缺血性卒中患者颅内外动脉狭窄与高血压、糖尿病的研究

目的 探讨缺血性卒中患者的颅内外动脉狭窄特点及程度与高血压病、糖尿病的病史及控制水平的 关系。 方法 回顾性分析住院治疗的存在颅内外动脉狭窄且并发高血压或糖尿病的大动脉粥样硬化性急 性缺血性卒中患者资料。将高血压患者分为高年限组（病史>5年）和低年限组（病史≤5年）,血压 控制良好组和不良组;将糖尿病患者也分为高年限组（病史>5年）和低年限组（病史≤5年）,血糖 控制良好组和不良组。比较不同组间颅内外动脉狭窄分布情况、血管狭窄程度。 结果 共入组216例急性缺血性卒中患者,其中57例颅外动脉狭窄,105例颅内动脉狭窄,54例颅内 外动脉均狭窄。轻度狭窄发生73例,中度狭窄发生101例,重度狭窄及闭塞发生42例。高血压病患者 共140例,高年限组动脉狭窄最常见于颅内动脉（54.5%）,低年限组血管狭窄的部位多见于颅外动脉 （51.3%）,差异有统计学意义（P＜0.001）。两组间动脉狭窄程度差异也有统计学意义。糖尿病患者共 76例,高年限组发生动脉狭窄最常见于颅内动脉（72.2%）,低年限组血管狭窄的部位多见于颅外动脉 （65%）,差异有统计学意义,两组间动脉狭窄程度差异也有统计学意义。高血压控制不良组发生重度 狭窄或闭塞的概率高于血压控制良好组（20.7% vs 8.6%）;血糖控制情况不良组发生重度狭窄或闭 塞的概率高于血糖控制良好组（40.9% vs 6.3%）。 结论 随着高血压病年限的增长,急性缺血性卒中患者颅内动脉狭窄的发生率增高,其中以中度狭 窄程度多见;血压控制不良的患者发生重度狭窄或闭塞的比率高。随着糖尿病年限的增长,颅内动 脉狭窄的发生率增高,其中以中度狭窄程度多见,血糖控制不良者发生重度狭窄或闭塞的比例高。     

脑卒中后糖尿病和糖调节异常的临床研究

目的调查脑卒中患者中糖尿病和糖调节异常的发病情况，探讨口服葡萄糖耐量试验（OGTT）的临床意义。方法对2004年1月-2006年6月收治入院的547例脑卒中患者进行空腹血糖、糖化血红蛋白（GHbAlc）等检测，登记患者的临床资料，对既往未诊断糖尿病而空腹血糖在5．6～6．9mmol／L的患者在适当时候进行OGTT，糖代谢分类采用2003年美国糖尿病学会建议标准。结果547例脑卒中患者住院前糖尿病的诊断率为13.9％，住院后检查发现糖尿病的患病率34．4％，糖调节异常26．5％；脑梗死、脑出血、蛛网膜下腔出血糖尿病的伴发率分别为45．1％、20．5％、13．2％，糖调节异常的伴发率分别30．2％、23．2％、16．2％；227例空腹血糖在5．6～6．9mmol／L的患者中，OGTT检查后发现，19．8％患者可诊断为糖尿病，42.3％提示糖耐量异常。结论脑卒中患者合并高比例的糖尿病和糖调节异常；缺血性卒中发病率高于出血性卒中：空腹血糖在5．6～6．9mmol／L的患者中，OGTT可以发现大量的糖尿病和糖耐量异常患者。     

