Contrast-induced encephalopathy presenting with refractory status epilepticus following endovascular coiling of an intracranial aneurysm: A case report and literature review

Abstract

Acute symptomatic seizures as the main manifestation of contrast-induced encephalopathy are relatively uncommon. A 50-year-old woman was admitted to our hospital with an unruptured right middle cerebral artery bifurcation aneurysm and underwent elective endovascular stent-assisted coiling. The interventional procedure was uneventful; however, she developed generalized tonic–clonic seizures consistent with status epilepticus on the first postoperative day. A computed tomography scan obtained on postoperative day 1 revealed mild edema in the right cerebral hemisphere, suggestive of contrast-induced encephalopathy. Following prompt antiepileptic therapy and supportive care, the patient achieved complete neurological recovery without residual deficits. By reporting this case and reviewing relevant literature, we summarize the clinical characteristics of contrast-induced encephalopathy presenting primarily with seizures, thereby providing clinical evidence to assist clinicians in the early diagnosis and optimal management of this condition.

Keywords

Contrast-induced encephalopathy seizure intracranial aneurysm cerebral angiography case report

Introduction

Contrast-induced encephalopathy (CIE) is an uncommon complication associated with the administration of iodine-based contrast agents during angiographic procedures.¹ The clinical manifestations of CIE are heterogeneous, ranging from mild neurological deficits, including motor weakness and sensory disturbances, to severe presentations such as seizures, visual disturbances, aphasia, and loss of consciousness.^2,3 Most CIE-related symptoms are transient and resolve spontaneously within 24–48 h; however, in rare cases, symptoms may persist for up to 2 weeks.⁴ Transient cortical blindness is the most common clinical manifestation of CIE,⁵ although severe prolonged neurological deficits have also been reported.⁶

Seizures are a recognized but infrequent manifestation of CIE. According to previous reviews, the incidence of seizures among all CIE cases is 14.2%, with a potentially higher incidence following cerebral angiography than following coronary angiography.⁷ Herein, we present a case of probable CIE characterized by refractory status epilepticus (SE) on the second postoperative day after endovascular coiling of an unruptured intracranial aneurysm. Notably, the initial computed tomography (CT) scans revealed no specific abnormalities, highlighting the need for clinical vigilance in recognizing this complication despite its generally favorable prognosis. This case report, together with a literature review, aims to enhance understanding of the clinical variability and management of CIE presenting with SE.

Case presentation

A 50-year-old woman was admitted to our institution for treatment of an unruptured right middle cerebral artery (MCA) bifurcation aneurysm. Physical examination on admission was unremarkable. She had a medical history of hypertension, which was well controlled with oral amlodipine. No other vascular risk factors, such as smoking, alcohol consumption, diabetes mellitus, dyslipidemia, family history of cardiovascular disease, or obesity, were identified. Computed tomography angiography (CTA) revealed a right MCA aneurysm (Figure 1(a)). The patient underwent uneventful endovascular stent-assisted coiling, with a total procedural duration of 110 min and administration of 120 mL of iodine contrast agent. On the evening after the operation, the patient developed a headache and nausea and vomited twice. Limb muscle strength was normal at that time. Emergency postoperative emergency CT scans (Figure 1(b) and (c)) showed no signs of intracerebral hemorrhage, subarachnoid hemorrhage, or focal hypodensity suggestive of ischemia. After symptomatic treatment with celecoxib, the headache was slightly relieved. As the patient presented with no severe neurological deficits, her symptoms improved after symptomatic treatment, and cranial CT showed no abnormal findings, CIE was not considered a primary diagnosis at that time, although the condition might already have developed.

Figure 1.

(a) Three-dimensional volume rendering of CTA showing a right MCA bifurcation aneurysm. (b–i) Postoperative day 0 CT showing no signs of intracerebral hemorrhage, subarachnoid hemorrhage, or focal hypodensity suggestive of ischemia. CTA: computed tomography angiography; MCA: middle cerebral artery; CT: computed tomography.

