抑郁症与精神分裂症患者心率变异性的对照分析

目的探讨抑郁症与精神分裂症患者的心率变异性（HRV）的差异。方法对36例首次发作的抑郁症患者及年龄、性别与之相匹配的41例首次发作的精神分裂症患者分别进行短时程HRV检测,并对其心率变异指标SDNN、MSD、rMSSD、PNN50、LF、HF、LF/HF结果进行分析。结果抑郁症患者的时阈指标rMSSD（P〈0.05）、PNN50（P〈0.01）较精神分裂症显著降低,而两者之间的频阈分析指标无明显差异。结论抑郁症患者的自主神经功能失调较精神分裂症患者更严重。     

抑郁症焦虑症患者心率变异性特点的对比研究

目的探讨抑郁症、焦虑症患者自主神经功能的特点。方法随机选择42例抑郁症患者,10例焦虑症患者和17例健康对照者分别接受短时心率变异性分析,记录相关考察指标,进行统计学分析。结果心率变异性分析的各项考察指标中,各观察组均有一项或多项低于正常对照组（P〈0．05）;且各组之间互相对比分析P〈0．05。结论抑郁症、焦虑症患者均存在心率变异性的降低,其自主神经功能活性降低。抑郁症患者因伴或不伴有焦虑症状,其心率变异指标不同,可以指导治疗。     

抑郁症与长期住院精神分裂症患者事件相关电位P300对照研究

目的对照抑郁症与长期住院精神分裂症患者之间事件相关电位P300的特点。方法对69例抑郁症患者(DD组),69例长期住院精神分裂症患者(SD组)以及70例健康对照患者(HC组)进行对照研究,记录中央点(Cz电极)N1、P2、N2、P3成分。结果三组之间N1、P2、N2、P3的潜伏期,P3波幅的差异有统计学意义(P<0.01)。SD组N1、P2、N2、P3潜伏期延长较HC组有统计学意义(P<0.01),P3波幅减低有统计学意义(P<0.01);DD组较HC组N2、P3潜伏期延长,P3波幅减低均有统计学意义(P<0.01);SD组N1、P2、N2、P3潜伏期延长较DD组有统计学意义(P<0.01),P3波幅差异无统计学意义(P=0.787)。结论长期住院精神分裂症认知受损程度较抑郁症明显,P300可以对抑郁症与精神分裂症的鉴别提供参考。     

齐拉西酮对首发男性精神分裂症患者心率及变异性的影响

目的 研究齐拉西酮对首发精神分裂症男性患者的心率及变异性影响,为临床安全用药提供参考.方法 将2011年1月～2012年10月收治的首发精神分裂症男性患者61例纳入研究,给予齐拉西酮治疗;健康体检者63例作为对照组,比较治疗前两组心率及变异性的指标差异以及齐拉西酮治疗8周前后心率变异性的指标差异,了解齐拉西酮对精神分裂症男性患者的心率变异性影响.结果 在基线时,研究组和对照组相比,HR及HRV所有指标(SDNN、SDNNi、PNN50、SDANN)的差异均有统计学意义(P＜0.01);研究组治疗8周前后比较,除SDNNi外,其余指标的差异均有统计学意义(P＜0.01);研究组治疗8周后,与对照组比较,除PNN50外,其余指标的差异均有统计学意义(P＜0.01).结论 精神分裂症患者存在心率变异性下降,交感神经张力增加,迷走神经张力降低,有可能增加心源性猝死的几率,齐拉西酮的治疗可能加重其影响;故对于使用齐拉西酮治疗的精神分裂症男性患者需要加强观察以及实行心率变异性的监测,以加强医疗安全.     

不同第二代抗精神病药物对精神分裂症患者心率变异性影响

目的 探讨氯氮平、利培酮、齐拉西酮和奥氮平四种药物对精神分裂症患者心率变异性的影响.方法 将165例精神分裂症患者随机分入氯氮平、利培酮、齐拉西酮和奥氮平治疗组.采用24小时动态心电图在治疗前和治疗8周末分别检测各组的心率变异性(Heart rate variability,HRV)参数变化.结果 治疗8周末与基线期相比,氯氮平组心率显著加快[(86.4±11.8)vs.(76.3±8.1)];氯氮平和齐拉西酮组SDNN值、SDANN、PNN50值显著降低,而利培酮及奥氮平组SDNNI值、PAN50值、rMSSD值显著增高,差异均有统计学意义.结论 在对心率变异性的影响上,奥氮平、利培酮明显优于齐拉西酮和氯氮平,有更好的心脏保护作用.     

