Predictive power of abnormal electroencephalogram for post-cerebral infarction depression.

Electroencephalography is a sensitive indicator for measuring brain condition, and can reflect early changes in brain function and severity of cerebral ischemia. However, it is not yet known whether electroencephalography can predict development of post-cerebral infarction depression. A total of 321 patients with ischemic stroke underwent electroencephalography and Hamilton Depression Rating Scale assessment to analyze the relationship between electroencephalography and post-cerebral infarction depression. Our results show that electroencephalograms of ischemic stroke patients with depression exhibit low-amplitude alpha activity and slow theta activity. In contrast, electroencephalograms of ischemic stroke patients without depression show fast beta activity and slow delta activity. These findings confirm that low-amplitude alpha activity and slow theta activity can be considered as independent predictors for post-cerebral infarction depression.

Neurotropin® alleviates hippocampal neuron damage through a HIF-1α/MAPK pathway.

AIMS: The main purpose was to verify the potent capacity of Neurotropin® against neuronal damage in hippocampus and to explore its underlying mechanisms. METHODS: HT22 cells were treated with 40 µmol/L Aß25-35 in the presence of various concentrations of Neurotropin® or in its absence. The cell viability was assessed with a CCK-8 assay, and flow cytometry was used to measure cell apoptosis, intracellular ROS levels, and mitochondrial membrane potential. Aß plaques were examined by Bielschowsky silver staining, and the activities of antioxidants were detected in hippocampus of APP/PS1 mice after Neurotropin® treatment. The expression of proteins, including HIF-1α, Bcl-2, Bax, and MAPKs signaling molecules was evaluated by Western blot. RESULTS: Neurotropin® significantly reversed the cell injury induced by Aß25-35 through increasing cell viability and mitochondrial membrane potential, decreasing intracellular ROS and cell apoptosis of HT22 cells (P<.05). Furthermore, Neurotropin® markedly reduced the formation of Aß plaques and upregulated the activities of antioxidants (P<.05). Additionally, the protein expression of HIF-1α, p-ERK1/2, p-JNK, and p-P38 was significantly inhibited in hippocampus of APP/PS1 mice. CONCLUSIONS: Neurotropin® exhibited a potent neuroprotective effect on inhibiting Aß-induced oxidative damage and alleviating Aß deposition in hippocampus via modulation of HIF-1α/MAPK signaling pathway.

[Comparative assessment of clinical features and imaging findings for patients with vascular parkinsonism and idiopathic Parkinson's disease].

OBJECTIVE: To compare the differences of clinical features and imaging findings between vascular parkinsonism (VP) and idiopathic Parkinson's disease (PD). METHOD: The clinical features and imaging findings from 54 patients with VP and 53 patients with PD were compared. RESULTS: The main clinical manifestations of patients with VP were hemiplegia, rigidity and bulbar palsy with obviously pyramidal tract system damage and less rest tremor. Patients with PD showed remarkable tremor-cogwheel rigidity. In the aspect of imageology, there were obvious imaging changes in patients with VP, mainly manifested lacunar infarction located in unilateral or bilateral basal ganglia and white matter of frontal lobe. Furthermore, some ischemic changes could be seen in the cerebral peduncle and lateral cerebral ventricle. In patients with PD, ischemic changes were invisible. As to the therapeutic effect to the anti-Parkinson's disease, patients with PD showed better effect than VP patients. CONCLUSION: As a self-sustaining clinical syndrome, the clinical manifestations and imaging findings in patients with VP are different from those with PD.

[Clinical study of susceptibility-weighted magnetic resonance imaging in lacunar cerebral infarction].

OBJECTIVE: To evaluate the clinical application of susceptibility-weighted magnetic resonance imaging (SWAN) in lacunar cerebral infarction imaging. METHODS: Forty-two cases of lacunar cerebral infarction, including 18 complicated by high blood pressure, 4 by type 2 diabetes and 12 by both high blood pressure and type 2 diabetes, underwent examinations with SWAN and conventional MRI sequences (including GRE sequence T(1) and T(2), T(2) gradient echo, T(2) FLAIR, DWI). The imaging data were analyzed in comparison with the clinical data of the patients. RESULTS: In 23 patients with lacunar cerebral infarction, intracerebral micro-hemorrhage displayed point-like, round and oval low signal on SWAN. A total of 123 lesions were identified, distributing from the cortical, subcortical, basal ganglia, thalamus, brain stem to the cerebellum. The conventional sequences were more sensitive in detecting the majority of lacunar cerebral infarction than SWAN, while the latter showed better performance in displaying cerebral micro-hemorrhage, tiny blood vessels and small vascular malformations as well as other small vascular diseases. SWAN was superior to other sequences in showing lacunar cerebral infarction complicated by cerebral micro-hemorrhages. CONCLUSION: MRI SWAN can better display lacunar cerebral infarction associated with cerebral micro-hemorrhages and small veins in the infract region. Identification of the micro-hemorrhages in lacunar cerebral infarction can be critical in determining the proper treatments. Patients with lacunar cerebral infarction are likely to have cerebral micro-hemorrhages in close relation to the number of lacunar infarction sites. The cerebral micro-hemorrhages and lacunar cerebral infraction are both signs of micro-vessel damage of the brain.

[Relationship between cystatin C and cerebral infarction].

OBJECTIVE: To study the relationship between cystatin C and cerebral infarction and explore the role of cystatin C in the protection against cerebral infarction. METHOD: Eighty-three patients with cerebral infarction and 71 randomly selected age- and gender-matched patients in the Department of Neurology (control group) were enrolled in this study. Fasting whole blood (3 ml) was obtained from the patients in both groups and the sera were separated to determine the levels of cystatin C using particle reinforced immunoturbidimetric assay. RESULTS: The serum cystatin C level was significantly lower in the cerebral infarction group than in the control group (1.62-/+0.31 vs 2.23-/+0.22 mg/L, P<0.01). CONCLUSIONS: Cystatin C is closely related to cerebral infarction probably as a protective factor against cerebral infarction.