On postoperative day 1, the patient presented with left limb weakness of grade II according to the Manual Muscle Test and a high fever, with a peak temperature of 39.3°C. Routine blood tests revealed a mild increase in white blood cell count, while C-reactive protein (CRP) levels were within the normal range. No significant abnormalities were found in electrolyte levels or liver or renal function. The patient’s blood pressure remained stable throughout the postoperative period, with no hypertensive episodes. Repeat CTA confirmed patency of the right MCA (Figure 2(a)) and revealed mild edema in the right cerebral hemisphere (Figure 2(b)). The fever and leukocytosis resolved spontaneously without antibiotic treatment. Based on the clinical presentation, imaging findings, and temporal association with contrast administration, a diagnosis of CIE was considered. Treatment with mannitol (125 mL intravenously every 12 h) was initiated to reduce intracranial pressure, together with butylphthalide (25 mg intravenously twice daily) to improve cerebral microcirculation.

Figure 2.

(a) Postoperative day 1 CTA showing the patency of the right MCA. (b) Postoperative day 1 CT showing mild edema in the right cerebral hemisphere. (c) Postoperative day 1 bedside EEG demonstrating high-amplitude spike-and-wave complexes, confirming status epilepticus. (d) Postoperative day 4 EEG showing no significant abnormal electrical activity. (e) Six-month follow-up EEG demonstrating normal electrical activity. (f, g) Six-month follow-up brain CT scans showing no residual hemorrhage, ischemia, or edema. CTA: computed tomography angiography; MCA: middle cerebral artery; CT: computed tomography; EEG: electroencephalogram.

At 10:30 on postoperative day 1, the patient developed SE. Immediate intravenous administration of diazepam (10 mg) failed to control the seizure activity and was followed by intravenous sodium valproate (800 mg over 30 min). However, the seizures persisted. Due to persistent refractory SE, the patient was transferred to the intensive care unit for sedation with propofol (2 mg/kg intravenously, followed by continuous infusion at 1 mg/kg/h for 12 h). Emergency bedside electroencephalogram (EEG) confirmed ongoing seizure activity (Figure 2(c)).

Following 48 h of sedation and dual antiepileptic therapy (sodium valproate 800 mg intravenously daily and levetiracetam 500 mg intravenously twice daily), the patient’s condition stabilized with no recurrent seizures. Complete discontinuation of sedative agents was associated with full recovery of consciousness and limb muscle strength. Repeat EEG showed no significant abnormal electrical activity (Figure 2(d)). The patient was discharged on oral sodium valproate (500 mg once daily) for 6 months of maintenance therapy. At the 6-month follow-up, the patient remained seizure free. Follow-up EEG (Figure 2(e)) and brain CT showed no residual edema, hemorrhage, or ischemia (Figure 2(f) and (g)).

Discussion

CIE is a rare and reversible neurotoxic complication of iodine-based contrast agent administration, with a favorable prognosis in most cases, as symptoms typically resolve within 24–48 h.⁸ The clinical manifestations of CIE range from mild symptoms, such as headache and vomiting, to severe neurological impairments, with transient cortical blindness being the most common presentation.⁵ According to the more recently published diagnostic criteria for CIE, the diagnosis is confirmed by the onset of neurological symptoms within 24 h of contrast administration, with exclusion of vascular occlusion/ischemia, intracranial hemorrhage, pre-existing seizure disorder, biochemical derangement, intracranial malignancy, and recent head trauma.⁹

A comprehensive literature review was performed to identify cases of CIE with seizure as the primary clinical manifestation. The search was conducted in PubMed, Embase, and Web of Science databases from January 2000 to December 2024, using the keywords “contrast-induced encephalopathy,” “CIE,” “seizure,” “convulsion,” “angiography,” and “endovascular intervention.” Inclusion criteria were as follows: (a) patients diagnosed with CIE; (b) seizure as the main clinical manifestation; and (c) availability of detailed clinical, imaging, and follow-up data. Exclusion criteria were as follows: (a) cases with incomplete clinical data; (b) cases in which seizures were attributed to other etiologies (e.g. ischemia, infection, or metabolic disturbances); and (c) reviews, meta-analyses, or non-English articles. A total of 28 eligible cases were identified (including our case), which were analyzed for clinical characteristics, risk factors, imaging findings, and treatment outcomes (Table 1).^10–29

Table 1.

Reported cases of contrast agent-induced encephalopathy with seizure as the main clinical manifestation.

