Vertebral artery wall inflammation suspected as the cause of cryptogenic ischemic stroke developing during the recovery period of COVID-19.

Coronavirus disease-2019 (COVID-19) can cause acute ischemic stroke (AIS) due to large vessel occlusion (LVO). Some cases of COVID-19-related LVO are known to be resistant to mechanical thrombectomy and have different characteristics from non-COVID-19-related LVO. Inflammation of the occluded arterial wall is suspected as one of the causes of such differences, but the exact mechanism is not fully understood. A 52-year-old man suffered from AIS due to left vertebral artery (VA) occlusion during the recovery period after mild COVID-19. Successful recanalization of the left VA was achieved with antithrombotic therapy, but a late and reversible edematous lesion appeared in part of the brainstem adjacent to the left VA, with abnormal enhancement in both the left VA wall and medulla oblongata on postcontrast magnetic resonance imaging. We suggest that the left VA wall inflammation, induced by COVID-19, caused the ischemic stroke and extended to the brainstem, and an incidental thrombosed unruptured aneurysm of the left VA accelerated these changes. This case provides the first evidence of LVO after COVID-19 in which the pathological conditions in the brainstem adjacent to the affected artery could be observed with neuroimaging and inflammation of the arterial wall was indirectly confirmed. Physicians should be aware that unconventional ischemic stroke may develop in some patients during the recovery period after COVID-19.

Unexpected intraabdominal hemorrhage due to segmental arterial mediolysis following subarachnoid hemorrhage: A case of ruptured intracranial and intraabdominal aneurysms.

BACKGROUND: Segmental arterial mediolysis (SAM) is an uncommon vascular disease, which manifests as catastrophic intraabdominal hemorrhage caused by rupture of visceral dissecting aneurysms in most cases. The etiology of SAM is still unclear, but SAM may be a vasospastic disorder and the responsible pressor agent is norepinephrine. Recently, abdominal SAM coexisting with intracranial dissecting aneurysms has been reported, but the relationship between intraabdominal and intracranial aneurysms in SAM remains unclear, as no cases of concomitant abdominal SAM and ruptured intracranial saccular aneurysm have been reported. CASE DESCRIPTION: A 49-year-old woman underwent emergent clipping for a ruptured saccular aneurysm at the left C1 portion of the internal carotid artery. Intraoperatively, norepinephrine was continuously administered intravenously under general anesthesia. Four days after the subarachnoid hemorrhage (SAH), the patient suddenly developed shock due to massive hematoma in the abdominal cavity. Imaging showed multiple aneurysms involving the splenic artery, gastroduodenal artery, common hepatic artery, and superior mesenteric artery. Coil embolization of the splenic artery was performed immediately to prevent bleeding. Subsequent treatment for cerebral vasospasm following SAH was performed with prevention of hypertension, and the patient recovered with left temporal lobe infarction. The diagnosis was abdominal SAM based on the clinical, imaging, and laboratory findings. CONCLUSION: Norepinephrine release induced by SAH and/or iatrogenic administration of norepinephrine may have promoted abdominal SAM in this case. Abdominal SAM may occur subsequent to rupture of ordinary saccular aneurysm, and may provoke catastrophic abdominal hemorrhage in the spasm stage after SAH.

[Dural arteriovenous fistula manifesting as subarachnoid hemorrhage at the craniocervical junction. A case report].

A 65-year-old man suddenly developed severe headache, vertigo, and sensory disturbance of the right side. On the CT, a high density round mass was identified in the dorsal portion of the pons. The patient's level of consciousness decreased one hour later. A repeat CT showed diffuse subarachnoid hemorrhage and hydrocephalus. Angiography demonstrated a dural arteriovenous fistula (DAVF) at the craniocervical junction. The main feeding artery was the left C2 radicular artery, and the fistula was drained by a leptomeningeal vein that proceeded upward and had a venous ectasia in its distal portion. Transarterial embolization could not be performed because the feeding artery could not be cannulated using a microcatheter. 3D-CT angiography showed a single draining vein at the anterior portion of the left vertebral artery. Four weeks later, ventricular drainage was instituted following surgical disruption of the arteriovenous fistula's draining vein. Postoperative angiography demonstrated complete obliteration. In the present case, surgical clipping of the draining vein was safe and effective; surgical resection of the DAVF or cautery of the surrounding dura was not necessary. Intraoperative digital subtraction angiography (DSA) was as useful as the Doppler technique.