Midazolam and somatosensory evoked potentials

The effect of midazolam, a water-soluble benzodiazepine, on the somatosensory evoked potentials (SEPs) following strong electrical stimulation of the upper lip, was investigated in Wistar albino rats. SEPs were recorded from the surface of the skull in the contralateral temporal area. A computer was used to obtain the averaged SEPs. The rats received intraperitoneal dosages of 1.25, 2.5, or 5.0 mg/kg of midazolam, or physiological saline. Relative amplitudes of the P₁N₁ wave were reduced significantly after midazolam injection. Amplitude recovered to the control level about 120 min after the injection in the 1.25 mg/kg group. In 2.5 and 5.0 mg/kg groups, midazolam-induced suppression did not recover within 120 min. No significant differences were found in the latencies of P₁ and N₁ before and after midazolam injection. It is suggested that midazolam has a mild analgesic effect due to central suppression of the pain perception following noxious stimuli.     

Spinal somatosensory evoked potentials after epidural isoproterenol in awake sheep

Purpose

The use of 10–15 μg epinephrine as an epidural test-dose is controversial. Isoproterenol would be a better alternative. However before 5μg isoproterenol can be incorporated in an epidural test-dose, neurotoxicological studies have to be performed. The present study was designed to assess spinal somatosensory evoked potentials (spinal SSEP) before and after epidural isoproteronol.

Methods

Spinal SSEPs were recorded before, 30 min after, and 72 hr after 50 μg isoproterenol were given epidurally (L_3–4) to six chronically instrumented awake sheep. The spinal SSEPs after epidural (L_3–4 administration of 15 ml lidocaine 2% were used to evaluate the model. The SSEPs were generated by transcutaneous stimulation of the sciatic nerve in the thigh. Spinal SSEPs were recorded directly from the spinal cord at vertebra T₁₂ using a monopolar epidural electrode referenced to a subcutaneous needle electrode in the adjacent paraspinal area.

Results

Thirty minutes and 72 hr after epidural injection of 50 μg isoproterenol the latency and the amplitude of the SSEP waves were similar to baseline values. After lidocaine, no SSEPs could be generated in three sheep while in three sheep the latency of wave 2 (W2) was prolonged and the amplitude diminished.

Conclusion

Administration of epidural isoproterenol did not affect spinal SSEPs in this study indicating an absence of neurotoxic side effects.     

Etidocaine and extradural somatosensory evoked potentials after posterior tibial nerve stimulation

We have examined the effects of lumbar extradural administrationof 1% etidocaine 10 ml on somatosensory evoked potentials toposterior tibial nerve stimulation measured in the cervicalextradural space. Eight patients, anaesthetized with propofoland nitrous oxide, were studied before hysterectomy and a controlgroup received a similar anaesthetic and 0.9% sodium chloridesolution 10 ml in the lumbar extradural space. Etidocaine decreasedsignificantly overall amplitude of the evoked potentials andthe amplitudes of all peaks, between 30 and 50 min after extraduralinjection. The effects of etidocaine on spinal cord conductionwere greater than those found previously for lignocaine andbupivacaine, suggesting that it is the local analgesic of choicefor inhibiting afferent conduction.     

Dexmedetomidine infusion and somatosensory evoked potentials.

Intraoperative neurophysiologic monitoring requires information on the effects of anesthetic drugs because these drugs can directly alter evoked potentials, thus interfering with monitoring. We report on our evaluation of the effect of the recently introduced alpha2-adrenergic agonist, dexmedetomidine, on the somatosensory evoked potentials in two patients undergoing cervico-occipital fusion. Our results suggest that, although dexmedetomidine can affect the later cortical peaks of somatosensory evoked potentials (SSEPs), consistent and reproducible potentials can be recorded.     

诱发电位监测脊髓缺血性损害的实验研究

目的：探索术中诱发电位对脊髓缺血性损害的监测作用。方法：12只犬,随机分为3组,分别行单纯主射造影剂、使用明胶海绵和碘油作栓塞剂栓塞单侧肋间动脉（左T8／9）造成脊髓缺血,术中应用运动诱发电位（MEPs)和体感诱发电位（SEPs)监测,观察术中,术后MEPs与SEPs的变化,比较各各组术后运动分级和病理检查结果。结果：注射造影剂或栓塞剂时SEPst MPEs潜伏期均有不同程度的延长,波幅均有不同程度的下降,但单纯造影组5min后恢复,明胶海绵组30min恢复,碘油组30min仍未见恢复。MEPs变化与运动功能分级一致,SEPs和MEPs都与病理形态相关。结论：SEPs、MEPs对脊髓缺血性损害具有良好的监测作用;MEPs 的改变与术后脊髓运动功能相关。     

Effect of epidural bupivacaine on somatosensory evoked potentials after dermatomal stimulation

The effect of lumbar epidural analgesia with plain bupivacaine, 0.5%, on early (less than 0.5 sec) somatosensory evoked potentials (SEP) to electrical stimulation of the T-10, L-1, and S-1 dermatomes and the posterior tibial nerve was examined in eight patients. A decrease of the cortical amplitude and an increase in latency were seen, most pronounced at the L-1 level, but with only minor effect on the S-1 dermatome. No correlation was found between segmental level of analgesia and decrease in amplitude of the evoked potentials. Thus despite clinically adequate surgical anesthesia, the neural pathways as assessed by SEP were incompletely blocked except at the L1 dermatome near the epidural injection site.     