Table 1a. Demographic characteristics, surgical procedures, risk factors, and contrast agent-related information of patients.
References	Sex	Age	Procedure	Risk factors	Contrast medium	Contrast medium class	Volume (mL)
Spina et al.¹⁰	F	44 years	PCI	End-stage kidney diseaseHTDM	Iohexol	Non-ionic low osmolar	190
	F	69 years	PCI	CKDDMPrevious contrast reaction	Iodixanol	Non-ionic iso-osmolar	320
	F	73 years	PCI	HT	Diatrozoate	Ionic high osmolar	800
	M	49 years	CAG	CKDHT	Diatrizoate	Ionic high osmolar	610
Gonzalez-Pardo et al.¹¹	F	2 months	CC	NR	Iopromide	Non-ionic low-osmolar	15
Zhang et al.¹²	M	Over 50 years	DSA	HTDMHyperlipidemia	NR	NR	NR
Zhao et al.¹³	F	50 years	DSA	NR	Iopromide	Non-ionic low-osmolar	6
Kamimura et al.¹⁴	F	70 years	DSA	NR	Iopamidol	Non-ionic low osmolar	43
Kahyaoglu et al.¹⁵	M	66 years	Lower extremity angiography	NR	Iohexol	Non-ionic low osmolar	250
Nakao et al.¹⁶	F	68 years	SAC	HT	iopamidol	Non-ionic low-osmolar	260
Nakao et al.¹⁶	F	66 years	Coiling	NR	Iomeprol	Non-ionic low-osmolar	80
Liu et al.¹⁷	F	84 years	CAG	HTParoxysmal atrial fibrillationChronic bronchitis	Iopromide	Non-ionic low osmolar	20
Liu et al.¹⁷	F	57 years	PCI	CKDHTDM	Iodixanol	Non-ionic iso-osmolar	130
Willman et al.¹⁸	M	60 years	CAG	HTDMHypercholesterolemia	Iomeron	Non-ionic low-osmolar	220
Zhu et al.¹⁹	M	54 years	CAA	NR	NR	NR	200
Ren et al.²⁰	F	74 years	Coiling	NR	Ioversol	Non-ionic iso-osmolar	240
Zhang et al.²¹	F	62 years	Coiling	HT	Iodixanol	Non-ionic iso-osmolar	400
Table 1a. Demographic characteristics, surgical procedures, risk factors, and contrast agent-related information of patients.
References	Sex	Age	Procedure	Risk factors	Contrast medium	Contrast medium class	Volume (mL)
Park et al.²²	F	58 years	DSA	HT, Hypothyroidism,Peripheral artery occlusive diseaseDepressive disorder	Iodixanol	Non-ionic iso-osmolar	220
Sansone et al.²³	F	6 years	CC	HTAortic isthmic coarctation	Iodate	Non-ionic high-osmolar	500
Donepudi et al.²⁴	F	73 years	AAG	HTHyperlipidemiaCKDMyocardial infarction	Iodixanol	Non-ioniciso-osmolar	248
Leong et al.²⁵	F	59 years	AAG	Renal impairmentHT	Diatrizoate	Ionic high osmolar	150
	F	53 years	Carotid artery angiography	NR	Diatrizoate	Ionic high osmolar	60
	F	70 years	CAG	HT	NR	Ionic	1500
	F	72 years	AAG+CAG+Carotid arteries angiography	Renal impairment	Diatrizoate meglumine;Iothalamate meglumine	Ionic high osmolar	200
Yang et al.²⁶	M	51 years	CAA	HTDM coronary artery disease	Iohexol	Non-ionic iso-osmolar	<50
Lei et al.²⁷	M	76 years	CAG	HTDMTransient ischemic attacks	Iodixanol	Non-ionic iso-osmolar	150
Frye et al.²⁸	M	18 months	CC	NR	Ioversol	low-osmolar nonionic	NR
Pašara et al.²⁹	M	75 years	CAG	Heart transplantCKD	Iodate	Non-ionic low-osmolar	140
Our case	F	50 years	SAC	HT	Iodixanol	Non-ionic iso-osmolar	120
Table 1b. Clinical manifestations, seizure classification, imaging findings, onset time, symptom duration, treatment regimens, and prognosis of patients.
References	Presentation	Classification of seizure type	Neuroimaging	Epileptic seizure	Symptom duration	Control epilepsy	Duration of epilepsy	Complete resolution
Spina et al.¹⁰	Left-sided weakness seizure activity	NR	CT: contrast enhancement of right cerebral hemisphere	4 h after the procedure	72 h	LorazepamLevetiracetamHemodialysis	NR	Yes
	Partial seizureHomonymous hemianopiaHemisensory lossHemiparesis	Focal motor seizure secondary to generalized tonic–clonic seizure	CT: cerebral edema	12 h after the procedure	24 h	Lorazepam	NR	Yes
	Myoclonus, seizure with respiratory arrest, slurred speech, gait instability	NR	CT: contrast enhancement of right frontoparietal lobe EEG diffuse slowing	NR	24 h	NR	NR	Yes
	SeizuresEncephalopathy	NR	CT: contrast enhancement of left frontal gyri	NR	4 h	NR	NR	Yes
