急性脑梗死患者睡眠结构的变化

目的 研究急性脑梗死患者睡眠结构的变化及影响因素.方法 采用加拿大产stellate Harmoaie system视频多导睡眠仪对86例急性脑梗死患者的睡眠进行全夜监测,并与63例正常相同年龄范围人群对照.结果 与对照组相比,急性脑梗死患者的总睡眠时间(TST)、睡眠效率(SE)、快速动眼期(REM)均明显减少(P＜0.01),而觉醒期(WASO)明显增加(P＜0.01).65.1%(56/86)脑梗死合并伴有睡眠呼吸紊乱(SRDB),伴有SRBD患者的S1期睡眠明显增加(P＜0.05),快速动眼期(REM)明显减少(P＜0.05),而且重度SRBD的脑梗死患者的总睡眠时间(TST)、Sl期睡眠、REM潜伏期(RL)明显高于轻度SRBD患者.与皮层下,脑干、小脑比较,大脑皮层梗死者的睡眠质量最差(P＜0.05).神经功能缺损的程度与快速眼动(REM)睡眠时间呈负相关(r2=0.537,P=0.00).结论 急性脑梗死患者存在着明显的睡眠效率低和睡眠结构的紊乱,与睡眠呼吸紊乱程度、梗死的部位及神经功能缺损程度有关.常规筛查和评估脑梗死后的睡眠功能,尽早干预,有可能改变脑梗死的不良转归.     

Sleep in major depression: relation to memory performance and outcome after interpersonal psychotherapy

BACKGROUND: Earlier findings suggest both a link between sleep and memory consolidation and a relationship between abnormal sleep at baseline and poor treatment outcome in major depression after interpersonal psychotherapy (IPT). METHODS: Pre-treatment polysomnography was examined in 32 patients with a major depressive episode (mean age = 39.5 years, 20 women). Declarative memory was tested by the Rey-Osterrieth Complex Figure Test and a paired associative word list and procedural learning was assessed by a mirror tracing skill. All patients were treated with IPT according to the manual and did not receive any antidepressant medication. Twenty-three patients took part in a minimum of 12 sessions of IPT. Remission was defined as 2 consecutive weeks with a score <8 on the Hamilton Rating Scale of Depression. RESULTS: Declarative visual memory performance was associated with total sleep time and total amount of rapid eye movement sleep. In IPT remitters (n = 14), there was a trend towards a decrease in rapid eye movement density (first period) and a significant decrease in delta power in pre-treatment sleep in comparison to non-remitters (n = 9). Treatment outcome after IPT was also associated with declarative memory performance at baseline (as a trend). CONCLUSIONS: Further indications of a role of sleep in memory processes and of the importance of specific sleep parameters as markers for a positive treatment response to psychotherapy were found.     

Admission glucose level in relation to mortality and morbidity outcome in 252 stroke patients

In a prospective study to correlate admission glucose level with neurologic outcome in stroke, 252 acute stroke patients without prior disability and admitted within 24 hours of onset of ictus were assessed. The stroke was classified into one of three types--cortical infarct, lacunar infarct, or intracerebral hemorrhage--by clinical, computed tomographic, and necropsy findings. Fifty-one diabetic patients were excluded from the entire cohort to form a nondiabetic category for analysis. We found that admission glucose level showed a significantly higher degree of correlation with mortality and morbidity (measured as arm function, leg function, and activities of daily living) when cortical (n = 118) and lacunar (n = 58) infarcts were pooled compared with when they were assessed separately. For intracerebral hemorrhage (n = 76), admission glucose level correlated with mortality but not morbidity. This trend persisted despite exclusion of diabetic patients. These results are consistent with previous observations of a correlation between a high admission glucose level and the severity of stroke. The importance of segregating cortical from lacunar infarcts, two groups with a different natural history and prognosis, in any future analysis is emphasized.     

