Objective To evaluate the teaching effects of applying clinical pathway in clinical practice teaching of neurology. Methods The undergraduate interns majoring in clinical medicine were randomly divided into clinical pathway teaching method group (n=34) and traditional teaching method group (n=34). Both groups were taught by senior physicians with the same teaching content and teaching material. A control study between the two groups in theoretical knowledge, operational skills and satisfaction degrees of teaching was carried out. Results The results of clinical pathway teaching method group in theoretical knowledge[(55.2±3.70) vs. (51.8±4.6)] and operational skills [(36.3±3.2) vs. (31.3±2.19)] were both sig-nificantly better than those of traditional teaching method group (P<0.05). The satisfaction degree of teach-ing of clinical pathway teaching method group is relatively higher . Conclusions The clinical pathway teaching method enhances the scientific property and systematic property of teaching contents, obtaining a favorable teaching effect.

Objective To evaluate the effect of vertebral artery kinking on cerebral hemodynamics. Methods The patients with vertebral artery kinking on digital subtraction angiograph (DSA) were selected from 223 patients with vertebral-basilar artery transient ischemic attack, then the changes of vertebral artery hemodynamics were evaluated using transcranial color Doppler (TCD). Results There were 84 patients with vertebral artery kinking among 223 patients with vertebral-basilar artery transient ischemic attack. Patients with vertebral artery kinking were older and had more vascular risk factors than patients without vertebral artery kinking. Compared with the control group, patients showed decreased blood flow rate such as peak velocity (Vp) and mean velocity (Vm), increased pulsatility index (PI) and resistant index (RI) in vertebral artery kinking group. Conclusions Vertebral artery kinking is common abnormal artery among patients with vertebral-basilar artery transient ischemic attack, it leads to hemodynamic changes. Age and vascular risk factors are potential causes of vertebral artery kinking.

Objective To observe the effects of sleep deprivation(SD)on learning and memory and phos-phorylated cyclic AMP responsive element binding protein(pCREB) expression in hippocampus of mice,and to explore the mechanism of cognitive change after SD. Methods Twenty female C57BL/6J mice were randomly divided into sleep deprivation group(SD, n = 10) and normal cage control group (CC,n = 10). Touch method was used to establish the sleep deprivation model. 30 days after SD,all the animals were subjected for Morris Water Maze (MWM) to test mean escape latency and percentage of time spent in the target quadrant. pCREB level in hippocampus was tested with Western blot. Results The mean escape latency in SD group in the second and third day of MWM was (29.31 ±4.93) s and (25.33 ±5.06)s, respectively, and was longer than that in CC group ((26.05 ±5.96)s and (19.35 ±7. 85)s,respectively). Mice in SD group spent less time in the target quadrant than that in CC group((23.61 ±9.86)% and (37.46 ±7. 51)%,.respectively, P<0.05). Results of Western blot for pCREB revealed that the pCREB level in hippocampus in sleep deprivation group was significantly lower than that in control group(0.71 ±0.03 and 0.82 ±0.06, respectively, P<0.01) . Conclusion The impairment of spatial learning and memory ability in sleep deprivation animals may be associated with the reduction of pCREB in hippocampus.