Gonzalez-Pardo et al.¹¹	Clonic movements of the left upper limbPersistent sucking movementsSeizure	Focal onset motor seizure (clonic + automatisms)	CT: slight diffuse increase in the density of predominantly frontal, parietal, and occipital cortices in the right cerebral hemisphere	12 h after the procedure	11 days	NR	NR	Yes
Zhang et al.¹²	Slurred speechRight limb weaknessUnconsciousness High fever (39.5°C)	Focal onset seizure with impaired consciousness	CT: swelling of the left frontal, temporal, parietal, and occipital lobe brain tissue and higher density of the left cerebral hemisphere than the right cerebral hemisphere	7 h after the DSA	6 days	Diazepam 10 mgSodium valproate 1.2 g	NR	Yes
Zhao et al.¹³	Fever (38.5°C) Disturbance of consciousnessFrequent blinkingStiffness in the extremities	Focal onset seizure with impaired awareness, motor seizure (tonic–clonic)	CT: no obvious abnormalityMRI: no obvious abnormality	Immediately after angiography	10 days	Intravenous rehydrationMannitol dehydrationOther supportive treatment	NR	Yes
Kamimura et al.¹⁴	Tonic–clonic seizures	Focal onset seizure with impaired awareness progressing to tonic–clonic seizure	CT: high-density signaling in the cortexMRI: high signal intensity in temporal lobe	3 h after angiography	1 days	LevetiracetamMethylprednisolone pulse therapy	NR	Yes
Table 1b. Clinical manifestations, seizure classification, imaging findings, onset time, symptom duration, treatment regimens, and prognosis of patients.
References	Presentation	Classification of seizure type	Neuroimaging	Epileptic seizure	Symptom duration	Control epilepsy	Duration of epilepsy	Complete resolution
Kahyaoglu et al.¹⁵	ConfusionCortical blindness	Focal onset seizure with impaired consciousness	CT: normal	1 h after the procedure	24 h	HydrationSedative medication	NR	Yes
Nakao et al.¹⁶	Decreased vision in both eyesDrowsinessGeneralized convulsions	NR	CT: subarachnoid contrast enhancement in bilateral occipital lobe sulci with loss of gray–white differentiation and sulcal effacement	1 day after the procedure	6 days	Levetiracetam 1 g/dayPhenobarbital 750 mg/dayMethylprednisolone 500 mg/day	NR	Yes
Nakao et al.¹⁶	Right hemiparesis, aphasia, altered sensorium	NR	NR	NR	12 months	NR	NR	Yes
Liu et al.¹⁷	Tonic–clonic seizures	Generalized tonic–clonic seizure	CT: high-density regions in the subarachnoid space	First: 10 min after transfer to the CCUSecond: 18 h post CAG	2 months	First: sodium valproate 60 mg per hourMannitol 125 mL every 6 hNimodipine 10 mg once a daySecond: 10 mg of dexamethasone once per day for 2 days	2–3 min	Yes
Liu et al.¹⁷	Tonic–clonic seizures	Generalized tonic–clonic seizure	CT: right parenchymal edema	Approximately 1 day after the procedure	72 h	Antiepileptic medicationHemodialysis	NR	Yes
Willman et al.¹⁸	AphasiaTonic–clonic seizure	Generalized tonic–clonic seizure	CT: a large area of parenchymal edema, sulcal effacement, and variable subarachnoid hyperdensity in the right hemisphere	On the morning of the day after the procedure	2 months	NR	NR	Yes
Zhu et al.¹⁹	Flexion and spasticity in the right armTonic–clonic seizures	Generalized tonic-clonic seizure	MRI: brain edema and high signal in the meninges	Half an hour later after the procedure	22 days	Continuous intravenous infusion of midazolam for 48 hLevetiracetam	Lasting from 10 s to several minutes	Yes
Table 1b. Clinical manifestations, seizure classification, imaging findings, onset time, symptom duration, treatment regimens, and prognosis of patients.
References	Presentation	Classification of seizure type	Neuroimaging	Epileptic seizure	Symptom duration	Control epilepsy	Duration of epilepsy	Complete resolution
