Median Nerve Somatosensory Evoked Responses Research Articles

Les potentiels évoqués somesthésiques comme évaluation objective du bloc sensitif du nerf médian après un bloc sous-claviculaire

Median nerve somatosensory evoked responses (MnSSER) alterations were compared to clinical tests (cold and pinprick) variations, in 20 ASA I adult patients following infraclavicular block obtained with 40 mL ropivacaine 0.5% to assess first, the difference of time course of the respective electrophysiological and clinical signs, and second, the objectivity and the reproducibility of MnSSER changes. Four MnSSER derivations (Erb's point; cutaneous projection of peripheral end of brachial plexus; posterior neck at C6 level, frontal and controlateral parietal scalp) were monitored and recorded for retrospective analysis. Continuous data acquisition were started before ropivacaine injection (baseline) and maintained for 30 min thereafter. Every three minutes after ropivacaine injection, cold and pinprick tests were performed in the hand median nerve cutaneous supply zone and were assessed using a sensory visual score (varying from 0-10). Data were compared using analysis of variance. Although MnSSER values were stable during baseline period, after ropivacaine administration, severe progressive amplitude depressions of selected MnSSER were detected in every patient. While clinical cold and pinprick tests became positive (score > 8) only 15.8 +/- 1.2 min and 20.1 +/- 1.8 min respectively after ropivacaine administration, the mean time to observe the earliest MnSSER 20% amplitude decrease at Erb's point derivation was reduced to 5.6 +/- 1.1 min (P < 0.01). Selected MnSSER amplitude reduction indicates objectively the onset of median nerve anesthesia following infraclavicular brachial plexus block before the appearance of clinical signs.

Recovery of memory after general anaesthesia: clinical findings and somatosensory evoked responses

Mid-latency somatosensory evoked responses are used to monitor the integrity of the sensory pathways intra-operatively. They can quantify the effects of anaesthetics on the central nervous system. Mid-latency auditory evoked responses have been related to cognition during anaesthesia, but there are no detailed studies using median nerve somatosensory evoked responses (MnSSER). We studied 49 patients during recovery from general anaesthesia (isoflurane/nitrous oxide or propofol) to assess implicit and explicit memory function in relation to mid-latency MnSSER. The MnSSER recordings were made before anaesthesia, during steady-state anaesthesia, and at the end of the recovery period. The patients were interviewed 24 h later about their memory for the immediate wake up phase. Statistical analysis was by multivariate analysis of variance. Out of 49 patients, 23 recalled the recovery period, 11 had implicit memory for an object shown to them during the recovery period, and 15 did not have any memory for the recovery period. At RECOVERY the patients with recall had significantly shorter MnSSER latencies N45 and P50 and inter-wave conduction times LatN35-LatP45 than patients without memory (P<0.05). We conclude that MnSSER components warrant further investigation for studying the effects of anaesthetic drugs on cognitive function.

Cortical arousal in critically ill patients: an evoked response study.

Assessing the level of sedation in critically ill patients remains a challenge for the intensivist in order to avoid over or under-sedation. Clinical scoring systems may fail in patients with concomitant neurological disorders or requiring muscle relaxants. We evaluated auditory (AER) and median nerve somatosensory evoked responses (MnSSER) in critically ill patients sedated with sufentanil and propofol, in order to quantify the level of sedation during therapeutic interventions. Prospective clinical study. Anaesthesiological intensive care unit (ICU) in a university hospital. Thirty-two patients following major abdominal or thoracic surgery requiring sedation during their stay on the ICU. During physiotherapy and following nursing care (tracheal suctioning) AER and MnSSER were recorded. The level of sedation was evaluated clinically in relation to vital parameters. Data were analysed by multivariate analyses of variance (Hotellings T2), Friedman test. In comparison to baseline levels the AER latency Nb decreased, while the amplitude NaPa increased during physiotherapy and after tracheal suctioning (p < 0.001). In contrast, the MnSSER latency P25 decreased and the amplitude P25N35 increased after tracheal suctioning only (p < or = 0.001). Clinical sedation scores decreased and mean arterial blood pressure increased during physiotherapy and nursing care. Changes of AER or MnSSER waves indicated cortical arousal in ICU patients during nursing care and physiotherapy. Further studies with evoked responses are recommended to evaluate whether bolus injections of sedatives and/or analgesics reduce cortical arousal and thereby minimise the patient's stress during nursing care.

Midlatency median nerve evoked responses during recovery from propofol/sufentanil total intravenous anaesthesia.

