The number of total shoulder arthroplasty (TSA) surgeries has substantially increased in the past decade.1,2 An estimated 66,485 such procedures are conducted each year in United States.1 Patients presenting for TSA are generally older and have multiple comorbidities,2 representing an aging population that wishes to remain active. For such patients, quality of life is often significantly compromised due to the inability to raise their arms leading to difficulties in dressing, personal hygiene, and general care of themselves and their families.3 Shoulder arthroplasty is thus a potentially life-changing procedure that offers promise of greatly improved mobility and a significant reduction in costs for supportive care.3 As such, the occurrence of an intraoperative peripheral nerve injury (PNI) can be devastating and have profound consequences that greatly limit the benefits of TSA.
Postoperative clinically apparent neuropathy after TSA occurs in 4.3% to 8.2% of patients,4,5 resulting in a wide range of symptoms from transient paresthesia to permanent muscle weakness and wasting.6 Most injuries during TSA are due to inadvertent stretching of the brachial plexus over its mobility limits from extreme shoulder and arm positions during surgical exposure or implantations rather than direct surgical transection of nerves.7,8 A timely detection/intervention of such stretch-related nerve insults is likely to minimize the extent of nerve injuries during TSA.9
Previous studies9,10 using intraoperative evoked potential monitoring have reported an exceedingly high incidence of intraoperative alerts, signifying high burden of nerve insults during TSA. The authors9 suggested that patients at high risks of nerve injury should be considered for routine monitoring. Intraoperative evoked potential monitoring has also been studied to prevent nerve injury in shoulder rotator cuff repair surgery,11 proximal humeral fracture fixation surgery,12 shoulder arthroscopy,13 closed humeral nailing,14 as well as acetabular surgery.15 However, because the conventional evoked potential monitoring is a relatively expensive and labor-intensive monitoring modality, routine monitoring is not performed in most surgical centers. Clearly, practicability is one of the key concerns for developing a new monitoring modality for intraoperative detection of PNI during TSA.
This single-arm (intervention arm) pilot study is a substudy under a previously registered protocol (NCT02237599) aimed at exploring the utility of an automated somatosensory potential (SSEP) device(EPAD; SafeOp Surgical, Hunt Valley, MD) in different surgical populations. The primary objective of this study was to assess the feasibility of this automated SSEP technology to provide a timely alert and allow intervention to minimize intraoperative nerve insults during TSA surgery. Secondary objectives were to obtain pilot data on the incidence of abnormal SSEP signals in our institute, and to assess their association with predisposing patient factors, as well as the intraoperative events. Detecting the pattern of intraoperative nerve alerts at each surgical stage, as well as identifying which surgical interventions could reverse abnormal SSEP at each surgical stage were also our goals. As a proof of concept pilot study, the outcome benefit of the automated SSEP device was not the primary objective of this study and will be evaluated in a subsequent randomized prospective study.
Twenty-one adult patients undergoing either anatomic or reverse TSA were prospectively recruited from June 2016 to March 2017. There was no restriction on the surgical approach, patient positioning or types of retractors used. The exclusion criteria included specific contraindications to SSEP monitoring such as skin burns and trauma at SSEP electrode sites, as well as lack of written consent, emergency surgery, and language barrier.
After obtaining informed consent, a brachial plexus catheter (BPC) was inserted with topical anesthesia under ultrasound guidance using an interscalene approach by the anaesthesiologists, but further local anesthetics were withheld till the end of surgery to enable SSEP monitoring. A baseline clinical examination of the sensory and motor function of the upper limb was performed after BPC insertion to ensure any changes in neurological symptoms were not due to needle injury during BPC insertion.
The anesthetic regimen was unrestricted (other than avoidance of local anesthetic into BPC) because only subcortical SSEP was monitored.16 Anesthesia was induced with variable dosages of fentanyl, midazolam, propofol, and rocuronium and was maintained with either desflurane or sevoflurane during surgery. After anesthesia induction and with the airway secured, the patient was positioned in semisitting position; the nonoperative arm was positioned on an arm board and the operative arm was surgically prepared by the surgeons for operation.
