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1.
目的:探讨DISC1内含子9甲基化水平与认知功能在首发精神分裂症患者与伴精神病性症状的双相情感障碍患者间的差异性。方法:选取2016-2018年就诊于河北省精神卫生中心的30例首发精神分裂症患者和30例伴有精神病性症状的双相情感障碍患者,分别给予MATRICS共识认知成套测验(MCCB)、阳性与阴性症状量表(PANSS)、汉密尔顿抑郁量表(HAMD)、杨氏躁狂量表(YMRS)进行评定,并检测DISC1内含子9位点的甲基化水平。结果:认知功能评定显示,在30~39岁中,首发精神分裂症组患者与伴精神病性症状的双相情感障碍患者在持续操作测验(CPT)存在显著差异且具有统计学意义(t=-3.254,P0.05);在40~50岁中,首发精神分裂症组患者在连线测试(TMT)(t=-3.235,P0.01)和持续操作测验(CPT)上(t=-2.318,P0.05)与伴精神病性症状的双相情感障碍患者间存在差异且具有统计学意义。杨氏躁狂量表(YMRS)评定显示,首发精神分裂症患者与伴精神病性症状的双相情感障碍患者间的差异性有统计学意义(t=-3.952,P0.001)。阳性与阴性症状量表(PANSS)、汉密尔顿抑郁量表(HAMD)评定以及不同年龄段DNA甲基化水显示,两组间均无统计学差异(P0.05)。首发精神分裂症患者DISC1内含子9位点甲基化水平均与TMT、CPT、stroop色词测验及简易视觉空间记忆均无明显相关性。但伴精神病性症状的双相情感障碍患者DISC1内含子9位点甲基化水与CPT间存在正相关(r=0.549,P0.05),与TMT、stroop色词测验及简易视觉空间记忆无明显相关性。结论:伴精神病性症状的双相情感障碍患者部分认知功能优于首发精神分裂症患者,但在其各自DISC1内含子9位点甲基化水平上无显著差异。伴精神病性症状的双相情感障碍患者DISC1内含子9位点甲基化水平与CPT间存在正相关,而首发精神分裂症患者与其认知功能无明显相关性。  相似文献   

2.
目的:比较伴与不伴焦虑症状抑郁症患者的自杀风险,分析抑郁症患者自杀风险的危险因素。方法:对2010年9月1日至2011年2月28日"中国双相情感障碍患者诊断评估服务"研究项目的数据进行二次分析,纳入分析的抑郁症患者共1172例,根据简明国际神经精神访谈(M.I.N.I)焦虑模块,分为伴焦虑症状抑郁症组728例(62.1%)及不伴焦虑症状组444例(37.9%)。采用M.I.N.I自杀模块评估自杀风险,比较伴与不伴焦虑症状抑郁症患者的自杀风险,通过logistic回归分析探讨抑郁症患者自杀风险的相关因素。结果:伴焦虑症状抑郁症患者中有自杀风险者331例(45.5%);不伴焦虑症状者中有自杀风险者54例(12.2%)。与不伴焦虑症状抑郁症患者比较,伴焦虑症状者自杀风险更高(P0.001)。Logistic回归分析显示,抑郁发作频繁(OR=2.07)、伴精神病性症状(OR=2.01)、伴焦虑症状(OR=3.18)、伴忧郁型特征(OR=2.90)与抑郁症患者的自杀风险相关。结论:伴焦虑症状抑郁症患者可能有更高的自杀风险。发作频繁、伴精神病性症状、伴焦虑症状或伴忧郁型特征可能是抑郁症患者自杀风险的危险因素。  相似文献   

