自然睡眠与药物诱导睡眠对脑电图睡眠脑波的影响

目的：观察药物诱导睡眠脑电图和睡眠剥夺脑电图的差别，初步探讨药物诱导和睡眠剥夺对睡眠脑波的影响。方法：选择2003-06／2004-06重庆三峡中心医院门诊和住院的3个月～12岁的患儿，临床有两项诊断中至少有一项诊断为癫痫或临床拟诊癫痫共383例。随机分为睡眠剥夺一自然睡眠组200例，药物诱导睡眠组183例。睡眠剥夺组不用药物，采用禁睡4～10h后描记脑电图，年龄越小禁睡时间越短。药物诱导睡眠组服用100g／L水合氯醛，剂量采用1mL／岁，最多10mL，待快入睡时描记脑电图。使用视频数字脑电图仪按国际10-20系统放置8-16个头皮盘状电极，参考电极置于双耳垂或Cz，均作单、双极导联描记。记录30-90mitt的脑电图，包括常规脑电图-睡眠脑电图-觉醒后脑电图或睡眠脑电图一觉醒后脑电图。对比分析觉醒、睡眠时程、着重观察有无非快速眼球运动睡眠期Ⅰ-Ⅱ期睡眠和睡眠纺锤的变化及癫痫放电频率。结果：两组患383例均收集到脑电图，全部进入结果分析。①两组觉醒状态时快波活动：药物诱导睡眠组中73．8％(135／183)的儿童觉醒状态时快波活动增多，睡眠剥夺一自然睡眠组的儿童觉醒状态时仅5．0％(10／200)快波活动增多。②睡眠状态中的睡眠时相：药物诱导睡眠组中24．0％(44／183)能见到非快速眼球运动睡眠期Ⅰ～Ⅱ期睡眠。睡眠剥夺-自然睡眠组85．0％(170／200)见到较完整的睡眠时程，包括非快速眼球运动睡眠期Ⅰ-Ⅳ期。③睡眠纺锤：药物诱导睡眠组37．7％(69／183)可见，睡眠剥夺-自然睡眠组76．O％(152／200)可见。④癫痫样放电：药物诱导睡眠组发现有22．4％(41／183)，睡眠剥夺-自然睡眠组发现有66．O％(132／200)。⑤睡眠纺锤与临床诊断的关系：药物诱导睡眠组中发现睡眠纺锤缺失62．3％(114／183)，其中临床拟诊“癫痫?”34例；拟诊“继发性癫痫?脑性瘫痪”26例；拟诊“继发性癫痫?大脑发育不全”28例；拟诊“癫痫?非典型热性惊厥?”17例；拟诊“癫痫?屏气发作”5例；拟诊“癫痫?癔病?”4例。有22．4％(41／183)发现癫痫样放电，其中有26．8％(11／41)可见极度纺锤波。睡眠剥夺-自然睡眠组中睡眠纺锤缺失24．O％(48／200)，其中临床拟诊“癫痫?”17例；拟诊“癫痫?脑性瘫痪”15例；拟诊“癫痫?大脑发育不全”8例；拟诊“癫痫?非典型热性惊厥?”6例；拟诊“癫痫?癔病?”2例。有66．O％(132／200)发现癫痫样放电的患儿中有30．3％(40／132)可见极度纺锤波。结论：药物诱导睡眠很快进入深睡期，不利于观察癫痫样放电等异常波最容易出现的非快速眼球运动睡眠期Ⅰ-Ⅱ期睡眠，同时由于药物的作用，快波增多，睡眠纺锤活动亦被掩盖，直接影响对睡眠脑波的分析。     

癫痫诊断中睡眠剥夺和药物诱导睡眠脑电图的临床价值

目的:对癫痫诊断中睡眠剥夺、药物诱导睡眠脑电图的临床应用价值进行分析。方法:以我院80例癫痫患者为调查样本,将其随机分为人数相等的两组,观察组患者给予睡眠剥夺诱导睡眠,研究组给予药物诱导睡眠,对两组患者睡眠脑电图扫描情况进行比较,并对两种睡眠诱导方式进行比较。结果:两组患者清醒期睁眼抑制、枕区α波优势、脑电图快波检测情况无统计差异(P>0.05)。观察组与研究组完整睡眠时相率无统计差异(P>0.05);观察组癫痫样放电率高于研究组,统计有差异(P<0.05)。结论:睡眠剥夺能够提升睡眠脑电图阳性率,但药物诱导操作简便,临床中可酌情选择。     