Ren et al.²⁰	Headaches Slurred speechLeft-hand muscle strength loss dysphoriaTongue deviationTonic–clonic seizures	Generalized tonic–clonic seizure	CT: edema within the right cerebral hemisphere involving the parietal and temporal lobes without hemorrhage	3 days after the procedure	6 days	Diazepam 10 mgSodium valproate 0.5 g MidazolamDehydration therapy	NR	Yes
Zhang et al.²¹	UnconsciousnessBlindnessHemiplegiaOphthalmoplegiaFever	Generalized tonic–clonic seizure	CT: widespread edema in the right cerebral hemisphere	On the following day after the procedure	3 days	Methylprednisolone pulse 80 mg/dayDiazepam 10 mg/day	NR	Yes
Park et al.²²	Tonic–clonic seizure	Generalized tonic–clonic seizure	CT: sulcal obliteration of right cerebral hemisphereMRI: gyral swelling and hyperintensity in the right cerebral hemisphere	A few hours after the procedure	6 days	HydrationIntravenous dexamethasone, mannitol, and anticonvulsant	A few seconds	Yes
Sansone et al.²³	Tonic–clonic seizure	Generalized tonic–clonic seizure	CT: cerebral sulci were of increased density	First: 5 min after extubation Second: 2 h later	10 days	DiazepamPhenobarbitalPhenytoinDexamethasone	NR	Yes
Donepudi et al.²⁴	A focal motor seizure in her left leg, arm, and face	Focal motor seizure (clonic) with impaired consciousness	CT: increased hyperdensity and enhancement of right cortex	An hour after ICU admission	7 days	Lorazepam 4 mgPropofolLevetiracetam 1000 mg twice daily	Lasting about 20 min	Yes
Table 1b. Clinical manifestations, seizure classification, imaging findings, onset time, symptom duration, treatment regimens, and prognosis of patients.
References	Presentation	Classification of seizure type	Neuroimaging	Epileptic seizure	Symptom duration	Control epilepsy	Duration of epilepsy	Complete resolution
Leong et al.²⁵	Cortical blindnessHeadacheMyoclonus	Focal seizures	CT: bilateral parieto-occipital contrast enhancement	2 h after the procedure	3 days	Diazepam intramuscular injectionIntravenous injection of phenytoin sodiumDiuresis	NR	Yes
	Partial motor seizure	Partial motor seizure	CT: right temporo-parietal contrast enhancement	Soon after the last injection	24 h	Diphenylhydantoin 250 mgDiazepam 10 mgHydrocortisone Sodium succinate100 mg	5 min	Yes
	Seizure	Focal aware motor seizure	CT: hyperdensity of right frontal	NR	24 h	NR	NR	Yes
	Partial motor seizure	Partial motor seizure	CT: scattered high-density areas in the parietal–frontal lobes of both cerebral hemispheres	Immediately after the injection of the contrast agent	24 h	DiazepamDiphenylhydantoin	2 min	Yes
Yang et al.²⁶	Gaze to the rightImpaired consciousness (GCS 7)Tonic–clonic seizureUnconsciousness	Generalized tonic–clonic seizure	CT: left frontal, temporal, and parietal lobes showed low-density shadows and brain sulci and gyri become shallow	During the procedures	7 days	Diazepam 20 mgMidazolam	NR	death
Lei et al.²⁷	Slight tremor in the upper limbsSeizures	Focal aware motor seizure (clonic)	NR	2 hours after the procedure	6 h	NR	2 seconds	Yes
Frye et al.²⁸	Left arm and leg clonic movementsLethargyIrritabilitySeizure	Focal motor seizure with impaired consciousness (clonic)	CT: right holohemispheric parenchymal and subarachnoid hyperdensity	Approximately 12 h after the procedure	6 days	LorazepamPhenobarbital	Less than 3 min	Yes
Pašara et al.²⁹	Unresponsive, head and gaze deviated to the left, with oroalimentary and gestural automatisms	Focal motor seizure with impaired consciousness (clonic)	CT: no obvious abnormality	2 h after the procedure	24 h	Levetiracetam	NR	Yes
Our case	Stiffness of limbs, loss of consciousnessElevated lactic acid (9.15 mmol/L)Tonic–clonic seizure	Tonic–clonic seizure	CT: right parenchymal edema	2 days after the procedure	24 h	DiazepamSodium valproateMethylprednisolone	20–30 s	Yes