抑郁症对老年2型糖尿病患者心率变异性的影响

目的 探讨抑郁症对老年2型糖尿病患者心率变异性的影响.方法 对70例老年2型糖尿病患者进行汉密尔顿抑郁量表(HAMD)测定及动态心电图测定,分为糖尿病合并抑郁症组(研究组)30例,糖尿病不合并抑郁症组(对照组)40例,比较两组患者动态心电图检查中心率变异性的变化.结果 研究组与对照组正常窦性R-R间期总体标准差分别为(81.97±11.63)ms和(111.82±14.11)ms、24 h每5 min窦性R-R间期均值标准差分别为(76.17±14.07) ms和(102.34±16.56) ms、正常连续窦性R-R间期差值均方根分别为(14.67±5.42) ms和(20.13±8.34) ms、相邻R-R间期差值＞50 ms的个数所占的百分比分别为4.65％±2.43％和7.32％±3.15％,差异均有统计学意义(P＜0.01).结论 研究组心率变异性较对照组降低,表明抑郁症增加老年2型糖尿病患者自主神经功能损害.     

躯体化症状为主的抑郁症心率变异性对照研究

目的：探讨躯体化症状为主的抑郁症患者自主神经系统的特点及抑郁症躯体化表现的发生机制。方法：对30例躯体化症状为主的患者（A组）和30例情绪症状为主的患者（B组）及30例健康正常者（C组）分别进行汉密尔顿抑郁量表（HAMD）和汉密尔顿焦虑量表（HAMA）评定及短时（10min）心率变异性（HRV）分析。结果：A、B、C3组HRV分析指标RR间期标准差（SDNN）分别为（50.84±19.92）ms、（94.93±28.80）ms、（105.77±22.05）ms,A组显著低于C组（t=5.68,P〈0.01）,较B组低（t=3.73,P〈0.05）;3组LF/HF分别为（6.26±2.11）ms、（3.51±2.44）ms、（1.80±1.07）ms,A组显著高于C组（t=6.35,P〈0.01）,较B组高（t=2.50,P〈0.05）;A组HAMD评分（28.30±6.26）分高于B组（24.35±6.69）分,二者差异有显著性（t=3.14,P〈0.05）;A组HAMA评分（22.70±4.92）分显著高于B组（13.05±4.71）分,二者差异有显著性（t=6.17,P〈0.01）;HAMD焦虑/躯体化因子分与HRV指标SDNN、LF、HF、VLF和LF/HF均呈中度相关（r分别为0.49、0.61、0.58、0.50、0.63）（P〈0.05或P〈0.01）。结论：躯体化症状表现为主的抑郁症患者多伴有焦虑,自主神经功能紊乱。     

