唑吡坦治疗失眠症双盲研究

目的：比较国产唑吡坦片和进口唑吡坦片治疗失眠症的疗效和不良反应。方法：对32例失眠症患者随机分为两组,分别服用国产或进口唑吡坦。采用睡眠障碍量表（SDRS）、汉密尔顿焦虑量表（HAMA）、临床总体印象量表（CGI）和副反应量表（TESS）评定疗效和不良反应。结果：SDRS评定国产唑吡坦组减分率为49．7％,与进口唑吡坦组49．8％相近,主要不良反应为头痛、口干、便秘和出汗等,病人均能耐受。结论：国产唑吡坦治疗失眠症的疗效和进口唑吡坦相当。     

唑吡坦按需治疗失眠症的临床研究

目的　探讨唑吡坦非每夜给药 (按需治疗 )对慢性失眠症的疗效及不良反应。方法　比较唑吡坦非每夜给药 (按需治疗 )和唑吡坦每夜给药 (持续治疗 )的疗效和不良反应。对慢性失眠者 40例进行对照研究。结果　持续治疗和按需治疗疗效相近 ,治疗过程中无反跳现象及撤药反应。结论　唑吡坦按需治疗方法有效可行 ,对不需每夜服药 ,又害怕对药物产生依赖的患者提供了一个较好的长期治疗方案。     

唑吡坦按需治疗失眠症的临床研究

目的 探讨唑吡坦非每夜给药(按需治疗)对慢性失眠症的疗效及不良反应。方法 比较唑吡坦非每夜给药(按需治疗)和唑吡坦每夜给药(持续治疗)的疗效和不良反应。对慢性失眠者40例进行对照研究。结果 持续治疗和按需治疗疗效相近，治疗过程中无反跳现象及撤药反应。结论 唑吡坦按需治疗方法有效可行，对不需每夜服药，又害怕对药物产生依赖的患者提供了一个较好的长期治疗方案。     

酒石酸唑吡坦片治疗急性脑卒中后失眠的临床疗效

目的分析酒石酸唑吡坦片在急性脑卒中后失眠治疗中的应用价值。方法选取我院2014-07—2016-08收治的急性脑卒中后失眠的90例患者,随机分为2组,对照组44例给予常规治疗,观察组46例给予酒石酸唑吡坦片治疗,比较2组患者治疗效果及不良反应。结果对照组治疗总有效率70.45%,观察组93.48%,差异有统计学意义(P0.05);治疗后,观察组阿森斯失眠量表评分、MESSS评分均显著低于对照组,Barthel指数显著高于对照组(P0.05)。对照组无不良反应,观察组不良反应发生率为4.35%,2组比较差异无统计学意义(P0.05)。结论将酒石酸唑吡坦片用于急性脑卒中后失眠的临床治疗,可有效改善患者失眠症状,提高患者的日常生活能力,且不会增加不良反应的发生风险,值得临床推广。     

酒石酸唑吡坦快速缓解木僵的临床研究

目前,临床对木僵的药物治疗起效较慢,国际上报道用酒石酸唑吡坦能够快速缓解木僵状态[1],而国内似未见报道(检索1997-2008年4月中国期刊全文数据库).我们在临床应用酒石酸唑吡坦缓解木僵,获得了满意的效果.     

唑吡坦引起遗忘和睡行症1例报告

1病例 女性,43岁,门诊号782286,主诉敏感多疑15年,诊断精神分裂症,用氯丙嗪治疗缓解,长期维持氯丙嗪治疗,近11个月氯丙嗪25mg/中,75mg/晚,因为间歇性失眠,不定期服唑吡坦（思诺思）15mg/晚,平均每3天服一次,4个月前某晚服唑吡坦15mg后,未睡前却打了4个电话,     

托吡酯和左乙拉西坦单药治疗癫痫患儿的疗效及不良反应对比

目的对比单用托吡酯或左乙拉西坦治疗儿童癫痫的疗效及不良反应,以期为儿童癫痫的临床合理用药提供依据。方法收集我院2014-08—2016-02收治的120例癫痫患儿为研究对象,根据给予不同药物进行随机分组,分别为托吡酯治疗组60例,左乙拉西坦治疗组60例。持续治疗6个月后,观察2组治疗效果,同时记录不良反应。结果维持治疗6个月后,乙拉西坦临床有效率明显高于托吡酯,差异有统计学意义(P0.05)。2组治疗中均发生不良反应,但总体症状轻,属于轻度不适,可较快恢复,差异无统计学意义(P0.05)。结论单药托吡酯或左乙拉西坦治疗儿童癫痫具有显著临床疗效,安全性较高,均可作为儿童癫痫治疗的首选药物。     