Sleep and stroke

More than 50% of stroke patients have sleep-disordered breathing (SDB), mostly in the form of obstructive sleep apnea (OSA). SDB represents both a risk factor and a consequence of stroke. The presence of SDB has been linked with poorer long-term outcome and increased long-term stroke mortality. Continuous positive airway presure is the treatment of choice for OSA. Oxygen and other forms of ventilation may be helpful in other (e.g., central) forms of SDB. SDB can improve spontaneously after stroke. About 20 to 40% of stroke patients have sleep-wake disorders (SWD), mostly in form of insomnia, excessive daytime sleepiness/fatigue, or hypersomnia (increased sleep needs). Depression, anxiety, SDB, stroke complications, and medications may contribute to SWD and should be addressed first therapeutically. Brain damage per se, often at thalamic or brainstem level, can be also a cause of persisting SWD. In these patients, hypnotics, dopeminergic agents, and stimulants (e.g., modafinil) can be attempted.     

Confusional state in stroke: relation to preexisting dementia, patient characteristics, and outcome

BACKGROUND AND PURPOSE: Acute confusional state (ACS) is frequent in hospitalized stroke patients. We previously showed that 16% of patients admitted for a stroke have preexisting dementia. The extent to which preexisting cognitive decline is associated with a risk of ACS at the acute stage of stroke remains to be systematically examined. The aim of this study was to evaluate the prevalence of ACS in acute stroke patients, to study the influence of preexisting cognitive decline and other patient characteristics, and to evaluate the influence of ACS on outcome. METHODS: We diagnosed ACS using DSM-IV criteria and the Delirium Rating Scale with a cutoff of 10 in 202 consecutive stroke patients aged 40 years or older (median age, 75 years; range, 42 to 101 years). Cognitive functioning before stroke was assessed with the Informant Questionnaire on Cognitive Decline in the Elderly. RESULTS: Forty-nine stroke patients (24.3%; 95% CI, 18.3% to 30.2%) had an ACS during hospitalization. Using logistic regression analysis, we found preexisting cognitive decline (P=0.006) and metabolic or infectious disorders (P=0.008) to be independent predictors of ACS. Functional, but not vital, prognosis was worse in patients with ACS at discharge and 6 months after stroke. CONCLUSIONS: ACS occurs in one fourth of stroke patients older than 40 years. Its occurrence requires inquiry for a preexisting cognitive decline, which usually remains unrecognized in the absence of a systematic evaluation.     

Sleep disorders and stroke

The purpose of this review is to highlight existing literature on the epidemiology, pathophysiology, and treatments of stroke sleep disorders. Stroke sleep disorders are associated with many intermediary vascular risk factors leading to stroke, but they may also influence these risk factors through direct or indirect mechanisms. Sleep disturbances may be further exacerbated by stroke or caused by stroke. Unrecognized and untreated sleep disorders may influence rehabilitation efforts and poor functional outcomes following stroke and increase risk for stroke recurrence. Increasing awareness and improving screening for sleep disorders is paramount in the primary and secondary prevention of stroke and in improving stroke outcomes. Many vital questions about the relationship of sleep disorders and stroke are still unanswered and await future well-designed studies.     

Sleep disorders and stroke

Obstructive sleep apnea (OSA) is a very common condition in patients with stroke and is found in over half of stroke patients. There is a complex relationship between OSA and stroke, attributable to shared risk factors. There are numerous mechanisms by which OSA may contribute to increased stroke risk, including promotion of atherosclerosis, hypercoagulability, and adverse effects on cerebral hemodynamics. Obstructive sleep apnea is also a risk factor for hypertension, and likely for atrial fibrillation and diabetes, conditions that in turn are risk factors for stroke. OSA is also associated with poor outcomes following stroke. Further epidemiological studies are needed to assess the relationship between OSA and stroke better. Clinical trials using continuous positive airway pressure as a treatment for OSA in stroke patients are needed to determine whether treatment of this condition alters outcome following stroke.     

Sleep apnea and stroke

The concept of sleep apnea as a risk factor for primary stroke derives mainly from evidence implicating sleep-disordered breathing (SDB) in the causation or aggravation of systemic hypertension and heart disease. Evidence of an association between SDB and sustained systemic hypertension is available from several large studies, though the exact mechanism involved is unknown. Another study found a 37% increase in risk of developing cardiovascular disease among middle-aged men attending a sleep clinic. The same study also found that treatment of SDB reduced the cardiovascular risk. Other mechanisms less well studied linking SDB with cerebrovascular risk include reduction in cerebral blood flow, altered cerebral autoregulation, impaired endothelial function, and accelerated proinflammatory states.     