Median nerve somatosensory evoked responses (MnSSER) are frequently used to monitor the integrity of the somatosensory pathway during surgery. We investigated MnSSER components during the wakeup phase from anaesthesia with propofol/sufentanil, because detailed information is lacking about the reversibility of anaesthetic induced changes of MnSSER. The aim of the study was to document precisely the MnSSER waves in relation to the clinical awakening. The hypothesis was that anaesthetic induced MnSSER changes are reversed when the patient becomes responsive after anaesthesia. In 20 gynaecological patients anaesthesia was maintained with propofol 8 mg kg(-1) h(-1) supplemented by bolus injections of sufentanil. MnSSER were recorded at C4' (N20, P25, N35, P45, N50) following electrical median nerve stimulation on the day before surgery, after the end of surgery during anaesthesia and every 5 min during recovery, till the patients were responsive again and able to identify a shown object. While the primary cortical MnSSER complex N20P25 regained baseline values, the cortical latencies > or =35 ms remained prolonged (P<0.001) and the amplitudes P45N50 were suppressed (P< or =0.013), when the patients were responsive after 26+/-7 min following anaesthesia. However, the amplitudes P25N35 exceeded their corresponding baseline value (P<0.01) Persistent changes of MnSSER waves > or =35 ms reflect impaired signal processing along the somatosensory pathway following propofol/sufentanil anaesthesia when the patients are responsive again. Further studies combining MnSSER recording with distinct neuro-psychological tests are needed to define the clinical relevance of these findings.

Surgical Stimulation Increases Median Nerve Somatosensory Evoked Responses During Isoflurane-Nitrous Oxide Anaesthesia

Median nerve somatosensory evoked responses (MnSSER) were recorded in 15 healthy adult patients, ASA I-II, before and during orthopaedic surgery. After induction of anaesthesia with fentanyl 0.1-0.15 mg, etomidate 0.3 mg kg-1 and vecuronium 0.1 mg kg-1, anaesthesia was maintained with 0.6% isoflurane (end-tidal) and 66% nitrous oxide in oxygen. MnSSER were recorded after establishment of steady-state anaesthesia at baseline, during preparation (n = 11) and continuously after the start of surgery. For the last measurement period, four patients were excluded from analysis because additional fentanyl was required. MnSSER were recorded at Erb's point, at C6 (neck) and at the respective contralateral primary somatosensory projection area (C3' or C4'). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. During intense surgical stimulation (e.g. periosteal stimulation) the peak-to-peak amplitude N20P25 increased significantly by more than 45% (P < 0.05), whereas latencies of all components did not change over time. These data indicate that MnSSER may be reliably monitored in the intraoperative period during steady-state isoflurane-nitrous oxide anaesthesia. In addition, concurrent changes in haemodynamic variables during nociceptive stimulation support the hypothesis that reversal of isoflurane-nitrous oxide-induced suppression of MnSSER may indicate increased nociceptive input when depth of anaesthesia is inadequate.

Surgical stimulation increases median nerve somatosensory evoked responses during isoflurane-nitrous oxide anaesthesia

Median nerve somatosensory evoked responses (MnSSER) were recorded in 15 healthy adult patients, ASA I-II, before and during orthopaedic surgery. After induction of anaesthesia with fentanyl 0.1-0.15 mg, etomidate 0.3 mg kg-1 and vecuronium 0.1 mg kg-1, anaesthesia was maintained with 0.6% isoflurane (end-tidal) and 66% nitrous oxide in oxygen. MnSSER were recorded after establishment of steady-state anaesthesia at baseline, during preparation (n = 11) and continuously after the start of surgery. For the last measurement period, four patients were excluded from analysis because additional fentanyl was required. MnSSER were recorded at Erb's point, at C6 (neck) and at the respective contralateral primary somatosensory projection area (C3' or C4'). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. During intense surgical stimulation (e.g. periosteal stimulation) the peak-to-peak amplitude N20P25 increased significantly by more than 45% (P < 0.05), whereas latencies of all components did not change over time. These data indicate that MnSSER may be reliably monitored in the intraoperative period during steady-state isoflurane-nitrous oxide anaesthesia. In addition, concurrent changes in haemodynamic variables during nociceptive stimulation support the hypothesis that reversal of isoflurane-nitrous oxide-induced suppression of MnSSER may indicate increased nociceptive input when depth of anaesthesia is inadequate.

Effect of the Acute Administration of High Dose Pentobarbital on Human Brain Stem Auditory and Median Nerve Somatosensory Evoked Responses

Brain stem auditory (BAERs) and median nerve somatosensory evoked responses (MnSSERs) were recorded from normal neural pathways during the induction of pentobarbital coma in six patients undergoing elective excision of complex arteriovenous malformations. Each patient received a 33-minute infusion of pentobarbital at a rate of 0.6 mg/kg (total dose, 19.8 mg/kg). This regimen resulted in burst suppression or isoelectricity of the electroencephalogram in all patients. Although statistically significant changes in latency and amplitude occurred, both BAERs and MnSSERs were readily recordable in all patients throughout the infusion. For the BAER, there were significant increases in the latencies of Waves III and V. However, these increases are sufficiently small that misinterpretation of these changes as an evolving neurological injury is unlikely, e.g., Wave V latency increased from 6.25 +/- 0.25 (SD) to 6.58 +/- 0.16 ms (P less than 0.006). For the MnSSER, changes of greater potential clinical relevance were observed. There were substantial increases in the latencies of the early components of the primary cortical response and in the central conduction time (e.g., CCT of 6.1 +/- 0.6 ms preinduction vs. 7.7 +/- 1.1 ms at t = 33 min, P less than 0.003), and the amplitude of the early cortical response (N20-P25) decreased by a mean of 45% (P less than 0.02). By contrast, subcortical components of the MnSSER (brachial plexus, upper cervical spine) were only minimally affected. We conclude that, in patients who are initially neurologically intact, BAERs and MnSSERs can be monitored effectively during pentobarbital coma and that the loss of these responses should not be ascribed to the effects of this drug alone. However, the interpretation of evoked response changes, particularly MnSSER changes, that occur during pentobarbital administration should take into account the dose-related changes in latency and amplitude that we have observed.