唑吡坦对失眠症患者睡眠影响的多导睡眠图研究

目的 应用多导睡眠图(PSG)探讨唑吡坦对失眠症患者睡眠脑电活动的影响.方法 对27例符合国际疾病分类标准第10版(ICD-10)非器质性失眠症诊断标准的患者连续进行3晚PSG描记,其中第3晚睡前予10 mg唑吡坦,观察用药后PSG的变化.正常对照组33名,作1夜适应和1夜基础PSG监测.结果 与基线睡眠比较,患者服用唑吡坦后睡眠效率提高[(91%±4%)vs(87%±8%),P＜0.05],觉醒时间减少[(24±6)min vs(39±16)min,P＜0.01],S1减少[(18%±6%)vs(30%±18%),P＜0.01],S2增加[(60%±5%)vs(44%±18%),P＜0.01],睡眠潜伏期缩短[(36±18)min vs(22±11)min,P＜0.01].结论 唑吡坦对失眠症患者夜间多导睡眠图脑电有影响.     

托吡酯对癫痫患者血清NPY、BD-NF表达及临床效果分析

目的探讨托吡酯治疗癫痫患儿的临床效果及对血清神经肽Y(NPY)、脑源性神经营养因子(BD-NF)水平的影响。方法选取2013年1月至2016年1月在本院诊治的癫痫患儿100例,采用SPSS16.0软件生成随机数字分为托吡酯组和左乙拉西坦组各50例,两组均治疗3个月后进行疗效评价。结果治疗前,托吡酯组和左乙拉西坦组患儿的血清NPY、BD-NF水平差异无统计学意义(P0.05);治疗3个月后,托吡酯组的NPY、BD-NF水平均低于左乙拉西坦组,差异均有统计学意义(P0.05),托吡酯组总有效率84.00%(42/50),左乙拉西坦组总有效率66.00%(33/50),差异具有统计学意义(P0.05);托吡酯组总有效率78.00%(39/50),左乙拉西坦组总有效率64.00%(32/50),差异具有统计学意义(P0.05);治疗过程中,托吡酯组不良反应发生率12.00%(6/50),左乙拉西坦组不良反应发生率24.00%(12/50),2组比较差异无统计学意义(P0.05)。结论托吡酯治疗癫痫患儿的临床效果优于左乙拉西坦,能更显著的降低患儿血清NPY、BD-NF水平     

曲唑酮片联合唑吡坦治疗失眠对SDRS PSQI评分及PSG指标的影响

目的 分析曲唑酮片联合唑吡坦治疗失眠对睡眠障碍评定量表(SDRS)、匹兹堡睡眠质量指数(PSQI)及多导睡眠图(PSG)的影响.方法 纳入120例于2018-05—2021-10于郑州大学第二附属医院接受治疗的失眠患者,A组40例施予曲唑酮片治疗,B组40例施予唑吡坦治疗,C组40例施予曲唑酮片联合唑吡坦治疗,对比3组SDRS、PSQI评分及PSG各指标.结果 治疗后7 d、14 d、28 d,C组SDRS评分分别为(14.04±5.57)分、(10.15±4.32)分、(7.82±3.62)分,均较A组(18.73±6.41、12.15±5.53、11.37±4.55)、B组(18.32±5.92、12.42±4.37、11.23±4.65)低,差异均有统计学意义(P<0.05);C组PSQI评分分别为(12.29±1.29)分、(12.35±1.04)分、(7.14±0.63)分,均较A组(15.83±1.34、14.32±1.27、12.29±1.29)、B组(15.84±1.43、14.45±1.15、12.35±1.04)低,差异均有统计学意义(P<0.05);C组中PSG睡眠效率、睡眠总时间、醒觉时间、入睡时间(82.53±6.74、389.24±33.34、80.27±32.63、29.24±4.77)各项指标优于A组(74.18±6.83、333.61±34.69、120.53±33.48、36.08±4.17)、B组(73.84±7.03、334.63±35.75、120.63±34.15、35.93±3.84),差异均有统计学意义(P<0.05).结论 失眠患者给予曲唑酮片联合唑吡坦治疗效果显著,有助于改善患者的SDRS、PSQI评分及PSG指标.     

Three Cases of Zolpidem Dependence Treated with Fluoxetine: The Serotonin Hypothesis

Zolpidem is an Imidazopyridine hypnotic that is believed to act selectively at al subunit-containing gamma-aminobutyric acid type A (GABA_A) receptors and thus to have minimal abuse and dependence potential. We present three cases of Zolpidem abuse and dependence in which the drug was used not for sedation but for stimulation and anxiolysis. All of the patients were treated with fluoxetine (a selective serotonin reuptake inhibitor) and managed to discontinue the abuse and remain abstinent from the drug. The efficacy of this kind of medication on the abuse of a GABAergic agonist, in this case dependence on zolpidem, leads to a serotonergic and GABAergic system interaction hypothesis.     

