Early Detection of Contrast-Induced Encephalopathy Using Somatosensory Evoked Potential Monitoring during Coil Embolization of an Intracranial Aneurysm

Abstract

Objective: Contrast-induced encephalopathy (CIE) is a rare complication of endovascular procedures with an incompletely understood pathophysiology. Its intraoperative detection under general anesthesia can be challenging. We present a case of CIE occurring during aneurysm embolization, demonstrating varying severity across procedures and suggesting that somatosensory evoked potentials (SEPs) may help in early recognition.

Case Presentation: A 63-year-old woman underwent endovascular coil embolization for a ruptured distal anterior cerebral artery aneurysm under general anesthesia, with intraoperative transcranial SEP monitoring. Contrast injection from the cervical internal carotid artery (ICA) during the procedure caused transient SEP attenuation, leading to mild post-procedural paresis and sensory impairment in the patient, both of which resolved within days. Six months later, DSA from the common carotid artery confirmed coil compaction. The patient underwent the examination and showed no signs of developing neurological symptoms. Repeat embolization was performed in the following month. During the 2nd procedure, contrast injection from the C1 segment of the ICA resulted in complete loss of left lower limb SEP. Immediately after the procedure, she exhibited mild left lower limb paresis and sensory impairment. Immediate postoperative cone-beam CT revealed contrast enhancement in the right hemisphere, leading to a diagnosis of CIE. On the following day, she developed left hemispatial neglect, along with worsening left hemiparesis and sensory impairment, despite no apparent abnormalities on MRI. The deficits improved with steroid therapy and were resolved by day 6.

Conclusion: Intraoperative SEP monitoring may be useful for the early detection of CIE during aneurysm embolization.

Introduction

Contrast-induced encephalopathy (CIE) is a rare complication with an incompletely understood pathophysiology. Its diagnosis usually relies on neurological symptoms and imaging findings after procedures or treatments, making intraoperative recognition particularly challenging under general anesthesia. Several risk factors have been proposed, including hypertension, renal dysfunction, a history of stroke, endovascular treatment for aneurysms in the posterior circulation, and prolonged procedure time; however, these vary among studies, complicating preoperative risk assessment.^1–4) We present a case of CIE that occurred during endovascular coil embolization of an intracranial aneurysm, with varying severities observed during 2 therapeutic angiographic procedures. Notably, no symptoms suggestive of CIE were observed following a diagnostic angiographic procedure performed between the 2 treatments. This case suggests that somatosensory evoked potentials (SEPs) may serve as a valuable tool for the early intraoperative detection of CIE.