伴焦虑抑郁症患者的睡眠质量及心率变异性的初步研究

目的 探讨伴焦虑抑郁症患者睡眠质量与心率变异性（HRV）的特征。方法 选取2021年11 月— 2022 年 6 月于河北医科大学第一医院精神卫生中心住院和门诊就诊的 80 例抑郁症患者为研究对象。采用汉密尔顿焦虑量表（HAMA）评估患者焦虑症状的严重程度,将 HAMA 评分＞ 14 分设为伴焦虑抑郁症组（n=50）,将 HAMA 评分≤ 14 分设为不伴焦虑抑郁症组（n=30）。采用匹兹堡睡眠质量指数量表（PSQI）评估患者的睡眠质量。采用 HRV 测量仪测量 HRV,分析两组患者的低频（LF）、高频（HF）、低频 /高频（LF/HF）、心搏中 RR 间期的标准差（SDNN）和相邻 RR 间期差值均方根（RMSSD）。采用汉密尔顿抑郁量表（HAMD）评估患者抑郁症状的严重程度。采用独立样本t检验比较两组睡眠质量和 HRV 的差异,采用二项 Logistic 回归分析抑郁症患者伴发焦虑的影响因素。结果 伴焦虑抑郁症组和不伴焦虑抑郁症组的年龄、性别、吸烟饮酒史和体重指数（BMI）比较,差异无统计学意义（P＞ 0.05）;伴焦虑抑郁症组的PSQI-Ⅴ（睡眠节律紊乱）、PSQI-Ⅶ（日间功能障碍）因子得分为（1.3±0.6）、（2.3±0.7）分,高于不伴焦虑抑郁症组的（1.0±0.6）、（1.8±1.0）分,差异有统计学意义（P＜ 0.05）;伴焦虑抑郁症组的 HAMD 总分、焦虑躯体化因子得分、认知障碍因子得分、迟滞因子得分、睡眠障碍因子得分为（19.6±3.6）、（6.5±2.2）、（5.0±2.1）、（7.3±1.9）、（3.5±1.8）分,高于不伴焦虑抑郁症组的（14.7±4.2）、（5.0±2.1）、（3.7±2.4）、（5.4±2.1）、（2.6±1.9）分,差异有统计学意义（P＜ 0.05）。HRV 分析结果显示,伴焦虑抑郁症组的 LF 为（5.2±1.2）ms,高于不伴焦虑抑郁症组的（4.5±1.4）ms,差异有统计学意义（P=0.011）,伴焦虑抑郁症组的 HF 和 RMSSD 为（4.0±1.1）、（22.8±10.5）ms,低于不伴焦虑抑郁症组的（5.4±1.2）、（28.3±9.7）ms,差异有统计学意义（P＜ 0.05）。二项 Logistic 回归分析显示,HAMD 总分高（OR=1.439,95%CI：1.157～1.789）、LF 高（OR=2.640,95%CI：1.275～5.467）与抑郁症患者焦虑风险增加有关,而 HF 高与抑郁症伴焦虑症状风险降低有关（OR=0.286,95%CI：0.142～0.577）。结论 伴焦虑症状的抑郁症患者的抑郁情绪更重,存在睡眠质量及自主神经功能紊乱。     

抑郁症与精神分裂症患者静息态功能磁共振成像与认知功能的差异

目的:探讨抑郁症与精神分裂症患者脑功能活动及认知功能损害的特点及其相关性。方法:对健康对照组、抑郁症组及精神分裂症组（每组各36例）患者进行数字符号测试（digital symbol test,DST）、数字广度测试（digital span test,DSPT）和语言流畅性测试（verbal fluency test...     

精神分裂症和抑郁症患者自杀行为的临床特征分析和护理

目的 探讨精神分裂症和抑郁症患者自杀行为的临床特征。方法 采用现症检查的方法对我院住院的精神分裂症和抑郁症患者进行随机抽样，并对资料进行χ^2检验。结果 偏执型精神分裂症与伴有抑郁症状的精神分裂症和兴奋、激惹、有冲动行为的精神分裂症患者易出现自杀。结论 精神分裂症和抑郁症患者自杀行为的临床特征不同，应采取有针对性的治疗措施。     

CNS- and ANS-arousal predict response to antidepressant medication: Findings from the randomized iSPOT-D study

Arousal systems are one of the recently announced NIMH Research Domain Criteria to inform future diagnostics and treatment prediction. In major depressive disorder (MDD), altered central nervous system (CNS) wakefulness regulation and an increased sympathetic autonomic nervous system (ANS) activity have been identified as biomarkers with possible discriminative value for prediction of antidepressant treatment response. Therefore, the hypothesis of a more pronounced decline of CNS and ANS-arousal being predictive for a positive treatment outcome to selective-serotonin-reuptake-inhibitor (SSRI) treatment was derived from a small, independent exploratory dataset (N = 25) and replicated using data from the randomized international Study to Predict Optimized Treatment Response in Depression (iSPOT-D). There, 1008 MDD participants were randomized to either a SSRI (escitalopram or sertraline) or a serotonin-norepinephrine-reuptake-inhibitor (SNRI-venlafaxine) arm. Treatment response was established after eight weeks using the 17-item Hamilton Rating Scale for Depression. CNS-arousal (i.e. electroencephalogram-vigilance), ANS-arousal (heart rate) and their change across time were assessed during rest. Responders and remitters to SSRI treatment were characterized by a faster decline of CNS-arousal during rest whereas SNRI responders showed a significant increase of ANS-arousal. Furthermore, SSRI responders/remitters showed an association between ANS- and CNS-arousal regulation in comparison to non-responders/non-remitters while this was not the case for SNRI treatment arm. Since positive treatment outcome to SSRI and SNRI was linked to distinct CNS and ANS-arousal profiles, these predictive markers probably are not disorder specific alterations but reflect the responsiveness of the nervous system to specific drugs.     

