Objective To investigate whether fluoxetine has therapeutic effect of clinical score and brain derived neurotrophic factor (BDNF) expression in serum of experimental autoimmune encephalomyelitis (EAE)model. Methods Rats were randomly divided into solvent control group (n=6) ,model control group ( n= 10)and fluoxetine group ( n= 10). The EAE model was prepared by injecting guinea pig spinal cord homogenate subcutaneously. The clinical score was daily measured according to the sign and symptoms of rats in the behavior examination. The serum BDNF level was measured by EL1SA. Results 1. Except for the solvent control group,the first sign of EAE(Piloerection) was detected on 4th day after immunization of rats from both model control group and fluoxetine group,then EAE rats had distal tail weakness on 8th day, and gradually developed into completely tail paralysis and limb paralysis. EAE rats' clinical score reached the peak on 16th day after immunization. 2. The clinical score of fluoxetine group became scientifically lower than model group since 18th day after immunization ( Fluoxetine group :3.27 ± 0. 33; Model control group :4.66 ± 0. 55, P ＜ 0. 05 ). 3. Compared with the model control group,fluoxetine did not significantly increase the expression of serum BDNF in EAE model ( Fluoxetine group:62.27 ± 0.43; Model control group :61.67 ± 0.85, P ＞ 0.05 ). Conclusion Fluoxetine reduced the clinical score of EAE since 18th day after immunization,which indicates fluoxetine could promote the recovery of neurological function in EAE rats. BDNF may not contribute to protective effect of fluoxetine in EAE animal.

Objective To investigate the correlation between total burden of cerebral small vessel disease (CSVD) and cognitive impairment in patients with acute basal ganglia infarction. Methods Patients with acute basal ganglia infarction for the first time were enrolled, and the general data of the enrolled patients were collected. Patients were assessed by Montreal cognitive assessment (MoCA). Based on MoCA assessment, patients were then divided into cognitive impairment (CI) group and non-cognitive impairment (NCI) group. CSVD total load scores were conducted afterwards in order to analyze the correlation between the total load of different degrees of cerebral small vessel disease and cognitive impairment. Results A total of 178 patients were enrolled in this study: 135 in the CI group and 43 in the NCI group. There were significant differences in age (t=4.11, P=0.04) but not in high-density lipoprotein (t=2.92, P=0.09), and glycosylated hemoglobin C (t=3.02, P=0.08) between the two groups. The infarct volume was larger in the CI group (CI group: 424.72±36.55, NCI group: 227.02±34.62, t=4.022, P=0.046). There were significant differences in a sing1e lentiform nucleus (χ2=19.08, P<0.01), caudal Nucleus(χ2=9.97, P<0.01), infarction at the site of internal capsule(χ2=3.85, P=0.05), the infarct site involved lentiform nucleus, internal capsule and caudate nucleus at(χ2=4.30, P=0.04), and numbers of patients with moderate-to-severe internal carotid artery stenosis (χ2=4.14, P=0.04) as well as numbers of patients with moderate-to-severe intracranial artery stenosis (χ2=4.19, P=0.04). Similarly, there were significant differences in CSVD total burden (t=3.62, P<0.01), deep white matter hyperintensity (t=9.02, P<0.01), and cerebral microbleeds (t=5.54, P=0.02) between CI group and NCI group. The comparisons on MoCA score, visuospatial and execution, attention, language, generalization and abstraction, memory and orientation but not naming were statistically significant between the two groups. The logistic regression equation showed that CSVD total burden (OR=0.316, 95%Cl: 0.185~0.541, P<0.001), age (OR=0.924, 95%Cl: 0.884~0.967, P=0.001) and infarct volume (OR=0.924, 95%Cl: 0.884~0.967, P=0.001), (95%Cl: 1.000~1.003, P=0.047) was significantly associated with cognitive impairment in patients with acute basal ganglia infarction. Conclusion High CSVD total load score, older age and larger infarct volume may be risk factors for cognitive impairment in patients with acute basal ganglia infarction.