The monitoring device used, EPAD (SafeOp Surgical), is a novel simplified, automated SSEP monitoring device (Food and Drug Administration approved), designed to detect intraoperative PNI. The technical setup of automated SSEP monitor was described in Figure 1. Surface adhesive electrodes were placed on the cervical spine at C5 level (C5) and on the forehead (Fz) for monitoring N13 cervical potential. After the operative arm was surgically prepared (Fig. 2), surface adhesive electrodes for stimulation of median, ulnar, and radial nerves of the operative arm were attached at the wrist (Fig. 2) on the operative arm, as well as the median nerve of contralateral arm, followed by covering with an occlusive transparent dressing (Tegaderm, 3M Co; St Paul, MN), and wrapping with a sterile strap. After confirming the physical setup of the EPAD device, the automated SSEP monitoring was initiated by the attending anesthesiologist. An automatic impedance check was performed by the EPAD device at the beginning of each case and baseline subcortical SSEP and the corresponding amplitude and latency of the baseline wave forms were then obtained automatically and continuously throughout the entire procedure (Fig. 3). Surgery commenced after a satisfactory baseline SSEP was obtained. The setup and monitoring were performed solely by the attending anesthesiologist without any additional neurophysiologist or technician.
As per convention, an abnormal SSEP was defined as either a 50% reduction in amplitude or a 10% prolongation of the latency in one of the potentials as compared with the baseline.18 When a nerve alert was signalled by the automated SSEP device, the stage of surgery was noted and the surgeon was informed with the aim of reversing the signal changes. Possible surgical interventions included repositioning the operative arm into a more neutral position, avoidance of excessive traction, removal of retractors, use of a smaller implant to avoid overcorrection/traction, and expedited surgery. The choice of surgical interventions was at the discretion of the surgeon based on the possible causes and stage of surgery. A subsequent offline review and analysis was performed from the downloaded continuous SSEP data of the EPAD device.
A standard data collection form was used to collect all perioperative data, including patient demographics, surgical characteristics, and intraoperative technical issues, important intraoperative events, and factors that related to the abnormal SSEP changes such as application of retractors, prosthesis implantation, and hypotension. The duration of abnormal SSEP changes and maneuvers which successfully restored the signal were recorded. At the stage of skin closure, local anesthetics (10 mL of 0.5% ropivacaine) were injected into the BPC. SSEP monitoring was continued until the dressing was applied. The effects of brachial plexus block onset on SSEP signal changes were recorded. As part of our routine practice, all patients received local anesthetics continuously via the BPC for the first few postoperative days. Thus, no neurologic examination was performed in the early postoperative period.
All patients were assessed by the attending orthopedic surgeon on postoperative week 6 for the detection of peripheral neuropathy and if symptomatic, were referred to neurology for further nerve conduction and electromyography (EMG) assessment.
Patient and surgical demographics were summarized. The patterns of intraoperative nerve alerts were summarized per affected nerve (median, ulnar, and radial), as well as per surgical stage (glenoid preparation, humerus preparation, humeral implantation, and postreduction). Univariate logistic regression analysis was performed to explore possible predictors of the occurrence of intraoperative nerve insults (or abnormal SSEP). The examined predictors include reverse TSA, age, female, body weight, body mass index, preexisting peripheral neuropathy, preexisting cervical spine disease, preexisting motor deficit of the operative arm, osteoarthritis, and diabetes.
