33 resultados para Deficit


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In recent years, the deficit of inhibition has become an important reason for explaining addiction. Response inhibition resembles the compulsive drug seeking behavior and it is the basement of addiction inhibition deficits. However, there were no enough evidence for the relationship between addiction and response inhibition deficits and the results of the neuro mechanisms studies remains unclear. Few studies has focused on the exploring the heroin users. Among those paradigms for study response inhibition deficits, stop signal is a very suitable model for the representation of compulsive drug seeking, but only a few researches has worked on this paradigm. In this study, we selected about 100 heroin abusers and had behaviour and neuro imaging scannings for investigating the response inhibition deficits. The behaviour researches found: first, the chronic heroin users had longer reaction time than control group and this reaction time were not affected by stop signals in heroin users. Second, heroin users had less waiting time than control group and they were more impulsive but less flexibility. Their erro monitoring and flexibale adjustment ability decreased. Third, the SSRT of heroin users was significantly longer than control group. These results suggested that the inhibition of heroin users were impaired. Further investigation showed that the SSRT of heroin users had positive correlation of four factor scores of ASI and the macro correlation coefficient was factor three of drug use. This correlation suggested that drug use was the main reason of inhibition deficits. fMRI results mainly focused on the ANOVA analysis for group difference. First, there was no intensity difference in M1 and SMA brain areas between the two groups. Second, heroin users had less activation in right dorsalateral prefrontal cortex, right inferior prefrontal cortex and anterior cingulated cortex, while in bilateral striatum and amygdala, heroin users had more activation than control group. The right prefrontal cortex was indentified as the main inhibition brain area. The anterior cingulated cortex has relationship with erro monitoring and amygdale was an important brain area for impulsivity and emotion control. The network of these brain areas was envovled in impulsivity and inhibition and it was suggested the mainly damaged network for heroin users’ disinhibition. We also investigated the gray matter changes of heroin users and found that chonic heroin use made their gray matter density decreased in prefrontal cortex (including bilateral dorsalateral prefrontal cortex, obital frontal cortex, inferior prefrontal cortex) and anterior cingulated cortex. The gray matter density in these brain regions had negative correlation with drug use duration. In conclusion, we indentified the disinhibition of heroin users and its neuro mechanism. Their compulsivity brain areas had more activation than control group and their inhibition brain areas had less activation than normal control. On the other side, the biological mechanism of this activation changes was the gray matter density decrease in these brain areas.

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Developmental dyslexia (DD) is a common kind of learning disorder, which affects 5-18% of people. It seems important to explore the deficit in visual magnocellular pathway in Chinese developmental dyslexia, for many researches demonstrated that one of the core deficits of Chinese developmental dyslexia was orthographic deficit which was associated with the deficit in visual magnocellular pathway. Two studies were done to detect the differences among Chinese developmental dyslexics, average readers of the same chronological age (CA controls) and average readers of the same reading level (RL controls) in reaction time, accuracy and visual mismatch negativity (vMMN) elicited by the moving gratings responded by visual magnocellular pathway. There were two grating-conditions which were low contrast/low spatial frequency condition and high contrast/high spatial frequency condition respectively. In ERP study, a modified “cross-modal delayed response” paradigm was used to elicit the vMMN. The results showed that the developmental dyslexics responded slower than CA controls, had more errors than RL controls, and had smaller amplitudes of vMMNs than the two controls in visual magnocellular pathway condition, but not in control condition. That is to say, Chinese developmental dyslexics had deficits in visual magnocellular pathway.

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By now, there are still many unsolved questions about associative priming. This study used process dissociation paradigm, perceptual identification task and speeded naming task,together with near infrared spectroscopy, to investigate priming for new associations and its brain mechanisms systematically. The results showed there was interaction between level of processing and unitization in affecting associative priming. When comparing with shallow encoding unrelated word pairs, the activation of both sides of prefrontal lobe was stronger, which suggested prefrontal lobe had relations with memory for new associations. Medial temporal lobe and frontal lobe lesioned patients were tested respectively using methods of perceptual identification task and speeded naming task. Both brain regions participated in associative priming. Medial temporal lobe mediated unitization between unrelated items. Frontal lobe contributed to priming for new associations by elaborative processing, inhibiting irrelevant information, selective attending to tasks, and establishing some effective strategies. In addition, normal subjects needed to aware the relationship between study and test to form associative priming and densely memory deficit patients could not form memory for new associations. In conclusion, the results further demonstrated that perceptual representation system could not support priming for new associations alone. Medial temporal lobe and frontal lobe played roles in priming for new associations, and there was some relation between associative priming and conscious retrieval processing.