男性抑郁症与勃起功能障碍共病分析

目的 探讨男性抑郁症患者与勃起功能障碍(ED)的共病情况及其影响因素.方法 对60例年龄26～50岁的男性抑郁症患者采用国际勃起功能指数问卷(IIEF-5)、汉米尔顿抑郁量表(HAMD)进行评估,同时对单相与双相抑郁患者组以及抑郁症与ED共病组及非共病组IIEF-5、HAMD量表评分进行比较,并对抑郁症与ED的共病的影响因素进行Logistic回归分析.结果 ①抑郁症患者与ED共病率为78.3%,主要为轻度ED;②双相抑郁患者与ED共病率以及IIEF-5与HAMD评分均显著高于单相抑郁患者;③21～30,31～40,41～50岁年龄段的抑郁症患者,其与ED共病率分别为65.5%、85.7%、85.0%,三者共病率比较有显著性差异.④服用SSRI类药物及米氮平的抑郁症患者,与ED共病率分别为77.5%及78.9%,两者比较无显著性差异;⑤HAMD评分＞17患者组的IIEF-5评分及与ED共病率均显著高于HAMD评分≤17患者组;⑥抑郁症与ED共病组HAMD量表评分显著高于非共病组;⑦Logistic回归分析表明HAMD评分及体重指数为抑郁症患者与ED共病的危险因素.结论 男性抑郁症患者与ED的共病率高,抑郁程度重及体重指数高可能是抑郁症患者与ED共病的危险因素.     

癫痫伴抑郁症患者认知功能的影响因素分析

目的分析癫痫伴抑郁症患者认知功能的影响因素。方法回顾性分析我院2005年9月至2009年3月门诊就诊的180例癫痫伴抑郁症患者的临床资料。结果180例癫痫伴抑郁症患者中,认知功能障碍者82例（45．6％）,其发生与性别、婚姻状况、癫痫病灶部位及癫痫发作类型差异无统计学意义（P〉0．05）,而与发病年龄、文化程度、病程、癫痫发作频率及发作持续时间差异有统计学意义（P〈0．05）。结论癫痫伴抑郁症患者认知功能的影响因素为发病年龄、文化程度、病程、发作频率及发作持续时间,临床应该尽量避免这些因素的影响。     

癫痫伴抑郁症患者认知功能影响的危险因素分析

目的分析癫痫伴抑郁症患者认知功能影响的危险因素,以指导临床工作。方法回顾性分析某院2005年9月至2009年3月门诊就诊的180例癫痫伴抑郁症患者的临床资料。结果180例癫痫伴抑郁症患者中,认知功能障碍者82例（45．6％）,其发生与性别、婚姻状况、癫痫病灶部位及癫痫发作类型差异无统计学意义（P〉0．05）,而与发病年龄、文化程度、病程、癫痫发作频率及发作持续时间差异有统计学意义（P〈0．05）。结论癫痫伴抑郁症患者认知功能影响的危险因素为发病年龄、文化程度、病程、发作频率及发作持续时间,临床应该尽量避免这些危险因素的发生,提高患者的生活质量。     

糖尿病与抑郁症共病研究进展

糖尿病和抑郁症均为临床常见慢性疾病,二者的相关性已成为研究热点。国内外学者针对糖尿病与抑郁症共病的危险因素、生物学特征和症状开展了大量研究。本文综述两种疾病的相关性以及糖尿病与抑郁症共病的治疗进展,以提高对糖尿病人群发生抑郁症的警惕性,早期诊断,早期治疗。     

物质使用障碍与抑郁症共病

物质使用障碍(Substance Use Disorder,SUD)与抑郁症均是全球主要的公共卫生问题,二者常常合并发生.本文试着从SUD与抑郁症共病的流行病学、发病机制、诊断及治疗等方面进行综述,从而引导临床医生对该共病的认识及治疗.     

