不宁腿综合征

不宁腿综合征为临床常见中枢神经系统感觉运动障碍性疾病,发病机制尚不明确,与遗传因素或多巴胺能系统功能失调有关。发病原因与缺铁性贫血、妊娠、免疫系统疾病、肾衰竭、糖尿病、周围神经病等有关。临床主要表现为感觉障碍、运动症状,并于休息时、傍晚或夜间出现或加重。以铁离子、多巴胺制剂、多巴胺受体激动药、抗癫痂药及阿片类药物为主要治疗药物,     

不宁腿综合征

不宁腿综合征为临床常见中枢神经系统感觉运动障碍性疾病,发病机制尚不明确,与遗传因素或多巴胺能系统功能失调有关。发病原因与缺铁性贫血、妊娠、免疫系统疾病、肾衰竭、糖尿病、周围神经病等有关。临床主要表现为感觉障碍、运动症状,并于休息时、傍晚或夜间出现或加重。以铁离子、多巴胺制剂、多巴胺受体激动药、抗癫药及阿片类药物为主要治疗药物。     

不宁腿综合征的临床分析

目的讨论不宁腿综合征的临床表现、诊断与治疗。方法回顾分析不宁腿综合征8例。结果不宁腿综合征以双下肢感觉异常为突出表现,静息时出现或加重,活动及被动运动症状缓解或消失,夜间症状突出而导致睡眠障碍,不宁腿综合征常常被误诊为其他疾病。结论不宁腿综合征诊断主要依据特征性的临床表现,左旋多巴制剂及多巴胺受体激动剂疗效肯定。     

不宁腿综合征的临床分析

目的 讨论不宁腿综合征的临床表现、诊断与治疗.方法 回顾分析不宁腿综合征8例. 结果不宁腿综合征以双下肢感觉异常为突出表现,静息时出现或加重,活动及被动运动症状缓解或消失,夜间症状突出而导致睡眠障碍,不宁腿综合征常常被误诊为其他疾病. 结论不宁腿综合征诊断主要依据特征性的临床表现,左旋多巴制剂及多巴胺受体激动剂疗效肯定.     

长期误诊为焦虑抑郁障碍的不宁腿综合征1例

正1病例患者,男,47岁,汉族,高中文化,公司职员。因失眠焦虑伴情绪低落7年就诊。患者7年前工作调动,压力大,逐渐出现失眠,夜间入睡困难,夜眠浅,时睡时醒,每晚睡4～5 h,白天精神差,头昏昏沉沉,尚能坚持工作生活,症状持续1年余,至当地某医院就诊,诊断失眠,予安定片治疗,症状较前略改善,后一直坚持服药,失眠持续存在。5年前患者病情加重,易醒转,醒后无法再次入睡,白天焦虑不安,反复担     

继发性不宁腿综合征

本文回顾继发性不宁腿综合征的相关研究结果,介绍其常见病因。经研究显示,有多种因素可能与继发性不宁腿综合征的发生发展和严重程度相关,如肾衰竭、脊髓和周围神经病变、妊娠所致铁和叶酸缺乏及相应性激素变化;帕金森病多巴胺能系统功能紊乱;某些药物（抗抑郁药、抗精神病药、组胺受体阻断药）;吸烟、饮酒;咖啡因;偏头痛等。临床应详细询问病史,去除病因,提高患者生活质量。     

帕金森病合并不宁腿综合征的相关因素分析

目的研究帕金森病(Parkinson's disease,PD)患者合并不宁腿综合征(restless leg syndrome,RLS)的特点,进一步探讨PD患者易合并RLS的相关因素。方法选取门诊诊断为PD的102例患者,根据是否合并RLS将入选病例分为不伴RLS的PD组和伴RLS的PD组,分别比较两组的一般状况、病史、临床表现、严重程度评分以及治疗等临床资料,进行单因素统计分析。结果102例PD患者中有28例合并有RLS,发生率为27·5%。其中有1例为诊断PD之前即存在RLS,其余均在出现PD症状后才出现RLS症状。两组在HAMD评分上有统计学差异(P0.05),而在一般状况,主要症状,左旋多巴的治疗以及蒙特利尔,UPDRS评分等方面均未见统计学差异(P0.05)。PD患者中RLS的发生与抑郁情绪有着较密切的关系,另外发现PD发病年龄与RLS的严重程度呈负相关。PD患者的发病年龄越小,RLS的程度越严重。结论PD患者抑郁状态时合并RLS的可能性较大。PD合并RLS患者,PD的发病年龄越小,RLS程度越严重。     

