Intra-aneurysmal embolization for subarachnoid hemorrhage due to rupture of an aneurysm located at the anterior spinal artery and vertebral artery: illustrative case.

BACKGROUND: A vertebral artery-anterior spinal artery (VA-ASA) aneurysm is very rare. The authors report a case of successful coil embolization of a ruptured aneurysm of the VA-ASA. OBSERVATIONS: A 54-year-old man with World Federation of Neurosurgical Societies grade II subarachnoid hemorrhage presented with an aneurysm located at the region involving the origin of ASA on the VA. Endovascular treatment was chosen to prevent rerupture and preserve the perforating branches. The catheter shape was modified with steam forming to allow access to the aneurysm. Partial embolization was performed to preserve the ASA. The authors also prevented further rupture. On day 16, angiography showed thrombosis within the aneurysm and preserved blood flow in the ASA despite a neck remnant. The patient was discharged home with a modified Rankin Scale score of 0. Careful follow-up has been continued. LESSONS: Endovascular coiling in the acute phase of rupture of a VA-ASA aneurysm achieved favorable results. The aneurysm could be safely treated by selecting the appropriate device and catheter geometry.

Concurrent TERT promoter and BRAF V600E mutation in epithelioid glioblastoma and concomitant low-grade astrocytoma.

Epithelioid glioblastoma (E-GBM) is a rare variant of glioblastoma (GBM), characterized by epithelioid cells with eosinophilic round cytoplasm devoid of stellate cytoplasmic processes. A number of studies have demonstrated that more than half of E-GBMs harbor a valine to glutamic acid substitution at position 600 of the serine/threonine-protein kinase BRAF (BRAF V600E). However, there are no previous reports on E-GBM with telomerase reverse transcriptase (TERT) promoter mutation in addition to BRAF V600E mutation. Here, we report an E-GBM case in an 18-year-old man with BRAF V600E and TERT promoter mutations. The tumor composed of 80% E-GBM and 20% diffuse astrocytoma-like components, and BRAF V600E and TERT promoter mutations were detected in both. E-GBM generally arises as a primary lesion; however, a few previous cases have been demonstrated to accompany low-grade areas. Demonstration of concurrent BRAF V600E and TERT promoter mutations in low- and high-grade lesions strongly suggested their identical origin, and acquisition of each mutation may be an early event, possibly playing a pivotal role in the genesis and subsequent progression to E-GBM.

[Intra-tumoral hemorrhage caused by foramen magnum meningioma: a case report].

Intratumoral bleeding from a meningioma is very rare. We herein report a case of a foramen magnum meningioma which presented in association with intratumoral bleeding. A 49-year-old female who had been suffering from occipital headache and shoulder pain on neck motion was referred to our hospital to undergo treatment for a tumor located in the posterior fossa. Magnetic resonance imaging (MRI) demonstrated a foramen magnum meningioma which originated at the lower clivus and extended to the C2 level of the vertebral column. Marked compression and distortion of the medulla oblongata and spinal cord was also noted. Surgery was therefore planned. The patient thereafter suffered from a sudden onset of headache, vomiting and hoarseness, and was transferred to our hospital. A computed tomography (CT) showed intratumoral bleeding, which extended to the subarachnoid space and the fourth ventricle. The tumor, as well as the massive hematoma, were both immediately removed. The histological diagnosis was meningothelial meningioma. We also reviewed the pertinent literature and propose the possible mechanism for such tumor bleeding in this particular location in which the blockage of the cerebrospinal fluid caused a craniovertebral pressure gradient, which thus resulted in intratumoral bleeding.