50例脑动脉重度狭窄（闭塞）分布及相关危险因素分析

目的研究脑动脉重度狭窄（闭塞）的血管分布及其相关危险因素,为缺血性脑卒中的发病机制、临床诊断、治疗以及预防提供重要依据。方法通过对50例DSA和（或）CTA诊断为脑动脉重度狭窄（或闭塞）的缺血性脑卒中患者计算其重度狭窄或闭塞动脉数目及其分布,同时测血压、血糖（GLU）、尿酸（UA）、甘油三酯（TC）、总胆固醇（TG）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）、极低密度脂蛋白（VLDL-C）、外周血白细胞数（WBC）、血小板数（PLT）、血小板分布宽度（PDW）、平均血小板体积（MPV）、大血小板比率（P—LCR）及纤维蛋白原（FIB）,与无脑动脉狭窄纽比较以上相关因素的差异。结果颅内动脉重度狭窄率（84．6％）明显高于颅外动脉（15．4％）,比较脑动脉存在重度狭窄与无狭窄的两组缺血性脑卒中患者,其舒张压、UA、TC、LDL-C、VLDL-C、WBC、PLT、PDW、MPV、P—LCR差异均无统计学意义（P〉0．05）,而收缩压、FIB、GLU、TG、HDL-C、年龄因素差异有统计学意义（P〈0．05或P〈0．01）,Logistic回归发现高血压、糖尿病与缺血性脑卒中脑动脉重度狭窄呈明显相关性（P〈0．05）。结论缺血性脑卒中患者颅内动脉重度狭窄发生率高于颅外动脉,HDL-C水平与脑动脉狭窄呈负相关,高血压、糖尿病与脑动脉重度狭窄有关,而高血压是脑动脉重度狭窄的独立危险因素。     

缺血性卒中患者动脉狭窄分布及变化趋势

目的 探讨缺血性卒中狭窄的分布及变化趋势。方法 缺血性卒中患者230例行全脑血管造影,根据年龄分为＜60岁组（121例）和≥60岁组（109例）,比较不同组患者脑供血动脉狭窄程度的差异。结果 ≥60岁组颈动脉颅外段和后循环颅外段狭窄的比率较＜60岁组高（P＜0.01）;＜60岁组颅内动脉闭塞较≥60岁组多见（P＜0.01）,＜60岁组颅内动脉闭塞较同组颅外动脉闭塞多见（P＜0.01）。结论 不同年龄缺血性卒中患者狭窄血管的空间分布及变化趋势不同。     

特发性脑动脉夹层28例致缺血性卒中机制分析

目的 通过回顾分析特发性脑动脉夹层（cerebral artery dissection,CAD）患者影像学和血管学资料研究其缺血性卒中机制,为治疗策略提供依据。方法 选取28例特发性CAD所致急性缺血性卒中患者,根据缺血性卒中病灶形态和分布来确定CAD致缺血性卒中机制;根据夹层病变的位置分为颅内组和颅外组,对两组患者夹层致缺血性卒中机制进行比较。结果 共28例患者纳入研究,男19例,女9例。颅外组17例,其中颈内动脉夹层15例,椎动脉V1段夹层2例。颅内组11例,其中大脑中动脉M1段夹层3例,基底动脉夹层2例,椎动脉V4段夹层6例。颅内组高血压和糖尿病患者分别为7例（63.6%）和5例（45.5%）,颅外组均为1例（5.9%）,颅内组高血压和糖尿病患病比例多于颅外组（P =0.002,0.022）。颅外组和颅内组单纯栓塞性缺血性卒中分别有12例（70.6%）和2例（18.2%）,两组比较差异有统计学意义（P =0.018）。颅内组由夹层病变闭塞局部穿支动脉所致缺血性卒中7例（63.6%）,由夹层闭塞穿支合并血流动力学机制所致1例（9.1%）,单纯血流动力学机制所致1例（9.1%）。结论 颅外CAD致缺血性卒中机制与颅内CAD有所不同,前者主要导致栓塞性缺血性卒中,而后者致缺血性卒中机制主要为夹层病变闭塞局部穿支动脉。     

