Millard-Gubler Syndrome in a Patient with Pontine Infarction: A Case Report

Millard-Gubler Syndrome is a rare neurological condition caused by damage to the sixth and seventh cranial nerves, as well as the corticospinal tract in the brainstem. It is characterized by the presence of ipsilateral facial paralysis and contralateral hemiplegia. We report a 55-year-old male patient who presented with sudden onset of left-sided weakness. Imaging revealed a pontine infarct. The patient therefore, was diagnosed with Millard-Gubler Syndrome also known as Ventral Pontine Syndrome based on his symptoms and imaging findings. He was treated with Aspirin and Atorvastatin and was referred to neurology for further consultation and to physiotherapy for his weakness. This case report highlights the importance of prompt recognition and diagnosis of Millard-Gubler Syndrome in patients with pontine infarction. Early identification especially with the use of high-resolution MRI can facilitate appropriate management and treatment, ultimately improving patient outcomes.

what drives progressive motor deficits in patients with acute pontine infarction?

Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be respon- sible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.

Sodium ozagrel and atorvastatin for type 2 diabetes patients with lacunar cerebral infarction

BACKGROUND The main pathological factor of cerebral infarction is atherosclerosis,which is the pathological process of chronic inflammatory diseases such as vascular smooth muscle hyperplasia,inflammatory cell infiltration,extracellular matrix increase,and thrombosis.At present,the focus of clinical treatment is anti-platelet aggregation and improving blood status,and current research is limited to improving symptoms only.AIM To observe the effect of sodium ozagrel and atorvastatin on type 2 diabetes patients with lacunar cerebral infarction.METHODS Eighty-two patients with type 2 diabetes and lacunar cerebral infarction admitted to our hospital from January 2018 to February 2020 were equally categorized into two groups according to their treatment method.The control group was administered atorvastatin,and the observation group was administered sodium ozagrel combined with atorvastatin.The National Institutes of Health stroke scale(NIHSS)score,activities of daily living(ADL)score,blood glucose,lipid levels,inflammatory factors,high-mobility group box 1(HMGB1)levels,paraoxonase-1(PON-1)levels,erythrocyte sedimentation rate(ESR),and macrophage migration inhibitory factor(MIF)levels were recorded before and after treatment.The total effective rate and adverse reaction rate of the two groups were analyzed.RESULTS The total effective rate of the observation group(94.00%)was significantly higher than that of the control group(80.00%)(χ2=3.998;P=0.046).The blood glucose indexes,total cholesterol levels,triglyceride levels,low-density lipoprotein cholesterol levels,high-sensitivity C-reactive protein levels,interleukin-1βlevels,tumor necrosis factor-αlevels,HMGB1 Levels,ESR,MIF levels,platelet aggregation rates,and plasma viscosity of the two groups decreased after treatment;however,high-density lipoprotein cholesterol and PON-1 Levels increased after treatment.After treatment,the blood glucose indexes;blood lipid indexes;inflammatory factors;HMGB1,PON-1,and MIF levels;ESR;platelet aggregation rate;and plasma viscosity of the observation group were better than those of the control group(P<0.05).After treatment,all patients in the observation group had higher ADL scores and lower NIHSS scores than those in the control group(P<0.05).CONCLUSION Sodium ozagrel with atorvastatin can reduce inflammatory reactions;regulate ESR and HMGB1,PON-1,and MIF levels;control blood glucose and lipid indexes;and alleviate nerve injury without increasing adverse effects of atorvastatin alone.

Correlation of ischemic ophthalmopathy with lacunar infarction

AIM:To investigate the correlation of ischemic ophthalmopathy(IO)with lacunar infarction(LI),an ischemic lesions in the cerebrovascular system.METHODS:Totally 204 cases of IO without any nervous system symptom and previously diagnosed LI served as the observational group.All 204 cases without IO,nervous system symptoms and previous LI served as the control group.Age and sex between the two groups matched well.LI was diagnosed by magnetic resonance imaging(MRI)and the results of the two groups were statistically analyzed and compared.RESULTS:IO included 174 eyes of 156 patients with non-arteritis anterior ischemic optic neuropathy(NAION),42 eyes of 36 patients with central retinal artery occlusion(CRAO)or branch retinal artery occlusion(BRAO)and 12 eyes of 12 patients with ocular ischemia syndrome(OIS).The detection rate of LI(72.54%)in IO group was obviously higher than that(15.68%)in the control group(P<0.001).IO was positively correlated with LI(r=0.573,P<0.05).In addition,most infarction sites located in the basal ganglia(67.57%),which were not the vital areas of cerebrum and not easy to be found due to their small size.The majority of those first visited IO patients(72.54%)without nervous system symptom and previously diagnosed LI had already suffered from LI.CONCLUSION:According to our studies,there is a positive correlation between IO and LI.IO can be used as an important predictor for the present of LI,especially obvious signs of the patient.

