Complex figure copying is a commonly used neuropsychological test. Here we explored the neural basis of the factors underlying complex figure copying (CFC), using data from the Birmingham Cognitive Screen (BCoS) in a large group of sub-acute, ischemic stroke patients (239). We computed two analyses: in the first we assessed the contribution of co-morbid deficits (i.e. in gesture processing, object use, visual neglect, pictures naming and sustained attention) to the lesions associated with CFC. In a second analysis a Principle Component Analysis (PCA) was used to isolate different underlying task components and to link to clinical neuroimaging scans. A voxel-based morphometry (VBM) analysis showed that poor CFC performance was associated with lesions to bi-lateral thalamus, lingual, right fusiform and right inferior parietal cortices (rIPC). The latter association with the posterior parietal cortex was diminished after controlling for neglect. Follow up analysis showed the neglect partially mediated the correlation of CFC and rIPC. The PCA revealed three main underlying components: (1) a component associated with high-level motor control common to different measures of apraxia and linked to the left postcentral gyrus, the right thalamus and middle frontal gyrus; (2) a visuo-motor transformation component unique to the CFC and associated with lesions to the posterior occipital and sensory cortices; (3) a component associated with multistep object use tasks which was correlated with lesions to the left inferior frontal orbital gyrus, the right fusiform and cerebellum. Using clinical symptoms, cognitive profiles and lesion mapping we showed that beyond visual perception, CFC performance is supported by three functional networks: one for high-level motor control, a visuo-motor transformation component, and multistep object use network.
Interventions to improve working memory, e.g. by combining task rehearsal and non-invasive brain stimulation, are gaining popularity. Many factors, however, affect the outcome of these interventions. We hypothesize that working memory capacity at baseline predicts how an individual performs on a working memory task, by setting limits on the benefit derived from tDCS when combined with strategy instructions; specifically, we hypothesize that individuals with low capacity will benefit the most. Eighty-four participants underwent two sessions of an adaptive working memory task (n-back) on two consecutive days. Participants were split into four independent groups (SHAM vs ACTIVE stimulation and STRATEGY vs no STRATEGY instructions). For the purpose of analysis, individuals were divided based on their baseline working memory capacity. Results support our prediction that the combination of tDCS and strategy instructions is particularly beneficial in low capacity individuals. Our findings contribute to a better understanding of factors affecting the outcome of tDCS when used in conjunction with cognitive training to improve working memory. Moreover, our results have implications for training regimens, e.g., by designing interventions predicated on baseline cognitive abilities, or focusing on strategy development for specific attentional skills.
Objective The present study aims to assess the cognitive function of healthy full-term puerperae and compare it with the cognitive function of healthy non-pregnant women in order to analyze possible influencing factors. Methods The study subjects were divided into two groups: the maternal (case) group (n = 80) and the control group (n = 30). A total of 50 healthy single-birth full-term primiparous women and 30 women undergoing a second pregnancy were assigned to the maternal group, while 30 non-pregnant women matched by general data were assigned to the control group. Subject cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) (Beijing version) and the Birmingham Cognitive Screen (BCoS) (Mandarin version); related influencing factors were analyzed. Results In the maternal group, the results showed a MoCA score of 26.52 ± 2.13 points and a cognitive impairment incidence of 26% in primiparous women, along with a MoCA score of 25.83 ± 2.49 points and a cognitive impairment incidence of 36.7% in women undergoing a second pregnancy. All scores were lower in the maternal group than in the control group, which had a MoCA score of 27.47 ± 1.28 points and cognitive impairment incidence of 6.7% (p < 0.05). The differences in MoCA score and cognitive impairment incidence between the primiparous sub-group and the second pregnancy sub-group were not statistically significant (p > 0.05). The visual space and executive function MoCA scale scores were lower in the maternal group than in the control group (p < 0.01). Furthermore, the scores were lower in the maternal group than in the control group in the following BCoS items: instant story recall, total apple deletion number, auditory attention, rule conversion, and gesture imitation (p < 0.05). Conclusion Women in the postpartum period may develop cognitive dysfunction; however, the difference in cognitive impairment incidence between the primiparous sub-group and the second pregnancy sub-group in this study was not statistically significant. The educational level, labor analgesia, and total labor time (min) were found to be influencing factors in the postpartum cognitive function decline (p < 0.05).
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