支架技术在急性缺血性卒中合并颅内外动脉狭窄中的应用

目的探讨支架技术在急性缺血性卒中合并颅内外动脉狭窄中应用的可行性、安全性及有效性。方法回顾性纳入2014年4月至2016年10月在山东大学附属济南市中心医院神经外科就诊的29例急性缺血性卒中合并颅内外动脉狭窄的患者。经数字减影血管造影（DSA）证实责任动脉闭塞,患者取栓后仍有重度狭窄,遂行球囊扩张、支架置入血管成形术。记录患者治疗前、后7d美国国立卫生研究院卒中量表（NIHSS）评分、30d卒中或短暂性脑缺血性发作的复发率及90d改良Rankin量表评分（mRS）。临床随访分别在术后30d和90d进行。结果29例患者的技术成功率为100％,支架治疗后平均残留狭窄率为（10．4±8．1）％。所有患者均得到随访,30d内再次卒中1例。NIHSS评分：治疗前为（19．5±3．5）分,治疗后7d为（5．8±2．1）分,治疗前后的差异有统计学意义（P〈0．05）。90d患者的病死率为0％,其中28例（97％）90dmRS评分≤2分,预后良好。结论急性缺血性卒中合并颅内动脉狭窄患者应用支架技术的并发症发生率较低且安全、有效;但残余狭窄以及合并基础性疾病、医嘱依从性差被认为是卒中再发的危险因素。     

缺血性卒中患者颅内动脉狭窄的相关危险因素分析

目的 探讨颅内动脉狭窄的狭窄程度、相关危险因素与缺血性脑卒中的关系,为缺血性卒中的防治提供重要依据.方法 90例缺血性卒中患者根据全DSA检查结果分为非狭窄组(狭窄<30%)与颅内动脉狭窄组(狭窄≥30%或闭塞),分析颅内动脉狭窄程度与年龄、性别、高血压、糖尿病、高脂血症、冠心病、家族史、总胆固醇(CHO)、三酰甘油(TG)、高密度脂蛋白胆同醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白 A1(ApoA1)、载脂蛋白B(ApoB)、血清脂蛋白(Lpa)等相关危险因素的关系.结果 (1)本组患者颅内动脉狭窄发生率为67.78%,发生率最高为大脑巾动脉,其次颈内动脉颅内段和椎基底动脉颅内段,发生率最低为大脑后动脉.(2)有高血压、糖尿病的缺血性卒中患者容易发生颅内动脉狭窄,其同归系数、OR值、P值分别为1.659、5.256、0.002,1.657、5.241、0.046.(3)颅内动脉狭窄组HDL-C含量[(0.99±0.30)mmol/L]比非狭窄组[(1.30±0.50)mmol/L]明显降低,差异有统计学意义(t=3.603,P=0.001).(4)年龄、性别、吸烟、既往卒中史、脑血管病家族史、TC、TG、LDL-C、ApoA1、ApoB、Lpa在两组间比较差异无统计学意义(P>0.05).结论 缺血性卒中患者颅内血管狭窄的主要危险因素有高血压、糖尿病,保护因素有HDL-C.     