Case Presentation

A 63-year-old woman who had no notable medical history presented to our hospital with a sudden-onset headache. Non-contrast brain CT revealed a hyperdense area near the interhemispheric fissure, leading to a diagnosis of World Federation of Neurosurgical Societies Grade 1 subarachnoid hemorrhage (SAH) (Fig. 1A). CTA revealed an aneurysm in the distal left anterior cerebral artery (ACA) (Fig. 1B). The left A1 segment was hypoplastic, and the right A1 segment was dominant, resulting in both A2 segments being supplied via the right internal carotid artery (ICA). Considering these findings, endovascular treatment was planned using a right ICA–right A1 route to access the distal left ACA aneurysm. On the same day, endovascular coil embolization was performed under general anesthesia, with intraoperative transcranial SEP monitoring. We routinely monitor SEP intraoperatively using the Endeavor CR system (Natus Medical, Middleton, WI, USA). Electrical stimulation of the median or posterior tibial nerve elicited SEPs (stimulation intensity: 20–50 mA; pulse duration: 0.2 ms), which were recorded from C3′–Fz and C4′–Fz for the upper limbs, and Cz–Fz for the lower limbs. A Flowgate2 (Stryker, Fremont, CA, USA) 8-Fr balloon catheter was inserted through the right radial artery into the right cervical ICA. A total of 43 mL of iohexol (300 mgI/mL) was administered over 7 contrast injections, including 3D rotational angiography (3DRA), without significant changes in SEP. DSA confirmed an aneurysm measuring 5.41 × 8.56 × 4.81 mm in the distal left ACA (Fig. 1C). Using a coaxial system consisting of a Guidepost catheter (Tokai Medical Products, Aichi, Japan), a Phenom 17 microcatheter (Medtronic, Irvine, CA, USA), and a CHIKAI black 14 micro guidewire (ASAHI INTECC, Aichi, Japan), the Phenom 17 microcatheter and the CHIKAI black 14 micro guidewire were advanced to the left A2 segment. After reaching the left A2 segment, contrast injection through the Flowgate2 catheter caused the left lower limb SEP amplitude to decrease to 20% of the baseline value. This SEP decline occurred following the administration of 5 mL of contrast agent, resulting in a total contrast volume of 48 mL at that point. Compared with the pre-advancement state, contrast enhancement in the left ACA was reduced, likely due to the presence of the microcatheter system extending into the left A2 segment, whereas no contrast stagnation or vasospasm was observed in the right ACA (Fig. 1D). As the SEP amplitude rapidly recovered to 50%, the procedure was continued (Fig. 2). Using a simple coiling technique, a total of 63 cm of coils was deployed, achieving a volume embolization ratio of 43% and leaving a residual neck. The procedure was completed in 80 min, using a total of 150 mL of contrast medium (Fig. 1E). At the end of the procedure, SEP amplitude had recovered to 70%, with no changes observed in the SEP of either the upper limbs or the right lower limb (Fig. 2). Cone-beam CT (CBCT) performed immediately after the procedure showed no increase in SAH or focal contrast enhancement (Fig. 1F). Upon awakening from anesthesia, the patient exhibited mild paresis (manual muscle test, 4/5) and sensory impairment in the left lower limb; however, MRI, including diffusion-weighted imaging, FLAIR, and T2^*-weighted imaging, did not reveal any corresponding abnormalities (Fig. 1G–1I). The neurological symptoms resolved within 4 days postoperatively, with no evidence of vasospasm or hydrocephalus, and the patient was discharged on postoperative day 18 with a modified Rankin Scale (mRS) score of 0.

Fig. 1 (A) Non-contrast brain CT shows a faint high-density area in the interhemispheric fissure. (B, C) Brain CTA and DSA show an aneurysm in the distal part of the left ACA. Hypoplasia of the left A1 segment is observed, with the right A1 being dominant. (D) DSA of the right internal carotid artery performed immediately after the decrease in somatosensory evoked potential waveforms shows decreased visualization of the left ACA, likely due to the presence of the microcatheter system extending into the left A2 segment. However, no occlusion, vasospasm, or reduction in contrast flow is observed in the right ACA. (E) The final DSA from the first treatment shows a neck remnant with preservation of the parent artery. (F) Immediate posttreatment cone-beam CT reveals no increase in subarachnoid hematoma or focal contrast enhancement. (G) Diffusion-weighted MRI on posttreatment day 1 does not show any abnormally high signal intensity indicating an acute infarction. (H) FLAIR imaging shows pre-existing high signal intensity in the white matter, without evidence of new hyperintense lesions or localized edema. (I) T2^*-weighted imaging shows a hypointense area in the interhemispheric fissure suggestive of subarachnoid hematoma, with no other apparent abnormalities. ACA, anterior cerebral artery

Fig. 2 After 8 contrast injections from the cervical portion of the right internal carotid artery, using a total of 48 mL of contrast agent, the SEP of the left lower limb decreased to 20% of its previous value (white arrow). The SEP of the left lower limb rapidly improved to 50% and gradually recovered to 70% by the end of the procedure (white arrowheads). No changes were observed in the SEP of either the upper limbs or the right lower limb. Lt., left; Rt., right; SEP, somatosensory evoked potential

