OBJECTIVE: Superficial temporal artery–middle cerebral artery (STA-MCA) bypass is a common approach for treating moyamoya disease (MMD); however, the selection of recipient vessels is still controversial, and its relationship with postoperative cerebral hyperperfusion (CHP) has not been revealed. The aim of the study was to investigate the relationship between the hemodynamic sources of the recipient parasylvian cortical arteries (PSCAs) and the occurrence of postoperative CHP. METHODS: The authors retrospectively analyzed the clinical data from 68 adult patients (75 hemispheres) with MMD who underwent STA-MCA bypass. Based on their hemodynamic sources from the MCA and non-MCAs, the PSCAs were classified as M-PSCAs and non–M-PSCAs, and their distributional characteristics were studied. Moreover, the patients’ demographics, incidence of postoperative CHP, and post- and preoperative relative cerebral blood flow values were examined. RESULTS: The digital subtraction angiography analysis demonstrated that 40% (30/75) of the recipient PSCAs had no hemodynamic relationship with the MCA. The post- and preoperative relative cerebral blood flow values of the M-PSCA group were significantly higher than those of the non–M-PSCA group (p < 0.001). Multivariate analysis revealed that the hemodynamic source of PSCAs from the MCA was significantly associated with the development of focal (p = 0.003) and symptomatic (p = 0.021) CHP. Twelve (85.7%) of the 14 patients with symptomatic CHP and all 4 (100%) patients with postoperative hemorrhage were from the M-PSCA group. CONCLUSIONS: This study revealed that direct anastomoses of PSCAs with anterograde hemodynamic sources from the MCA had a high risk of postoperative CHP during STA-MCA bypass in adult patients with MMD.

Moyamoya disease (MMD) is a chronic steno-occlusive cerebrovascular disease that often leads to hemorrhagic and ischemic strokes; however, its etiology remains elusive. Surgical revascularization by either direct or indirect bypass techniques to restore cerebral hypoperfusion is the treatment of choice to date. This review aims to provide an overview of the current advances in the pathophysiology of MMD, including the genetic, angiogenic, and inflammatory factors related to disease progression. These factors may cause MMD-related vascular stenosis and aberrant angiogenesis in complex manners. With a better understanding of the pathophysiology of MMD, nonsurgical approaches that target the pathogenesis of MMD may be able to halt or slow the progression of this disease.

Background: Although multiple signaling cascades and molecules contributing to the pathophysiological process have been studied, the treatments for stroke against present targets have not acquired significant clinical progress. Although CARD3 (caspase activation and recruitment domain 3) protein is an important factor involved in regulating immunity, inflammation, lipid metabolism, and apoptosis, its role in cerebral stroke is currently unknown. Methods and Results: Using a mouse model of ischemia‐reperfusion (I‐R) injury based on transient blockage of the middle cerebral artery, we have found that CARD3 expression is upregulated in a time‐dependent manner during I‐R injury. Further animal study revealed that, relative to control mice, CARD3‐knockout mice exhibited decreased inflammatory response and neuronal apoptosis, with reduced infarct volume and lower neuropathological scores. In contrast, neuron‐specific CARD3‐overexpressing transgenic (CARD3‐TG) mice exhibited increased I‐R induced injury compared with controls. Mechanistically, we also found that the activation of TAK1 (transforming growth factor‐β–activated kinase 1) was enhanced in CARD3‐TG mice. Furthermore, the increased inflammation and apoptosis seen in injured CARD3‐TG brains were reversed by intravenous administration of the TAK1 inhibitor 5Z‐7‐oxozeaenol. Conclusions: These results indicate that CARD3 promotes I‐R injury via activation of TAK1, which not only reveals a novel regulatory axis of I‐R induced brain injury but also provides a new potential therapeutic approach for I‐R injury.