抑郁症合并代谢性疾病的共病机制及其治疗药物的研究进展

抑郁症是严重危害人类身心健康的常见病,随着"生物–心理–社会"的现代医学模式转变,发现其常与其他重大疾病如糖尿病、高血脂、心脏病、高血压等代谢综合征组分并存,合并疾病发病率高且预后不良,以及造成对家庭和社会的高负担,关于其发病机制和防治措施的研究方兴未艾。抑郁症和代谢性疾病的发病可能存在一定共病基础和因果关系,旨在重点探讨脂质代谢紊乱和血管内皮功能障碍在抑郁症合并代谢性疾病的病理发展和共病机制中的作用,同时归纳总结现有治疗药物对脂质代谢异常和内皮功能障碍的影响,为临床用药的优选及其共病患者的治疗方式提供综述基础。     

老年抑郁症和焦虑障碍共病的研究概况

老年人口中抑郁症和焦虑障碍共病很常见,共病病人的临床症状更重,预后更差。作者复习近期的老年抑郁症和焦虑障碍共病的相关研究,总结此领域近年来的研究概况。     

脑源性生长因子参与疼痛-抑郁共病的研究进展

疼痛和抑郁症存在共病联系,两者之间可能存在共同的神经解剖机制及分子机制。近年来研究发现,中枢神经系统中的脑源性生长因子(brain-derived neurotrophic factor,BDNF)在疼痛-抑郁共病过程中发挥重要作用,BDNF也逐渐成为疼痛及抑郁症的研究热点及治疗靶点。该文就BDNF参与疼痛-抑郁共病的机制及外周血BDNF在疼痛、抑郁症的诊治中的意义做论述。     

糖尿病抑郁共病治疗管理研究进展

糖尿病患者有较高的抑郁症患病风险,可对患者的主观幸福感和生活质量产生不利影响,并可能增加降糖治疗不顺从性。糖尿病患者的抑郁可通过心理治疗及药物方式得到有效缓解,及时有效地治疗抑郁症可以显著提高糖尿病患者的生活质量,减轻患者的心理负担,促进降糖治疗的有效开展。针对糖尿病抑郁共病的相关危险因素、共病诊断、慢性病治疗管理等方面的研究进展作一综述。     

用集中注意法对抑郁症患者进行押韵汉字的分听研究

目的：探讨抑郁症患者相对于健康被试的大脑半球机能不对称特点，以及共病和非共病焦虑障碍抑郁症患者，不同文化水平抑郁症患者的大脑半球机能不对称是否有差别。方法：用集中注意法及两种押韵词，对58名健康被试，115名抑郁症患者进行耳优势测试。结果：健康被试真词测听未见明显耳优势而假词测听呈现出右耳（左半球）优势。2．抑郁症患者真词测听未见耳优势而假词测听呈现增强的右耳（左半球）优势。3．真词测听，共病焦虑障碍组无耳优势，非共病组有增强的右耳（左半球）优势；假词测听，两组均表现为右耳（左半球）优势，非共病组强于共病组。4．真词测听，高低教育组无差异；假词测听，低教育组右耳（左半球）优势强于高教育组。5．HAMD，HAMA，SCL-90评分与真，假词偏侧指数无相关性。结论：1．健康中国人对真词的加工与认知无耳优势，表明健康中国人在加工真词时需要左右两侧半球的协同参与；对假词的加工与认知则表现出右耳（左半球）优势，表明更为纯粹的言语材料的加工以左半球为主。2．抑郁症患者对汉字词的加工与认知，表现出较健康人强的右耳（左半球）优势。3．共病和非共病焦虑障碍者对汉字词的加工与认知，表现出较健康人强的右耳（左半球）优势，而非共病者较共病者右耳（左半球）优势强。4．低教育抑郁症患者比高教育者的右耳（左半球）优势强。5．患者的言语偏侧化指数与症状严重程度无相关性。6．假词为较为理想的分听材料。     

