强迫症工作记忆受损机制的研究与展望

强迫症(obsessive-compulsive disorder,OCD)是一种以强迫思维和强迫行为为主要表现的精神障碍,以有意识的自我强迫和反强迫同时存在为特征[1]。笔者在临床工作中发现,轻度OCD患者一般不主动求医,当症状严重或继发抑郁情绪时才在家人陪同下就诊;患者社会功能损害严重,疗效不理想且预后较差,自杀率相对较高。大量研究表明OCD患者存在以记忆损害为主的功能障碍[2],且与强     

强迫障碍认知行为治疗的研究进展

强迫障碍(obsessive-compulsive disorder,OCD)是以强迫思维和(或)强迫动作为特征的一种焦虑障碍,其症状明显影响患者的日常生活能力,且病程迁徙,常导致严重的功能损害.过去的10余年中,OCD药物治疗[主要是氯米帕明和选择性5-羟色胺(5-HT)再摄取抑制剂]和认知行为治疗(cognitive-behavioral therapy,CBT)都取得了重要进展.     

强迫障碍认知行为治疗的研究进展

强迫障碍(obsessive-compulsive disorder,OCD)是以强迫思维和(或)强迫动作为特征的一种焦虑障碍,其症状明显影响患者的日常生活能力,且病程迁徙,常导致严重的功能损害.过去的10余年中,OCD药物治疗[主要是氯米帕明和选择性5-羟色胺(5-HT)再摄取抑制剂]和认知行为治疗(cognitive-behavioral therapy,CBT)都取得了重要进展.     

强迫障碍认知行为治疗的研究进展

强迫障碍(obsessive-compulsive disorder,OCD)是以强迫思维和(或)强迫动作为特征的一种焦虑障碍,其症状明显影响患者的日常生活能力,且病程迁徙,常导致严重的功能损害.过去的10余年中,OCD药物治疗[主要是氯米帕明和选择性5-羟色胺(5-HT)再摄取抑制剂]和认知行为治疗(cognitive-behavioral therapy,CBT)都取得了重要进展.     

脑深部电刺激术在强迫症外科治疗中的应用

强迫症(obsessive-compulsive disorder,OCD)是临床常见的精神类疾病,以强迫观念或强迫行为为主要表现,症状较轻时可以采用认知行为治疗,较重时需要药物治疗,但部分患者药物治疗无效,称为药物难治性强迫症,需要外科手术治疗。以往常采用脑深部核团毁损术治疗,但副作用较大,疗效不够满意,而脑深部电刺激(deep brain stimulation,DBS)治疗OCD较毁损术具有微创、不破坏脑结构、可程控的优势,开辟了OCD外科治疗神经调控领域。本文对DBS治疗OCD的作用机制、外科治疗效果及其进展等进行综述。     

强迫症患者小脑结构及功能磁共振技术研究进展

强迫症(Obsessive-compulsive disorder,OCD)是一种常见的以强迫思维和(或)强迫行为为主要临床表现的精神障碍,至今病因及发病机制不明。近年来磁共振技术凭借其优点已被广泛用于精神障碍的研究,已有磁共振研究结果发现OCD患者的小脑结构及功能发生了改变。本文对目前OCD患者小脑结构和功能在磁共振技术相关研究结果进行综述。     

强迫症治疗的研究进展

强迫症（obscssive-compulsive disorder,OCD）指的是以反复出现的强迫思维或强迫行为为主要临床表现的病症。病人深知这些症状不合理,没必要,无意义,但欲无法摆脱和控制,因而焦虑和痛苦,OCD相对于其他神经症而言,具有病程较长,治疗难度较大,心理功能和社会功能损害较重的特点,OCD在一般人群中的发病率为1‰,近年来,专     

强迫障碍药物治疗现状

强迫障碍（OCD）是一种以强迫思维及强迫行为为主要表现的慢性进行性精神障碍,终身患病率约1％-3％。据WHO统计,OCD是世界范围内10种最致残疾病之一,常导致严重精神残疾,生活质量差,给家庭造成严重负担。OCD还与其它精神疾病如抑郁症、焦虑障碍、抽动障碍、疑病症、躯体变形障碍（BDD）及进食障碍等有较高的共病率,临床疗效不佳。现就OCD的有关药物治疗简述如下：     