Association of ALOX5AP and PDE4D with the risk of lacunar infarct in people from Jiangsu Province,China

The genes for 5-1ipoxygenase activating protein （ALOX5AP） and phosphodiesterase 4D （PDE4D） have been demonstrated as susceptibility genes for lacunar in the Icelandic and Pakistani populations, but little is known about the role of these genes in Chinese populations. The present study utilized polymerase chain reaction and ligase detection reaction to detect single nucleotide polymorphisms （SNPs） in 280 consecutive stroke patients and 258 unrelated population-based controls from Nanjing, Jiangsu Province, China. The allele frequency, genotypes, and haplotypes of the two SNPs （rs456009 and rs966221） in PDE4D were similar between the two groups. However, A allele frequency of rs4073259 （A/G） and rs4769055 （A/C） in the ALOX5AP gene exhibited differences in two groups, and especially the haplotype of the SNP was significantly different between the two groups. Results suggested that the ALOX5AP gene might be involved in lacunar infarct, while PDE4D gene was not a risk factor for lacunar infarct in individuals from Jiangsu Province, China.

Correlative factors of cognitive impairment in patients with lacunar infarcts

Objective To study the relationships between cognitive impairment in patients with lacunar infarcts and quantitative CT measures and to determine the independent correlative factors of cognitive impairment.Methods Neuropsychological examination was conducted for 128 patients with acute lacunar infarct.Number,location,and volume of infarcts,cerebral atrophy index and severity of white matter lesions(WMLs) were measured and recorded.Results The number of lacunar infarcts in cognitive impairment (CI) group was significantly larger than that in cognitive normal(CN) group.Mean width of sulcus and sylvian fissure,index of frontal horn and ventricular-brain ratio(VBR) were significantly different in both groups.There were more patients with 3 grades or 4 grades WMLs in CI group(62%) than those in CN group(22%).The total volume of lacunar infarcts showed no statistically significant difference.Logistic regression analysis indicated that the number of lacunar infarcts in frontal subcortex and thalamus,the volume of infarcts in anterior periventricular white matter,width of cerebral sulcus and sylvian fissure were correlated with cognitive impairment respectively.Additionally,age and education were correlative factors of cognitive impairment in patients with lacunar infarct.Conclusion Correlative factors of cognitive impairment in patients with lacunar infarct are not merely one feature,but a combination of infarct features(number,location,and volume),cortical atrophy and host factors(age and education).

The relation between prognosis and nocturnal blood pressure variation in hypertensive patients with lacunar infarct

Objective We conducted a study using MRI and ambulatory blood pressure monitoring(ABPM) to determine whether an in-apporpriately low nocturnal blood pressure, or an excess fall in nocturnal blood pressure, might be responsible for lacunar infarct. Method ABPM and Casul blood pressure(CBP) were examined in 35 hypertentives with lacunar infarct(LI)and 33 hypertentives without lacunar infarct as control group. Results There is no significant difference of CBP between two groups. But the mean nighttime systolic blood pressure (nSBP) and diastolic blood pressure (nDBP) in patients with lacunar infarct were significantly smaller than in patients without lacunar infarct. The ratio of nSBP/dSBP and nDBP/dDBP in SI were smaller than in control group respectively. Conclusions The results indicate that an inap-propriately low nocturnal blood pressure, or an excessive fall in nocturnal blood pressure, is associated with lacunar infarct. It is necessary not only to control high blood pressure but also to pay attention to circadian changes of blood pressure during the course of anti-hypertensive treatment.

