A 10-year-old Japanese boy entered the emergency room, with complaints of headache and a loss of consciousness in the 2nd week of August, 2022. During this period, the Omicron BA.5 variant of SARS-CoV-2 was the most prevalent strain in Japan. He had no history of hypertension but self-limited infantile epilepsy at age one with normal neuroimaging and electroencephalography results. A computer tomography (CT) image at age one suggested no apparent aneurysmal lesion. Fourteen days before admission, he had fever and vomiting with positive test for SARS-CoV-2. After intravenous hydration, he obtained a prompt recovery on the next day. The child had not been previously vaccinated against COVID-19. On admission, left-sided tonic seizure persisted and was terminated after infusions of diazepam. The Glasgow Coma Scale was E2V3M3. A polymerase chain reaction test on the nasopharyngeal sample was negative for SARS-CoV-2. An urgent head CT revealed hydrocephalus with massive intraventricular hemorrhage and the parenchymal edema. A hyperdense round-shape lesion was identified at the left pontocerebellar cistern, adjacent to the hyperdense material in the basal cistern. These indicated the diagnosis of aneurysmal SAH (WFNS clinical scale: Grade 4). An additional computed tomography angiography (CTA) detected a large saccular aneurysm sized 15 mm of the left posterior cerebral artery (PCA). The 3D-reconstruction image confirmed a large aneurysm in the P2 segment. Intensive care was started after immediate bilateral external ventricular drainage. Pupils began to dilatate from Day 2 of admission. The follow-up CT showed progressive brain edema. Left vertebral-angiography revealed poor perfusion to the arteries distal to basilar artery due to the increased intracranial pressure. Additional interventions with coil occlusion and decompressive craniectomy did not reduce the intracranial pressure to less than 80 mmHg. He died on Day 7th of admission (21 days after the onset of COVID-19). Autopsy had not been performed following caregivers’ refusal to consent. To exclude vasculitis or vasculopathy, we retrospectively analyzed cerebrospinal fluid (CSF) using “FilmArray” meningitis and encephalitis panel (Biofire Diagnostics, Utah, USA). The test was negative for 14 pathogens, including enterovirus and varicella zoster virus []. A genetic diagnostic panel for connective tissue disorders including Ehlers-Danlos syndrome, Marfan syndrome, Loeys-Dietz syndrome reported no pathogenic variants []. We measured concurrent cytokine concentrations in serum and the CSF with a flow-cytometric bead assay (BD Biosciences, San Jose, NJ). The CSF sample was obtained one day after the onset of SAH (15 days post-COVID-19) from ventricular drain 24 h after the procedure without evidence of rebleeding. Interleukin (IL)-6 level was > 750 times higher in the CSF showing 273,680 pg/mL compared to concurrently obtained serum sample measuring 356 pg/mL. CSF levels of IL-1β (CSF: 352 pg/mL; serum: 0 pg/mL) and IL-8 (CSF: 310,360 pg/mL; serum: 2,638 pg/mL) were also predominantly elevated. Tumor necrosis factor-α was undetectable in CSF or serum samples. We reviewed literature on aneurysmal SAH and COVID-19 up to September 2022 (PUBMED search for the keywords: SAH, COVID-19 and aneurysm). We identified a total of 22 cases from 10 articles [–, –]. The clinical information is summarized in Table. All but one adolescent case [] were adult patients. The present patient was the youngest of all reported cases. The severity of COVID-19 was varied, ranging from asymptomatic to respiratory distress with systemic involvement (“Severe”). Only one patient had a previously detected aneurysm []. Twenty of 23 cases (87%) were SARS-CoV-2-positive during the acute stage of SAH. The remaining 3 (13%) including ours suffered from the later-onset SAH (> 2 weeks after infection). Aneurysmal size ranged from 1.4–21 mm (mean: 8.7 mm). The only one patient (Ref9-10) with PCA aneurysm showed a large aneurysmal size (21 mm) [], as observed in our case.