A 36-year-old man presented with preceding headache, dysarthria, and right upper limb weakness. Magnetic resonance imaging demonstrated cerebral infarction extending from the left basal ganglia to the corona radiata. Digital subtraction angiography (DSA) revealed a string sign at the left middle cerebral artery (MCA) M1 segment, leading to a diagnosis of left MCA dissection. Thrombocytosis on admission, combined with bone marrow biopsy findings and a JAK2 mutation, led to a diagnosis of essential thrombocythemia (ET). Three months later, stenosis appeared at the right MCA M1 segment, raising suspicion for a second cerebral artery dissection, although a definitive diagnosis could not be established. A few cases have been reported of patients with ET presenting with cerebral artery dissection or in situ intracranial thrombosis. ET may contribute to these vascular events through enhanced platelet aggregability and endothelial injury, with JAK2 mutation potentially accelerating this pathophysiology. Although ischemic stroke in ET is most commonly attributed to microthromboembolism, multiple cerebrovascular lesions developing within a short period, as in the present case, can occur. Evidence regarding this entity remains scarce, and further case accumulation and pathophysiological investigation are warranted.

We report a rare case of an 80-year-old woman who developed delayed subarachnoid hemorrhage and rapid formation of a blood blister-like aneurysm (BBA) on the anterior wall of the right internal carotid artery (ICA) following endovascular mechanical thrombectomy for right ICA occlusion. Stent-assisted coil embolization was planned; however, rebleeding occurred the day before the procedure, resulting in death. In this case, endothelial injury caused by aspiration catheter manipulation or stent retriever traction may have contributed to BBA formation. To the best of our knowledge, reports on BBA formation after endovascular mechanical thrombectomy are extremely rare, with only one documented case. This case highlights the need for vigilance in endovascular treatment, emphasizing careful device selection, vessel-protective techniques, detailed assessment of final angiographic images, and early postoperative imaging follow-up to detect potential BBA formation in related vascular regions.

A 44-year-old man presented with fever and left-sided weakness preceded by a 1-month history of watery diarrhea. Brain computed tomography revealed a right parietal subcortical hemorrhage caused by cerebral venous sinus thrombosis, and he was admitted to our department. Truncal computed tomography demonstrated splanchnic venous thrombosis and edematous changes in the ascending colon. Despite antibiotic therapy, fever and watery diarrhea persisted. Subsequent colonoscopy suggested ulcerative colitis. After initiation of 5-aminosalicylic acid therapy, fever and diarrhea improved, and coagulation abnormalities normalized. He was finally diagnosed with cerebral venous sinus thrombosis secondary to ulcerative colitis. Cerebral venous sinus thrombosis preceding the diagnosis of inflammatory bowel disease is rare. In patients with cerebral venous sinus thrombosis with gastrointestinal symptoms, inflammatory bowel disease should be considered in the differential diagnosis, and early diagnostic evaluation is crucial.

A 96-year-old woman experienced cerebral infarctions in the territory of left middle cerebral artery (MCA) and a right cerebellar infarction. No atrial fibrillation was detected before or during the course of the illness. Speckle-tracking echocardiography revealed an apical sparing pattern, and ^99mTc pyrophosphate myocardial scintigraphy showed abnormal myocardial uptake, leading to a diagnosis of transthyretin (amyloid transthyretin: ATTR) cardiac amyloidosis. Cardiac amyloidosis can cause functional atrial standstill even in sinus rhythm, potentially leading to cerebral embolism. Since disease-modifying drugs are now available, it is necessary to properly diagnose this disease.

We report a case of vascular perforation during mechanical thrombectomy for medium vessel occlusion (MeVO). Although hemostasis was achieved by occlusion of the parent vessel, the patient developed delayed subarachnoid hemorrhage due to pseudoaneurysm rupture. The patient was a 79-year-old woman who was transported to our hospital 2 h after her last known normal time, presenting with right hemiplegia, aphasia, and left conjugate deviation. Head MRA revealed cerebral infarction caused by occlusion of the M2 superior trunk of the left middle cerebral artery. Intravenous thrombolysis and mechanical thrombectomy were performed. Vessel perforation occurred during the third lesion crossing, and occlusion of the parent vessel of the M2 superior trunk was performed to achieve hemostasis. Blood flow subsequently resumed, and a delayed pseudoaneurysm was identified at the perforation site. Follow-up imaging revealed early development of subarachnoid hemorrhage secondary to pseudoaneurysm rupture. MeVO carries a high risk of bleeding depending on vascular anatomy, requiring more gentle device selection and procedural techniques. Furthermore, once a pseudoaneurysm develops, the rupture rate is high due to its fragile structure, necessitating careful imaging evaluation and prompt therapeutic intervention.