Restless legs syndrome secondary to pontine infarction:Clinical analysis of five cases

Objective: Pontine infarction is a common type of stroke in the cerebral deep structures, resulting from occlusion of small penetrating arteries, may manifest as hemi-paralysis, hemi-sensory deficit, ataxia, vertigo, and bulbar dysfunction, but patients presenting with restless legs syndrome (RLS) are extremely rare. Herein, we reported five cases with RLS as a major manifestation of pontine infarction.Methods: Five cases of pontine infarction related RLS were collected from July 2013 to February 2016. The diagnosis of RLS was made according to criteria established by the International RLS Study Group (IRLSSG) in 2003. Neurological functions were assessed according to the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS). Severity of RLS was based on the International RLS Rating Scale (IRLS-RS). Sleep quality was assessed by Epworth Rating Scale (ERS), and individual emotional and psychological states were assessed by Hamilton Depression Scale (HDS) and Hamilton Anxiety Scale (HAS).Results: The laboratory data at the onset including hemoglobin, serum concentration of homocysteine, blood urea nitrogen (BUN), creatinine, electrolytes, and thyroid hormones were normal. The electroencephalogram (EEG), lower-extremity somatosensory evoked potential (SEP), and nerve conduction velocity (NCV) in four limbs were normal. The average period of follow-up was 34.60 ± 12.76 months. The MRI examination showed acute or subacute pontine infarction lesions, 3 cases in the rostral inner side, 1 case in the rostral lateral and inner side, and 1 case in rostral lateral side. The neurological deficits included weakness in 4 cases, contralateral sensory deficit in 1 case, and ataxia in 2 cases. All 5 patients presented with symptom of RLS at or soon after the onset of infarction and 4 patients experienced uncomfortable sensations in the paralyzed limbs contralateral to the ischemic lesion. Their neurological deficits improved significantly 2 weeks later, but the symptoms of RLS did not resolve. Among them, 3/5 patients were treated with dopaminergic drugs. At the end of the follow-up, RLS symptom eventually resolved in 3 patients but persisted in two. The IRLS-RS, NIHSS and mRS scores were significantly lower at the onset than those at the last follow-up (P=0.035, 0.024 and 0.049, respectively). However, there was no significant difference in the ERS, HDS and HAS scores (P=0.477, 0.226 and 0.778, respectively).Conclusion: RLS can be an onset manifestation of pontine infarction, clinicians should be aware of this potential symptom. RLS usually occurs in the paralyzed limbs contralateral to the infarction lesion. The pathogenesis still needs further investigation.

Multimodal magnetic resonance imaging for assessing lacunar infarction after proximal middle cerebral artery occlusion in a canine model

Background A new lacunar infarction model was recently established in beagle dogs through proximal middle cerebral artery （MCA） occlusion by thrombus. This study aimed to characterize the model by multimodal magnetic resonance imaging （MRI） and to investigate its potential role for the future stroke research. Methods The left proximal MCA was embolized with an autologous thrombus in six beagles. Diffusion-weighted imaging （DWI） and T2-weighted imaging （T2Wl） were performed every half hour during the first six hours after occlusion, followed by three time points at 12 hours, 24 hours, and one week. Perfusion-weighted imaging （PWI） and magnetic resonance angiography （MRA） were carried out at six hours, 24 hours and one week. The PWI-DWI mismatch ratio was defined as （PWI-DWl）/DWl ischemic volume. Results Lacunar infarcts induced by MCA occlusion were located in the left caudate nucleus and internal capsule. All the lesions could be detected within two hours by DWI. Lesion volume on DWl increased in a time dependent manner, from （87.19±67.16） mm3 at one hour up to （368.98±217.05） mm3 at 24 hours （P=0.009）, while that on PWl gradually decreased from （7315.00±2054.38） mm3at six hours to （4900.33±1319.71） mm3 at 24 hours and （3334.33±1195.11） mm3 at one week （P=0.002）. The mismatch ratio was 41.93±22.75 at six hours after ischemia, showing ＂extensive mismatch＂, and decreased to 18.10±13.74 at 24 hours （P=0.002）. No MCA recanalization was observed within 24 hours after MCA occlusion. Conclusions Lacunar infarction induced by proximal MCA occlusion could be detected early by DWl and was characterized by extensive PWI-DWl mismatch. Multimodal MRI is useful to demonstrate the natural evolution of PWI-DWl mismatch. This ischemic model could be further used for investigating early thrombolysis in lacunar stroke showing extensive mismatch.

