A 74-year-old woman was admitted to our hospital due to headaches, nausea, and vomiting for three days. The patient possessed no history of hypertension, coronary artery disease, or diabetes. Her laboratory profile, including renal and hepatic function, was normal. The physical examination indicated a positive meningeal irritation sign. A cranial computed tomography (CT) scan of the brain depicted a subarachnoid hemorrhage in the right cerebral hemisphere (Fig.
1a). The patient’s symptoms had entirely resolved post-treatment with nimodipine and mannitol. The patient received a computed tomography angiography (CTA) examination for further assessment. The results showed no evident aneurysm or vascular malformation (Fig.
1b). The patient underwent digital subtraction angiography (DSA) under local anesthesia with a total of 120 ml of ioversol to identify the cause. DSA revealed a 4 mm ∗ 3 mm aneurysm inside the M1 segment of the right middle cerebral artery (MCA) (Fig.
1c). No complications were observed during or after the procedure. After six days, the patient received a therapeutic embolization procedure for a cerebral aneurysm with 120 ml of ioversol under general anesthesia (Fig.
1d). The Xper-CT was performed immediately after the process, showing cortical and subarachnoid enhancement (Fig.
2A). Later, the patient returned safely to the wards post-surgery. Approximately seven hours post-procedure, the patient manifested mild bearable headaches. This is followed by slurred speech, left-hand muscle strength loss (level 0/5), dysphoria, tongue deviation, and a positive left Babinski sign within four hours. An immediate brain CT scan detected edema within the right cerebral hemisphere involving the parietal and temporal lobes without hemorrhage (Fig.
2B). Since DSA did not reveal cerebrovascular stenosis and Xper-CT revealed enhanced cortical and subarachnoid, the patient was suspected of CIE. We used 5 mg of dexamethasone and 250 ml of glycerol fructose to decrease brain edema. Meanwhile, glucose sodium chloride helped eliminate the contrast agent. On the following day post-procedure, there was no improvement in neurologic impairment symptoms, although the CT revealed an improvement in right brain edema (Fig.
2C). On the third day, the patient’s symptoms further deteriorated, with several generalized tonic-clonic seizures. Despite being promptly treated with 10 mg diazepam through intravenous injection and 0.5 g sodium valproate extended-release oral tablets, the symptoms were poorly controlled. Then, the patient was transferred to the intensive care unit for further treatment, where she received a head CT scan the next day (Fig.
2D). Midazolam was continuously infusioned to treat epilepsy. Simultaneously, we initiated intensive dehydration therapy. Human serum albumin, methylprednisolone, and glycerol fructose helped reduce intracranial pressure. Thus, all neurologic deficits and brain edema (Fig.
2E) improved significantly on postoperative Day 6 while she was transferred back into the general ward. The patient was discharged on the 8th day after the second DSA with only a tongue deviation.