3.
目的:分析伴精神病性特征抑郁症患者自杀未遂的危险因素.方法:对2010年9月1日-2011年2月28日“中国双相障碍患者诊断评估服务”研究项目的数据进行二次分析,1068例抑郁症患者中伴精神病性特征抑郁症患者112人(10.5%).采用简明国际神经精神访谈(M.I.N.I)中抑郁发作模块、自杀模块和精神病性疾患模块,分析伴精神病性特征抑郁症患者自杀未遂的危险因素.结果:伴精神病性特征抑郁症患者较不伴精神病性特征抑郁症患者的自杀未遂风险高(OR =2.22),多因素logistic回归分析显示被控制体验(OR =3.54)、幻听(OR =3.84)和无价值感/罪恶感(OR =4.78)的患者更易有自杀未遂风险.结论:本研究提示伴精神病性特征抑郁症患者的自杀未遂风险高,存在被控制体验、幻听和无价值感/罪恶感症状的患者发生自杀行为的危险性可能更高.  相似文献   

4.
伴抑郁症状的精神分裂症临床分析   总被引:1,自引:0,他引:1  
目的 了解精神分裂症的抑郁症状临床特征。方法 对76例件抑郁症状的精神分裂症,140例不伴抑郁症状的精神分裂症进行临床对照分析。结果 抑郁症状在精神分裂症中颇为普遍,抑郁症状与精神病性症状关系密切,抑郁症状与复发率、住院时间、自杀有关;与性别、年龄、精神疾病总痛程比较,差异均无显著性;加用与不加用抗抑郁剂比较,在治疗起效时间、症状改善时间方面的差异均有非常显著性(P<0.01)。结论 对伴抑郁症状的精神分裂患者治疗上加用抗抑郁剂是缩短疗程的有效途径。  相似文献   

5.
目的:探讨抑郁症伴精神病性症状患者童年期虐待及与依恋类型的关系。方法:选取安徽省精神卫生中心门诊及住院抑郁症患者160例,其中抑郁症伴精神病性症状患者和抑郁症不伴精神病性症状患者各80例,采用儿童期虐待问卷-简易版(CTQ-SF)和亲密关系经历量表(ECR)评估童年期虐待与依恋类型。结果:伴精神病性症状患者组CTQ-SF各维度得分及ECR的2个分量表得分均高于不伴精神病性症状患者组(均P0.05)。安全型依恋是抑郁症伴精神病性症状的保护性因素(OR=2.25),而不安全依恋是抑郁症伴精神病性症状危险因素(OR=14.84),其中恐惧型依恋的风险最大(OR=8.79)。结论:童年期虐待和不安全依恋可能是抑郁症伴精神病性症性症状患者发病的相关因素。  相似文献   

6.
目的 探讨抗抑郁药对伴焦虑抑郁症状的精神分裂症的辅助治疗作用及不良反应.方法 对符合CCMD-Ⅲ关于精神分裂症的诊断且伴焦虑抑郁症状的住院患者进行随机分组,研究组(64例)给予抗精神病药加抗抑郁药(西酞普兰20mg/d)治疗;对照组(67例)单给抗精神病药治疗;两组于入组时、4周末、8周末分别评定简明精神病量表(BPRS)、汉密顿抑郁量表(HAMD)和汉密顿焦虑量表(HAMA),以副反应量表(TESS)评定不良反应,然后进行比较.结果 两组的BPRS总分和HAMD、HAMA总分在治疗后均显著下降(P<0.01);研究组4周末疗效更佳(P<0.05~0.01);8周末疗效两组相近(P>0.05);两组的不良反应无显著性差异(P>0.05).结论 抗抑郁药在急性期对伴焦虑抑郁症状的精神分裂症有辅助治疗作用,不良反应轻微.  相似文献   

7.
目的:比较伴与不伴躯体化症状老年期抑郁患者前瞻记忆(PM)与回溯记忆(RM)的差异。方法:对30例伴躯体化症状老年期抑郁患者以及年龄、受教育程度相匹配的30名不伴躯体化症状老年期抑郁患者,实施前瞻记忆和回溯记忆的问卷调查。结果:伴躯体化症状老年期抑郁患者PM评分为(20.00±5.86)分,对照组PM评分为(16.83±3.98)分,两组之间差异有统计学意义(t=2.451,P0.05),伴躯体化症状老年期抑郁患者RM评分为(17.10±4.05)分,对照组RM评分为(15.80±3.61)分,两组之间差异无统计学意义(t=1.313,P0.05)。结论:伴躯体化症状老年期抑郁患者相对不伴躯体化症状老年期抑郁患者存在更为严重的前瞻记忆损害。  相似文献   