Effects of zolpidem on cyclic alternating pattern, an objective marker of sleep instability, in Japanese patients with psychophysiological insomnia: a randomized crossover comparative study with placebo

OBJECTIVE: A placebo-controlled randomized crossover study to investigate the effects of zolpidem on sleep stability in Japanese insomniac patients was performed using the cyclic alternating pattern (CAP) rate, a polysomnographic marker that reflects sleep instability. METHODS: Seventeen patients (5 M and 12 F, mean age: 40.4+/-13.6 years) who met the International Classification of Sleep Disorders (ICSD) criteria for psychophysiological insomnia were evaluated. During the first period, patients were administered the placebo on the first night, followed by either zolpidem or the placebo on the second night (treatment night). The second crossover period was conducted after a minimum 3-day observation. Improvement in the overnight CAP rate was the primary endpoint. Secondary endpoints included the CAP variables, conventional sleep variables, EEG arousals, subjective evaluation of sleep quality (measured by means of a visual analogue scale and the St. Mary's Hospital Sleep Questionnaire), and drug safety. RESULTS: Zolpidem significantly decreased the overnight CAP rate values (57.6 vs. 39.0%, p=0.009) and improved "sleep depth" (p=0.044) and "sleep quality" (p=0.023) subjective questionnaire scores. Zolpidem also significantly improved VAS (p=0.036). The amount of time spent in sleep stages 3+4 was significantly increased by zolpidem without affecting the amounts of stage 2 and rapid eye movement (REM) sleep. Significant negative correlations were found when the sleep quality score was matched to the CAP rate (p=0.022). No serious adverse events occurred during the study. DISCUSSION: In Japanese patients with psychophysiological insomnia, zolpidem increased sleep stability by significantly improving the overnight CAP rate. Zolpidem also improved sleep depth and sleep quality, both subjectively and objectively.     

Differential sensitivity to Zolpidem of IPSPs activated by morphologically identified CA1 interneurons in slices of rat hippocampus

Hippocampal pyramidal cells express several alpha-subunits, which determine the affinity of GABAA (gamma-aminobutyric acid) receptors for benzodiazepine site ligands. This study asked whether inhibitory postsynaptic potentials (IPSPs) elicited by specific interneuronal subclasses were differentially sensitive to the alpha1-preferring agonist Zolpidem, i.e. whether different receptors mediate different inhibitory connections. Paired intracellular recordings in which the presynaptic cell was an interneuron and the postsynaptic cell a CA1 pyramid were performed in slices of adult rat hippocampus. Resultant IPSPs were challenged with Zolpidem, cells filled with biocytin and identified morphologically. IPSPs elicited by fast spiking (FS) basket cells (n = 9) were enhanced more than IPSPs elicited by regular spiking (RS) basket cells (n = 10). At FS basket cell synapses the efficacy of Zolpidem was equivalent to that of Diazepam, while RS basket cell IPSPs are enhanced 50% less by Zolpidem than by Diazepam. Thus, while alpha1 subunits may dominate at synapses supplied by FS basket cells, RS basket cell synapses also involve alpha2/3 subunits. Two bistratified cell IPSPs tested with Zolpidem did not increase in amplitude, despite powerful enhancements of bistratified cell IPSPs by Diazepam, consistent with previous indications that these synapses utilize alpha5-containing receptors. Enhancements of basket cell IPSPs by Zolpidem and Diazepam were bi- or triphasic with steep amplitude increases separated by plateaux, occurring 10-15, 25-30 and 45-55 min after adding the drug to the bath. The entire enhancement was, however, blocked by the antagonist Flumazenil (n = 7). Flumazenil, either alone (n = 3), or after Zolpidem, reduced IPSP amplitude to approximately 90% of control, suggesting that alpha4-containing receptors were not involved.     

Clinically Significant Response to Zolpidem in Disorders of Consciousness Secondary to Anti-N-Methyl-d-Aspartate Receptor Encephalitis in a Teenager: A Case Report

BackgroundAnti-N-methyl-d-aspartate receptor encephalitis has been associated with a prolonged neuropsychiatric phase that may last for months to years.PatientWe report the case of a 16-year-old girl who was diagnosed with anti-N-methyl-d-aspartate receptor encephalitis resulting from left ovarian mature teratoma 2 weeks after presentation with psychosis. Following tumor removal and immunotherapy, recovery from a minimally conscious state was accelerated significantly by zolpidem that was used for her sleep disturbance. Our patient was discharged home 8 weeks after admission with marked improvement in her neurological function. Zolpidem has been reported to improve arousal in disorders of consciousness but there are no previous reports of its benefit among patients with anti-N-methyl-d-aspartate receptor encephalitis.ConclusionZolpidem would be a reasonable consideration as an adjunctive treatment in anti-N-methyl-d-aspartate receptor encephalitis after tumor removal and immunotherapy to accelerate recovery and rehabilitation.     

