ABSTRACT
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.
ABSTRACT
Objective:To explore the effect of functional electrical stimulation on cognition and on the expression of the brain-derived neurotrophic factor (BDNF), synaptophysin (SYN) and microtubule-associated protein 2 (MAP2) using a rat model of vascular dementia.Methods:Ninety pathogen-free male Wistar rats were randomly divided into a sham operation group, a placebo stimulation group and an electrical stimulation group. Both the placebo and electrical stimulation groups underwent bilateral occlusion of the common carotid artery to establish a model of vascular dementia. In the sham operation group the arteries were exposed without occlusion. Each group was then sub-divided into 3, 7 and 14 days subgroups with 10 rats in each subgroup. Beginning seven days after the surgery, the rats in the electrical stimulation group were given 30-minutes of stimulation every day while those in the sham operation group and the placebo stimulation group were given false electrical stimulation. After 3, 7 or 14 days the rats′ cognitive functioning was quantified using the Morris water maze test. The rats were then sacrificed and the expression of BDNF mRNA was measured using in situ hybridization. MAP2 and SYN levels were quantified immunohistochemically.Results:After 14 days the average latency in the placebo stimulation group was significantly longer than in the other groups. On the sixth day the average time in the target zone among the placebo stimulation group was significantly shorter than the other two groups′ averages. After only 3 days of simulation, the average expression of BDNF mRNA in the CA1 area of the hippocampus was significantly lower in the placebo stimulation group than among the others. After 7 days of stimulation the placebo group′s average was significantly lower than that of the sham operation group. The average expression of MAP2 had decreased significantly in the placebo stimulation group compared with the other two groups after 7 and 14 days of simulation. After 7 days the average expression of SYN in the placebo stimulation group was significantly lower than in the sham operation group, and after 14 days it was significantly lower than in the other two groups.Conclusions:Functional electrical stimulation may improve learning and memory in rats modelling vascular dementia through increasing BDNF, SYN and MAP2 expression levels.