8.
目的:了解伴阻塞性睡眠呼吸暂停(OSA)首发抑郁症患者的嗅觉功能,分析嗅觉功能的相关因素。方法:对143例首发抑郁症患者进行多导睡眠监测(PSG)、T&T嗅觉检查。以PSG结果呼吸暂停低通气指数(AHI)≥5次/h为抑郁伴OSA组(n=87),AHI<5次/h为单纯抑郁组(n=56)。采用多元逐步回归分析伴OSA首发抑郁症患者嗅觉功能的相关因素。结果:抑郁伴OSA组的嗅觉识别阈值、嗅觉障碍发生率高于单纯抑郁组(均P<0.05),以嗅觉减退为主(93.9%,46/49)。伴重度OSA的首发抑郁症患者嗅觉识别阈值、嗅觉障碍发生率高于轻、中度组(均P<0.05)。多元逐步回归分析显示,AHI指数和HAMD得分与嗅觉识别阈值正相关(β=0.05~0.30,均P<0.01)。结论:本研究显示伴阻塞性睡眠呼吸暂停首发抑郁症患者较单纯首发抑郁症患者嗅觉障碍更显著,以嗅觉减退为主。  相似文献   

9.
目的了解河北省抑郁障碍患者精神药物的治疗现状。方法使用自制调查问卷,按一定的抽样比例,选择河北省37家专科医院或综合医院精神科进行调查。结果1共调查住院和门诊抑郁障碍病人223例;单一药物治疗97例(43.5%),联合2种及其以上药物治疗124例(55.6%),未用药2例(0.9%);2门诊患者帕罗西汀的使用频度明显高于住院患者(P0.01),其它药物在门诊与住院患者的使用中没有明显差异;三环类抗抑郁剂多虑平、阿米替林住院患者用药剂量明显高于门诊患者(P0.05,P0.01);3合并使用苯二氮类药113例(50.7%),使用频率依次为阿普唑仑、氯硝西泮、劳拉西泮、艾司唑仑;使用剂量在正常范围,持续时间超过60天者占30.8%(43/140);4伴精神病性症状的抑郁症37例(16.6%),伴精神病性症状者治疗多合并精神药物73.0%(27/37)。结论河北省抑郁障碍治疗基本合理,但应注意减少合并用药及缩短苯二氮卓类药物使用时间。  相似文献   

10.
目的探讨舍曲林对抑郁障碍的冠心病患者的治疗效果及其临床意义。方法对48例伴抑郁障碍冠心病患者,进行8周的随机对照研究。实验组、对照组各24例。以BECK抑郁问卷(BDI)和汉密尔顿抑郁量表(HAMD)评定疗效,心电图监测冠心病缓解情况。结果实验组抑郁症状的减轻明显优于对照组(P<0.05~0.01),根据BDI评分实验组的显效率明显高于对照组(62.5%,33.3%,P<0.05),根据HAM D评分,实验组的治愈率高于对照组(45.8%,25.0%,P<0.05),实验组冠心病相关症状的显效率比对照组更明显。结论舍曲林能有效的减轻冠心病患者的抑郁症状,这种治疗更有利于冠心病的控制。  相似文献   

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12.

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

  • Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
  • The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
  • To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.
Quadriceps weakness is a common consequence of traumatic knee joint injury1,2 and chronic degenerative knee joint conditions.3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.5 The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,6 biomechanical deficits,7 and possibly reinjury.5 Furthermore, researchers8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,1012 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators15 have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,7 produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,1618 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.5 The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.19 Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.1618 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.20 Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.  相似文献   

13.
即早基因c-fos与脑血管病及学习记忆   总被引:5,自引:1,他引:5  
即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.  相似文献   

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OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.  相似文献   

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