Rhythm and blues: Animal models of epilepsy and depression comorbidity

Clinical evidence shows a strong, bidirectional comorbidity between depression and epilepsy that is associated with decreased quality of life and responsivity to pharmacotherapies. At present, the neurobiological underpinnings of this comorbidity remain hazy. To complicate matters, anticonvulsant drugs can cause mood disturbances, while antidepressant drugs can lower seizure threshold, making it difficult to treat patients suffering from both depression and epilepsy. Animal models have been created to untangle the mechanisms behind the relationship between these disorders and to serve as screening tools for new therapies targeted to treat both simultaneously. These animal models are based on chemical interventions (e.g. pentylenetetrazol, kainic acid, pilocarpine), electrical stimulations (e.g. kindling, electroshock), and genetic/selective breeding paradigms (e.g. genetically epilepsy-prone rats (GEPRs), genetic absence epilepsy rat from Strasbourg (GAERS), WAG/Rij rats, swim lo-active rats (SwLo)). Studies on these animal models point to some potential mechanisms that could explain epilepsy and depression comorbidity, such as various components of the dopaminergic, noradrenergic, serotonergic, and GABAergic systems, as well as key brain regions, like the amygdala and hippocampus. These models have also been used to screen possible therapies. The purpose of the present review is to highlight the importance of animal models in research on comorbid epilepsy and depression and to explore the contributions of these models to our understanding of the mechanisms and potential treatments for these disorders.     

Antidepressant therapy in epilepsy: can treating the comorbidities affect the underlying disorder?

There is a high incidence of psychiatric comorbidity in people with epilepsy (PWE), particularly depression. The manifold adverse consequences of comorbid depression have been more clearly mapped in recent years. Accordingly, considerable efforts have been made to improve detection and diagnosis, with the result that many PWE are treated with antidepressant drugs, medications with the potential to influence both epilepsy and depression. Exposure to older generations of antidepressants (notably tricyclic antidepressants and bupropion) can increase seizure frequency. However, a growing body of evidence suggests that newer (‘second generation’) antidepressants, such as selective serotonin reuptake inhibitors or serotonin-noradrenaline reuptake inhibitors, have markedly less effect on excitability and may lead to improvements in epilepsy severity. Although a great deal is known about how antidepressants affect excitability on short time scales in experimental models, little is known about the effects of chronic antidepressant exposure on the underlying processes subsumed under the term ‘epileptogenesis’: the progressive neurobiological processes by which the non-epileptic brain changes so that it generates spontaneous, recurrent seizures. This paper reviews the literature concerning the influences of antidepressants in PWE and in animal models. The second section describes neurobiological mechanisms implicated in both antidepressant actions and in epileptogenesis, highlighting potential substrates that may mediate any effects of antidepressants on the development and progression of epilepsy. Although much indirect evidence suggests the overall clinical effects of antidepressants on epilepsy itself are beneficial, there are reasons for caution and the need for further research, discussed in the concluding section.     

Current and emerging drug therapies for the treatment of depression in adults with epilepsy

Introduction: Depression is the most frequent psychiatric comorbidity among people with epilepsy. It can impact on quality of life and increases the risk of morbidity and premature mortality.

Areas covered: The authors review the available data on current and emerging drug treatments for depression in epilepsy. Sources have been identified through Medline/PubMed searches while ongoing clinical trials have been identified through a ClinicalTrials.gov search.

Expert opinion: SSRIs are the drug class with the largest amount of data. Though promising, the level of evidence provided by these studies is still low as the majority have relevant methodological limitations. Antiepileptic drugs under development have the unique opportunity to be of multi-use in the treatment of epilepsy and depression. The serotoninergic system has already been identified as a potential area of interest, but new targets are still needed in epilepsy and depression. For this reason, it is important that basic scientists working on these two conditions develop collaborative projects and integrate findings.     

The effects of chronic norepinephrine transporter inactivation on seizure susceptibility in mice.