In total, 21 TSA patients were prospectively recruited and were successfully monitored as part of routine anesthetic care without recourse to a technician or neurophysiologist. Minimal technical issues were encountered, and satisfactory signals were SSEP obtained in all patients. Because of automated device setup procedures (eg, automated impedance check and baseline signal acquisition) and since only 6 surface electrodes were required (one each for stimulation median, ulnar, and radial nerves of the operative arm and median nerve of contralateral arm, as well as for recording in C5 and Fz position), the average preparation time for electrodes placement and obtaining baseline SSEP signals was ~5 minutes. The qualities of the raw SSEP signals were good and were comparable with a standard neurophysiological monitoring machine (Fig. 4). No technical issues were found in maintaining surgical sterility or with automatic impedance check and electrocautery suppression by the device. The average impedance of the cervical surface electrode was 3817±1922 Ω (normal range: <5000 Ω).19 One patient had impedance of 8808 Ω but adequate SSEP signals were still obtained and permitted continuous monitoring.
Patient demographics and surgical data are presented in Tables 1 and 2. The majority of patients (66.7%) underwent reverse TSA. No patients had clinically documented preexisting peripheral neuropathy or neurological deficits. A summary of baseline SSEP signals is listed in Table 3. The average anesthesia (time from arrival in OR until extubation) and surgical duration (time from skin incision until dressing completed) were 145.9±27.5 minutes and 109.5±28.7 minutes, (mean±SD) respectively.
Five (24%) patients developed abnormal SSEP signal changes (Table 3). Median nerve (4 patients) was most commonly affected, followed by radial nerve (3 patients) and ulnar nerve (1 patient). The mean duration of abnormal SSEP signal of median, ulnar, and radial nerve on the operative arm (mean±SD) were 27.4±27.3, 7.8±15.6, and 29.9±28.0 minutes, respectively. Most abnormal nerve alerts occurred at the stage of glenoid preparation and humeral implantation (Table 3). All operative arm cases were due to the extreme external rotation and extension of shoulder; repositioning of arm into a more neutral position, repositioning of the surgical retractor, or expedited surgery were undertaken with resolution of abnormal SSEP signals in all except 1 patient who had irreversible abnormal signals of median and radial nerves till the end surgery. As we applied all possible interventions at once when there was an abnormal nerve alert, we could not identify which intervention was contributing the reversal of abnormal nerve alert. One patient had abnormal SSEP in the nonoperative arm, which was reversed within 1 minute after detection and repositioning of the arm board.
In the univariate logistic regression analysis, we failed to identify any predictor for developing intraoperative nerve insults other than stage of surgery (Supplementary Table 1, Supplemental Digital Content 1, http://links.lww.com/JNA/A54). No further multivariate logistic regression analysis was performed.
In total, 19 of 21 patients had abolishment of SSEP signals after injection of local anesthetics into BPC at the end of surgery. However, 2 patients had no changes in SSEP signals after local anesthetic injection and both had severe pain after emergence from general anesthesia in postanesthetic care unit (PACU), one of whom had visual analogue pain score of 10/10; the other who had visual analogue pain score 8/10. Both patients required repositioning of BPC in PACU, with significant improvement of their pain scores. In patients with complete initial abolishment of SSEP signals, there were no complaints of pain in PACU. No patient had postoperative wound infection. No patients were found to have clinical apparent peripheral neuropathy at 6 weeks postoperatively, and no patients were referred for EMG assessment.
The primary objective of this pilot study was to assess the feasibility of automated SSEP technology to provide timely detection/intervention of intraoperative nerve insults in patients undergoing TSA. Our pilot experience suggests that such approach using automated SSEP monitoring in TSA is clinically practical as it did not affect the sterility of the surgical field, was readily accomplished by the attending anesthesiologist without an additional monitoring technician, and it did not significantly prolong operative time.
Although this was a small, single-arm pilot study, we did observe the reversibility of most intraoperative nerve insults reflecting the fact that simple maneuvers such as repositioning of the operative arm can reverse abnormal SSEP signals (ie, restore normal nerve conduction) during TSA. Although not designed for assessing efficacy, in this study no patient developed postoperative clinical apparent peripheral neuropathy, compared with an average incidence of postoperative peripheral neuropathy in our institute of ~4% to 5% (personal communication with surgeons). One patient had persistent abnormal SSEP till the end of surgery but was neurologically normal at postoperative 6 weeks. This could be due to the injury being recovered at the time of assessment or the initial injury was mild (so that it did not led to a permanent injury). This favorable experience supports our hypothesis that intraoperative nerve injury in TSA is largely reversible and that timely detection facilitates guided interventions that can reverse or shorten the duration of nerve conduction abnormalities.