Lacunar infarction with leukoaraiosis may aggravate cognitive dysfunction

This study semi-quantitatively analyzed the effects of leukoaraiosis.Patients with moderate or severe lacunar infarction were found to exhibit low scores on the Montreal Cognitive Assessment Scale （F=12.02,P=0.000）,and prolonged P300 Cz2.0 latency （F=16.04,P=0.000）.Correlation analysis revealed that the occurrence of leukoaraiosis was negatively correlated with Montreal Cognitive Assessment scores （r=-0.416,P=0.000）,and positively correlated with P300 Cz2.0 latency （r=0.538,P=0.000）.These findings indicate that leukoaraiosis aggravates cognitive impairment in patients with lacunar infarction,such that more severe leukoaraiosis is associated with more severe cognitive decline.

延髓外侧梗死致尿潴留1例并文献复习

延髓外侧梗死是常见的脑干梗死综合征之一,但在临床上其导致尿潴留的病例并不多见。本文回顾性分析山东中医药大学第二附属医院收治的延髓外侧梗死致尿潴留的患者1例,患者以头晕、行走不稳为主要症状,同时发现存在急性尿潴留的临床表现,完善影像学检查后诊断为延髓外侧梗死;神经源性膀胱(尿潴留)。及时予以患者静脉溶栓、导尿及其他对症治疗,约1个月后其自主排尿功能完全恢复。尽管延髓外侧梗死导致尿潴留的病例不常见,但应充分了解并提高对此类情况的认知,做到全面预判,提前告知患者及其家属尿潴留的可能性及其预后,反之,在颅脑CT显示不佳、MRI完善不及时的情况下,对于眩晕症状明显而其他定位体征较少,同时又合并急性尿潴留的患者,也能给予脑干-延髓外侧部分-可能受损的提示,提高对后循环梗死的警惕和重视,给予及时、适当的处理,避免延治失治。

多发腔隙性脑梗死后血管性认知障碍的发生情况及影响因素分析

目的探讨多发腔隙性脑梗死后血管性认知障碍发生的独立风险因素。方法采用回归分析研究多发腔隙性脑梗死患者的年龄、文化程度、婚姻状况、民族、吸烟史、饮酒史、运动状况、饮食状况、家族痴呆史、家族高血压史、家族脑卒中史、家族糖尿病史、合并心脏病、合并高血压、合并高血脂、合并糖尿病、脑梗死位置和NIHSS评分对多发腔隙性脑梗死后血管性认知障碍发生的影响。结果450例患者中40例(8.89%)发生血管性认知障碍。年龄、婚姻状况、运动状况、家族痴呆史、家族脑卒中史、合并高血压、合并高血脂、脑梗死位置和NIHSS评分是多发腔隙性脑梗死后血管性认知障碍发生的独立风险因素(P<0.05)。结论年龄、婚姻状况、运动状况、家族痴呆史、家族脑卒中史、合并高血压、合并高血脂、脑梗死位置和NIHSS评分对多发腔隙性脑梗死后血管性认知障碍的发生有显著影响,应在临床实践中加以重视,以制定有效的干预措施。

腔隙性脑梗死合并脑微出血的危险因素与脑白质病变的相关性

目的 探讨腔隙性脑梗死(LI)合并脑微出血(CMBs)的危险因素及与脑白质病变(WML)的关系。方法 于2020年3月至2022年6月在海南省老年病医院收集LI患者134例,根据磁敏感加权成像(SWI)检测CMBs,分为CMBs组(49例)和非CMBs组(85例),利用脑白质病变量表评分(WMLs)分析LI患者脑白质病情情况与CMBs相关性,采用Logistic回归模型分析LI患者并发CMBs的危险因素。结果 134例LI患者合并CMBs发生率为36.57%(49/134例)。CMBs组WML发生率、WMLs评分明显高于非CMBs组(P<0.05);多因素Logistic回归分析显示,血尿酸、高血压史、高密度脂蛋白(HDL)、WML发生率和WMLs评分是LI患者发生CMBs的独立影响因素。且CMBs病灶数量与WMLs评分存在明显正相关(r=0.412,P<0.05)。结论 LI患者发生CMBs发生影响因素众多,控制血压、血脂水平以及降低血尿酸对于预防LI患者发生CMBs具有重要意义,且脑白质病变程度与CMBs严重程度紧密相关。

Cognitive impairment in cerebral small vessel disease induced by hypertension

Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.