Low-normal free triiodothyronine and high leukocyte levels in relation to stroke severity and poor outcome in acute ischemic stroke with intracranial atherosclerotic stenosis

Background: It is uncertain that the effect of free triiodothyronine (FT3) within normal ranges on initial severity and early functional outcomes in acute ischemic stroke (AIS) patients with Intracranial Atherosclerotic Stenosis (ICAS). The predictive values of white blood cell (WBC) and FT3 are also unclear in symptomatic ICAS (sICAS) patients.

Methods: We consecutively reviewed 848 ischemic stroke patients admitted into Xiangya Hospital within 72?h after symptom onset. sICAS was defined as AIS patient with degree of ICAS ≥50% proved by magnetic resonance angiography, computed tomography angiography or digital subtraction angiography. WBC and FT3 were assessed within 24?h after admission. Neurological severity was evaluated on admission using the National Institutes of Health Stroke Scale (NIHSS). Stroke outcomes were defined by the modified Rankin Scale (mRS) on the 14th day after admission.

Results: Logistic regression analysis showed that hypertension, lower FT3 and higher WBC concentrations independently associated with severe stroke [FT3 (odds ratio(OR)?=?0.543, 95% confidence interval(95% CI): 0.383–0.769); hypertension (OR = 0.436, 95% CI: 0.238–0.800); WBC (OR = 1.17; 95% CI:1.041–1.316]. Besides, lower FT3, higher FT4, higher WBC and higher plasma glucose concentrations independently associated with unfavorable outcomes [FT3 (OR = 0.460; 95% CI: 0.306–0.690); FT4 (OR = 1.151; 95% CI: 1.055–1.255); WBC (OR = 1.178; 95% CI: 1.039–1.334); Plasma glucose (OR = 1.160; 95% CI: 1.002–1.342)].

Conclusions: Lower FT3 levels within normal ranges and higher WBC count are independently associated with the severity and early poor prognosis of sICAS simultaneously, FT3 and WBC count might be important biomarkers for sICAS patients.     

睡眠呼吸暂停综合征与脑卒中

本文综述睡眠呼吸暂停综合征与脑卒中的关系及其防治。近年来国内外大量流行病学研究表明,睡眠呼吸暂停综合征(SAS)可显著增加脑卒中发生和死亡的风险,被认为是脑卒中发生的独立危险因素。由SAS产生的呼吸暂停、低氧血症、高碳酸血症引起的血压改变、脑血流动力学改变、脑自动调节功能减退及血液流变学改变是患者发生脑卒中的主要机制。目前在脑卒中的防治中已越来越关注对SAS的早期诊断和治疗。多道睡眠描记术(Poly- somnography,PSG)是诊断SAS的“金标准”。针对SAS的治疗中,经鼻持续气道正压通气为首选治疗措施。     

Sleep problems in the aged in relation to senility

Abstract As a part of an epidemiologic survey of dementia in a community of aged persons, correlation between sleep complaints and physical illness and senility were studied. A total of 3302 randomly sampled aged individuals (aged 65 yean) were studied using a questionnaire. In this sample the prevalence of poor sleep and habitual snoring did not increase with age. The prevalence of excessive daytime sleepiness showed an increase with age. Male predominance of habitual snoring and female predominance of poor sleep were observed. Female predominance of excessive daytime sleepiness was noted among the aged 70 and over. Age-related excessive daytime sleepiness was significantly correlated with senility.     

Sleep disturbances in relation to fatigue in major depression

Objective

This study aimed to investigate the independent correlations of subjective sleep disturbances (insomnia and daytime sleepiness) with the severity of fatigue in patients with major depression.