家族聚集性儿童青少年强迫症发病的影响因素研究进展

强迫症（obsessive-compulsive disorder,OCD）的病因尚未明确，遗传和环境因素共同参与了儿童青少年OCD家族聚集性的发生。OCD家族史阳性的患者起病年龄更早，OCD患者一级亲属的发病率更高，家庭成员之间的强迫症状维度存在高度一致性，计划功能受损作为OCD的内表型，可能参与了OCD的遗传。不良的家庭教养方式、父母人格特征、应激事件、家庭顺应作为儿童生长环境因素可能也参与了家族聚集性OCD的发生，儿童对父母行为的模仿和学习，容易出现与父母类似的强迫特质，成为OCD发病的高危因素。但临床样本收集数量少、缺乏针对儿童青少年OCD的研究给当前探索带来困难。未来研究需更深入地探索OCD家族聚集性的可能原因，及早识别遗传及环境对OCD的影响并及时干预。     

神经肽在强迫症中的作用

以往研究认为强迫症(Obsessive-Compulsive Disease,OCD)的发生机制主要与5-羟色胺(5-hydroxytryptamine,5-HT)系统的异常有关,但目前尚存在争议,有多项证据不支持这个观点,如有证据显示患者中枢5-HT异常已恢复,但症状没有立即好转;SRIs(5-羟色胺再摄取抑制剂)对33％～50％的OCD患者治疗无效;药物刺激OCD患者产生的5-HT功能异常结果不一致;急性色氨酸脱失可导致脑内5-HT急剧下降,但并没有使SRIs治愈的OCD患者症状恶化。近年来的研究发现OCD患者还存在神经肽异常,包括精氨酸血管加压素(AVP),催产素、促肾上腺皮质激素(ACTH)、促肾上腺皮质激素释放因子(CRF)、生长抑素和阿片肽等,现综述如下。     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.     

The influence of comorbid depression on seizure severity

PURPOSE: To determine the relation between depressive symptoms and seizure severity among people with epilepsy. METHODS: A postal questionnaire was used to survey a nationwide community sample about seizures and depression. The Seizure Severity Questionnaire (SSQ) assessed the severity and bothersomeness of seizure components. The Centers for Epidemiological Studies-Depression scale categorized levels of depression. RESULTS: Respondents categorized as having current severe (SEV, n = 166), mild-moderate (MOD, n = 74), or no depression (NO, n = 443) differed significantly in SSQ scores (all p < 0.0001). People with SEV or MOD reported significantly worse problems than did those with NO depression for overall seizure recovery (mean, 5.3, 4.9, 4.5, respectively); overall severity (5.0, 4.5, 4.2); and overall seizure bother (5.3, 4.8, 4.4) (all p < 0.005). Cognitive, emotional, and physical aspects of seizure recovery also were rated worse among people with SEV than with NO depression (all p < 0.05). Symptoms of depression were significantly correlated with higher levels of all components of generalized tonic-clonic seizure severity (r = 0.33-0.48; all p < 0.0001), and partial seizures (r = 0.31-0.38; all p < 0.01). CONCLUSIONS: Clinically depressed people with epilepsy reported higher levels of perceived severity and bother from seizures, as well as greater problems with overall seizure recovery than did nondepressed people experiencing similar types of seizures. The pervasive influence of depressive symptoms on reports of seizure activity suggests that people with epilepsy should be screened for depression. These data highlight the importance of detecting and treating depression among people with epilepsy.     

Une phénoménologie de la dépendance à l'alcool. Une expérience primordiale de la « nostrité »

The phenomenological approach to alcoholism interestingly focuses on specific dynamics of interpersonal relationships displaying the founding of the Self from a primary “us” and its original basis in the human feast. Priorities for treatment intervention recommend to involve social setting and relationships of the patients, reaching their active participation to a motivational and long term group treatment, underlying the specific therapeutic effect of world exchanges. Biopsychosocial determination of alcoholism could be primarily based on components of interpersonal relationships. Regarding social background, drinking is one of the most famous supports for the achievement of the feast, a founding marker of present time. Taking an existential point of view, the feast appears as the heart of mankind because it presents a primary “us”, a plural state which indicates the beginning and founding of the Self from the others. During the feast, we regularly have to reach our Self from the “us” while avoiding two main dangers, drunkenness, an increase in the dizziness of upright verticality, and addiction, an opposite vertical surrender to alcohol and falling into in the alcoholic relapse, both situations imply a spatial domination and the disappearance of others. Treatment programs of alcohol addicts need to integrate the necessity of reaching the existential basic trust from the support of a group to the appropriation of the community which can be defined as an original “usness”.