Epilepsy and depression are comorbid disorders, but the mechanisms underlying their relationship have not been identified. Traditionally, many antidepressants have been thought to increase seizure incidence, although this remains controversial, and it is unclear which medications should be used to treat individuals suffering from both epilepsy and depression. Since the neurotransmitter norepinephrine (NE) has both antidepressant and anticonvulsant properties, we speculated that NE transporter (NET) inhibitor antidepressants might be therapeutic candidates for comorbid individuals. To test this idea, we assessed the effects of chronic administration (via osmotic minipump) of the selective NET inhibitor reboxetine on flurothyl-induced seizures in mice. We found that reboxetine had both proconvulsant and anticonvulsant properties; it lowered both seizure threshold and maximal seizure severity. NET knockout (NET KO) mice essentially phenocopied the effects of reboxetine on flurothyl-induced seizures, and the trends were extended to pentylenetetrazole and maximal electroshock seizures (MES). Furthermore, reboxetine had no further effect in NET KO mice, demonstrating the specificity of reboxetine for the NET. We next tested the chronic and acute effects of other classes of antidepressants (desipramine, imipramine, sertraline, bupropion, and venlafaxine) on seizure susceptibility. Only venlafaxine was devoid of proconvulsant activity, and retained some anticonvulsant activity. These results suggest that chronic antidepressant drug treatment has both proconvulsant and anticonvulsant effects, and that venlafaxine is a good candidate for the treatment of epilepsy and depression comorbidity.     

Definitions of secondary depression: effects on comorbidity and outcome in anxiety disorders.

The impact of different definitions of secondary depression on comorbidity and treatment outcome findings in anxiety disorder patients was examined by reviewing existing studies. Few data were found specifically on alternative definitions of secondary depression. However, other relevant findings yielded several conclusions: (a) different definitions of depression dramatically affect comorbidity findings, (b) widely divergent comorbidity findings are obtained in studies that use the same (temporal) definition of secondary depression, (c) few data exist on how different definitions of depression affect treatment outcome findings for anxiety disorders, and (d) some data show that patients' reports of whether or not their depressive symptoms temporally followed their anxiety symptoms are unreliable, suggesting that investigators who want to study secondary depression need to first determine that they have a reliable way to assess it.     

Childhood and adolescent risk factors for comorbid depression and substance use disorders in adulthood

The comorbidity of major depression and substance use disorders is well documented. However, thorough understanding of prevalence and early risk factors for comorbidity in adulthood is lacking, particularly among urban African Americans. With data from the Woodlawn Study, which follows a community cohort of urban African Americans from ages 6 to 42, we identify the prevalence of comorbidity and childhood and adolescent risk factors of comorbid depression and substance use disorders, depression alone, and substance use disorders alone. Prevalence of comorbid substance use disorders and major depression in adulthood is 8.3% overall. Comorbidity in cohort men is twice that for women (11.1% vs. 5.7%). Adjusted multinomial regression models found few differences in risk factors for comorbidity compared to either major depression or a substance use disorder on its own. However, results do suggest distinct risk factors for depression without a substance use disorder in adulthood compared to a substance use disorder without depression in adulthood. In particular, low socioeconomic status and family conflict was related to increased risk of developing major depression in adulthood, while dropping out of high school was a statistically significant predictor of adult-onset substance use disorders. Early onset of marijuana use differentiated those with a substance use disorder with or without depression from those with depression without a substance use disorder in adjusted models. In conclusion, comorbid substance use disorders and depression are highly prevalent among these urban African Americans. Insight into the unique childhood and adolescent risk factors for depression compared to substance use disorders is critical to intervention development in urban communities. Results suggest that these programs must consider individual behaviors, as well as the early family dynamic.     

Plasticity of Presynaptic and Postsynaptic Serotonin 1A Receptors in an Animal Model of Epilepsy-Associated Depression