The Effect of High-Dose Fentanyl on Human Median Nerve Somatosensory-Evoked Responses

Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 win and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 ± 9.1 μg·kg-1), followed by a continuous infusion at 10-20 μg·kg-1·hr-1 (total dose 63.6 ± 10.1 μg·kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 ± 1.55 ms preinduction versus 22.18 ± 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 ± 1.30 μV preinduction versus 1.31 ± 0.74 μV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t - 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be ministerpreted as neurologic injury in evolution.

Effect of the acute administration of high dose pentobarbital on human brain stem auditory and median nerve somatosensory evoked responses.

Brain stem auditory (BAERs) and median nerve somatosensory evoked responses (MnSSERs) were recorded from normal neural pathways during the induction of pentobarbital coma in six patients undergoing elective excision of complex arteriovenous malformations. Each patient received a 33-minute infusion of pentobarbital at a rate of 0.6 mg/kg (total dose, 19.8 mg/kg). This regimen resulted in burst suppression or isoelectricity of the electroencephalogram in all patients. Although statistically significant changes in latency and amplitude occurred, both BAERs and MnSSERs were readily recordable in all patients throughout the infusion. For the BAER, there were significant increases in the latencies of Waves III and V. However, these increases are sufficiently small that misinterpretation of these changes as an evolving neurological injury is unlikely, e.g., Wave V latency increased from 6.25 +/- 0.25 (SD) to 6.58 +/- 0.16 ms (P less than 0.006). For the MnSSER, changes of greater potential clinical relevance were observed. There were substantial increases in the latencies of the early components of the primary cortical response and in the central conduction time (e.g., CCT of 6.1 +/- 0.6 ms preinduction vs. 7.7 +/- 1.1 ms at t = 33 min, P less than 0.003), and the amplitude of the early cortical response (N20-P25) decreased by a mean of 45% (P less than 0.02). By contrast, subcortical components of the MnSSER (brachial plexus, upper cervical spine) were only minimally affected. We conclude that, in patients who are initially neurologically intact, BAERs and MnSSERs can be monitored effectively during pentobarbital coma and that the loss of these responses should not be ascribed to the effects of this drug alone. However, the interpretation of evoked response changes, particularly MnSSER changes, that occur during pentobarbital administration should take into account the dose-related changes in latency and amplitude that we have observed.

The effect of high-dose fentanyl on human median nerve somatosensory-evoked responses.

Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 min and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 +/- 9.1 micrograms X kg-1), followed by a continuous infusion at 10-20 micrograms X kg-1 X hr-1 (total dose 63.6 +/- 10.1 micrograms X kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 +/- 1.55 ms preinduction versus 22.18 +/- 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 +/- 1.30 microV preinduction versus 1.31 +/- 0.74 microV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t = 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be misinterpreted as neurologic injury in evolution.

The effect of high dose sodium thiopental on brain stem auditory and median nerve somatosensory evoked responses in humans.

Median nerve somatosensory evoked potentials (MnSSEPs), brain stem auditory evoked responses (BAERs), and the cortical electro-encephalogram (EEG) were recorded in six patients during a 62-min infusion of sodium thiopental (STP) at a rate of 1.25 mg X kg-1 X min-1 (total dose, 77.5 mg/kg). The EEG became isoelectric after 22 +/- 8 (SD) min of STP infusion. Dose-related changes in the latencies and amplitudes of various evoked response wave forms were observed. However, in no instance was any component of either the MnSSEP or the BAER rendered unobtainable by STP administration. For the MnSSEP, progressive increases in the central conduction time (5.33 +/- 0.41 ms preinduction vs. 7.46 +/- 1.2 ms at t = 60 min) and in the latency of the cortical primary specific complex were observed simultaneously with significant reductions in the amplitude of the latter (2.10 +/- 0.85 muV preinduction vs. 0.85 +/- 0.55 muV at t = 60 min). Changes in the latency and amplitude of the response recorded over the upper cervical spine (C2) were not statistically significant in this small population. For the BAER, progressive and significant increases in the latencies of Waves I, III, V (e.g., Wave V latency: 6.16 +/- 0.24 vs. 6.87 +/- 0.31 ms) and in the I-III, III-V, and the I-V interwave latencies were observed. The amplitudes of the BAER components were not significantly altered. The authors conclude that the administration of a dose of STP in excess of twice that required to produce EEG isoelectricity can be compatible with effective monitoring of MnSSEPs and BAERs. However, STP produces dose-related changes in both evoked response wave forms, which must be considered in the interpretation of responses elicited during STP anesthesia.