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Objective:To investigate the correlation between paroxysmal slow-wave events (PSWEs) and cerebral small vessel disease (CSVD) and CSVD-related cognitive impairment.Methods:Patients with CSVD visited Weihai Municipal Hospital from March 2021 to April 2022 were included, and sex- and age-matched healthy controls were recruited for cross-sectional analysis. The patients with CSVD were further divided into cognitive impairment group and non-cognitive impairment group. The self-developed Python script was used to detect the PSWE parameters in electroencephalogram records. Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) were used to evaluate cognitive function. Multivariate logistic regression analysis was used to determine whether PWSE parameters were the independent related factors of CSVD and CSVD-related cognitive impairment. Multiple linear regression analysis was used to determine the correlation between the PSWE parameters and overall cognitive function (MoCA total score) in patients with CSVD. Results:A total of 76 patients with CSVD (including 41 patients with cognitive impairment and 35 patients without cognitive impairment) and 45 healthy controls were included. Compared with the healthy control group, PWSEs in the F3 (left frontal area) and O1 (left occipital area) regions of the CSVD group occurred more frequently and lasted longer (all P<0.05). Multivariate logistic regression analysis showed that the frequency (odds ratio [ OR] 1.080, 95% confidence interval [ CI] 1.023-1.140; P=0.005) and duration ( OR 1.006, 95% CI 1.001-1.011; P=0.023) of PWSEs in the left frontal area, as well as the frequency ( OR 1.052, 95% CI 1.010-1.095; P=0.014) and duration ( OR 1.003, 95% CI 1.000-1.006; P=0.028) of PWSEs in the left occipital region were the independent related factors for CSVD. The frequency ( OR 1.106, 95% CI 1.033-1.183; P=0.004) and duration ( OR1.010, 95% CI 1.003-1.017; P=0.004) of PWSEs in the left frontal area were the independent risk factors for cognitive impairment in patients with CSVD. Multiple linear regression analysis showed that the frequency ( β= –0.242, P=0.045) and duration ( β= –0.235, P=0.046) of PWSEs in the left frontal region were negatively correlated with the overall cognitive function score in patients with CSVD. Conclusions:The frequency and duration of PSWEs in some brain regions of patients with CSVD increase, and there is an independent correlation between PSWEs and cognitive impairment, suggesting that the damage of blood-brain barrier may participate in the pathogenesis of cognitive impairment in patients with CSVD.
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Objective:To investigate the correlation between heart rate variability (HRV) and cognitive impairment in patients with obstructive sleep apnea (OSA).Methods:Patients received polysomnography in Weihai Municipal Hospital from June 2019 to November 2020 were enrolled as the subjects of cross-sectional analysis. According to the Montreal Cognitive Assessment score, the patients with OSA were divided into a cognitive impairment group and a non-cognitive impairment group. Multivariate logistic regression analysis was used to determine whether HRV parameters were the independent influencing factors of cognitive impairment in patients with OSA. Multiple linear regression analysis was used to determine the independent correlation between HRV parameters and overall cognition as well as each cognitive domain in patients with OSA. Results:A total of 115 patients with OSA were included, including 80 males (69.6%), aged 58.25±9.88 years. Among them, there were 61 in the cognitive impairment group (53.0%) and 54 in the non-cognitive impairment group (47.0%). The standard deviation of the R-R interval in normal sinus beats (SDNN), the square root of the mean of the sum of the squares of the difference between adjacent NN intervals (RMSSD), the percentage of the number of pairs of adjacent R-R intervals differing by more than 50 ms (pNN50) and the power in high-frequency range (HF; 0.15-0.40 Hz) in the cognitive impairment group were significantly lower than those in non-cognitive impairment group (all P<0.05). Multivariate logistic regression analysis showed that SDNN (odds ratio [ OR] 0.551, 95% confidence interval [ CI] 0.380-0.798; P=0.002), RMSSD ( OR 0.516, 95% CI 0.342-0.779; P=0.002), pNN50 ( OR 0.900, 95% CI 0.834-0.971; P=0.006), LF ( OR 0.821, 95% CI 0.687-0.982; P=0.030) and HF ( OR 0.687, 95% CI 0.525-0.899; P=0.006) were the independent protective factors of cognitive impairment in patients with OSA. Multiple linear regression analysis showed that SDNN ( β=0.208, P=0.023), RMSSD ( β=0.228, P=0.011), pNN50 ( β=0.186, P=0.040), HF ( β=0.235, P=0.010) is independently correlated with overall cognitive function in patients with OSA. Conclusion:The decline of HRV parameters SDNN, RMSSD, pNN50 and HF is independently correlated with cognitive impairment in patients with OSA, suggesting that the decline of vagus nerve function may be involved in the mechanism of cognitive impairment in patients with OSA.