儿童重症肺炎支原体肺炎致不同类型脑梗死3例

总结3例儿童重症肺炎支原体肺炎致腔隙性脑梗死、大脑中动脉下干梗死、分水岭脑梗死的患儿临床特征及诊治结局。3例患儿均因发热、咳嗽为主诉收入院。住院期间出现活动不利等神经系统症状,完善头部影像学后确诊为脑梗死。病例1,男,5岁,腔隙性脑梗死同时合并有心房血栓及上肢动脉血栓。病例2,男,5岁,大脑中动脉下干梗死;病例3,女,4岁,分水岭脑梗死。病例2、3在行纤维支气管镜后出现神经系统症状。3例患儿D-二聚体水平均异常升高。肺炎支原体感染急性期可致各种类型脑梗死,不同类型脑梗死存在不同的致病机制。肺炎支原体肺炎诊疗过程中需检测D-二聚体水平、及时完善心脏超声,术前注意患儿出入量及灌注水平,避免脑梗死的发生。

口腔内感应电刺激对脑桥梗死后吞咽障碍患者的临床疗效观察

目的:探讨口腔内感应电刺激对脑桥梗死后吞咽障碍患者的吞咽功能的影响及临床疗效。方法:选取脑桥梗死后吞咽障碍患者50例。随机分为对照组和观察组,各25例。2组均实施常规吞咽康复训练,在此基础上,对照组接受神经肌肉低频电刺激,观察组接受口腔内感应电刺激,均持续4周。分别在治疗前、治疗4周后,采用改良洼田饮水试验评分(MWST)、Rosenbek渗漏-误吸量表(PAS)评级以及功能性经口摄食量表(FOIS)评分对2组患者吞咽功能进行评估。结果:治疗4周后,2组PAS评级较治疗前降低(P<0.05),2组FOIS评分较治疗前升高(P<0.05),且观察组PAS评级低于对照组(P<0.05),FOIS评分高于对照组(P<0.05);与对照组相比,观察组临床总有效率更高(P<0.05)。结论:口腔内感应电刺激可有效改善脑桥梗死后吞咽障碍患者的吞咽功能,并且提高临床疗效。

腔隙性脑梗死患者脑白质病变情况与缺氧诱导因子1α相关性研究

目的:探究腔隙性脑梗死(LACI)患者脑白质病变情况与缺氧诱导因子1α(HIF-1α)的相关性。方法:收集196例LACI患者为研究对象,患者均完成MRI检查,并采用Fazekas量表评估纳入者脑白质病变情况;同时留取患者入院确诊时静脉血样,用于测定血清HIF-1α、半胱氨酸蛋白酶-3(Caspase-3);分析血清HIF-1α与脑白质病变情况的关系。结果:纳入者中72.45%出现脑白质病变,其中42.96%轻度病变,33.80%中度病变、23.24%重度病变。与非脑白质病变组相比,病变组患者年龄和高血压占比明显增大,血清HIF-1α和Caspase-3水平明显升高(均P<0.05)。脑白质不同程度病变者收缩压和血清HIF-1α和Caspase-3水平比较差异具有统计学意义(均P<0.01),重度病变者明显高于中度病变者,中度病变者高于轻度病变者(均P<0.05)。Logistic回归分析显示,收缩压和血清HIF-1α、Caspase-3水平均是影响LACI患者脑白质病变程度的危险因素(均P<0.05)。受试者工作特征(ROC)曲线分析显示,血清HIF-1α对LACI患者脑白质病变发生及重度脑白质病变均具有一定预测价值(AUC=0.840、0.874)。结论:LACI伴有脑白质病变患者体内HIF-1α呈高表达状态,且其表达水平升高与脑白质病变加重有关。