癫痫患者自然睡眠诱发脑电图92例分析

目的 :观察自然睡眠诱发脑电图对癫痫的诊断价值。方法 :对 92例临床拟诊癫痫的患者行常规脑电图和自然睡眠诱发脑电图检查。结果 :常规脑电图 30 % ( 2 7例 )出现痫样放电 ,而自然睡眠诱发脑电图 75 % ( 6 9例 )出现痫样放电。痫样放电检出率与年龄、临床发作类型、睡眠周期有关。结论 :自然睡眠诱发脑电图可显著地提高痫样放电的检出率 ,对癫痫的诊断与鉴别诊断有重要的参考价值     

剥夺性睡眠后自然睡眠脑电图在癫痫诊断中的意义

目的：探讨剥夺睡眠后自然睡眠脑电图对癫痫的诊断价值。方法：对86例临床诊断癫痫患进行常规及剥夺睡眠脑电描记，并进行随访。结果：本组86例癫痫患间歇期常规脑电图异常率为26．5％(23／86)，剥夺睡眠脑电图异常率为77．9％(67／86)，剥夺睡眠脑电图能够较明确提示癫痫病人发作类型，指导临床用药，并与非癫痫发作进行鉴别。结论：剥夺睡眠脑电图痫样放电检出率显提高，对癫痫的诊断与鉴别诊断有重要的参考价值。     

睡眠诱发脑电图在小儿癫痫诊断中的意义

目的 :探讨睡眠脑电图在小儿癫痫诊断中的意义。方法 :对 1998年 7月～ 1999年 7月疑为癫痫的患儿脑电图进行总结 ,对其中 130例确诊为癫痫的患儿进行自身对照回顾性研究 ,同一患者既作清醒状态脑电图 ,又作睡眠脑电图。睡眠脑电图均在自然或剥夺睡眠状态下进行。出现棘波、尖波、棘慢复合波、尖慢复合波或多棘慢复合波认为脑电图检查阳性。结果 :本年度疑为癫痫患者 6 0 5人次 ,清醒脑电图阳性率36 8% (99/ 2 6 9) ,睡眠脑电图阳性率 5 1 2 % (172 / 336 ) ,睡眠脑电图阳性率较清醒脑电图更高 (χ2 =12 5 ,P =0 0 0 0 4)。 130例中清醒脑电图阳性 38例 ,阳性率 2 9 2 % (38/ 130 ) ,同组患者睡眠脑电图阳性率净增加 92例(即不包括清醒阳性的 38例 ) ,净增 70 8% (92 / 130 )。结论 :睡眠脑电图能明显提高癫痫确诊率 ,疑为癫痫的患儿在作清醒状态脑电图同时应作睡眠脑电图。     

睡眠剥夺在癫痫患儿视频脑电图监测中的应用价值

[目的]探讨研究睡眠剥夺在癫痫患儿视频脑电图监测中的应用价值。[方法]将于本院收治的在癫痫患儿中抽出100例,并将其平均分成观察组和对照组。观察组在患儿视频脑电图监测中加以睡眠剥夺进行干预,对照组选择常规脑电图进行干预,比较两组患儿的临床效果。[结果]观察组检测出43例脑电图异常(86.00%),其中痫样放电(阳性检出率)35例(81.40%),均较对照组26例脑电图异常(52.00%)、痫样放电15例(57.69%)对应值高,且差异有统计学意义(P0.05)。[结论]在癫痫患儿诊断中加以睡眠剥夺视频脑电图监测进行干预,检测效果显著,是提高患儿脑电图异常及痫阳性检出率的有效措施。     

剥夺睡眠脑电图对儿童癫痫的诊断价值

目的探讨剥夺睡眠诱发试验对癫痫的诊断价值。方法对180例临床诊断为癫痫的患儿进行常规脑电图和剥夺睡眠脑电图,比较两者痫样放电率及与癫痫类型的关系。结果与常规脑电图比较剥夺睡眠脑电图可提高脑电图痫样放电率（痫样放电率从30％提高到76％,P〈0．01）。并观察到精神运动性癫痫阳性率高。结论剥夺睡眠脑电图可明显提高痫样放电检出率,应作为癫痫患儿的常规检查。     