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Objective@#To investigate the impact of obstructive sleep apnea hypopnea syndrome (OSAHS) on platelet function in patients with ischemic stroke.@*Methods@#Patients with ischemic stroke treated in the Department of Neurology, Weihai Municipal Hospital from January 2017 to November 2017 were collected prospectively. The presence or absence of OSAHS was determined by polysomnography. After oral administration of aspirin enteric coated tablets for 7±1 d, the maximum aggregation ratio (MAR) induced by arachidonic acid (AA) was determined by PL-12 Platelet Function Analyzer. MAR-AA ≥50% was defined as platelet hyperresponsiveness. Multivariate logistic regression analysis was used to evaluate the risk factors for platelet hyperresponsiveness in patients with ischemic stroke, and multiple linear regression analysis was used to determine the correlation between sleep parameters reflecting the severity of sleep apnea and MAR-AA.@*Results@#Among the 124 patients with ischemic stroke, 58 (46.77%) complicated with OSAHS, 66 (53.23%) without complicated with OSAHS; 84 (67.74%) had platelet hyperresponsiveness, and 40 (32.26%) had not platelet hyperresponsiveness. MAR-AA in the complicated OSAHS group was significantly higher than that in the non-complicated OSAHS group (48.98%±20.61% vs. 26.45%±15.15%; t=-6.858, P<0.001). Multivariate logistic regression analysis showed that OSAHS was an independent risk factor for platelet hyperresponsiveness in patients with ischemic stroke (odds ratio 9.551, 95% confidence interval 3.051-29.905; P<0.001). Multiple linear regression analysis showed that there was a significant linear relationship between apnea hypopnea index and MAR-AA (β=0.499, P<0.001).@*Conclusions@#OSAHS is an independent risk factor for platelet hyperresponsiveness in patients with ischemic stroke. Apnea hypopnea index is significantly correlated with MAR-AA.
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Objective To investigate the changes of platelet reactivity and its influencing factors after aspirin treatment in patients with ischemic stroke complicated with diabetes. Methods From September 2016to December 2017, patients with acute ischemic stroke admitted to the Department of Neurology, Weihai Municipal Hospital within 24 h of onset were enrolled. All patients took aspirin (100 mg/d) within 24 h ofadmission, and after taking the drug (7 ±2 d), the PL-11 platelet function analyzer was used to determine the maximum platelet aggregation ratio (MAR) induced by arachidonic acid (AA). The baseline data of the patients were documented. The factors affecting high platelet reactivity (HPR) were analyzed. Results A total of 398 patients with ischemic stroke were enrolled, including 137 in the diabetes group and 261 in the non-diabetes group. MARAA (43. 45％ ± 14. 11％ vs. 31. 55％ ± 19. 39％; t = 6. 996, P < 0. 001) and the incidence of HPR (34. 3％ vs. 19. 9％; χ2 = 9. 946, P = 0. 002) in the diabetes group were significantly higher than in those in the non-diabetes group. Of the 137 patients with ischemic stroke complicated with diabetes, 47 had HPR. The proportions of patients with hyperlipidemia, previous history of stroke or transient ischemic attack and baseline NIHSS score, HOMA-IR (homeostatis model assessment-insulin resistance),high-sensitivity C-reactive protein, fasting blood glucose, and glycosylated hemoglobin in the HPR group were significantly higher than those in the non-HPR group (all P < 0. 05). Multivariate logistic regression analysis showed that HOMA-IR (odds ratio [OR] 1. 153, 95％ confidence interval [CI] 1. 027-1. 295; P =0. 016), high-sensitivity C-reactive protein (OR 9. 416, 95％ CI 2. 271-39. 049; P = 0. 002), fasting blood glucose (OR 1. 125, 95％ CI 1. 025-1. 235; P = 0. 013), and glycosylated hemoglobin (OR 1. 458, 95％ CI 1. 170-1. 816; P = 0. 001) were the independent risk factors for HPR. Conclusion The platelet reactivity during aspirin therapy in patients with ischemic stroke complicated with diabetes mellitus was high, and platelet activity was associated with multiple mechanisms, such as inflammation, insulin resistance, and hyperglycemia.
