RÉSUMÉ
@#To summarize the clinical and imaging features of ipsilateral limb weakness caused by cerebral infarction，and to explore the possible physiological mechanism of the disease. Methods The clinical data of patients with ipside-limb weakness caused by acute cerebral infarction hospitalized in our department from January 1，2016 to December 30，2016 were collected，and the neurological symptoms and signs，magnetic resonance imaging （MRI） and other examination results of the patients were analyzed descriptively. Results 8 cases of ipsilateral hemiparesis （0.18%） were found in 4495 patients with acute cerebral infarction，all 8 patients were lacunar cerebral infarction，4 cases with previous medical history of cerebral infarction，3 cases have old infarcts in Contralateral cerebral hemisphere，DTI of 1 case showed pyramidal tract was not cross，the lesions of 2 cases were in the brain stem，2 cases in centrum semiovale，3 cases in capsule，One was in the putamen and one in the frontal cortex. Conclusion Most of the patients with ipside hemiparesis caused by cerebral infarction had a history of previous pyramidal tract injury，which was mostly lacunar lesions，mostly located in the configuration area of ipside-pyramidal tract.
RÉSUMÉ
Objective To investigate the relationship between exon 11 CAG triplet nucleotide repeats ([CAG]n) of myocyte enhancer binding factor-2A (MEF2A ) polymorphisms and ischemic stroke caused by large artery atherosclerosis (LAA). Methods Two hundred and five patients with first onset ischemic stroke caused by LAA, admitted to our hospital from June 2010 to December 2014, and 192 healthy controls were chosen in our study. The polymorphisms of exons 11 of MEF2A gene were genotyped by polymerase chain reaction-sequence-based typing (PCR-SBT). The relation of ischemic stroke caused by LAA with polymorphisms of (CAG)n was analyzed. Results Different (CAG)n alleles could be detected, with repeated sequences of 9-11. Frequencies for the different (CAG)n alleles in exon 11 CAG of MEF2A gene were not the same between the ischemic stroke patients and the controls (χ2=8.547, P=0.036). The distribution frequency of the (CAG)9 allele in the ischemic stroke group was significantly higher than that in the control group (χ2=6.650, P=0.010). Logistic regression analysis indicated that systolic pressure and (CAG)9 (OR=1.401, P=0.017, 95％CI: 1.063-1.847) were the independent risk factors of acute ischemic stroke caused by LAA. Conclusion The (CAG)n polymorphisms may be associated with ischemic stroke caused by LAA and the (CAG)9 allele may be one of the genetic susceptibility factors for this subtype of stroke.