Background and Purpose: Amaurosis fugax and central retinal artery occlusion (CRAO) are acute ocular ischemic events that are closely associated with ischemic stroke. To clarify current clinical practices and the challenges in establishing care pathways in Japan, we conducted a nationwide survey of stroke physicians. Methods: A web-based questionnaire was distributed to all members of the Japan Society of Vascular and Interventional Neurology (JSVIN) between August and September 2024. Results: A total of 82 stroke physicians (37%) responded. In case-based scenarios, most respondents reported performing MRI and carotid ultrasonography for both amaurosis fugax and CRAO at presentation. Even in the absence of significant imaging abnormalities, 60% and 54% recommended hospitalization, and 74% and 78% initiated antiplatelet therapy, respectively. These proportions increased when cerebral infarction or ipsilateral carotid stenosis was present. Only 20% indicated they would administer intravenous thrombolysis for CRAO presenting within 4.5 hours, demonstrating wide variability in treatment intentions. Conclusions: Stroke physicians in Japan commonly apply stroke-oriented diagnostic and therapeutic approaches to amaurosis fugax and CRAO. These findings highlight current practice patterns and may serve as a foundation for developing integrated care pathways and strengthening collaboration between stroke physicians and ophthalmologists.

A 72-year-old man was admitted to our hospital due to sudden onset of sensory aphasia. Head CT revealed a subcortical hemorrhage with a surrounding hypodense area in the left temporal lobe. Contrast-enhanced MRI revealed filling defects in the left transverse and sigmoid sinuses, and the cerebral hemorrhage was suspected to be caused by venous infarction due to dural venous sinus thrombosis. DSA on day 7 revealed a dural arteriovenous fistula in the superior sagittal sinus. Twelve months after the initial hemorrhage, a follow-up MRI revealed an abnormal vascular structure in the left temporal lobe. Subsequently, DSA demonstrated newly developed dural arteriovenous fistulas at the left transverse and sigmoid sinuses, as well as a de novo arteriovenous malformation in the left temporal lobe. The arteriovenous malformation was completely obliterated using transarterial and transvenous embolization.

The patient was a 67-year-old man. When he was admitted to our hospital for the treatment of ureteral stones, a decrease in blood oxygen saturation was incidentally observed, and type II respiratory failure was diagnosed. The detailed examinations by respiratory physicians found no causes for his respiratory failure. He was started on home oxygen therapy after discharge. Five months after his first admission, he was readmitted to our hospital with urinary retention and gait disturbance. Brain MRI and cerebral angiography showed a craniocervical junction dural arteriovenous fistula (CCJ dAVF), which was thought to have caused venous return disorder in the medulla oblongata. Because his respiratory condition rapidly deteriorated with dysphagia, we immediately performed direct surgery. Postoperative cerebral angiography showed disappearance of the arteriovenous shunt, and brain MRI showed improvement of edema in the medulla oblongata. Not only his neurological deficits but also his chronic respiratory failure gradually improved, and finally, he no longer needed home oxygen therapy. His respiratory failure may have been the initial symptom of CCJ dAVF, and we report this case with a literature review.

A 42-year-old woman presented with headache and seizures. Magnetic resonance imaging revealed occlusion of the superior sagittal sinus and adjacent cortical veins. She was diagnosed with cerebral venous thrombosis (CVT). In addition to anticoagulation therapy, a mechanical thrombectomy (MT) was performed, which resulted in complete recovery without neurological sequelae. However, several months later, she developed a secondary dural arteriovenous fistula (DAVF). Reports of DAVF secondary to CVT treated with MT are extremely rare. After CVT, regular follow-up imaging is necessary to monitor the development of secondary DAVF.

A 48-year-old woman developed headache and severe visual disturbance upon waking up. On arrival at our hospital, the patient was completely blind and had mild left-lower-limb paralysis. Diffusion-weighted brain magnetic resonance imaging revealed high-signal-intensity lesions in the bilateral occipital lobes, and a FLAIR high ventral pontine lesion was observed. Brain MRA revealed spasms in all cerebral arteries. We suspected reversible cerebral vasoconstriction syndrome and stroke, so the patient was treated with edaravone, lomerizine, and aspirin. Then, we treated the patient for Basedow’s disease. Brain imaging indicated worsening until the fifth day of illness but gradual improvement along with her neurological symptoms. On day 35 of hospitalization, her left-sided paralysis healed, and her vision returned to the manual valve level. Five months after onset, her visual acuity was 0.3, and she was able to perform independently at home. Basedow’s disease may induce spasms in the cerebral arteries.

Vertebral artery stump syndrome (VASS) involves thrombus formation in the blind stump of a proximally occluded vertebral artery (VA) supplied by collateral flow, leading to recurrent distal embolization. We report a case of recurrent basilar artery occlusion (BAO) caused by dissection-induced VASS, successfully managed with repeated thrombectomy and retrograde parent artery occlusion (PAO). A 54-year-old man presented with vertigo following left neck pain. Imaging revealed an acute infarction in the left posterior inferior cerebellar artery (PICA) territory and left VA occlusion. Diagnosis of VA dissection (VAD) was made based on preserved outer diameter on basi-parallel anatomical scanning. On Day 3, he developed altered consciousness, aphasia, and right hemiplegia due to BAO. Mechanical thrombectomy via the right VA achieved recanalization. The left VA was occluded at the V1 segment, with the V3 segment faintly visualized via collaterals. Anticoagulation was withheld due to post-procedural subarachnoid hemorrhage and extensive PICA infarction. On Day 4, BAO recurred. Angiography revealed retrograde filling and stagnation in the left VA stump, confirming VASS. Following a second thrombectomy, retrograde coil PAO of the left V3 stump, including the collateral inflow zone, was performed via the right VA. The patient’s consciousness improved immediately. Retrograde PAO of the arterial stump is an effective and necessary therapeutic option for recurrent BAO caused by VAD-associated VASS, particularly when anticoagulation is contraindicated due to hemorrhagic risks.