In addition, the technique as described did not adversely affect postoperative pain control and informed the anesthesiologists of the effectiveness of brachial plexus block before emergence. There has long been concern about the risk of nerve injury due to peripheral nerve blocks in shoulder arthroplasty.20,21 As described our technique enables us to examine the neurological function of the patient’s upper arm (eg, insertion of BPC without injection of local anesthetics), as well as obtain a normal baseline SSEP recordings before the commencement of the surgery in order to delineate the time of nerve injury should it occur.
An important advantage of automated SSEP monitor described here is that only subcortical SSEP are being monitored and it is much less susceptible to volatile anesthetic agents.16 Previous studies reported negligible suppressive effects on subcortical SSEP activities with up to 1.5 minimum alveolar concentration (MAC) of halogenated volatile agents, including halothane,22,23 isoflurane,24 sevoflurane,25 and desflurane,26 with or without the concomitant use of nitrous oxide. Cortical SSEP amplitude is reduced by 40% to 70% and the latency is prolonged by 10% to 15% with only 1 MAC of halogenated volatile agents.22–26 The suppressive effect of halogenated volatile agents on cortical SSEP is more pronounced with concomitant use of nitrous oxide.22–26 In this pilot study, up to 1 MAC of volatile agents was used without affecting the subcortical SSEP signals. In contrast, motor evoked potential (MEP) (as used in other TSA studies27) are sensitive to volatile anesthetics,16 and both MEP and EMG monitoring require avoidance of the use of muscle relaxants. Operators of MEP monitoring have also reported other complications including tongue biting, seizures, and needle stick injuries due to motor stimulation,28 and necessitates the interruption of surgery during intermittent transcranial stimulation.29
Furthermore, our technique avoids the complicated logistics/expertise involved in the conventional neurophysiological monitoring, including the large machine size, a nonintuitive user interface, the need for the presence of a designated technician and/or neurophysiologist for device setup/trouble shooting and data interpretation. This implies our technique may potentially reduce the costs associated with the conventional neurophysiological monitoring; thus potentially promote a wider application of nerve monitoring in high-risk procedures.
An important premise here is that since median, ulnar, and radial nerves are mixed sensory and motor nerves, detection of injury to sensory fibers will reflect simultaneous injury to motor fibers, while conversely, absence of sensory nerve changes can be evidenced as integrity of associated motor nerve fibers. SSEP monitoring for detection of PNI is thus fundamentally different to the use of SSEP monitoring for detection of intraoperative spinal cord injury in which the dorsal column is anatomically distinct from the corticospinal tract. Thus, concerns about the sensitivity of SSEP for detection of intraoperative spinal cord injury are not germane to the use of SSEP monitoring for detection of PNI.
Similar to other cadaveric and clinical studies,7,9,10 we also found most intraoperative nerve insults occurred during glenoid exposure and humeral implantation. This is likely attributed to the extreme external rotation and extension of shoulder,7 or excessive arm lengthening8 during these surgical stages. This is consistent with neurophysiology, in that stretching of a nerve by as little as 5% to 15% beyond its resting length30,31 can result in ischemic insult, and subsequent structural damage.30,31 Nerve topography and anatomy vary substantially in different body habitus and different positions during TSA,7 resulting in an “unpredictable and difficult to prevent” clinical phenomenon of PNI in TSA. As the mechanism of injury in TSA is largely due to extreme shoulder and arm positions during the procedure (ie, a stretch-related nerve injury),7,8 once identified, a simple intervention (eg, repositioning of the operative arm) is likely to minimize further nerve injury. Previous studies in TSA9 and in other surgical procedures32–35 suggest that repositioning of the arm can reverse a majority of abnormal nerve conduction due to excessive stretching or compression.