At the 6-month follow-up, right common carotid artery (CCA) angiography with 28 mL of contrast medium revealed coil compaction. No neurological abnormalities were observed post-angiography. Seven months after the initial embolization, the patient underwent repeat embolization under general anesthesia with SEP monitoring. A Fubuki XF guide catheter (ASAHI INTECC) was navigated from the right radial artery to the right cervical ICA. During the 3 contrast injections, including 3DRA, 23 mL of contrast medium was administered without any SEP changes. A 6-Fr SOFIA SELECT catheter (Terumo Neuro, Aliso Viejo, CA, USA) was advanced into the right C1 segment, and a Phenom 17 microcatheter was guided into the left ACA. Immediately after contrast injection of 5 mL using the SOFIA SELECT catheter, the left lower limb SEP signal disappeared (Figs. 3A and 4). DSA revealed no vascular occlusion or contrast stagnation (Fig. 3B). To enable contrast injection from the cervical ICA, as in the initial treatment, the catheter was replaced with a Guidepost catheter, after which the procedure was continued. The simple coiling technique was used again, with an additional 20 cm of coil deployed to achieve occlusion of the residual neck. The procedure was completed in 75 min, using a total of 143 mL of contrast agent (Fig. 3C). By the end of the procedure, the SEP of the left lower limb remained absent, whereas the SEP signals of the other limbs remained stable (Fig. 4). Postoperative CBCT revealed contrast enhancement in the right hemisphere (Fig. 3D). Upon awakening, the patient exhibited mild paresis (manual muscle test, 4/5) and sensory impairment in the left lower limb. On postoperative day 1, the neurological deficits progressed to left hemispatial neglect, left hemiparesis (manual muscle test, 3/5), and persistent sensory disturbance. MRI, including diffusion-weighted imaging, FLAIR, and T2^*-weighted imaging, showed no structural abnormalities that could account for the symptoms (Fig. 3E–3G). Given the clinical course, CIE was suspected at this point, and prednisolone (30 mg/day) was initiated. The symptoms began to improve on day 2 and returned to the preoperative state by day 5. After confirming neurological recovery, prednisolone was gradually tapered and discontinued. The patient was discharged without requiring a prolonged hospital stay (mRS 0).

Fig. 3 (A) DSA of the right ICA, performed using the SOFIA SELECT catheter (Terumo Neuro, Aliso Viejo, CA, USA) positioned in the C1 segment (white arrowhead), demonstrates coil compaction and enlargement of the opacified aneurysm neck. The right ICA and both anterior cerebral arteries are clearly visible, with no evidence of spasm or occlusion. (B) DSA of the right ICA, performed following contrast injection from the proximal cervical portion immediately after the disappearance of the somatosensory evoked potential waveform in the left lower limb, demonstrates no vascular occlusion, spasm, or reduction in contrast flow velocity. (C) Final DSA from the 2nd procedure reveals a slight neck remnant while preserving the parent artery. (D) Immediate posttreatment cone-beam CT demonstrates diffuse cortical enhancement in the right hemisphere. (E) Diffusion-weighted MRI on posttreatment day 1 reveals a faint high signal in the right subcortical frontal lobe, with no abnormalities that could explain left hemispatial neglect or left hemiparesis. (F) FLAIR imaging reveals pre-existing high signal intensity in the white matter, without evidence of new hyperintense lesions or localized edema. (G) No obvious abnormalities are observed on T2^*-weighted imaging. ICA, internal carotid artery

Fig. 4 During the 3 contrast injections from the cervical portion of the ICA, with a total contrast volume of 23 mL, no changes in SEP were observed. However, a single contrast injection (5 mL) from the SOFIA SELECT catheter (Terumo Neuro, Aliso Viejo, CA, USA) positioned in the C1 segment of the right ICA resulted in the disappearance of the SEP waveforms exclusively in the left lower limb (white arrow). No subsequent recovery of the SEP was observed in the left lower limb. ICA, internal carotid artery; Lt., left; Rt., right; SEP, somatosensory evoked potential

Discussion

This case suggests 2 key findings: intraoperative SEP monitoring is valuable for the early detection of CIE during aneurysm embolization, and the severity of CIE is affected by the location of contrast injection.

Intraoperative SEP monitoring may be useful for the early detection of CIE during aneurysm embolization. Although intraoperative neurophysiological monitoring is frequently used during aneurysm embolization to identify ischemia in real time,⁵⁾ there are few reports on its use in detecting CIE. A previous case report detailed the successful detection of CIE affecting the medulla and cervical spinal cord during the endovascular treatment of a posterior circulation aneurysm.⁶⁾ To the best of our knowledge, this is the 1st report demonstrating the utility of transcranial SEP monitoring for the early detection of CIE in a ruptured anterior circulation aneurysm. Although the exact mechanism of CIE remains unclear, it has been suggested to be caused by blood–brain barrier (BBB) disruption due to the high osmolarity of contrast agents; this can lead to neurotoxicity when the contrast leaks into the cerebral cortex or subarachnoid space.^7,8) Despite the ruptured aneurysm being located in the distal left ACA and the SAH being more prominent on the left side, SEP changes were localized to the left lower limb in both procedures. Endothelial damage due to an aneurysmal SAH may contribute to BBB dysfunction,⁹⁾ potentially exacerbating susceptibility to CIE. Although preoperative imaging did not reveal any definitive brain parenchymal damage related to the SAH, it is possible that the aneurysmal rupture affected not only the left but also the right medial part of the cerebral hemisphere, potentially leading to a disruption of the BBB. In addition to this mechanism, the right ACA territory may have had some underlying vulnerability to contrast-induced injury, possibly due to unidentified local or systemic factors. However, since motor evoked potential monitoring was not performed, intraoperative detection of motor deficits potentially related to the frontal lobe adjacent to the ruptured aneurysm was not possible, which represents a limitation of this study.

