motor performance in the rat model. In 20 rats subjected to graded spinal injury (10-100 g-cm), there was a differential injury threshold for ablation of exp-MEP and pyr-MEP. All peaks of the pyr-MEP were extinguished in the animals subjected to impact forces of 50 g-cm and above (n = 12). In contrast, the exp-MEP was completely abolished in only two animals at injuries of 80 g-cm or above. A residual exp-MEP response persisted in the remaining 18 animals. Motor performance was monitored in 16 additional animals for up to 1 week after spinal injury. The pyr-MEP was abolished in 100% of the rats subjected to a 50-g cm injury (n = 7), whereas the exp-MEP persisted up to the highest impact forces (80 g-cm). Hind leg paralysis was present in the five rats where the pyr-MEP was extinguished but with persistence of the exp-MEP. An 80% reduction in the amplitude of the pyr-MEP in four animals resulted in mild ataxia with motor improvement at the end of a week. An increase or a 70% loss in pyr-MEP peak amplitude resulted in no clinical motor deficits (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)