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Objective To observe the changes of spleen volume in patients with acute cerebral infarction, and to explore the relationship between the spleen volume and platelet reactivity , inflammatory factors'lymphocyte subsets.Methods This is a case control study.Thirty patients with acute cerebral infarction from January 2017 to June 2017 in Department of Neurology , Weihai Municipal Hospital were included.The spleen volume, arachidonic acid-induced maximum platelet aggregation ratio ( AA-MAR), interferon gamma (IFN-γ) and lymphocyte subsets of patients were monitored in 24 hours of stroke, at 48 hours of stroke, at four days of stroke and at seven days of stroke.Twenty patients without acute cerebral infarction with the same baseline data were selected as the control group , to determine the baseline of spleen volume, AA-MAR, IFN-γand lymphocyte subsets.A t test was used to describe the changes of spleen volume, AA-MAR, IFN-γand lymphocyte subsets at different time points , and Pearson's correlation analysis was used to estimate the relationship between the spleen volume and these variables .Results Compared with the control group ((120.12 ±10.28) cm3), the patients with acute cerebral infarction in 24 hours of stroke ((117.48 ±7.93) cm3) and at 48 hours of stroke ((111.61 ±9.21) cm3) had smaller spleen volume (t＝-2.142, P＜0.05; t＝-2.790, P＜0.01), whereas at four days ((121.31 ±8.16) cm3) and seven days of stroke ((126.11 ±10.31) cm3) had bigger spleen volume (t＝2.242, P＜0.05;t＝2.762, P＜0.01), with the spleen volume decreased first and increased later.Compared with the control group, the patients with acute cerebral infarction had more AA-MAR (control group:20.97%±8.21%;24 h:31.86%±9.54%,t＝3.165,P＜0.01;48 h:41.38%±8.55%,t＝3.254,P＜0.01;4 d:35.34%± 8.15%, t＝3.203,P＜0.01;7 d:29.38% ±10.46%,t＝2.494,P＜0.05) and IFN-γ(pg/L, control group:15.21 ±5.21;24 h:29.75 ±4.57,t＝3.262,P＜0.01;48 h:43.37 ±12.15,t＝3.304,P＜0.01;4 d:40.44 ±9.86, t＝3.291,P＜0.01;7 d:20.93 ±5.51, t＝2.417,P＜0.05) at different time points, with the most AA-MAR at 48 hours of onset, and the most IFN-γat four days of stroke.Compared with the control group, the patients with acute cerebral infarction had more T 4, B lymphocytes and natural killer lymphocytes at the four time points , while the level of T8lymphocytes did not show statistically significant difference even though also increased at the four time points.The correlation analysis results showed that in patients with acute cerebral infarction , the level of AA-MAR (r＝-0.397, P＜0.05; r＝-0.515, P＜0.01; r＝-0.382, P＜0.05) and IFN-γ(r＝-0.408, P＜0.05; r＝-0.479, P＜0.01; r＝-0.378, P＜0.05) was negatively corelated with the spleen volume in 24 hours of onset, at 48 hours of stroke and at four days of stroke; the level of T4, B and natural killer lymphocytes were negatively corelated with the spleen volume in 24 hours of stroke and at 48 hours of stroke.Conclusion After the acute cerebral infarction onset, the spleen volume tends to reduce and then increases , the levels of platelet reactivity , inflammatory factors and lymphocyte subsets are correlated with the spleen volume , and the spleen may aggravate the brain injury by releasing platelets inflammatory factors and lymphocyte subsets.