剥夺睡眠-睡眠脑电图对小儿癫痫的诊断价值（附86例报道）

目的探讨剥夺睡眠-睡眠联合诱发脑电图对小儿癫痫的诊断价值。方法对86例临床诊断为癫痫而间隙期常规脑电图检查正常的小儿癫痫患者进行剥夺睡眠-睡眠联合诱发脑电图描记。结果86例中间隙期常规EEG均未发现异常,剥夺睡眠-睡眠联合诱发EEG检查痫样放电率81．4％。结论剥夺睡眠-睡眠联合诱发脑电图痫样放电率明显提高,对小儿癫痫的诊断具有重要价值。     

视频EEG剥夺睡眠诱发试验对癫痫的诊断价值

目的探讨视频EEG剥夺睡眠诱发试验对癫痫的诊断价值。方法对134例临床诊断为癫痫及可疑癫痫病人施行视频脑电图剥夺睡眠（检查前禁睡20-36 h）诱发试验,分别记录剥夺睡眠后清醒状态（包括睁闭眼、过度换气等诱发试验）及剥夺睡眠后自然睡眠状态2-4 h的脑电图变化。结果134例病人中,73例诱发出癫痫样放电,其中64例根据发作期和发作间期脑电图特征,结合有关病史及临床表现确诊为癫痫。7例病人癫痫的发作类型得到了修正。结论与常规脑电图比较,视频脑电图剥夺睡眠诱发试验不但能提高癫痫的诊断率,且对癫痫的分型亦起到重要的作用。     

癫痫患者剥夺睡眠-睡眠诱发EEG与常规EEG对比分析

[目的]探讨剥夺睡眠-睡眠诱发脑电图(EEG)与常规EEG对癫痫诊断的价值.[方法]对138例临床确认的癫痫患者分别进行常规EEG和剥夺睡眠诱发EEG检查,将二次结果异常率与痫样放电率与睡眠周期比较.[结果]常规EEG痫样放电检出率为32.6%,异常率64.5%,剥夺睡眠-睡眠诱发EEG痫样放电检出率为84.1%,异常率84.1%,两者比较痫性放电率差异有显著性(P＜0.01).[结论]剥夺睡眠-睡眠诱发EEG可明显提高癫痫患者EEG的痫样放电率,痫样放电率在睡眠Ⅰ期Ⅱ期最高,少儿较成人检出率更高.     

Genes for normal sleep and sleep disorders

Sleep and wakefulness are complex behaviors that are influenced by many genetic and environmental factors, which are beginning to be discovered. The contribution of genetic components to sleep disorders is also increasingly recognized as important. Point mutations in the prion protein, period 2, and the prepro-hypocretin/orexin gene have been found as the cause of a few sleep disorders but the possibility that other gene defects may contribute to the pathophysiology of major sleep disorders is worth in-depth investigations. However, single gene disorders are rare and most common disorders are complex in terms of their genetic susceptibility, environmental effects, gene-gene, and gene-environment interactions. We review here the current progress in the genetics of normal and pathological sleep.     

Genes for normal sleep and sleep disorders

Sleep and wakefulness are complex behaviors that are influenced by many genetic and environmental factors, which are beginning to be discovered. The contribution of genetic components to sleep disorders is also increasingly recognized as important. Point mutations in the prion protein, period 2, and the prepro‐hypocretin/orexin gene have been found as the cause of a few sleep disorders but the possibility that other gene defects may contribute to the pathophysiology of major sleep disorders is worth in‐depth investigations. However, single gene disorders are rare and most common disorders are complex in terms of their genetic susceptibility, environmental effects, gene‐gene, and gene‐environment interactions. We review here the current progress in the genetics of normal and pathological sleep.     

BDNF in sleep,insomnia, and sleep deprivation

The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase.

• Key messages

• Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders.

• The interplay of stress and sleep impacts on BDNF level.

• Partial sleep deprivation (PSD) shows a fast action on BDNF level increase.