PCI: percutaneous coronary intervention; CAG: coronary angiography; DSA: digital subtraction angiography; SAC: stent-assisted coiling; CC: cardiac catheterization; CAA: carotid artery angioplasty; AAG: aortic arch angiography; HT: hypertension; DM: diabetes mellitus; CT: computed tomography; MRI: magnetic resonance imaging; EEG: electroencephalography; NR: not reported.

Analysis of the 29 reviewed cases revealed a female predominance, with 72.4% of cases occurring in women (9 men and 21 women, including our case). The median age was 59 years, and almost all patients were aged over 50 years. Reported risk factors included chronic hypertension (16 cases, 53.3%), diabetes mellitus (7 cases, 23.3%), and renal insufficiency (6 cases, 20.0%). Hypertension and diabetes are known to induce cerebral microvascular injury, increasing blood–brain barrier (BBB) permeability and predisposing patients to CIE.^30,31 Renal insufficiency prolongs contrast agent excretion, thereby increasing systemic neurotoxicity and the risk of CIE.

No definitive correlation was identified between contrast agent type or dose and the occurrence of CIE. Non-ionic iodine contrast agents are widely used in angiography due to their lower neurotoxicity and reduced vascular endothelial injury. However, our literature review demonstrated that CIE can occur with low-, medium-, or high-osmolar non-ionic iodine contrast agents.^{11,14,17,25,28} Although high contrast doses may increase neurotoxicity risk, CIE has also been reported with normal or even extremely low contrast doses (6 mL),¹² consistent with the present case, which involved a standard clinical dose range.

CIE presenting with seizure exhibits diverse clinical phenotypes, including generalized and focal seizures. Approximately one-third of patients, including our case, present with tonic–clonic seizures. Cerebral CT may demonstrate hemispheric or lobar edema, with ipsilesional contrast enhancement in some cases.^{10–12,16–18,20,24,25} However, CT findings may be unremarkable in a subset of CIE cases,^13,15 as observed in our patient, in whom only mild right hemispheric edema was noted on postoperative day 1 CT, with no significant abnormalities on subsequent scans. Therefore, CIE should still be considered in patients who present with seizures after cerebrovascular interventional therapy, even in the absence of abnormalities on CT or magnetic resonance imaging (MRI).³²

Peri-procedural ischemia was excluded based on postoperative CT findings (no focal hypodensity), CTA results (patent right MCA), and complete resolution of limb weakness without residual deficits. Infection was excluded based on normal CRP levels, absence of meningeal irritation or other infectious signs, and spontaneous resolution of fever and leukocytosis without antibiotic therapy. Hyperperfusion syndrome was excluded based on stable postoperative blood pressure and nonterritorial mild cerebral edema. Posterior reversible encephalopathy syndrome (PRES) was excluded due to the absence of bilateral parieto-occipital edema and no history of renal insufficiency or immunosuppression. Metabolic disturbances were excluded based on normal postoperative electrolyte levels and normal liver and renal function.

The core treatment principles for CIE include the following: (a) prompt control of acute symptoms, especially seizures; (b) enhancement of contrast agent excretion; (c) protection of the BBB; and (d) supportive care to prevent complications. Antiepileptic therapy is critical for seizure control: diazepam is used for acute seizure termination, while sodium valproate and levetiracetam are used for refractory seizures, often in combination for synergistic effects. In cases of refractory SE, propofol sedation may be required to suppress neuronal excitability.

Adjunctive therapies include mannitol (a hyperosmotic agent that reduces intracranial pressure via osmotic diuresis), butylphthalide (which improves cerebral blood flow and microcirculation), and hydration therapy (which accelerates contrast excretion by increasing renal blood flow and urine output). Glucocorticoids are sometimes used empirically to inhibit inflammation and promote BBB repair; however, their efficacy in CIE is not supported by high-level clinical evidence, and no consensus exists regarding optimal dose, duration, or agent type. Corticosteroids were not used in our case, as the patient demonstrated rapid clinical improvement with antiepileptic and supportive therapy, with no evidence of severe BBB disruption.

A recent case report by Pašara et al.²⁹ described a heart transplant patient with cardiac allograft vasculopathy who developed CIE following coronary angiography, presenting with seizures that were responsive to intravenous levetiracetam. This case aligns with our findings regarding delayed seizure onset, efficacy of levetiracetam, and absence of initial imaging abnormalities, highlighting the diagnostic challenges of CIE and the need for clinical vigilance.