Methods

Eighty-one currently depressed patients (70 females and 11 males), aged between 23 and 65 years, with a DSM-IV diagnosis of major depressive disorder were studied. Patients with physical diseases or other conditions associated with prominent fatigue were excluded. The 17-item Hamilton Depression Rating Scale (HDRS), the Athens Insomnia Scale (AIS), and the Epworth Sleepiness Scale (ESS) were used for the cross-sectional assessment of the severity of depression, insomnia, and sleepiness, respectively. Severity of fatigue was measured with the Fatigue Severity Scale (FSS). Pearson's and Spearman's coefficients were used in bivariate correlations between FSS score and the independent variables (age, gender, inpatient/outpatient status, HDRS score, AIS total score, AIS individual item scores, and ESS score). A stepwise multiple regression analysis was then performed, with FSS score as the dependent variable.

Results

The severity of fatigue was significantly correlated with female sex, HDRS score, AIS total score, awakenings during the night (AIS item 2), compromised sleep quality (AIS item 5), and ESS score. Sleep quality (AIS item 5) and daytime sleepiness (ESS) were the only significant predictors of the severity of fatigue in the multiple regression analysis.

Conclusions

Both sleep quality and daytime sleepiness correlate independently with fatigue severity, as measured with the FSS, in patients with major depression. The FSS does not appear to be a ‘pure’ measure of fatigue in depressed patients, a finding with potential implications for the choice of appropriate fatigue measures in this population.     

Sleep patterns in acute ischemic stroke

We studied polysomnographic recordings using an Oxford Medilog 9000 System in 18 patients with ischemic stroke in the middle cerebral artery territory. All patients underwent neurologic examination and brain CT scan within 5 h after the onset of symptoms. Polysomnographic recordings were started immediately thereafter and went on for three nights. Clinical and polysomnographic follow-up were performed 3 weeks after admission. The number and duration of REM phases were significantly reduced in the acute phase. This reduction correlated with the severity of neurological deficit at outcome and with the anatomical site of the lesion on CT scan. Our data provide evidence that polysomnographic recording is useful to detect symptoms of patients with different clinical outcomes during the acute phase of ischemic stroke.     

Leukoaraiosis and stroke outcome

We studied the influence of leukoaraiosis on the prognosis of stroke for the first year after onset. Three hundred and seventy consecutive stroke subjects were observed for 1 year. Data were collected prospectively in a questionnaire constructed in accordance with the Stroke Data Bank and analyzed using SPSS. Leukoaraiosis was observed in 17.6% of subjects. Subjects with leukoaraiosis were older than subjects without leukoaraiosis. Cerebrovascular risk factors were similar in both groups. During the first 30 days, the fatality rate of both groups was similar. However, at 1 year, the fatality rate in subjects with leukoaraiosis was higher. Stroke Severity, Weakness Score, and the Barthel Modified Activities for Daily Living score did not differ between groups at 30 days or 1 year. At both 30 days and 1 year, the MMSE score was lower in subjects with leukoaraiosis. Leukoaraiosis did not predict stroke recurrence within 1 year. Leukoaraiosis in stroke patients is an adverse predictor of cognitive functioning at 30 days and at 1 year and is an adverse predictor of survival at 1 year.     

Sleep architecture in school-aged children with primary snoring

ObjectiveWe aimed to examine if sleep architecture was altered in school-aged children with primary snoring (PS).MethodsChildren ages 6 to 13 years from 13 primary schools were randomly recruited. A validated obstructive sleep apnea (OSA) screening questionnaire was completed by their parents. Children at high risk for OSA and a randomly chosen low-risk group were invited to undergo overnight polysomnography (PSG) and clinical examination. Participants were classified into healthy controls, PS, mild OSA, and moderate to severe OSA (MS OSA) groups for comparison.ResultsA total of 619 participants underwent PSG (mean age, 10.0 ± 1.8 years; 396 (64.0%) boys; 524 (84.7%) prepubertal). For the cohort as a whole, there were no significant differences in measures of sleep architecture between PS and nonsnoring healthy controls. In the multiple regression model, percentage of nonrapid eye movement (NREM) stage 1 (N1) sleep had a significantly positive association, whereas percentage of slow-wave sleep (SWS) had a significantly negative association with sleep-disordered breathing (SDB) severity after controlling for age, gender, body mass index (BMI) z score, and pubertal status. In prepubertal children with PS, no significant disruption of sleep architecture was found. However, pubertal adolescent PS participants had significantly higher adjusted percentage of N1 sleep and wake after sleep onset (WASO) compared to healthy controls.ConclusionsPS did not exert significant adverse influences on normal sleep architecture in prepubertal school-aged children. Nevertheless, pubertal adolescents with PS had increased N1 sleep and WASO.     

