Effect of Western medicine therapy assisted by Ginkgo biloba tablet on vascular cognitive impairment of none dementia
ABSTRACT To discuss the clinical effects of Western medicine therapy assisted by Ginkgo biloba tablet (GBT) on patients with vascular cognitive impairment of none dementia (VCIND).
A total of 80 patients with VCIND were divided into two groups randomly: Conventional treatment group (control group) and combined treatment group. Conventional treatment group was given conventional treatment with anti-platelet aggregation. In this group, 75 mg aspirin was given three times a day for 3 months. While in combined treatment group, 19.2 mg GBT was given three times a day for 3 months together with conventional treatment (anti-platelet aggregation drugs). Montreal cognitive assessment (MoCA) and transcranial Doppler (TCD) were used to observe changes of cognitive ability and cerebral blood flow in VCIND patients before and after treatment in both groups. Then the clinical data were analyzed so as to compare the efficacy in two groups.
After 3 month-treatment in combined treatment group, the scores of executive ability, attention, abstract, delayed memory, orientation in the MoCA were significantly increased compared with those before treatment and those in control group after treatment. Besides, blood flow velocity of anterior cerebral artery increased significantly than that before treatment and that in control group after treatment.
GBT tablet can improve the therapeutic efficacy as well improve cognitive ability and cerebral blood flow supply of patients with VCIND.
- [Show abstract] [Hide abstract]
ABSTRACT: The ginkgo biloba extract EGb761 improves memory loss and cognitive impairments in patients with senile dementia. It also promotes proliferation of neural stem cells in the subventricular zone in Parkinson's disease model mice and in the hippocampal zone of young epileptic rats. However, it remains unclear whether EGb761 enhances proliferation of endogenous neural stem cells in the brain of rats with vascular dementia. In this study, a vascular dementia model was established by repeatedly clipping and reperfusing the bilateral common carotid arteries of rats in combination with an intraperitoneal injection of a sodium nitroprusside solution. Seven days after establishing the model, rats were intragastrically given EGb761 at 50 mg/kg per day. Learning and memory abilities were assessed using the Morris water maze and proliferation of endogenous neural stem cells in the subventricular zone and dentate gyrus were labeled by 5-bromo-2-deoxyuridine immunofluorescence in all rats at 15 days, and 1, 2, and 4 months after model establishment. The escape latencies in Morris water maze tests of rats with vascular dementia after EGb761 treatment were significantly shorter than the model group. Immunofluorescence staining showed that the number and proliferation of 5-bromo-2-deoxyuridine-positive cells in the subventricular zone and dentate gyrus of the EGb761-treated group were significantly higher than in the model group. These experimental findings suggest that EGb761 enhances proliferation of neural stem cells in the subventricular zone and dentate gyrus, and significantly improves learning and memory in rats with vascular dementia.Neural Regeneration Research 06/2013; 8(18):1655-62. DOI:10.3969/j.issn.1673-5374.2013.18.003 · 0.23 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Cognitive impairment is common among patients with stroke or other cerebrovascular disease and influences long-term outcome, including occupational functioning. Recognition and monitoring of mild cognitive impairment is thus essential to good patient care. The Montreal Cognitive Assessment (MoCA) has been suggested as a brief screening test of vascular cognitive impairment. This paper presents a critical review of the research literature evaluating the validity and utility of this test with the aim of informing future clinical and research practice. A total of 30 papers employing the MoCA in the context of cerebrovascular disease were identified. Reporting of the methods and results of such studies tended to fall short of the established reporting guidelines. Under-specification of the exclusion criteria applied and their impact make it difficult to assess the potential impact of sampling bias and loss to follow-up. Nevertheless, content validity evidence suggests that the MoCA covers most of the domains that represent cognitive impairment in cerebrovascular disease, with mixed evidence for its preferential sensitivity to the type of cognitive impairment encountered in the context of vascular disease. Evidence clearly supports the need to establish norms and cut-offs for the MoCA that are culturally appropriate and that are matched to the range of cognitive impairment that is present in the population being assessed. Recent modifications of the MoCA have been developed for assessing patients with visual impairment or restricted mobility, which may reduce the impact of 'untestability' on cognitive screening in the clinic or research context. The MoCA correlates well with other measures of cognitive and functional abilities in patients with cerebrovascular disease, and may also predict future response to rehabilitation and long-term occupational outcome. Further research is needed to provide evidence for the validity of the MoCA in longitudinal studies. However, it compares favourably to the Mini Mental State Examination as a screening test that is sensitive to the milder forms of cognitive impairment that often accompany cerebrovascular disease.Cerebrovascular Diseases 07/2013; 36(1):6-18. DOI:10.1159/000352051 · 3.70 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Post-stroke cognitive impairment occurs frequently in the patients with stroke. The prevalence of post-stroke cognitive impairment ranges from 20% to 80%, which varies for the difference between the countries, the races, and the diagnostic criteria. The risk of post-stroke cognitive impairment is related to both the demographic factors like age, education and occupation and vascular factors. The underlying mechanisms of post-stroke cognitive impairment are not known in detail. However, the neuroanatomical lesions caused by the stroke on strategic areas such as the hippocampus and the white matter lesions (WMLs), the cerebral microbleeds (CMBs) due to the small cerebrovascular diseases and the mixed AD with stroke, alone or in combination, contribute to the pathogenesis of post-stroke cognitive impairment. The treatment of post-stroke cognitive impairment may benefit not only from the anti-dementia drugs, but also the manage measures on cerebrovascular diseases. In this review, we will describe the epidemiological features and the mechanisms of post-stroke cognitive impairment, and discuss the promising management strategies for these patients.