BACKGROUND: Activation of leucocyte and endothelial cell in ischemic area of brain and the expression of adhesive molecule on the surface can cause aggregation and infiltration of leucocyte which deteriorated cerebral injury due to cytotoxicity. Ligustrazine can inhibit thrombosis and improve microcirculation.OBJECTIVE: To observe the effect of ligustrazine on adhesion of leucocyte and endothelial cell in focal area after cerebral ischemia-reperfusion injury.DESIGN: Randomized controlled animal study.SETTING: Second Division of Brain, Department of Neurology, Daping Hospital of the Third Military Medical University of Chinese PLA; Department of Psychiatry, the Second People's Hospital of Yuxi, Yunnan Province.MATERIALS: The experiment was carried out at the Second Cerebral Laboratory of Neurological Department of Daping Hospital Affiliated to the Third Military Medical University of Chinese PLA. A total of 32 male Wistar rats weighing 250-300 g were randomly divided into normal control group (n=8), cerebral ischemia-reperfusion group (n=12) and cerebral ischemia-reperfusion + ligustrazine group (n=12).METHODS: Rats in ligustrazine group were venously injected with 15 g/kg ligustrazine phosphoric acid, and rats in normal control group and cerebral ischemia-reperfusion group were venously injected with the same volume of saline. Cerebral ischemia-reperfusion injury and adhesive changes of leucocyte in focal area after administration of ligustrazine were observed with immunofluorescent labeling technique and micro-ultra-speed imaging system.MAIN OUTCOME MEASURES: ① Adhesive density index of leucocyte of arteriole in focal area after cerebral ischemia-reperfusion injury; ② Adhesive changes of leucocyte in focal area after administration of ligustrazine.RESULTS: All experimental animals were involved in the finalanalysis.① As compared with those in control group, adhesive density index of leucocyte of arteriole in focal area in cerebral ischemia-reperfusion group was increased, broken stress between leucocyte and endothelial cell was decreased remarkably, adhesion was increased obviously, and there was significant difference (P ＜ 0.01). ② As compared with those in cerebral ischemia-reperfusion group, adhesive density index and adhesion of leucocyte in ligustrazine group were decreased and reached the lowest values after 24 hours. Broken stress was increased and maintained at a higher level. There was no significant difference from that in normal control group till 24 hours.CONCLUSION: Ligustrazine can relieve adhesion between endothelial cell and leucocyte after cerebral ischemia-reperfusion injury.

Objective To investigate the efficacy of intra-arterial thrombolysis with stenting for acute cerebral infarction. Methods Using a prospective case-control design, 24 patients with acute cerebral infarction who remained angiostegnosis ( ＞ 50%) after intra-arterial thrombolysis were randomly divided into stent treatment group and drug treatment group. They were treated with stenting + drug treatment and conventional drug treatment. The rates of vascular complete revascularization and residual stenosis, and the modified Rankin scale scores at 3 months in both groups were evaluated. Results The rate of complete revascularization in the stent treatment group was significantly higher than that in the drug treatment group (54. 5% vs.0%,χ2 =6.382, P ＜0. 001), and the rate of residual stenosis was significantly lower than that in the drug treatment group ([4.5 ±5.2]% vs. [82. 5 ±10. 5]%, t =7.464, P＜0.001). The rate of favorable clinical outcome in the stent treatment group was significantly higher than that in the drug treatment group (100% vs. 76. 9%,χ2 = 14. 263, P = 0.038). Conclusion The efficacy of intra-arterial thrombolysis with stenting in the treatment of acute cerebral infarction is superior to that in the drug treatment group, and it is safer.

Objective To observe the dynamic changes of serum inflammatory factors after vertebral artery stenting and to investigate its clinical significance. Methods A total of 48 patients treated with vertebral artery stenting were included, and 48 patients only received cerebral angiography were used as a control group. The levels of soluble intercellular adhesion molecule-1 (sICAM-1), high-sensitivity C-reactive protein (hs-CRP) and tumor-necrosis factor-α (TNF-α) were detected before procedure (angiography), at 24 h, 48 h, 3 d, and 1 and 3 weeks after procedure (angiography). Results The serum levels of hs-CRP (4. 85 ± 0. 53 mg/L vs. 2. 57 ±0. 36 mg/L,P＜0. 05), TNF-α (2.42 ±0. 34 μg/L vs. 1. 08 ±0. 37 μg/L,P ＜0. 05) and sICAM-1 (449.43 ± 47. 16 μg/L vs. 269. 15 ± 37. 46 μg/L, P ＜ 0. 05) at 24 hours after procedure in the stenting group were significantly elevated compared with those before procedure. The Hs-CRP level (6.24 ± 0.59 mg/L) reached the peak at 48 hours after procedure. At week 3 (2. 51 ±0.29 mg/L), it returned to the level before procedure (2. 57 ±0. 36 mg/L); TNF-α level reached the peak at day 3 (2.30 ± 0.25 μg/L), and it remained higher level at week 3 (1. 89 ±0. 13 μg/L); the sICAM-1 level continued to rise at week 3 (296. 95 ± 59. 72 μg/L). The serum hs-CRP, TNF-α and sICAM-1 levels at 24 hours after procedure in the stenting group were significantly higher than those (3. 25 ±0.40 mg/L、J. 18 ±0. 19 μg/L and 336. 57 ± 50. 18μg/L) in the control group (all P＜0.05). Conclusions The serum hs-CRP, TNF-α, sICAM-1 levels were significantly elevated after vertebral artery stenting. It was suggested that the stenting caused a longer duration of inflammatory response.

