Objective To investigate the influence of infarction location on the executive function and self-efficacy of patients with ischemic stroke. Methods 320 patients with cerebral infarction at basal ganglia, parietal-occipital lobe, frontal lobe and other areas (80 cases respectively)and 80 healthy people were assessed with Wisconsin Card Sorting Test (WCST), Clock Drawing Test (CDT), Self-rating Depression Scale (SDS), Self-Rating Anxiety Scale (SAS) and General Self-efficacy Scale (GSES). Results The scores of WCST, CDT and GSES were significantly worse in the patients than in the controls, especially in those with infarction at frontal lobe and basal ganglia. There was no significant difference in scores of SDS and SAS among all the subjects (P>0.05). Conclusion There are executive function and self-efficacy impairment in ischemic stroke patients, especially for those with the focus at frontal lobe and basal ganglia.

Objective To investigate the characteristics of Behavioral Assessment of Dysexecutive Syndrome (BADS) and Wisconsin Card Sorting Test (WCST) for executive function assessment in patients with cerebral infarction. Methods 706 patients with cerebral infarction were assessed with BADS, WCST and Mini-Mental State Examination (MMSE). Results There was significant difference in the scores of BADS and WCST among the patients with normal cognition, mild cognition impairment and severe cognition impairment (P<0.05). There was no significant difference in the scores of BADS among the patients with different focuses of infarction (P>0.05), but there was in the scores of WCST (P<0.05). Conclusion BADS and WCST can be used to assess the executive impairment in the patients with cerebral infarction, and the focuses may affect the outcome of WCST.

AIM: To investigate the effect of extracellular signal-regulated kinase 1/2 signaling pathway after severe diffuse brain injury (DBI) in rats, and to provide base for treatment. METHODS: Male Sprague-Dawley rats were randomly divided into four groups: control group, traumatic group, low dose of inhibitor U0126 treatment group and high dose of inhibitor U0126 treatment group. DBI rat model was established according to the description of Marmarou's diffused brain injury. At 30 min and 1 h, 6 h, 24 h, 48 h and 72 h after injury, morphological changes were observed under light and electronic microscopes. The ERK1/2 phosphorylation and c-Fos were measured by Western blotting. Apoptosis was measured with TUNEL method. Learning and memory function were performed with Morris water maze from 3 days to 7 days after injury. RESULTS: After trauma, some neurons displayed histopathologic changes of necrosis and apoptosis, axon myelin sheath internalization and disconnection. ERK1/2 phosphorylation protein was apparently increased at 30 min after injury, approached peak at 6 h and continued to 24 h. c-fos protein was markedly increased at 30 min after injury, approached peak at 6 h and returned to bottom at 24 h. The number of apoptotic nerve cells increased at 6 h after and approached peak at 72 h. Latencies of searching safety island prolonged. Rats treated with U0126 had reduction in ERK1/2 activity, c-Fos protein, neuronal apoptosis and searching safety island latencies. CONCLUSION: The activated ERK1/2 signaling pathway plays an important role in processing of nerve cell apoptosis after severe DBI.