Nagada et al9 used EMG and MEP in 30 consecutive patients undergoing TSA and found 56.7% of patients had nerve insults during the surgery and that most insults (76.7%) could be reversed by arm repositioning but not removal of retractors. Five (16.7%) patients had postoperative EMG features of nerve injuries and all resolved at 6 months after surgery. These authors suggested that “patients who are at high risks of nerve injuries should be considered for routine monitoring.” In another large retrospective study27 of 284 patients undergoing TSA using MEP monitoring, abnormal nerve alert was found in 36.2% of patients, in which 2 (0.7%) and no patient(s) developed transient and persistent clinical detectable nerve injuries, respectively. The authors27 reported a sensitivity of 100% and a specificity of 94% of MEP in predicting postoperative nerve injury. Because of the reported high diagnostic values of MEP and no long-term nerve injury in this cohort,27 the authors also advocated the routine use of neurophysiological monitoring during the TSA procedure.
However, in a similar cohort study by Parisien et al,10 EMG, SSEP, and MEP monitoring were used in 36 anatomic and reverse TSA patients. They reported an exceedingly high incidence (100%) of nerve alerts reporting 203 alerts in 36 procedures or an average of 5.6 alerts/procedure. There were 17 patients (47%) with nerve alerts that persisted until the end of surgery, of whom 2 had clinically detectable nerve injuries immediately postoperatively and both of which were fully recovered at 6 months postoperatively. In this study, no postoperative EMG were performed. These authors commented that “the clinical utility of routine intraoperative nerve monitoring remains in question given the high level of nerve alerts and lack of persistent postoperative neurologic deficits”10 and that “Intraoperative neuromonitoring for shoulder arthroplasty will significantly increase the cost and length of surgery, thus we critically question the true benefit or value.”10
In contrast with these studies,9,10 we demonstrated a lower incidence of nerve insults of the operative arm (19% or 4/21 patients) during TSA using SSEP monitoring alone. This difference is likely in part related to the uses of EMG monitoring in the previous studies9,10 (a technique with low specificity [~24%]36 in spine surgery), and in part related to the different surgeons and surgical techniques. In addition, in our study, all patients were monitored without extra technician or research staff, and the setup time that was performed solely by the attending anesthesiologist and required ~5 minutes for each patient. These results effectively obviate the arguments of high cost and complex logistics for such monitoring and now require a prospective randomized trial to assess clinical efficacy and possible outcome benefits.
Concomitant evaluation of the EPAD device in comparison with a conventional neurophysiological machine was not feasible because asynchronized stimulations emanating from 2 separate machines will confound SSEP waveform extraction of both devices. Neither diagnostic accuracy nor outcome benefit were among primary goals of this pilot study which was focused primarily on assessing clinical utility.
One significant limitation is that any neuromonitoring is obviously unable to detect nerve injury occurring outside the monitored territory. As the current technique only monitors median, ulnar, and radial nerves, direct axillary nerve injury without involvement of the brachial plexus cannot be detected. However, a previous anatomic study37 has demonstrated that the main anterior circumflex branch of the axillary nerve is fixed to the humeral metaphysis and that excessive lengthening of the arm from the humeral prosthetic implant might result in axillary nerve injury during reverse TSA. Whether detection and mitigation of medial, ulnar, and radial nerve injury during stretching or positioning may also mitigate axillary nerve injury can only be resolved by a randomized trial.
This pilot study found that automated SSEP monitoring is easy to use and can be performed quickly and efficiently without a dedicated technician during TSA. A high incidence of nerve insults was detected during TSA especially during glenoid preparation and humeral implantation. This indicates that the practical challenges of performing intraoperative neuromonitoring during TSA have been largely overcome while confirming the feasibility of its routine use. Further randomized controlled studies are warranted to confirm the outcome benefit of routine automated SSEP monitoring in this setting.