This study has several limitations. First, as a single case report, the findings are subject to limited generalizability, and conclusions regarding CIE complicated by SE cannot be extrapolated to the broader population. Second, incomplete information regarding the patient’s pre-existing microvascular status represents a potential confounding factor that cannot be fully excluded. Third, cerebrospinal fluid analysis was not performed, which could have further supported the exclusion of infectious or inflammatory etiologies, although these were reasonably excluded based on clinical and laboratory findings. In addition, no postoperative MRI was performed, limiting the radiological evidence available for a definitive diagnosis. Fourth, “Not Reported (NR)” entries in the literature review introduced data gaps; although cases with NR in key variables were excluded, incomplete reporting may still have affected the comprehensiveness and internal validity of the analysis. Future multicenter, large-sample clinical studies and basic research are warranted to address these limitations and provide more robust evidence for the diagnosis and management of CIE.

Conclusion

Seizures, including refractory SE, are a clinically relevant manifestation of CIE and should be considered in the differential diagnosis of acute central nervous system dysfunction following intra-arterial contrast administration. CIE is a diagnosis of exclusion; in the presence of contrast-associated cerebral edema or enhancement, it should be strongly considered. Although seizures are less common than other manifestations of CIE, clinical vigilance is essential to ensure timely diagnosis and treatment, thereby preventing severe outcomes. This case report contributes to the growing body of literature on CIE, highlighting its clinical variability and the importance of individualized management.

Footnotes

Acknowledgments

The authors wish to express their sincere thanks to the patient and her family for their kind participation in this work.

Author contributions

LJ: Writing and figure organization. ZZ and SW: EEG examination, surgical procedure, and review; MW: Writing, review and editing; GS: Supervision, review and editing.

Data availability statement

The original contributions presented in the study are included in the article. Further inquiries can be directed to the corresponding author.

Declaration of conflicting interests

All authors declare no conflict of interest.

Ethics statement

Written informed consent was obtained from the patient for the publication of any potentially identifiable images or data included in this article.

Funding

This work was supported by grants from the Medical Health Science and Technology Project of Zhejiang Provincial Health Commission (WKJ-ZJ-2340), Zhejiang Province “Vanguard Geese Leading Plan” Project (2025C02151), and Zhejiang Clinovation Pride (CXTD202501002).

Generative AI statement

The authors declare that no generative AI was used in the creation of the manuscript.

ORCID iD

Ming Wang

References

Vinayak

Ahmed

Koshy

, et al. Contrast-induced encephalopathy following transcatheter aortic valve replacement: a case series. J Soc Cardiovasc Angiogr Interv 2024; 3: 101349.

Liang

Liu

, et al. Contrast-induced encephalopathy following cerebral angiography: a case report. Med Int (Lond) 2022; 2: 16.

Takada

Kamata

Yamashita

, et al. False-negative motor-evoked potential due to contrast-induced encephalopathy during coil embolization for intracranial aneurysm: a case report. Cureus 2024; 16: e73487.

Cristaldi

PMF

Polistena

Patassini

, et al. Contrast-induced encephalopathy and permanent neurological deficit: a case report and literature review. Surg Neurol Int 2021; 12: 273.

Yao

Zhu

Yang

, et al. Cardiorespiratory arrest after iso-osmolar iodinated contrast injection: a case report of contrast-induced encephalopathy following contrast-enhanced computed-tomography. Medicine (Baltimore) 2021; 100: e24035.

Mitsui

Wada

Saito

, et al. Clinical characteristics of contrast leakage and contrast-induced encephalopathy following endovascular treatment for unruptured intracranial aneurysm. J Neuroendovasc Ther 2024; 18: 287–292.

Vazquez

Graifman

Spirollari

, et al. Incidence and risk factors for acute transient contrast‐induced neurologic deficit: a systematic review with meta‐analysis. Stroke Vasc Interv Neurol 2022; 2: e000142.

Zhang

Yuan

, et al. Contrast-induced encephalopathy and permanent neurological deficit following cerebral angiography: a case report and review of the literature. Front Cell Neurosci 2022; 16: 1070357.

Mariajoseph

Lai

Praeger

, et al. The Australian diagnostic criteria for contrast-induced encephalopathy. Neuroradiology 2025; 67: 1163–1169.