Heart rate variability in bipolar mania and schizophrenia

Background

Autonomic nervous system (ANS) dysfunction and reduced heart rate variability (HRV) have been reported in a wide variety of psychiatric disorders, but have not been well characterized in bipolar mania. We recorded cardiac activity and assessed HRV in acutely hospitalized manic bipolar (BD) and schizophrenia (SCZ) patients compared to age- and gender-matched healthy comparison (HC) subjects.

Method

HRV was assessed using time domain, frequency domain, and nonlinear analyses in 23 manic BD, 14 SCZ, and 23 HC subjects during a 5 min rest period. Psychiatric symptoms were assessed by administration of the Brief Psychiatric Rating Scale (BPRS) and the Young Mania Rating Scale (YMRS).

Results

Manic BD patients demonstrated a significant reduction in HRV, parasympathetic activity, and cardiac entropy compared to HC subjects, while SCZ patients demonstrated a similar, but non-significant, trend towards lower HRV and entropy. Reduction in parasympathetic tone was significantly correlated with higher YMRS scores and the unusual thought content subscale on the BPRS. Decreased entropy was associated with increased aggression and diminished personal hygiene on the YMRS scale.

Conclusion

Cardiac function in manic BD individuals is characterized by decreased HRV, reduced vagal tone, and a decline in heart rate complexity as assessed by linear and nonlinear methods of analysis. Autonomic dysregulation is associated with more severe psychiatric symptoms, suggesting HRV dysfunction in this disorder may be dependent on the phase of the illness.     

Effects of depression and melatonergic antidepressant treatment alone and in combination with sedative–hypnotics on heart rate variability: Implications for cardiovascular risk

Objectives: To examine heart rate variability (HRV) in unmedicated patients with major depressive disorder (MDD) and its changes after treatment with agomelatine alone and in combination with sedative–hypnotics.

Methods: We recruited 152 physically healthy, unmedicated patients with MDD and 472 age- and sex-matched healthy volunteers. Frequency-domain measures of HRV were obtained during enrolment for all participants and again for MDD patients after 6 weeks of treatment with agomelatine alone and combining sedative–hypnotics.

Results: Compared to the controls, unmedicated patients exhibited significantly lower mean R-R intervals, low-frequency (LF) HRV, and high-frequency (HF) HRV, but higher LF/HF ratios. Fifty-six and 49 patients successfully completed agomelatine monotherapy and the combination therapy of agomelatine and sedative–hypnotics, respectively. Between-group analyses showed significant treatment-by-group interactions for LF-HRV, HF-HRV and LF/HF ratio. The results showed a significant increase in HF-HRV after agomelatine monotherapy, a significant decrease in LF-HRV and HF-HRV, and a increase in the LF/HF ratio after combination therapy.

Conclusions: MDD patients had reduced HRV, and the patterns of HRV changes differed between patients treated with agomelatine alone and in combination with sedative–hypnotics. Clinicians should consider HRV effects when adding sedative–hypnotics to agomelatine, which is important for depressed patients who already have decreased cardiac vagal tone.     

The NR1 N-methyl-D-aspartate subunit and brain-derived neurotrophic factor in temporal lobe epilepsy hippocampus: a comparison of patients with and without coexisting psychiatric symptoms

PURPOSE: The glutamate N-methyl-D-aspartate (NMDA) receptor and the neurotrophin brain-derived neurotrophic factor have been implicated in the pathophysiology of schizophrenia and depression. Since these psychiatric disorders are common in temporal lobe epilepsy (TLE), a comparison of TLE patients with and without coexisting psychiatric symptoms may be useful to unravel pathophysiologic mechanisms for psychosis or depression. METHODS: We used immunoautoradiography to assess the NR1 NMDA receptor subunit and brain-derived neurotrophic factor in resected TLE hippocampus. RESULTS: No changes relative to comparison controls were found for TLE patients with schizophrenia-like psychosis or depression. Increased NR1 was found in the dentate molecular layer in the dysphoria group and unmedicated depressed patients. CONCLUSIONS: An increase in NR1 protein in the dentate molecular layer suggests an upregulation of NMDA receptors in granule cells in TLE patients with dysphoria and depression. This finding is compatible with the theory that increased NMDA receptor function is involved in the pathogenesis of depression and that antidepressants may act by opposing this mechanism.     