基于孟德尔随机化方法研究血清尿酸水平与脑小血管病之间的因果关系

目的:探究血清尿酸(SUA)水平是否与脑小血管病(CSVD)存在因果关系。方法:从已发表的全基因组关联研究汇总数据获得SUA、腔隙性脑梗死(LI)、白质高信号(WMH)、各向异性分数(FA)和平均弥散率(MD)的数据,筛选出与SUA强相关(F>10)的单核苷酸多态性(SNPs)作为工具变量,用逆方差加权法、MR-Egger、加权中位数法方法进行因果分析,利用MR-Egger截距法和Cochran's Q检验进行异质性和水平多效性检验。结果:逆方差加权法表明SUA与LI(OR=1.086,95%CI 0.959~1.230,P=0.193)、WMH(OR=1.010,95%CI 0.956~1.066,P=0.725)、FA(OR=1.058,95%CI 0.848~1.320,P=0.617)和MD(OR=1.009,95%CI 0.790~1.288,P=0.943)无关,敏感性分析结果显示无异质性和水平多效性。结论:目前MR研究表明SUA水平与CSVD之间不存在因果关系,但仍需规范化、大样本的临床研究和基于大规模GWAS的MR研究更全面评估它们之间的关联性。

叙事护理在腔隙性脑梗死患者中的应用及对创伤后成长的影响

目的探讨叙事护理对腔隙性脑梗死(LI)患者的干预效果及对创伤后成长的影响。方法选取郑州大学第一附属医院2022年5月至2023年4月收治的86例LI患者,以随机数字表法分成干预组(43例)与对照组(43例),对照组接受常规心理护理,干预组接受叙事护理,比较两组应用效果。结果干预后,两组创伤后成长评定量表(PTGI)评分升高,干预组较对照组高(P<0.05)。干预后,两组社会影响量表(SIS)评分下降,干预组较对照组低(P<0.05)。干预后,两组面对评分升高,回避、屈服评分下降,干预组面对评分较对照组高,回避、屈服评分较对照组低(P<0.05)。干预后,两组脑卒中专门化生活质量表(SS-QOL)评分升高,干预组较对照组高(P<0.05)。结论LI患者采用叙事护理能够促进患者创伤后成长,减轻病耻感,改善应对方式,提高生活质量。

多发腔隙性脑梗死患者抑郁症状与睡眠-觉醒昼夜节律的关系

目的:探讨多发腔隙性脑梗死(MLI)患者抑郁症状与睡眠觉醒昼夜节律的关系。方法:选取2020年12月至2021年12月某院住院治疗的MLI患者277例,根据DSM-5卒中后抑郁症状的诊断标准和Zung氏抑郁自评量表(SDS)评分,分为MLI抑郁症状(PSD)组和MLI无抑郁症状(NPSD)组。应用智能睡眠监测系统监测睡眠参数,评估睡眠-觉醒昼夜节律日间稳定性(IS)和昼夜变异性(IV);应用昼夜节律类型(CTI)量表评估睡眠-觉醒昼夜调节能力。比较两组基本临床特征、睡眠参数、昼夜节律指标,应用多因素logistic回归分析探讨MLI患者抑郁症状与睡眠-觉醒昼夜节律的关系。结果:(1)PSD组年龄、NIHSS评分、高同型半胱氨酸血症(HHcy)、焦虑症状及梗死病灶位于额叶、颞叶、枕叶、丘脑、脑干的比例高于NPSD组(Z=-3.322,-2.897,χ^(2)=4.737,16.184,4.925,12.710,8.974,10.598,8.334;P<0.05);(2)PSD组IS、灵活性/刚性(CTI-FR)评分低于NPSD组,IV、困倦/活力(CTI-LV)评分高于NPSD组(Z=-3.255,-2.140,-2.489,-2.010,P<0.05);(3)PSD组夜间总睡眠时间(TST)、REM时间、REM%和夜间睡眠效率(SE)均低于NPSD组(Z=-3.511,t=-4.754,-3.768,Z=-4.904,P<0.05);PSD组入睡后清醒时间(WASO)、睡眠潜伏期(SL)及浅睡眠(LST)%高于NPSD组(Z=-2.817,-2.889,t=2.222,P<0.05);(4)多因素Logistic回归分析结果显示,REM%(OR=0.910,95%CI=0.853~0.971)、夜间SE(OR=0.893,95%CI=0.821~0.972)、IS(OR=0.807,95%CI=0.662~0.984)、CTI-FR(OR=0.751,95%CI=0.588~0.958)、CTI-LV(OR=1.102,95%CI=1.012~1.200)与MLI患者抑郁症状独立相关(均P<0.05)。结论:睡眠-觉醒昼夜节律与MLI抑郁症状密切相关,REM%、夜间SE、IS、CTI-FR降低或CTI-LV增高,MLI患者发生抑郁症状的危险性增高。