The authors would acknowledge the administrative support of Lawson Research Institute and SafeOp Surgical for provision of SSEP monitor and electrodes.
1. Schairer WW, Nwachukwu BU, Lyman S, et al. National utilization of reverse total shoulder arthroplasty in the United States. J Shoulder Elbow Surg. 2015;24:91–97.
2. Issa K, Pierce CM, Pierce TP, et al. Total shoulder arthroplasty demographics, incidence, and complications-a nationwide inpatient sample database study. Surg Technol Int. 2016;XXIX:240–246.
3. Vincent HK, Struk AM, Reed A, et al. Mid-term shoulder functional and quality of life outcomes after shoulder replacement in obese patients. Springer Plus. 2016;5:1–9.
4. Ho E, Cofield RH, Balm MR, et al. Neurologic complications of surgery for anterior shoulder instability. J Shoulder Elbow Surg. 1999;8:266–270.
5. Lynch NM, Cofield RH, Silbert PL, et al. Neurologic complications after total shoulder arthroplasty. J Shoulder Elbow Surg. 1996;5:53–61.
6. Menorca RM, Fussell TS, Elfar JC. Peripheral nerve trauma: mechanisms of injury and recovery. Hand Clin. 2013;29:317–330.
7. Lenoir H, Dagneaux L, Canovas F, et al. Nerve stress during reverse total shoulder arthroplasty: a cadaveric study. J Shoulder Elbow Surg. 2017;26:323–330.
8. Lädermann A, Denard PJFrankle MA, Marberry S, Pupello D. Influence of arm lengthening in reverse shoulder arthroplasty. Reverse Shoulder Arthroplasty. Cham: Springer; 2016:277–288.
9. Nagda SH, Rogers KJ, Sestokas AK, et al. Neer award 2005: Peripheral nerve function during shoulder arthroplasty using intraoperative nerve monitoring. J Shoulder Elbow Surg. 2007;16:S2–S8.
10. Parisien RL, Yi PH, Hou L, et al. The risk of nerve injury during anatomical and reverse total shoulder arthroplasty: an intraoperative neuromonitoring
study. J Shoulder Elbow Surg. 2016;25:1122–1127.
11. Delaney RA, Freehill MT, Janfaza DR, et al. 2014 Neer award paper: neuromonitoring
the latarjet procedure. J Shoulder Elbow Surg. 2014;23:1473–1480.
12. Warrender WJ, Oppenheimer S, Abboud JA. Nerve monitoring during proximal humeral fracture fixation: what have we learned? Clin Orthop Relat Res. 2011;469:2631–2637.
13. Pitman MI, Nainzadeh N, Ergas E, et al. The use of somatosensory evoked potentials for detection of neuropraxia
during shoulder arthroscopy. Arthroscopy. 1988;4:250–255.
14. Mills WJ, Chapman JR, Robinson LR, et al. Somatosensory evoked potential monitoring during closed humeral nailing: a preliminary report. J Orthop Trauma. 2000;14:167–170.
15. Calder HB, Mast J, Johnstone C. Intraoperative evoked potential monitoring in acetabular surgery. Clin Orthop Relat Res. 1994;305:160–167.
16. Banoub M, Tetzlaff JE, Schubert A. Pharmacologic and physiologic influences affecting sensory evoked potentials: implications for perioperative monitoring. Anesthesiology. 2003;99:716–737.
17. Chui J, Murkin JM, Turkstra T, et al. A novel automated somatosensory evoked potential (SSEP
) monitoring device for detection of intraoperative peripheral nerve injury
in cardiac surgery: a clinical feasibility study. J Cardiothorac Vasc Anesth. 2017;31:1174–1182.
