Résumé
Cognitive impairment often occurs in elderly patients with heart failure.In this paper, we reviewed the possible mechanism of cognitive impairment in elderly patients with heart failure.The possible pathological mechanism of cognitive impairment in elderly patients with heart failure was discussed from the aspects of decreased cardiac output, renal damage, atrial fibrillation, inflammatory reaction, neuroregulation, depression and high homocysteine level, and the effect of cognitive impairment on heart failure was also summarized, so as to improve both the clinicians' awareness of cognitive impairment and the level of diagnosis and treatment in elderly patients with heart failure.
Résumé
Objective To investigate the impairment and the effect factors of encoding of episodic memory in patients with cerebral infarction. Methods 112 cases cerebral infarction patients and 115 healthy elders as controls were tested for episodic memory encoding with episodic pictures accomplished in computer, and compare the differences of encoding of episodic memory between the two groups. Results The remember indexes ( REM )of encoding memory test in patient group was significantly lower than that in control group( (70.81 ± 6.08 )vs (84.67 ± 4.49), P ＜ 0.01 ). The REM in patients with different impaired areas was significantly different ( (65.88 ± 5.73 ), (68.92 ± 4.65 ), (73.39 ± 6.20), ( 73.53 ± 3.44), P ＜ 0. 01 ). The REM in frontal lobe infarction group was significantly lower than that in temporal lobe infarction group (P ＜ 0.05 ), and in temporal lobe infarction group was significantly lower than that in basal ganglia infarction group and corona radiate infarction group (P＜0.05, P＜0. 01). The REM in cortex infarction group was significantly lower than that in under cortex group ( ( 67.37 ± 5.40 ), ( 73.46 ± 4.99 ), P ＜ 0.01 ). The REM in small cerebral infarction group was significantly higher than that in large cerebral infarction group( (72.67 ±4.47 ), (67.56 ± 6.18 ), P＜0.01 ). The size of cerebral infarction diameter was related with the REM( r= -0.39, P＜0. 01 ). The REM among control group,infarction with atrophy group, and infarction without atrophy group were significantly different( (67.03 ± 6. 17 ),( 72.84 ± 5. 00 ), ( 84.67 ± 4.49 ), P ＜ 0. 01 ). The REM in infarction with atrophy group was significantly lower than that in infarction without atrophy group and control group( both P＜0.01 ) ,The REM in infarction without atrophy group was significantly lower than that in control group (P ＜ 0.01). Conclusion The encoding of episodic memory was impaired in cerebral infarction patients. The infarction parts,size of infarction area and atrophy was related with the impairment of encoding of episodic memory.
Résumé
Objective To elucidate the delayed neuron death and the expression of ?-amyloid protein (A?) in hippocampus after reperfusion of transiently ischemic lesion.Methods Immunohistochemical and HE technique was used to examine the delayed neuron death and expression of ?-amyloid protein at 6 h,2 d,3 d,7 d,14 d,35 d after reperfusion of transiently incomplete forebrain ischemia in rat hippocampus.Results Delayed neuron death was seen at 3 days after ischemia/reperfusin in CA 1 area of the hippocampus. A? immunoreactivity began enhanced at 2 d (A:0.082?0.011)after reperfusion, up to peak at 7 d(A:0.175?0.024), disapeared at 35 d.Conclusion Delayed neuron death was occurred after reperfusion of transiently incomplete forebrain ischemia in rat hippocampus,and at the same time, A? was up expression, which is suggested to be an important role of A? in neuron death after reperfusion of ischemic lesion.