Sleep architecture in patients with Juvenile Myoclonic Epilepsy

AimThe aim is to analyze the sleep architecture using polysomnography (PSG) in patients with Juvenile Myoclonic Epilepsy (JME): (newly diagnosed and those on valproate drug) attending epilepsy clinic at Alexandria University Hospitals.MethodsThis study involved 20 patients with JME on valproate (age: 22.40 ± 5.80 years; M:F = 6:14), 20 newly diagnosed patients (age: 18.55 ± 6.0 years; M:F = 6:14), and 20 matched healthy controls (age: 22.10 ± 5.0 years; M:F = 6:14). Clinical assessment, electroencephalogram (EEG), evaluation with comprehensive sleep questionnaire, and PSG were done for all patients.ResultsPSG showed significant alterations in sleep architecture in the total JME group in the form of reduced mean sleep efficiency (p = 0.001¹), increased mean Rapid eye movement (REM) onset latency (p = 0.046¹), decrease mean REM percentage (p = 0.011¹), increased mean wakefulness after sleep onset (p = 0.018¹), increase the index of total arousal (p = 0.005¹), increased mean periodic limb movement index (P = 0.001¹), and reduced apnea hypopnea index (P = <0.001) in comparison to control group. Valproate treated group showed increased sleep efficiency (p = 0.040¹), decreased REM arousal index (P = 0.012), longer stage 3 (P = 0.038), and prolonged stage 2 (P = 0.049¹) than the newly diagnosed group.ConclusionsSleep architecture was significantly disturbed in JME, with improvement in sleep efficiency in valproate treated patients.     

Sleep architecture in children with idiopathic generalized epilepsy

PURPOSE: Children with epilepsy experience sleep disturbances, behavioral and attentional problems at higher rates than their peers. However, the relation between sleep disturbances and the observed behavioral and attentional abnormalities is poorly defined. METHODS: Children with primary generalized epilepsy who were seizure free and between the ages of 5 and 18 years were matched with age- and gender-matched healthy controls and underwent two consecutive nights of nocturnal polysomnography with extended electroencephalography. Connor's Continuous Performance Test (CPT) was administered to assess daytime attentional function. Parents completed the Child Behavior Checklist (CBCL) to assess their emotional-behavioral status. Two sample t tests were used to examine group differences. Spearman correlations were used to examine the relation between sleep variables and behavior and attention variables. Multiple regression analysis was used to identify independent predictors of abnormal behavior and attention among patients. RESULTS: Eleven children with primary generalized epilepsy and eight age- and sex-matched controls participated in the study. Children with epilepsy had longer stage 1 sleep percentage (7.19 +/- 3.2 vs. 4.8 +/- 3.5; p = 0.05) and latency to rapid-eye-movement (REM) sleep (123.5 +/- 40.1 vs. 101.75 +/- 24.3; p = 0.018) compared with controls. Children with epilepsy had worse attention (CPT index, 10.94 +/- 6.55 vs. 3.42 +/- 4.04; p = 0.004) and exhibited significantly higher CBCL Total Behavior and Internalizing Behavior Problem scales. Whereas regression analysis showed no independent predictors of abnormal behavior and attention, a tendency toward association between CBCL total behavior scale and REM percentage (r= 0.55; p = 0.07), and between CPT overall index and stage 1 sleep percentage (r= 0.40; p = 0.10) was noted. CONCLUSIONS: Sleep architecture is abnormal in children with primary generalized epilepsy. Further studies are needed to determine whether abnormalities in sleep architecture contribute to poor daytime behavior and attention.