帕金森病合并不宁腿综合征26例临床分析

目的探讨帕金森病（Parkinson’s disease,PD）患者合并不宁腿综合征（restless leg syndrome,RLS）的临床特点,且进一步研究PD患者合并RLS的相关因素。方法选取确诊的119例PD患者,根据是否合并RLS分为伴RLS组和单纯PD组,分别比较2组的一般状况、病史、临床表现、严重程度、合并症、治疗情况等临床资料。结果 119例PD患者中26例合并RLS,发生率为20.8%,且RLS均出现在PD症状后。2组在UPDRS、HAMD、HAMA、PSQI上有统计学差异（P〈0.05）,而在一般状况、主要症状、左旋多巴治疗等方面均未见统计学差异（P〉0.05）。另外,发现左旋多巴的日剂量与RLS严重度之间存在正相关关系,即服用左旋多巴剂量越大,RLS程度越重。结论 RLS可能是PD病程中出现的一种并发症。PD运动症状较严重、并发症较多时合并RLS的可能性相对较大,随着多巴胺能药物剂量的加大,RLS的病情可能加重。     

继发性不宁腿综合征

本文回顾继发性不宁腿综合征的相关研究结果,介绍其常见病因。经研究显示,有多种因素可能与继发性不宁腿综合征的发生发展和严重程度相关,如肾衰竭、脊髓和周围神经病变、妊娠所致铁和叶酸缺乏及相应性激素变化;帕金森病多巴胺能系统功能紊乱;某些药物(抗抑郁药、抗精神病药、组胺受体阻断药);吸烟、饮酒;咖啡因;偏头痛等。临床应详细询问病史,去除病因,提高患者生活质量。     

帕金森病与不宁腿综合征

帕金森病为慢性进行性神经系统变性疾病，典型临床症状包括运动迟缓、静止性震颤、强直以及姿势平衡障碍。不宁腿综合征（restless legs syndrome，RLS）系指出现在腿部的不适感导致难以控制的移动下肢的冲动，多发生在夜间并由此而产生睡眠障碍。早在19世纪，《震颤麻痹》一书中就已首次提出帕金森病患在夜间会出现频繁的肢体运动。近年来不断有研究报道，帕金森病患不宁腿综合征的发病率高于普通人群，提示二之间可能存在某种联系。[第一段]     

Cognitive behavioral therapy for insomnia in restless legs syndrome patients

ObjectivesThe purpose of this study was to investigate the effects of cognitive behavioral therapy for insomnia (CBTI) in patients with Restless Legs Syndrome (RLS).MethodsThis is a randomized controlled study. The patients were sequentially selected and randomly assigned to either a CBTI group or a non-CBTI group. A total of 25 RLS patients with comorbid insomnia were recruited from a tertiary university hospital sleep center. Twelve were assigned to the CBTI group, and 13 were assigned to the non-CBTI group. The CBTI group received 4 sessions of behavioral therapy, while the non-CBTI group received one informative session on sleep hygiene. All patients completed sleep and psychiatric-related questionnaires. In addition, each individual completed a one-week sleep log for collecting subjective sleep data and actigraphy for objective sleep data.ResultsAfter conducting the CBTI, there were significant improvements in severity of insomnia symptoms, subjective sleep efficiency, total sleep time, latency to sleep onset, wake after sleep onset, objective latency to sleep onset, and anxiety in the CBTI group as compared to the non-CBTI group. The effect of CBTI on sleep-related data was maintained for up to three months.ConclusionsCBTI was effective in RLS patients by improving sleep quality and anxiety symptoms. CBTI may be considered in clinical practice for RLS patients with comorbid insomnia.     

Sleep spindles in children with restless sleep disorder,restless legs syndrome and normal controls

ObjectiveTo analyze and identify differences in sleep spindles in children with restless sleep disorder (RSD), restless legs syndrome (RLS) and normal controls.MethodsPSG (polysomnography) from children with RSD, RLS and normal controls were analyzed. Sleep spindle activity was detected on one frontal and one central electrode, for each epoch of N2 and N3 sleep. Sleep spindle density, duration and intensity (density × duration) were then obtained and used for analysis.ResultsThirty-eight children with RSD, twenty-three children with RLS and twenty-nine controls were included. The duration of frontal spindles in sleep stage N2 was longer in children with RSD than in controls. Frontal spindle density and intensity tended to be increased in RSD children. No significant differences were found for central spindles.ConclusionChildren with RSD had longer frontal spindles. This finding may contribute to explain the occurrence of excessive movement activity during sleep and the presence of daytime symptoms.SignificanceRecent research has demonstrated that children with RSD have increased NREM instability and sympathetic activation during sleep. Analyzing sleep spindles in children with RSD in comparison with children with RLS and controls adds to our understanding of the pathophysiology or RSD and its effects on daytime impairment.     

