scholarly journals Long-term outcome and recurrent episode of cerebral infarction

Nosotchu ◽  
1983 ◽  
Vol 5 (2) ◽  
pp. 124-130
Author(s):  
Jun-ichi Wada ◽  
Kazuo Ueda ◽  
Teruo Omae
Author(s):  
Richard Libman ◽  
Thomas Kwiakowski ◽  
Patrick Lyden ◽  
James C. Grotta ◽  
Barbara C. Tilley ◽  
...  

2016 ◽  
Vol 124 (5) ◽  
pp. 1221-1227 ◽  
Author(s):  
Eun-Hee Kim ◽  
Mi-Sun Yum ◽  
Young-Shin Ra ◽  
Jun Bum Park ◽  
Jae Sung Ahn ◽  
...  

OBJECT Moyamoya disease (MMD) is an idiopathic cerebrovascular occlusive disorder prevalent in East Asia. In the pathogenesis of MMD, the important role of genetic factors is being elucidated, and RNF213 has recently been identified as a susceptibility gene for MMD. The aim of this retrospective study was to investigate the RNF213 genotype in patients with MMD and to determine their genotype-phenotype associations. METHODS The study involved 165 Korean MMD patients from 155 unrelated families who were diagnosed with MMD at a single center from 1995 to 2013. Their demographic, radiological, and clinical findings were evaluated. Direct sequencing of the major RNF213 single nucleotide polymorphisms was performed. The association of the common RNF213 variant with MMD risk was evaluated using historical controls for comparison. Correlations between RNF213 genotype and phenotype were statistically analyzed. RESULTS The c.14429G>A (p.R4810K) variant was identified in 125 (75.8%) of 165 MMD patients. Most patients (112) were heterozygous, and 13 patients had 2 copies of the c.14429G>A variant. A novel heterozygous variant, c.12086A>G (p.Q4029R), was found in 1 additional patient. The minor allele frequency of the c.14429G>A variant was significantly higher in the MMD group (138 [41.8%] of 330 patients) than in the control group (8 [1.36%] of 588 subjects; p < 0.001). The c.14429G>A (p.R4810K) variant significantly increased the risk of MMD in Korean patients, with an OR of 52.11 (p < 0.001) compared with controls. Moreover, c.14429G>A (p.R4810K) genotypes occurred more frequently in patients with a family history of MMD. The homozygous variant was highly associated with early-onset MMD (age at onset < 5 years), cerebral infarction at diagnosis, and cognitive impairment in long-term outcome. CONCLUSIONS The findings indicate that the c.14429G>A (p.R4810K) allele of RNF213 is strongly associated with Korean patients with MMD. The homozygous c.14429G>A (p.R4810K) variant is particularly related to early-onset MMD, severe symptomatic manifestations at diagnosis, and poor prognosis. This genotypic variant may be a useful biomarker for early-onset MMD or unstable MMD with cerebral infarction, which requires early diagnosis and revascularization treatment.


2004 ◽  
Vol 110 (2) ◽  
pp. 107-112 ◽  
Author(s):  
H. Naess ◽  
H. I. Nyland ◽  
L. Thomassen ◽  
J. Aarseth ◽  
K.-M. Myhr

2000 ◽  
Vol 137 (3) ◽  
pp. 351-355 ◽  
Author(s):  
Con Sreenan ◽  
Ravi Bhargava ◽  
Charlene M.T. Robertson

2018 ◽  
Vol 2018 ◽  
pp. 1-11
Author(s):  
Yaohui Ni ◽  
Kefu Cai ◽  
Yujie Hu ◽  
Chuan-hui Wang ◽  
Yuanyuan Zhang ◽  
...  

Delayed administration of kallikrein after cerebral infarction can improve neurological function. However, the appropriate kallkrein treatment time after ischemic stroke has not been illuminated. In this study, we compared the long-term outcome among three kallikrein therapeutic regimens starting at different time points following mouse cerebral ischemia. Furthermore, the protective mechanisms involving neurogenesis, angiogenesis, and AKT-GSK3β-VEGF signaling pathway were analyzed. Human tissue kallikrein was injected through the tail vein daily starting at 8 h, 24 h, or 36 h after right middle cerebral artery occlusion (MCAO) until the 28th day. Three therapeutic regimens all protected against neurological dysfunction, but kallikrein treatment starting at 8 h after MCAO had the best efficacy. Additionally, kallikrein treatment at 8 h after MCAO significantly enhanced cell proliferation including neural stem cell and induced differentiation of neural stem cell into mature neuron. Kallikrein treatment starting at 8 h also promoted more angiogenesis than other two treatment regimens, which was associated with AKT-GSK3β-VEGF signaling pathway. Thus, we confirm that three delayed kallikrein treatments provide protection against cerebral infarction and furthermore suggest that kallikrein treatment starting at 8 h had a better effect than that at 24 h and 36 h. These findings provide the experimental data contributing to better clinical application of exogenous kallikrein.


2001 ◽  
Vol 120 (5) ◽  
pp. A624-A624 ◽  
Author(s):  
J ARTS ◽  
M ZEEGERS ◽  
G DHAENS ◽  
G VANASSCHE ◽  
M HIELE ◽  
...  

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