10.

Spina

Simon

Markus

, et al. Contrast‐induced encephalopathy following cardiac catheterization. Catheter Cardiovasc Interv 2017; 90: 257–268.

11.

Gonzalez-Pardo

Ordoñez

Roa

Contrast-induced encephalopathy in an infant. Radiol Case Rep 2021; 16: 1065–1067.

12.

Zhang

Wang

, et al. Unilateral contrast-induced encephalopathy with contrast medium exudation: a case report. World J Clin Cases 2023; 11: 2260–2266.

13.

Zhao

Huang

Chen

, et al. Rapid contrast-induced encephalopathy after a small dose of contrast agent: illustrative case. J Neurosurg Case Lessons 2021; 1: CASE2052.

14.

Kamimura

Nakamori

Imamura

, et al. Low-dose contrast-induced encephalopathy during diagnostic cerebral angiography. Intern Med 2021; 60: 629–633.

15.

Kahyaoglu

Agca

Cakmak

, et al. Contrast-induced encephalopathy after percutaneous peripheral intervention. Turk Kardiyol Dern Ars 2018; 46: 140–142.

16.

Nakao

Joshi

Hirose

, et al. Rare cases of contrast-induced encephalopathies. Asian J Neurosurg 2020; 15: 786–793.

17.

Liu

Jiang

, et al. Case report and literature review on low-osmolar, non-ionic iodine-based contrast-induced encephalopathy. Clin Interv Aging 2020; 15: 2277–2289.

18.

Willman

Ruuskanen

Hassan

, et al. The varied clinical and radiological manifestations of contrast-induced encephalopathy following coronary angiography. Int J Neurosci 2025; 135: 1006–1009.

19.

Zhu

Shang

Zhao

, et al. Case report: anti-neurexin-3alpha-associated autoimmune encephalitis secondary to contrast-induced encephalopathy. Front Neurol 2023; 14: 1060110.

20.

Ren

Wen

, et al. Contrast-induced encephalopathy after an embolization procedure for a cerebral aneurysm in a female with subarachnoid hemorrhage: a case report. BMC Neurol 2024; 24: 38.

21.

Zhang

Zhou

Wang

, et al. Case report: a 62-year-old woman with contrast-induced encephalopathy caused by embolization of intracranial aneurysm. Front Surg 2021; 8: 689713.

22.

Park

Ahn

Chang

, et al. A case of unusual presentation of contrast-induced encephalopathy after cerebral angiography using iodixanol. J Cerebrovasc Endovasc Neurosurg 2017; 19: 184–188.

23.

Sansone

Piazza

Butera

, et al. Contrast-induced seizures after cardiac catheterization in a 6-year-old child. Pediatr Neurol 2007; 36: 268–270.

24.

Donepudi

Trottier

A seizure and hemiplegia following contrast exposure: understanding contrast-induced encephalopathy. Case Rep Med 2018; 2018: 9278526.

25.

Leong

Fanning

NF.

Persistent neurological deficit from iodinated contrast encephalopathy following intracranial aneurysm coiling. A case report and review of the literature. Interv Neuroradiol 2012; 18: 33–41.

26.

Yang

Yue

, et al. Fatal contrast medium-induced adverse response to iohexol in carotid artery angioplasty: a case report. Medicine (Baltimore) 2019; 98: e16758.

27.

Lei

Shi

, et al. Recurrent epileptic seizures following cardiac catheterization with iodixanol: a case report. BMC Cardiovasc Disord 2020; 20: 79.

28.

Frye

Newburger

Nugent

, et al. Focal seizure and cerebral contrast retention after cardiac catheterization. Pediatr Neurol 2005; 32: 213–216.

29.

Pašara

Momčilović

Kovač

, et al. Contrast medium-induced encephalopathy following coronary angiography and evidence for reversal using intravenous levetiracetam in a heart transplant patient with cardiac allograft vasculopathy: a case report. Int J Clin Pharmacol Ther 2025; 63: 439–443.

30.

Wardlaw

Smith

Dichgans

Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol 2013; 12: 483–497.

31.

Quagliaro

Piconi

Assaloni

, et al. Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: the role of protein kinase C and NAD(P)H-oxidase activation. Diabetes 2003; 52: 2795–2804.

32.

Almasood

Alsenani

Alawlah

, et al. Contrast-induced encephalopathy presenting with fever after coronary angiography: a case report. Cureus 2022; 14: e32271.