Radiation-induced cerebrovascular disease is a major late complication in survivors of childhood brain tumors, often presenting decades after treatment. We report a 51-year-old man who received 60 Gy whole-brain irradiation for pineal germinoma at age 8 and subsequently developed progressive large- and small-vessel vasculopathy. More than 20 years after irradiation, he began experiencing recurrent lacunar infarctions, followed by intracerebral hemorrhage and a radiation-related internal carotid artery aneurysm. Neuroimaging demonstrated diffuse intracranial arterial stenosis, aneurysm formation, deep white matter hyperintensities, numerous cerebral microbleeds, and brain atrophy, indicating ongoing vascular injury more than 40 years after treatment.

Previous studies have shown that radiation-induced vasculopathy occurs at high frequency, particularly after high-dose or repeated irradiation, and that the accumulation of cerebral microbleeds is associated with future stroke. This case provides rare insight into the ultra–long-term natural history of radiation-induced vasculopathy and underscores the need for lifelong neurovascular surveillance and risk-factor management in childhood brain tumor survivors, especially those who received high-dose irradiation to suprasellar or optic pathway regions.

A 71-year-old man was admitted to our hospital with quadriplegia. MRI revealed a spinal subarachnoid hemorrhage (sSAH) compressing the cervical spinal cord. We performed an emergency C3 laminectomy, C4-6 open door laminoplasty, and hematoma evacuation. This surgical intervention prevented the progression of paresis. Based on his history of bronchial asthma, allergic rhinitis, peripheral blood eosinophilia, and anti-neutrophil cytoplasmic antibody (ANCA) positivity, eosinophilic granulomatosis with polyangiitis (EGPA) was suspected. The patient was definitively diagnosed with EGPA via skin biopsy and improved after steroid treatment. The evacuated hematoma showed eosinophil-predominant inflammation, indicating that sSAH was associated with EGPA. EGPA is a systemic disease that affects multiple organs and requires early diagnosis and treatment. However, sSAH is a rare complication of this disease. In some cases, sSAH provides the impetus for diagnosis. It is important to consider EGPA when reviewing the past medical history, including asthma and allergic rhinitis, as well as blood test results. Early surgical intervention is effective for sSAH.

A man in his 70s experienced a sudden loss of consciousness and collapsed forward at home. He was transported to a local hospital, where a persistent impairment of consciousness was noted. Neuroimaging revealed an acute infarction in the right lateral medulla and right cerebellar hemisphere, along with basilar artery occlusion. He was subsequently transferred to our institution for endovascular intervention. Non-contrast head CT and three-dimensional CT angiography demonstrated traumatic subarachnoid hemorrhage and a contrast defect at the vertebrobasilar junction. As basilar artery occlusion was suspected, intravenous thrombolysis with rt-PA was not performed, and endovascular treatment was attempted; however, recanalization could not be achieved. Antiplatelet therapy was initiated after admission, but it was later switched to anticoagulation upon the detection of atrial fibrillation. Despite these interventions, the patient developed progressive dysphagia and worsening ataxia. Retrospective review of the initial head CT revealed a clival fracture with entrapment of the basilar artery at the fracture site. Conservative management was continued, but his neurological condition did not improve, and he was transferred to a long-term care facility on hospital day 105, where he subsequently died. Basilar artery entrapment associated with a clival fracture is extremely rare. We present this case and review the relevant literature.

A 58-year-old woman underwent head MRI during the evaluation of dizziness, which revealed a left cerebellar infarction. Cervical MRA including the aortic arch suggested an aberrant right subclavian artery (ARSA). Further evaluation with cerebral angiography was conducted to identify a potential embolic source, and incidentally revealed an anomalous origin of the right vertebral artery arising from the right common carotid artery (VA-CC). The patient was diagnosed with atherothrombotic brain infarction due to left posterior inferior cerebellar artery stenosis and was started on aspirin, with outpatient follow-up planned. The coexistence of ARSA and VA-CC is extremely rare. In this report, we reviewed the epidemiology, embryological background, and anatomical characteristics of these vascular anomalies based on previous reports. Although these anomalies are often detected incidentally, cervical MRA including the aortic arch is useful for identifying them. Recognizing such vascular variations is important for ensuring procedural safety when performing diagnostic cerebral angiography or endovascular treatment.