Prof. Miki FujimuraJapan
Department of Neurosurgery, Hokkaido University Graduate School of Medicine
| 2021/01 to present | Professor and Chairman, Department of Neurosurgery, Hokkaido University |
| 1996 - 2000 | Dpt. Neurosurgery, Tohoku University Graduate School of Medicine |
| 2014 - 2017 | Associate Professor, Dpt. Neurosurgery, Tohoku University, Sendai, Japan |
| 2021.1 - present | Professor of Neurosurgery, Hokkaido University, Sapporo, Japan |
| 1994.05 - present | Neurosurgery |
Surgery for Cerebral Stroke
Miki Fujimura, M.D., Ph.D. is currently the Professor and Chairman at Department of Neurosurgery, Hokkaido University Graduate School of Medicine, Sapporo. He graduated from Tohoku University School of Medicine, Sendai, in 1994. He has been consistently interested in the management/research of cerebrovascular diseases and benign brain tumors, publishing more than 320 academic peer review articles in these fields. He is particularly focusing on Moyamoya disease, attending many international workshops and symposia organized by WFNS for this topic. He also worked with Professor Pak H. Chan at Stanford University.
Surgical management of Moyamoya disease; Standard surgical procedure and tips for complication avoidance
1110 08:05-08:15
AASNS / AANS Joint Session "Spetzler Symposium"/305
Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease with unknown etiology characterized by progressive stenosis at the internal carotid artery terminus and an abnormal vascular network formation at the base of the brain. Accurate diagnosis of MMD is clinically important because surgical revascularization including superficial temporal artery-middle cerebral artery (STA-MCA) bypass is markedly beneficial for MMD to prevent cerebral ischemia by improving cerebral hemodynamics. Recent evidence by Japan Adult Moyamoya Trial further indicated that STA-MCA bypass could effectively prevent re-bleeding in hemorrhagic MMD patients, especially in those who suffer posterior hemorrhage. Based on these backgrounds, there is a worldwide increase in the number of MMD patients undergoing surgical revascularization. I sought to demonstrate our surgical procedure of combined revascularization (STA-MCA bypass with indirect pial synangiosis) and its technical pitfall. I also highlight the intrinsic peri-operative hemodynamics of MMD after revascularization surgery such as transient focal cerebral hyperperfusion, which should be avoided by intensive perioperative care.
Basic pathology of Moyamoya disease; Impact of RNF213 susceptibility gene
1108 12:30-12:40
Cerebrovascular/304B
Moyamoya disease (MMD) is a chronic occlusive cerebrovascular disease characterized by progressive stenosis at the internal carotid artery terminus and an abnormal vascular network formation at the base of the brain. The etiology of MMD is still unknown, while increasing evidence suggest the impact of the intrinsic genetic variant of RNF213 p.R4810K single nucleotide polymorphism in the clinical presentations of MMD, such as the early onset-age and/or clinical severity. More recently, increasing evidence indicated that MMD patients with RNF213 p.R4810K variant have a higher potential to develop neovascular pial synangiosis derived from encephalo-myo-synangiosis after combined revascularization surgery compared to non-variant patients. Alternatively, MMD patients with RNF213 p.R4810K variant were found to have potentially higher risk for delayed cerebral cerebral hyperperfusion and prolonged vasogenic edema at the vascular territory supplied by bypass after combined revascularization procedure. The exact mechanism underlying such characteristic postoperative pathophysiology in MMD patients with RNF213 variant is undetermined, but recent basic research using genetically engineered animals demonstrated the degradation of capillary pericyte and the blood-brain- barrier dysfunction in RNF213-deficient mice, suggesting that the genetic variant of RNF213 could contribute to the characteristic postoperative hemodynamics and subsequent enhancement of indirect pial synangiosis in MMD patients after revascularization surgery. These findings may give clue to the involvement of RNF213 gene in the basic pathology of MMD, and thereby could facilitate the precision medicine of MMD.