Depression is a common comorbidity of temporal lobe epilepsy and has highly negative impact on patients'' quality of life. We previously established that pilocarpine-induced status epilepticus (SE) in rats, concurrently with chronic epilepsy leads to depressive impairments, and that the latter may stem from the dysregulation of hypothalamo–pituitary–adrenocortical (HPA) axis and/or diminished raphe–hippocampal serotonergic transmission. We examined possible involvement of presynaptic and postsynaptic serotonin 1A (5-HT1A) receptors in epilepsy-associated depression. Based on their performance in the forced swim test (FST), post-SE animals were classified as those with moderate and severe depressive impairments. In moderately impaired rats, the activity of the HPA axis (examined using plasma corticosterone radioimmunoassay) was higher than in naive subjects, but the functional capacity of presynaptic 5-HT1A receptors (measured in raphe using autoradiography) remained unaltered. In severely depressed animals, both the activity of the HPA axis and the function of presynaptic 5-HT1A receptors were increased as compared with naive and moderately depressed rats. Pharmacological uncoupling of the HPA axis from raphe nucleus exerted antidepressant effects in severely impaired rats, but did not modify behavior in both naive and moderately depressed animals. Further, the function of postsynaptic 5-HT1A receptors was diminished in the hippocampus of post-SE rats. Pharmacological activation of postsynaptic 5-HT1A receptors improved depressive deficits in epileptic animals. We suggest that under the conditions of chronic epilepsy, excessively hyperactive HPA axis activates presynaptic 5-HT1A receptors, thus shifting the regulation of serotonin release in favor of autoinhibition. Downregulation of postsynaptic 5-HT1A receptors may further exacerbate the severity of epilepsy-associated depression.     

Autonomous neurobiological pathways to late-life major depressive disorder: clinical and pathophysiological implications.

The objective of our study was to elucidate distinct paths to depression in a model that incorporates age, measures of medical comorbidity, neuroanatomical compromise, and cognitive status in a sample of patients with late-life major depressive disorder (MDD) and nondepressed controls. Our study was cross-sectional in nature and utilized magnetic resonance imaging (MRI) estimates of brain and high-intensity lesion volumes together with clinical indices of cerebrovascular and nonvascular medical comorbidity. Neuroanatomic and clinical measures were incorporated into a structural covariance model in order to test pathways to MDD. Our data indicate that there are two paths to MDD; one path is represented by vascular and nonvascular medical comorbidity that contribute to high-intensity lesions that lead to depression. Smaller brain volumes represent a distinct path to the mood disorder. Age influences depression by increasing atrophy and overall medical comorbidity but has no direct impact on MDD. These findings demonstrate that there are distinct biological substrates to the neuroanatomical changes captured on MRI. These observations further suggest that neurobiological mechanisms acting in parallel may compromise brain structure/function, thereby predisposing individuals to clinical brain disorders such as depression.     

Ameliorating effects of aripiprazole on cognitive functions and depressive-like behavior in a genetic rat model of absence epilepsy and mild-depression comorbidity

Aripiprazole (APZ) is regarded as a first-line atypical antipsychotic used for the treatment of first and multiple episodes of schizophrenia to improve positive- and negative-symptoms. Its therapeutic indications were extended to acute manic and mixed episodes associated with bipolar disorder. In addition, APZ was approved as an adjunct therapy for major depressive disorder in 2007. Compared to other antipsychotic drugs, APZ has a unique pharmacological profile. It is a partial agonist at D(2) dopamine receptors and serotonin 5-HT(1A) and 5-HT(7) receptors, whereas it is an antagonist at serotonin 5-HT(2A) and 5-HT(6) receptors. Since epilepsy is often accompanied with neurological comorbidities such as depression, anxiety and cognitive deficits caused by both the disease and/or drug treatment, we wished to examine the effects of a sub-chronic treatment (>14 consecutive days) with APZ (0.3, 1 and 3?mg/kg; i.p.) on both absence seizures and WAG/Rij rat's behavior using different standard paradigms: Open field (OF) test, elevated plus maze (EPM) test, forced swimming (FS) test, sucrose consumption (SC) test and Morris water maze (MWM). WAG/Rij rats represent a validated genetic animal model of absence epilepsy with mild-depression comorbidity, also including other behavioral alterations. APZ treatment showed some anti-absence properties and regarding the behavioral comorbidity in this rat strain, we observed that APZ possesses clear antidepressant effects in the FS and SC tests also increasing memory/learning function in the Morris water maze test. In the two anxiety models used, APZ showed only minor effects. In conclusion, our results indicate that APZ might actually have a potential in treating absence seizures or as add-on therapy but more interestingly, these effect might be accompanied by positive modulatory actions on depression, anxiety and memory which might be also beneficial in other epileptic syndromes. This article is part of a Special Issue entitled 'Cognitive Enhancers'.