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     

Direct tramadol application on sciatic nerve inhibits spinal somatosensory evoked potentials in rats

We sought to determine the possible neural conduction blockade of tramadol and whether there is evidence of localized neural toxicity with spinal somatosensory evoked potential (SSEP) measurements. Male Wistar rats were used. SSEP, elicited by supramaximally stimulating the hind paw and recorded from the thoracolumbar and the first and second lumbar interspinous ligaments, was monitored. SSEPs were obtained before drug application as the pretreatment baseline and measured every 15 min after treatment for 2 h and at 60-min intervals thereafter until SSEP returned to baseline or for another 4 h. Two small strips of Gelfoam (0.6 x 1.0 cm(2)) soaked with the drug were placed under and over the left sciatic nerve for a 30-min period. Gelfoam was prepared with tramadol hydrochloride (Tramal; the US trade name is Ultram) 5, 2.5, and 1.25 mg, diluted if needed with saline to a total volume of 100 microL (5%, 2.5%, and 1.25%, respectively). The control data were obtained from the right side limb with normal saline by following the same method. Spinal SSEPs were measured after 48 h to detect the late neural damage. The results showed that direct tramadol application on sciatic nerves dose-dependently reduced both the amplitude and conduction velocity of SSEPs when compared with the pretreatment baseline. All SSEPs returned to pretreatment baseline, and no significant changes of SSEP between bilateral limbs were noted at the 48-h measurements. No evidence of irreversible conduction blockade indicative of local neural toxicity was seen. Pretreatment with naloxone 1 mg/kg failed to block the changes of SSEP produced by 2.5% tramadol 100 microL. We conclude that tramadol exerts a local anesthetic-type effect on peripheral nerves.     

Early somatosensory evoked potentials in supratentorial brain tumors

Early somatosensory evoked potentials were recorded in 33 patients with supratentorial brain tumors (9 benign tumors, 17 glioblastomas and 7 metastases). All the cases were studied with CT scan and all but 2 were surgically explored and histologically classified. Evoked potentials were statistically analyzed regarding the nature and site of the tumors. The temporal malignant tumors showed the most significant alterations in latencies, particularly for waves P25, N34 and P44.     

The origin,and application of somatosensory evoked potentials as a neurophysiological technique to investigate neuroplasticity

Somatosensory evoked potentionals (SEPs) can be used to elucidate differences in cortical activity associated with a spinal manipulation (SM) intervention. The purpose of this narrative review is to overview the origin and application of SEPs, a neurophysiological technique to investigate neuroplasticity. Summaries of: 1) parameters for SEP generation and waveform recording; 2) SEP peak nomenclature, interpretation and generators; 3) peaks pertaining to tactile information processing (relevant to both chiropractic and other manual therapies); 4) utilization and application of SEPs; 5) SEPs concurrent with an experimental task and at baseline/control/pretest; 6) SEPs pain studies; and 7) SEPs design (pre/post) and neural reorganization/neuroplasticity; and 8) SEPs and future chiropractic research are all reviewed. Understanding what SEPs are, and their application allows chiropractors, educators, and other manual therapists interested in SM to understand the context, and importance of research findings from SM studies that involve SEPs.     

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.     

Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair

OBJECTIVE: To compare transcranial motor evoked potentials (tc-MEPs) and somatosensory evoked potentials (SSEPs) as indicators of spinal cord function during thoracoabdominal aortic aneurysm repair. SUMMARY BACKGROUND DATA: Somatosensory evoked potentials reflect conduction in dorsal columns. tc-MEPs represent anterior horn motor neuron function. This is the first study to compare the techniques directly during thoracoabdominal aortic aneurysm repair. METHODS: In 38 patients, thoracoabdominal aortic aneurysm repair (type I, n = 10, type II, n = 14, type III, n = 6, type IV, n = 8) was performed using left heart bypass and segmental artery reimplantation. tc-MEP amplitudes <25% and SSEP amplitudes <50% and/or latencies >110% were considered indicators of cord ischemia. The authors compared the response of both methods to interventions and correlated the responses at the end of surgery to neurologic outcomes. RESULTS: Ischemic tc-MEP changes occurred in 18/38 patients and could be restored by segmental artery reperfusion (n = 12) or by increasing blood pressure (n = 6). Significant SSEP changes accompanied these tc-MEP events in only 5/18 patients, with a delay of 2 to 34 minutes. SSEPs recovered in only two patients. In another 11 patients, SSEP amplitudes fell progressively to <50% of control without parallel tc-MEP changes or association with cross-clamp events or pressure decreases. At the end of the procedure, tc-MEP amplitudes were 84 +/- 46% of control. In contrast, SSEP amplitudes were <50% of control in 15 patients (39%). No paraplegia occurred. CONCLUSION: In all patients, tc-MEP events could be corrected by applying protective strategies. No patient awoke paraplegic. SSEPs showed delayed ischemia detection and a high rate of false-positive results.     

Effect of thoracic epidural bupivacaine on somatosensory evoked potentials after dermatomal stimulation

The effect of epidural bupivacaine (9 ml 0.5%) analgesia on early (less than 500 msec) somatosensory evoked potentials (SEPs) with electrical stimulation of the T-10 and L-1 dermatomes was examined in eight patients. Cortical amplitudes decreased only insignificantly after stimulation of both dermatomes, despite the presence of sensory analgesia (pin prick) from T-3.5 +/- 0.4 to L-2.9 +/- 0.4 (mean +/- SEM). Latency of the SEP components remained unchanged and sensory threshold increased only insignificantly during blockade. We conclude that thoracic epidural analgesia with conventional doses of bupivacaine provides only a limited blockade of fast conducting afferent nerve fibers.     

右美托咪定对特发性脊柱侧弯矫形术中体感诱发电位和运动诱发电位的影响

目的:研究右美托咪定（dexmedetomidine, Dex）对特发性脊柱侧弯矫形术中体感诱发电位（somatosensory evoked potentials, SEPs）和经颅电刺激运动诱发电位（transcranial electric motor evoked potentials, TCeMEPs）的影响...