High prevalence of restless legs syndrome in somatoform pain disorder

Patients with somatoform pain often complain of sleep disorders, but sleep disorders are not an integrated part of the diagnosis of this disorder. Restless legs syndrome is associated with painful symptoms and sleep disturbances. The aim of our study was to evaluate the prevalence of restless legs syndrome (RLS) in somatoform pain disorder. Method In this study 100 consecutive patients (mean age: 46.4; SD: 11.4; women: 58) diagnosed with somatoform pain disorder (SPD) were clinically investigated for the occurrence of RLS at the behavioral medicine clinic for pain outpatients in the department of psychiatry within the Medical University of Vienna. The pain parameters of SPD were assessed using a pain questionnaire and visual analogue scales (VAS). The severity of RLS was established using the questionnaire of the International Restless Legs Syndrome Study Group (IRLSSG). Results The prevalence of restless legs syndrome found in somatoform pain disorder was 42%. Interrupted sleep was found in 83.3% in somatoform pain disorder with comorbid RLS and in 64.1% in somatoform pain disorder without RLS. Patients with continuous somatoform pain had a significant higher occurrence of RLS (Sample: 55%; with RLS: 71.4% and without RLS: 43.1%). The pain parameters increased parallel to the severity of RLS. Additionally, RLS was associated with higher psychosocial disability in family life. Conclusions The prevalence of RLS is high in our sample of patients with somatoform pain disorder. There seems to be a difference in pain profile between patients with and without RLS. RLS may increase the pain level and prolong pain in somatoform pain disorder. RLS should be considered when a somatoform pain disorder is diagnosed.     

Secondary periodic limb movement disorder and restless legs syndrome

Periodic limb movement disorder (PLMD) and restless legs syndrome (RLS) are well-known entities from a clinical and polysomnographic point of view. PLMD and RLS are seen mostly as primary or hereditary diseases, but may occur in conjunction to other diseases such as uremia, polyneuropathy, Parkinson's disease, and deficiencies of iron and magnesium. This review will discuss the prevalence, etiology and pathophysiology of secondary PLMD and RLS.     

Ropinirole in a child with attention-deficit hyperactivity disorder and restless legs syndrome

A 6-year-old male being treated with limited efficacy by methylphenidate immediate release for attention-deficit hyperactivity disorder also presented with sleep disruption due to potential restless legs/periodic limb movement syndrome. Treatment with the dopamine agonist ropinirole resulted in a significant improvement in both his attention-deficit hyperactivity disorder symptoms and sleep problems.     

Higher nocturnal systolic blood pressure in patients with restless legs syndrome compared with patients with insomnia

BackgroundThere is evidence linking restless legs syndrome (RLS) with increased blood pressure (BP), but the mechanism of this relation remains unclear. Is the BP increased due to some features of RLS or to deterioration of sleep caused by RLS? This study compared values of nocturnal BP in patients with RLS and patients with insomnia. If increased BP in RLS is a consequence of disordered sleep, then it should be similar to increased BP in insomnia.MethodsPolysomnographic recordings of patients admitted to a sleep center with RLS or insomnia were analyzed. Demographic and clinical data, objective sleep parameters, and nocturnal BP were compared.ResultsRecordings of 35 patients with RLS and 33 patients with insomnia were analyzed. The groups did not significantly differ in terms of demographic traits or prevalence of other comorbidities. Patients with RLS had significantly higher systolic BP during the night (122.4 ± 13.8 vs 116.3 ± 13.4; p = 0.03) and during sleep (121.4 ± 13.3 vs 115.7 ± 13.3; p = 0.04). The only significant difference in sleep architecture was an increased number of periodic limb movements in sleep (PLMS) and PLMS with arousal in the RLS group (25.5 ± 24.6 vs 13.9 ± 22.7; p = 0.02 and 4.7 ± 5.4 vs 2.1 ± 3.4; p = 0.01).ConclusionOur results suggest that patients with RLS have higher nocturnal BP than patients with insomnia, and that increased PLMS is related to the increase in BP.     

Olanzapine-induced restless legs syndrome

Only nine patients with olanzapine-induced restless legs syndrome (RLS) have been reported in the literature to our knowledge. We describe two patients with olanzapine-induced RLS treated at our hospital and review the nine reported patients. There were five women and six men aged between 28 and 62 years in the overall group. RLS symptoms emerged at olanzapine doses between 2.5 and 20 mg. The symptoms improved in all patients when the dose was reduced and immediately disappeared when the medication was stopped. International Restless Legs Scale (IRLS) scores ranged from 10 to 35. Three patients had a family history of idiopathic RLS. Supplemental drugs were administered to control RLS symptoms in five patients. Ropinirole was effective in one patient, while two patients did not respond to the drug. Propoxyphene effectively relieved symptoms in one patient who did not respond to ropinirole or clonazepam. RLS symptoms did not recur following substitution of other antipsychotic drugs for olanzapine. In conclusion, olanzapine can induce RLS, particularly in patients with a family history of idiopathic RLS. More than half of the patients experienced severe to very severe symptoms. A dose-dependent relationship was observed between olanzapine and RLS symptoms. A gradual increase in dose may prevent olanzapine-induced RLS. The optimal treatment for olanzapine-induced RLS is discontinuation of olanzapine.