Zolpidem modified-release in insomnia

Zolpidem modified-release (MR) is the first hypnotic agent to be marketed in an extended-release formulation. Zolpidem MR is a two-layered, biphasic release tablet indicated for the management of induction of sleep and sleep maintenance. The pharmacokinetics of the drug are similar to those of immediate-release zolpidem. Two double-blind, placebo-controlled, parallel-group trials demonstrated efficacy in adults and elderly patients treated with zolpidem MR for 3 weeks without significant impairment in next-day psychomotor functioning. The most common adverse effects with zolpidem MR were dizziness, somnolence, and headache. A starting dose of zolpidem MR 12.5 mg is recommended for adults and 6.25 mg for elderly patients.     

Improvement of blepharospasm with Zolpidem.

Zolpidem (ZLP) is an imidazopyridine that binds to GABA receptors. We report on improvement of blepharospasm in 3 patients treated with ZLP. The GABAergic action of this drug on the output structures of the basal ganglia could explain the improvement of blepharospasm in these patients.     

Central nervous system side effects associated with zolpidem treatment

Zolpidem is one of the newer medications developed for the treatment of insomnia. It is an imidazopyridine agent that is an alternative to the typical sedative-hypnotic agents. Zolpidem use is gaining favor because of its efficacy and its side effect profile, which is milder and less problematic than that of the benzodiazepines and barbiturates used to treat insomnia. Still, side effects are not uncommon with zolpidem use. We report a series of cases in which the patients developed delirium, nightmares and hallucinations during treatment with zolpidem. We will review its pharmacology, discuss previous reports of central nervous system side effects, examine the impact of drug interactions with concurrent use of antidepressants, examine gender differences in susceptibility to side effects, and explore the significance of protein binding in producing side effects.     

Amnestic sleep-related eating disorder associated with zolpidem

OBJECTIVE: To describe the association of amnestic nocturnal eating behavior with use of zolpidem for insomnia. BACKGROUND: Sleep-related eating disorder is increasingly recognized in relationship to other diagnosable sleep disorders. Many of these disorders, like restless legs syndrome (RLS), give rise to complaints of insomnia. Zolpidem is the most commonly prescribed drug for insomnia complaints, and although it has sometimes been associated with side effects of transient amnesia and sleep walking, an association with sleep-related eating has not been previously emphasized. METHODS: Consecutive case series of five patients who were using zolpidem and evaluated with nocturnal eating behaviors. RESULTS: We evaluated five patients over 11 months with problematic amnestic nocturnal eating associated with zolpidem used for complaints of insomnia. All five patients had RLS, three had obstructive sleep apnea syndrome, two had sleep walking, and one had psychophysiologic insomnia. With discontinuation of zolpidem and effective treatment of their sleep disorders, nocturnal eating resolved. CONCLUSIONS: Zolpidem, at least in patients with underlying sleep disorders that cause frequent arousals, may cause or augment sleep-related eating behavior. This report demonstrates the importance of arriving at a specific diagnosis for insomnia complaints, and alerts the sleep practitioner to this unusual side effect of zolpidem.     

Zolpidem therapy for movement disorders

Zolpidem is a selective agonist of the benzodiazepine subtype receptor BZ1. The highest density of this receptor is in the output structures of the basal ganglia. The basal ganglia are pathologically involved in many movements disorders. Thus, zolpidem has accumulated attention for a possible drug to treat neurological signs and symptoms in Parkinsonian diseases. In this mini-review, I reviewed effects of zolpidem as movement disorders including Parkinson's disease, progressive supranuclear palsy, dystonia and so on. In addition, I reviewed a possible mechanism of zolpidem for movement disorders.     

The hypnotics triazolam and zolpidem have identical metabolic effects throughout the brain: implications for benzodiazepine receptor subtypes.

Using Sokoloff's 2-deoxyglucose autoradiography procedure, the effects of trizolam, a classical benzodiazepine (BZ) hypnotic, were compared to those of zolpidem, which preferentially binds to BZ1 receptor subtypes. Triazolam depressed metabolism in 40 of the more than 60 brain regions evaluated. Zolpidem depressed metabolism in all of these areas, including the spinal cord, an area where the BZ1 receptor subtype is not supposed to exist. Zolpidem and triazolam also depressed metabolism in the molecular layer of the dentate gyrus, an area low in BZ1 receptors. Neither drug affected metabolism in 21 areas, including the regions most specific for the BZ1 subtype (cerebellum, inferior colliculus, globus pallidus, and substantia nigra pars reticularis). It is concluded that: (i) zolpidem and triazolam depress energy metabolism of the same areas of the brain, (ii) zolpidem's effects may not be mediated solely through the BZ1 receptor subtype, and (iii) the BZ2 receptor may be functionally more significant than the BZ1 receptor.