The incidence of intracranial dural arteriovenous fistulas (DAVFs) has recently increased in Japan because of the widespread use of magnetic resonance imaging screening. Various classifications based on hemodynamics and embryology have been reported. These classifications are effective in predicting the clinical prognosis of DAVFs. Venous congestion due to shunt flow and sinus occlusion remains silent until it results in sudden-onset intracranial hemorrhage or venous infarction. Therefore, appropriate intervention based on the risk evaluation of venous circulation disturbance is necessary. The treatment options for DAVFs include endovascular surgery, open surgery, and stereotactic radiosurgery. The efficacy of endovascular surgery has significantly improved with the introduction of the Onyx embolization system. Although endovascular surgery is often the first-line treatment option, certain locations and hemodynamics may require surgical ablation. Proper selection and collaboration of each treatment modality are essential to improve the safety and effectiveness of DAVF treatment.

  The incidence of spinal arteriovenous shunts (SAVS) is low, and they are the critical causative disorder leading to severe myelopathy. Although spinal angiography is essential for the diagnosis and treatment of SAVS, the procedures of spinal angiography and analysis of spinal angiograms are challenging to master because of their rarity and complexity. Both dural and epidural arteriovenous fistulas with intradural venous reflux are more common in older men and develop into congestive myelopathy ; however, they have different angioarchitectures. Detailed and precise diagnosis using spinal angiography is mandatory for appropriate treatment. Cross-sectional imaging, such as slab maximum intensity projection, is helpful for an accurate diagnosis. There is a consensus on the need to block the intradural reflux of shunt flow when treating both diseases. However, the choice between direct surgery and endovascular treatment remains controversial.

  The pathophysiology of cerebrovascular diseases often involves the intracranial vessel wall. Recent developments in magnetic resonance imaging have enabled the visualization of the submillimeter structures of intracranial vessels. Vessel wall imaging using a sequence of T1 weighted black blood methods has emerged for the evaluation of various vascular pathologies, such as intracranial aneurysms, atherosclerosis, Moyamoya disease, vasculitis, and arteriovenous malformation. In this review, we describe the concept of vessel wall imaging and demonstrate the currently available clinical applications for cerebrovascular diseases, particularly with neurosurgical insights.

  With regard to the diagnosis and treatment of carotid artery stenosis, treatment indications have traditionally been discussed based on the presence of ischemic events and the degree of stenosis. Recently, plaque morphology reportedly plays a more important role compared to the degree of stenosis. Even if the degree of stenosis is the same, the presence of plaque with a large amount of intraplaque hemorrhage (IPH) or lipid-rich necrotic core (LRNC), and high inflammatory activity is considered as “vulnerable plaque” that can cause ischemic events. In contrast, plaque with fibrous components and a small amount of IPH or LRNC is considered as “stable plaque” which indicates a low risk of ischemic events. We believe that carotid plaque imaging is important for the identification of “vulnerable plaque,” which can be useful in clinical practice. In this review, we will summarize the carotid plaque imaging modalities and discuss the related potential clinical implications and future challenges.

  Aggressive pituitary tumors account for ＜2% of all pituitary tumors. We report a case of a pituitary tumor that recurred as an aggressive pituitary tumor long after initial treatment.

  A 72-year-old man underwent transsphenoidal resection and radiotherapy 24 years earlier for an adrenocorticotropic hormone (ACTH) -producing pituitary tumor. The patient presented to the emergency department with sudden headache, and a close examination revealed a lesion in the left temporal lobe. Therefore, a craniotomy was performed to remove the lesion, which was histopathologically diagnosed as a pituitary neuroendocrine tumor (PitNET), corticotroph tumor. Seven months after the surgery, the residual tumor enlarged rapidly and was diagnosed as an aggressive pituitary tumor. Radiotherapy was administered to the residual tumor, and the tumor size continues to reduce after 4 months.

  Although aggressive pituitary tumors and metastatic PitNETs are often treated with multidisciplinary therapies, the efficacy of each therapy has not yet been established. Further accumulation and review of similar cases are required.

  Cystic lesions within the sellar region encompass a spectrum of neoplastic and non-neoplastic entities, each of which require distinct therapeutic approaches and prognostic considerations. However, it is rare for these lesions to extend and cause bone destruction, and differentiating cystic sellar lesions from craniopharyngiomas, which require radical surgery, is crucial. We report a case of a Rathke's cleft cyst with bone destruction that was challenging to distinguish from a craniopharyngioma based on imaging, intraoperative findings, and pathology. A 25-year-old male presented with bitemporal hemianopia and anterior pituitary dysfunction. Magnetic resonance imaging revealed a cystic lesion extending from the sella turcica to the suprasellar region, clivus, and sphenoid sinus. The cyst exhibited high signal intensity on T1- and T2-weighted images, with slight enhancement of the cyst wall, but lacked an enhancing mass. Computed tomography indicated surrounding bone destruction and thinning, with areas suggestive of calcification. Preoperative differential diagnoses based on imaging included craniopharyngioma, mature teratoma, and xanthogranuloma. Endoscopic transsphenoidal surgery was performed, and revealed a motor oil-like fluid with cholesterol crystals within the cyst. Fenestration and biopsy of the cyst wall were conducted. Pathological examination identified fibrous connective tissue with inflammatory cell infiltration, covered by ciliated columnar epithelium, confirming Rathke's cleft cyst. This case underscores the potential for Rathke's cleft cyst and associated inflammatory changes, such as sellar xanthogranuloma, to induce significant bone destruction.