Increased cerebrospinal fluid interleukin-6 levels in patients with schizophrenia and those with major depressive disorder

Elevated peripheral levels of interleukin-6 (IL-6) are common findings in schizophrenia and depression. However, previous studies that measured cerebrospinal fluid (CSF) IL-6 levels in these disorders reported controversial results. The present study examined whether CSF IL-6 levels are altered in patients with schizophrenia and those with depression. Lumbar punctures were performed in 32 patients with schizophrenia, 30 with major depressive disorder (MDD), and 35 healthy controls. Serum samples were simultaneously collected from all subjects in the patient groups and from 32 of the control group. CSF and serum IL-6 levels were determined by enzyme-linked immunosorbent assay. Both the patients with schizophrenia and MDD had significantly higher CSF IL-6 levels compared to the controls (schizophrenia: P = 0.0027; MDD: P = 0.012). IL-6 levels were significantly higher in the CSF than in the serum. No significant correlation was observed between CSF and serum IL-6 levels. The present findings suggest that IL-6 of central origin is associated with the pathophysiology of schizophrenia and MDD, although confounding effect of smoking status can not be entirely excluded.     

Systematic review of appropriate cognitive assessment instruments used in clinical trials of schizophrenia,major depressive disorder and bipolar disorder

Cognitive dysfunction is increasingly recognized as a symptom in mental conditions including schizophrenia, major depressive disorder (MDD), and bipolar disorder (BPD). Despite the many available cognitive assessment instruments, consensus is lacking on their appropriate use in clinical trials. We conducted a systematic literature review in Embase, PubMed/Medline and PsychINFO to identify appropriate cognitive function instruments for use in clinical trials of schizophrenia, MDD, and BPD. Instruments were identified from the articles. Instruments and articles were excluded if they did not address schizophrenia, MDD, or BPD. Instrument appropriateness was further assessed by the criteria of the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) initiative: test–retest reliability, utility, relationship to functional status, potential changeability to pharmacological agents, and tolerability and practicality for clinical trials. The database search yielded 173 articles describing 150 instruments used to assess cognitive function. Seventeen additional instruments were identified through Google and clinicaltrials.gov. Among all these, only 30 (18%) were deemed appropriate for use in the diseases of interest. Of these, 27 were studied in schizophrenia, one in MDD and two in BPD. These findings suggest the need for careful selection of appropriate cognitive assessment instruments, as not all may be valid in these disorders.     

Abnormal fatty acid pattern in the superior temporal gyrus distinguishes bipolar disorder from major depression and schizophrenia and resembles multiple sclerosis

This study investigated the fatty acid composition of the postmortem superior temporal gyrus (STG), a cortical region implicated in emotional processing, from normal controls (n=15) and patients with bipolar disorder (BD, n=15), major depressive disorder (MDD, n=15), and schizophrenia (SZ, n=15). For comparative purposes, STG fatty acid composition was determined in a separate cohort of multiple sclerosis patients (MS, n=15) and normal controls (n=15). Compared with controls, patients with BD, but not MDD or SZ, exhibited abnormal elevations in the saturated fatty acids (SFA) palmitic acid (16:0), stearic acid (18:0), the polyunsaturated fatty acids (PUFA) linoleic acid (18:2n-6), arachidonic acid (20:4n-6), and docosahexaenoic acid (22:6n-3), and reductions in the monounsaturated fatty acid (MUFA) oleic acid (18:1n-9). The total MUFA/SFA and 18:1/18:0 ratios were lower in the STG of BD patients and were inversely correlated with total PUFA composition. MS patients exhibited a pattern of fatty acid abnormalities similar to that observed in BD patients including elevated PUFA and a lower 18:1/18:0 ratio. Collectively, these data demonstrate that BD patients exhibit a pattern of fatty acid abnormalities in the STG that is not observed in MDD and SZ patients and closely resembles MS patients.