An Unusual Cause of Intraoperative Somatosensory-Evoked Potential Signal Loss during Intracranial Aneurysm Clipping

Abstract

Multimodal neuromonitoring plays a pivotal role in the prevention of perioperative stroke during microsurgical occlusion of an aneurysm. Several modalities are available for the same, and by appropriately combining them, depending on the vascular territory of interest, their diagnostic precision can be maximized. Any intraoperative change in evoked potentials during aneurysm clipping should be addressed immediately. A root cause analysis using a checklist can identify and rectify reversible causes, avoiding morbidity. In this report, we present a case of surgical clipping of a right middle cerebral artery aneurysm where the intraoperative somatosensory-evoked potential changes occurred secondary to an ipsilateral extradural hemorrhage. This is the first report describing such a rare phenomenon, and addressing it promptly led to a complete neurological recovery.

Keywords

aneurysm - intraoperative neuromonitoring - somatosensory-evoked potential - extradural hemorrhage

Introduction

Intraoperative neuromonitoring (IONM) is the standard of care to prevent the risk of perioperative stroke following aneurysm clipping. New ischemic insults, which can occur due to various surgical, physiological, and anesthetic factors, can be promptly detected and reversed with the help of IONM. This report describes an unusual cause of IONM signal loss and its management during microvascular aneurysm clipping.

Case Description

A 50-year-old woman patient was scheduled for a craniotomy and clipping of the right middle cerebral artery (MCA) bifurcation aneurysm under general anesthesia, with IONM. Her neurological examination was unremarkable, with a Glasgow coma scale (GCS) score of 15/15, and she exhibited no sensorimotor or cranial nerve deficits. Diagnostic cerebral angiography revealed two aneurysms located at the bifurcations of the right and left MCAs, respectively. Anesthesia was induced and maintained with target-controlled infusion of propofol, 1 µg/kg/h fentanyl, and 0.05 mg/kg/h vecuronium to maintain a bispectral index of 40 to 50. The patient was positioned supine in a Mayfield 3-pin fixator, and bilateral baseline median nerve somatosensory-evoked potential (SSEP) measurements were obtained.

Intraoperatively, the aneurysm dome was embedded within the brain parenchyma, necessitating the placement of a temporary clip on the M1 segment of the right MCA to facilitate the dissection of the aneurysm neck. The initial two temporary clip applications (7 and 8 minutes, with a 5-minute interval) did not produce any signal changes in SSEPs. Upon the third application, there was a reduction in left median SSEP amplitude within 2 minutes of clip application ([Fig. 1]).

Fig. 1 Stack of all the SSEP recordings during the entire procedure in (A) left median stimulation, (B) left tibial stimulation, and (C) right median stimulation (reference); SSEP, somatosensory-evoked potential.

The team was alerted, and an IONM checklist was carried out immediately, which did not show any technical or physiological abnormalities; consequently, the clip was removed. Following the clip removal, the amplitude increased gradually but did not return to the baseline level. Given the stability of the recovered signals, the dissection was continued, and the temporary clip was applied again, which immediately led to a marked reduction in the left median and tibial SSEPs ([Fig. 1]). Hence, the clip was removed, resulting in SSEP recovery with time, albeit with reduced amplitudes compared with baseline.

Considering a possible vasospasm resulting from vessel manipulation, blood pressure was augmented by 20% above baseline, resulting in a partial recovery of the SSEP amplitude. Further elevation of blood pressure was deemed inadvisable due to the potential risk of rupture of an unsecured aneurysm on the contralateral MCA. A permanent clip was applied, which did not induce any new changes in the SSEPs, and the indocyanine green angiography confirmed obliteration of the aneurysm and distal flow in the right MCA. Following hemostasis, the cranium was closed, anesthetic agents were discontinued, and neuromuscular blockade was reversed. Upon neurological evaluation, the patient's GCS was E1VTM5, with dense hemiplegia on the left side necessitating neuroimaging, which revealed a right parieto-occipital extradural hemorrhage (EDH) with a 9-mm midline shift.[Fig. 2] The patient underwent recraniotomy and evacuation of the EDH, after which she returned to her baseline neurological status (E4V5M6 without focal deficits) ([Fig. 2]).

Fig. 2 Hyperacute MRI stroke protocol T2 FLAIR sequence shows a biconvex hyperintense lesion in the right parieto-occipital region with midline shift to the left; FLAIR, fluid-attenuated inversion recovery; MRI, magnetic resonance imaging.

Discussion

For anterior circulation aneurysms, SSEPs, motor-evoked potentials (MEPs), and electroencephalography, either individually or in combination, are employed for intraoperative ischemia detection, whereas MEP and brain stem auditory-evoked responses are utilized in posterior circulation aneurysms.[1] In our case, given the aneurysm's location in the MCA, we monitored median nerve SSEPs.

A 10% increase in latency and/or a 50% decrease in the peak-to-peak amplitude of cortical SSEP is regarded as a warning criterion.[2] [3] Changes in SSEP signals can be multifactorial. Technical factors include alterations in electrode impedance, electrode dislodgement, disconnections, and electrical interference. Physiological parameters such as hypotension, anemia, hypothermia, hypoxia, hypocarbia, acidosis, and dyselectrolytemia significantly impact evoked potentials.[4] All anesthetic agents (inhalational > >intravenous) induce dose-dependent suppression of SSEPs, which is more pronounced with boluses than infusions.[5] During aneurysm surgery, brain retraction, prolonged temporary clipping, inadvertent clipping of the parent vessel or perforators, and vasospasm resulting from vessel handling can cause cortical ischemia and signal change.[6] [7] Therefore, troubleshooting changes in IONM signals should be conducted systematically using a checklist.

The troubleshooting ruled out technical, anesthetic, and physiological causes in this case, indicating a probable surgical insult. Due to the temporal correlation between the signal change and the placement of a temporary clip, we initially hypothesized that the repeated temporary occlusion might have induced ischemia. However, the clip removal did not restore the baseline SSEP amplitude. Also, the brain was relaxed following durotomy, thereby ruling out retractor-induced ischemia. Given the extensive sylvian dissection, vasospasm was considered a potential factor, and blood pressure augmentation (20% from baseline) and papaverine-soaked gel foam application to the MCA trunk were attempted. However, all these efforts did not aid in further recovery of the SSEP by the conclusion of the surgery, thereby excluding vasospasm as a cause.

The partial recovery of SSEP correlated with the new-onset left hemiplegia observed during neurological assessment, suggesting an intraoperative ischemic event. The imaging revealed a substantial right parieto-occipital EDH, which, on evacuation, resulted in complete neurological recovery. We propose that the intraoperative expansion of the EDH likely led to compression of the brain parenchyma and ischemia, thereby causing the persistent depression of SSEP. The source of this EDH could be theoretically attributed to the skull pin of the Mayfield fixation system. But hemodynamic stability was maintained during and after skull pin fixation, and there were no apparent intraoperative signs of EDH, such as a brain bulge. This could be due to the previously resolved subarachnoid hemorrhage, cerebrospinal fluid release from the cisterns, ipsilateral origin of the hematoma, and venous rather than arterial source of EDH, which is consistent with the delayed presentation.

Conclusion

Any intraoperative change in evoked potentials during aneurysm clipping should be addressed immediately. A root cause analysis using the IONM checklist can identify reversible causes of signal loss, which can be promptly rectified to avoid potential morbidity. Sometimes, the signal change can be due to a rare cause such as the one we encountered; hence, any change in IONM should not be overlooked.

Conflict of Interest

None declared.

• References

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Publication History

Article published online:
11 December 2025