BACKGROUND: The presence of cognitive impairment following stroke onset strongly indicates poor prognosis of the patients surviving the crisis.Understanding of the incidence of cognitive impairment after ischemic stroke and its confidence interval has practical significance in preventing is occurrence in stroke patients and its differentiation from age-related cognitive impairment.OBJECTIVE: To study the incidence of cognitive impairment in patients with the first onset of ischemic stroke.DESIGN: Single-factor analyses of the cases followed up for 3 months SETTING: Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA.PARTICTPANTS: Totally 434 inpatients with acute cerebral infarction [218 male and 216 female, aged 55 to 85 with a mean of (70.3±9.5) years]admitted within 48 hours after the onset in Department of Neurology, Daping Hospital of Third Military Medical University from May 8, 1999 to December 31, 2000. All patients participated in this study voluntarily.METHODS: The general background and clinical data of the patients were collected at the time of admission. A simplified intelligence test was performed both 7 to 10 days of the onset and 3 months after discharge. The scale employed for the test included 20 questions with a total of 30 items divided to test 5 aspects of the patients' cognition, namely orientation ability, memory, calculation ability, memory recall and linguistic ability (1 point was given for a correct answer, and 0 for an wrong one or an answer of "I don't know", with the total score of 30 for all items). A score of the simplified intelligence test less than the score of demarcation (specifically,below 17 for illiterate patients, below 20 for those receiving an education no more than 6 years, and below 24 for those having an education for no less than 7 years) for 3 months after cerebral stroke was regarded as the diagnostic criteria for cognitive impairment.MAIN OUTCOME MEASURES: The incidence of cognitive impairment was recorded 3 months after hospital discharge and single-factor analysis of the scores of simple intelligence test.RESULTS: All the 434 patients were included in result analysis. Totally 161 (37.1%) patients were diagnosed as having cognitive impairment, and 273 (62.9%) had normal cognitive function 3 months after hospital discharge. The mean age of the patients with cognitive impairment was significantly higher than that of the patients with normal cognitive function [(73.0±7.0) years vs (64.5±6.6) years, t=2.626, P ＜ 0.01]. The proportion of patients with cognitive impairment receiving education for no more than 6 years was significantly higher than that among patients with normal cognition (45.3% vs 22.7%, OR=2.823, with 95% confidence interval of 1.855 -4.297), and the score of simple intelligence test was significantly lower in the former patient group (16.3±8.7 vs 23.4±4.2, t=3.352, P ＜ 0.001).CONCLUSION: The incidence of cognitive impairment in this cohort is relatively high. The patients with cognitive impairment following cerebral infarction have obviously older age and poorer education, suggesting significant synergetic effect of age and education with cognitive impairment following cerebral infarction.

BACKGROUND: Pro-inflammatory cytokines can promote the expression nof intercellular adhesion molecule-1 (ICAM-1), and the adhesion of white cells to intravascular endothelium, thereby involving in the developing ischemic stroke.OBJECTIVE: To investigate the prognostic value of soluble intercellular adhesion molecule-1 (sICAM-1) and its relative factors in the developing ischemic stroke.DESIGN: Randomized controlled study based on patients.SETTING: Department of neurology, the field surgery research institute in a military hospital of Chinese PLA.PARTICIPANTS: Between January 1st and December 31st 2000, total 238patients with ischemic stroke received treatment at the Neurological Department of the Third Affiliated Hospital, the Third Military Medical University of Chinese PLA, including 117 males and 121 females, amongst which 186cases were confirmed of none-developing ischemic stroke and 52 cases developing ischemic stroke.INTERVENTIONS: After hospitalization, patients were subject to daily neurological examination, Canada stroke score(CSS), temperature and white blood cell(WBC) counting, sICAM was examined at 1, 3 and 7 days after hospitalization.correlative factors between developing ischemic stroke and non-developing ischemic stroke at 24 hours 3 days and 7 days after the onset of stroke.RESULTS: Within 24 hours from the onset of stroke, the number of WBC was[(8.4 ± 1.2) × 109 L-1] in developing ischemic stroke group, with blood glucose of[ (45.8 ± 5.1) g/L], fibrinogen of[ (64. 6 ± 5. 1) g/L] and sICAM-1 of[ (261.4 ± 9. 7) μg/L], which were obviously higher than the corresponding[(6.7±1.3) ×109 L-1, (36.2±5.5) g/L, (44.0±6.2) g/L,(223. 1 ± 8.4) μg/L] in non-developing ischemic stroke group, the difference was of statistical significance( t = 2. 368 - 2. 387, P ＜ 0. 01 ) . The results of multiple factor analysis on developing ischemic stroke indicated that serum sICAM-1 was a risk factor independent of higher blood glucose,fibrinogen and CSS, and was obviously correlated with developing ischemic stroke( OR =2.9, 95% CI= 1.4 -6. 3) . There was significant change in sICAM-1, the number of WBC, blood glucose and fibrinogen at 24 hours, 3days and 7 days, as well as the scores for CSS at hospitalization in developing ischemic stroke group, which were significantly different from non-developing ischemic group( t = 2. 345 - 2. 878, P ＜ 0.01 ).CONCLUSION: sICAM-1 was proved obviously correlated with developing ischemic stroke, and can be used as a prognostic factor.