18. Toleikis JR. Intraoperative monitoring using somatosensory evoked potentials. J Clin Monit Comput. 2005;19:241–258.
19. Cruccu G, Aminoff MJ, Curio G, et al. Recommendations for the clinical use of somatosensory-evoked potentials. Clin Neurophysiol. 2008;119:1705–1719.
20. Walton JS, Folk JW, Friedman RJ, et al. Complete brachial plexus palsy after total shoulder arthroplasty done with interscalene block anesthesia. Reg Anesth Pain Med. 2000;25:318–321.
21. Boardman ND, Cofield RH. Neurologic complications of shoulder surgery. Clin Orthop Relat Res. 1999;368:44–53.
22. Peterson DO, Drummond JC, Todd MM. Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans. Anesthesiology. 1986;65:35–40.
23. Pathak KS, Ammadio M, Kalamchi A, et al. Effects of halothane, enflurane, and isoflurane on somatosensory evoked potentials during nitrous oxide anesthesia. Anesthesiology. 1987;66:753–757.
24. Wolfe DE, Drummond JC. Differential effects of isoflurane/nitrous oxide on posterior tibial somatosensory evoked responses of cortical and subcortical origin. Anesth Analg. 1988;67:852–859.
25. Rytky S, Huotari AM, Alahuhta S, et al. Tibial nerve somatosensory evoked potentials during EEG suppression in sevoflurane anaesthesia. Clin Neurophysiol. 1999;110:1655–1658.
26. Bernard JM, Péréon Y, Fayet G, et al. Effects of isoflurane and desflurane on neurogenic motor- and somatosensory-evoked potential monitoring for scoliosis surgery. Anesthesiology. 1996;85:1013–1019.
27. Aleem AW, Wilent WB, Narzikul AC, et al. Incidence of peripheral nerve injury
during shoulder arthroplasty when motor evoked potentials are monitored. J Clin Monit Comput. 2017. [In press].
28. Tamkus A, Rice K. Risk of needle-stick injuries associated with the use of subdermal needle electrodes during intraoperative neurophysiologic monitoring. J Neurosurg Anesthesiol. 2014;26:65–68.
29. Tamkus A, Rice K. The incidence of bite injuries associated with transcranial motor-evoked potential monitoring. Anesth Analg. 2012;115:1–5.
30. Ogata K, Naito M. Blood flow of peripheral nerve effects of dissection, stretching and compression. J Hand Surg Br. 1986;11:10–14.
31. Wall EJ, Massie JB, Kwan MK, et al. Experimental stretch neuropathy
. changes in nerve conduction under tension. J Bone Joint Surg Br. 1992;74:126–129.
32. Larson SJ. Incidence of position related neuropraxia
in 4489 consecutive patients undergoing spine surgery. role of SSEP
monitoring? J Neurosurg. 2016;124:A1146–A1209.
33. Ying T, Wang X, Sun H, et al. Clinical usefulness of somatosensory evoked potentials for detection of peripheral nerve and brachial plexus injury secondary to malpositioning in microvascular decompression. J Clin Neurophysiol. 2015;32:512–515.
34. Jellish WS, Sherazee G, Patel J, et al. Somatosensory evoked potentials help prevent positioning-related brachial plexus injury during skull base surgery. Otolaryngol Head Neck Surg. 2013;149:168–173.
35. Chung I, Glow JA, Dimopoulos V, et al. Upper-limb somatosensory evoked potential monitoring in lumbosacral spine surgery: a prognostic marker for position-related ulnar nerve injury. Spine J. 2009;9:287–295.
36. Gunnarsson T, Krassioukov AV, Sarjeant R, et al. Real-time continuous intraoperative electromyographic and somatosensory evoked potential recordings in spinal surgery: correlation of clinical and electrophysiologic findings in a prospective, consecutive series of 213 cases. Spine. 2004;29:677–684.
37. Lädermann A, Stimec BV, Denard PJ, et al. Injury to the axillary nerve after reverse shoulder arthroplasty: an anatomical study. Orthop Traumatol Surg Res. 2014;100:105–108.