The position of the catheter during contrast injection may have influenced the severity of CIE. Fuga et al. reported that contrast injection from an intradural artery and repeat embolization are risk factors for CIE.¹⁰⁾ Contrast injection using a distally placed distal access catheter (DAC) can cause increased pressure and volume on the distal arteries, leading to BBB breakdown and contrast leakage, and subsequently triggering CIE. In our case, contrast injection from a distally placed DAC in the ICA immediately led to a decline in left lower limb SEPs, which did not improve. Postoperatively, the patient developed severe neurological symptoms on the following day. After the initial treatment, transient mild paresis and sensory impairment in the left lower limb were observed; however, intraoperative cerebral angiography revealed no evidence of wedging, vasospasm, or arterial occlusion. As the patient had SAH, evaluation of cortical enhancement using CBCT immediately after the procedure was inconclusive. Postoperative imaging also showed no obvious abnormalities that could account for the symptoms, and the etiology remained unidentified at that time. Subsequently, CIE was observed during retreatment, suggesting that the initial symptoms may also have been attributable to CIE. Contrast injection from the cervical ICA also induced CIE, but it was milder, as evidenced by partial intraoperative SEP recovery. Despite multiple ICA angiography injections during the 1st procedure, SEP recovery was observed, possibly because of reduced contrast inflow into the right ACA via the A1 segment. These findings suggest that contrast injection from a distally positioned DAC may have contributed not only to the onset but also to the severity of CIE, possibly due to the administration of highly concentrated contrast medium with limited dilution by circulating blood. This may also be associated with the abrupt decrease in SEP amplitude observed during the procedure.

Recent studies have reported that a prolonged procedure⁴⁾ and higher contrast volume³⁾ are associated with CIE in unruptured aneurysm embolization. However, in our case, the procedure duration was 80 min for the initial treatment and 75 min for the retreatment, and the total volumes of contrast medium used were 150 and 143 mL, respectively, which are not considered excessive. Notably, the onset of SEP decline occurred after the administration of a relatively small volume of contrast agent—48 mL from the cervical ICA during the initial treatment, and 23 mL from the cervical ICA followed by 5 mL from the C1 segment during the retreatment—suggesting that even a small amount of contrast agent could induce CIE in areas where the BBB is compromised. The relationship between previous CIE episodes and the safety of subsequent contrast-enhanced imaging remains unclear. However, in this case, CTA performed prior to the 1st treatment and CCA angiography conducted between the 2 therapeutic procedures did not induce CIE, further supporting the notion that the site of contrast injection plays a crucial role in CIE onset.

Intraoperative SEP monitoring may be useful for the early detection of CIE during aneurysm embolization. Furthermore, the position of the catheter during contrast injection may have influenced the severity of CIE. Although most cases of CIE are transient and resolve without permanent neurological sequelae, rare cases of persistent deficits or mortality have been documented.^11,12) Therefore, when an intraoperative decline in SEP occurs without signs of ischemia, CIE should be considered, and modifications to contrast injection techniques or the decision to proceed with the procedure should be carefully evaluated.

Conclusion

Intraoperative SEP monitoring may contribute to the early detection of CIE during aneurysm embolization. Additionally, the position of the catheter during contrast injection may have played a role in the observed severity of CIE.

Acknowledgments

We would like to thank Editage (www.editage.com) for English language editing.

Informed Consent

We obtained informed consent from the patient and her family to publish this clinical report.

Disclosure Statement

The authors declare that they have no conflicts of interest.

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