BACKGROUND:With the trend of population aging,the morbidity of cognitive dysfunction has been gradually increased.People start to pay attention to the impact of smoking to cognitive dysfunction. OBJECTIVE:To investigate the effects of smoking on cognitive dysfunction in elder people,and explore the possibility of intervention. DESIGN:Randomized cluster sampling. SETTING:Neurology Department of a hospital. PARTICIPANTS:A total of 3 012 old people aged above 60 year were selected from two resident committees by drawing from Gaoxin district,Yubei district and Yuzhong district of Chongqing in which there were 1 668 males and 1 344 females. METHODS:Mini mental state examinate(MMSE) was used to assess cognitive function.t test and Logisitc regression were used to analyze the information. RESULTS:MMSE assessment was conducted to 3 012 people,the total smoking rate was 35% .The abnormality rate of cognitive function in aged people of Chongqing was 11.95% .Among smoking population,11.8% of the currently smoking people and 4.5% of previously smoking people suffered from the cognitive dysfunction while 5.3% of the non smoking people got cognitive dysfunction. CONCLUSION:Smoking is closely correlated with cognitive dysfunction(χ 2=6.59,P=0.047) and education background, age, occupation and sex are the influencing factors of cognitive dysfunction.Current smoking people get higher risk to suffer cognitive dysfunction(RR=2.33,95% CI=1.37- 5.82).Smoking is an important risk factor for cognitive dysfunction in aged people so that it will be an effective strategy for aged people to reduce the incidence of cognitive dysfunction by quitting smoking.

Objective To investigate the influence of carotid artery stenting (CS)of asymptomatic critical internal carotid artery (ICA)stenosis patients on cognitive function .Methods One hundred and fifty‐six asymptomatic patients with internal carotid arter‐y stenosis(carotid stenosis severity≥70% )were enrolled ,in whom CS was attempted .Functional assessments including alzheimer disease assessment scale‐cognitive subtest (ADAS‐Cog) ,mini‐mental state examination (MMSE) ,and trail making test A(TMTa) and B(TMTb) were done prior to 1 weeks and 3 months after the procedure .Results Successful CS was achieved in all of patients (100% ) ,only 1 patient was lost to follow‐up .There were significant improvement in ADAS‐Cog score(pre 6 .60 ± 2 .04 vs .post 5 .16 ± 1 .63 ,P<0 .01) ,MMSE score (pre 26 .32 ± 1 .06 vs .post 27 .05 ± 1 .46 ,P< 0 .01) ,TMTa (pre 108 .94 ± 17 .42 vs .post 94 .70 ± 20 .27 ,P<0 .01) ,TMTb (pre 178 .65 ± 21 .77 vs .post 148 .92 ± 23 .65 ,P<0 .01) .There was new cerebral infarction dur‐ing 3 months after surgery .Conclusion Asymptomatic critical internal carotid artery (ICA)stenosis may be one reason of cognitive impairment ,and successful CS could improve cognitive function in asymptomatic ICA stenosis .