Cerebral aneurysm surgery became well-established after the introduction and widespread use of the surgical microscope, endoscopy, and monitoring techniques. However, recent advancements in endovascular techniques have changed the treatment environment. In the past, superiority or inferiority of surgery compared to endovascular treatment was the main issue in determining management strategies for cerebral aneurysms, as shown by the International Subarachnoid Aneurysm Trial or the Barrow Ruptured Aneurysm Trial. Today, however, this competition is transforming into a more collaborative relationship as hybrid surgeons who are familiar with both open surgery and endovascular treatment are increasing in number. It will be crucial to individualize the treatment strategy for each aneurysm patient using modern imaging techniques, computational flow dynamics, and molecular biology.

  Various novel devices to overcome recanalization following endovascular coiling of cerebral aneurysms have been developed. Among the so-called next generation of coils, hydrogel-coated coils were shown to be more effective than bare platinum coils in the GREAT trial. Neck-bridging stents have expanded the indications for aneurysm coiling and have been shown to significantly reduce recanalization. Use of flow diverter devices has almost completely overcome the recanalization phenomenon. The concept of treating an aneurysm by flow diversion through the parent vessel without accessing the aneurysm lumen has totally changed our treatment paradigm. However, antiplatelet therapy remains mandatory to avoid ischemic complications. In the near future, intrasaccular devices that leave no foreign material in the vessel are expected, which would possibly negate the need for antiplatelet therapy.

  The incidence of subarachnoid hemorrhage has been decreasing worldwide except for in Japan. Cerebral aneurysmal rupture is the main cause of subarachnoid hemorrhage. Surgical interventions that reduce or block intraluminal blood flow in these aneurysms have been developed to prevent rupture ; however, regrowth and de novo development of cerebral aneurysms have not been completely controlled because their pathogenesis has not been fully elucidated. Moreover, recent clinical and basic science studies have suggested that macrophage-mediated chronic inflammation plays a crucial role in the development of cerebral aneurysms. Medical interventions that suppress the inflammatory process in aneurysmal walls have been proposed as a potential treatment strategy based on promising results in animal models. Prophylactic intervention that considers the pathogenesis of cerebral aneurysms is expected to be developed.

  The outcome of patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) remains poor. In addition to early aneurysm treatment, immediate control of elevated intracranial pressure associated with early brain injury (EBI), treatment of systemic complications, and management of delayed cerebral ischemia (DCI) are required to improve patient outcome. The main causes of poor outcome are EBI and DCI. Treatment of DCI is challenging ; there is little evidence-based guidance. In addition, DCI unrelated to vasospasm is difficult to monitor in patients with poor-grade SAH. New therapies for EBI and DCI unrelated to vasospasm are needed ; the main target may be microcirculatory disturbances.

  Neuro-Sweet disease (NSD) is a rare multisystem inflammatory disorder which typically involves skin and eye lesions. Diagnosis is usually made via skin biopsy, which can be difficult in cases without skin or eye lesions.

  We experienced two such cases of possible NSD. On magnetic resonance imaging, one case showed gadolinium enhancing lesions in the postcentral gyrus with surrounding edema ; the other case showed gadolinium enhancement of the leptomeninges of the temporal lobe. In both, a malignant brain tumor, such as primary central nervous system lymphoma (PCNSL) or malignant glioma, was suspected and surgery was performed using a microscope and neuronavigation. Intraoperative frozen section histopathology examination showed no malignancy, so fluorescence-guided resections were performed. These specimens showed small lymphocytes and neutrophils but no atypical cells. Monoclonality was not determined by immunohistochemistry and flow cytometry. Human leukocyte antigen (HLA) -B54 was positive. Both cases received a diagnosis of possible NSD.

  The differential diagnosis of PCNSL includes NSD. HLA typing can suggest the diagnosis and should be performed once PCNSL is ruled out. Fluorescence-guided resection was useful in our cases to minimize the extent of resection.