急性缺血性卒中患者颅内动脉粥样硬化性狭窄与不同血糖水平代谢综合征的相关性分析

目的 探讨急性缺血性卒中患者颅内动脉粥样硬化性狭窄与不同血糖水平代谢综合征的相关性。 方法 选取2013年6月-2016年6月入住本院神经内科的急性缺血性卒中患者352例为研究对象,根 据颅内血管狭窄情况分为狭窄组227例和非狭窄组125例;选取同期非颅内动脉粥样硬化性狭窄体检 者310例为对照组。研究对象中合并代谢综合征的患者分为3个亚组：糖耐量正常组、伴糖尿病组、伴 高血糖组（包括空腹血糖受损、糖耐量降低）。同时测定代谢综合征患者血脂水平,分析不同血糖 水平代谢综合征与颅内动脉粥样硬化性狭窄的相关性。 结果 352例急性缺血性卒中患者共确诊代谢综合征195例（55.39%）,其中狭窄组和非狭窄组代谢 综合征的发生率均明显高于对照组,比较差异有显著性（P <0.05）;狭窄组代谢综合征的发生率明显 高于非狭窄组,比较差异有显著性（P <0.05）。狭窄组中伴糖尿病的代谢综合征患者比例明显高于非 狭窄组和对照组,比较差异有显著性（P <0.05）;狭窄组中伴高血糖和糖耐量正常的代谢综合征患 者比例与非狭窄组比较,差异均无显著性（P＞0.05）。Logistic回归分析显示：代谢综合征与颅内动脉 粥样硬化性狭窄存在明显相关性;代谢综合征伴糖尿病、伴低高密度脂蛋白（high density lipoprotein, HDL）、高甘油三酯（triglyceride,TG）与颅内动脉粥样硬化性狭窄发生风险呈明显正相关。 结论 在急性缺血性卒中患者中,代谢综合征尤其是糖尿病、高TG血症及低HDL血症和颅内动脉粥 样硬化性狭窄密切相关。     

缺血性卒中患者颅内外血管狭窄率研究

目的:研究缺血性卒中患者颅内外血管狭窄或闭塞的发生率,并对其相关病因进行分析。方法:对经CT/MRI/DWI诊断的缺血性卒中患者的人口构成情况进行登记,了解其相关危险因素。并经TCD和/或MRA了解其颅内外血管狭窄或闭塞的情况。结果:579例缺血性卒中患者中,颅内外血管狭窄的发生率为70.98%(411/579例);411例大动脉狭窄或闭塞患者中,以大脑中动脉狭窄或闭塞最常见(64.48%),其次为颈内动脉(50.36%)。大动脉狭窄或闭塞的主要原因为动脉粥样硬化,引起动脉粥样硬化的危险因素的发病率依次为:高血压病(77.24%),吸烟(63.68%)。通过Logistic回归分析发现,糖尿病、高血压、吸烟是血管狭窄的主要相关危险因素(P值均<0.05)。结论:国内缺血性卒中患者颅内外血管狭窄或闭塞的发生率高,其主要病因为动脉粥样硬化,糖尿病是大动脉狭窄或闭塞的最主要危险因素。     

多发颅内动脉粥样硬化性狭窄对轻型卒中和短暂性脑缺血发作早期卒中复发风险影响研究

目的 探讨多发颅内动脉狭窄对轻型缺血性卒中和TIA早期卒中复发的影响。 方法 纳入氯吡格雷用于急性非致残性脑血管事件高危人群的疗效（Clopidogrel in High -risk Patients with Acute Non-disabling Cerebrovascular Events,CHANCE）研究影像亚组1089例非心源性高危 TIA和轻型缺血性卒中患者。根据患者入院时MRA序列的检查结果分为无颅内动脉狭窄、单发颅内动 脉狭窄和多发颅内动脉狭窄3组。随访患者90 d卒中复发（缺血性和出血性卒中）事件。采用Cox回归 分析多发颅内动脉狭窄对轻型缺血性卒中和TIA患者90 d卒中复发风险的影响。 结果 无颅内动脉狭窄、单发颅内动脉狭窄和多发颅内动脉狭窄组分别有608例、298例和183 例患者;90 d卒中发生风险比例分别为5.43%、9.06%和18.03%。与无颅内动脉狭窄患者相比,伴 有颅内动脉狭窄（包含单发和多发颅内动脉狭窄）患者卒中复发风险显著高于非颅内动脉狭窄患者 （12.50% vs 5.40%,P＜0001）。其中,多发颅内动脉狭窄卒中复发风险最高（18.03%）,是无颅内动脉 狭窄患者的3.578倍（HR 3.578,95%CI 2.189～5.850）。 结论 多发颅内动脉狭窄是非心源性TIA和轻型卒中患者早期卒中复发的独立危险因素。     

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”.