大动脉粥样硬化狭窄性脑梗死的危险因素

目的 研究大动脉粥样硬化狭窄性脑梗死的危险因素.方法 186例脑梗死患者根据大动脉狭窄情况分为狭窄组(124例)及无狭窄组(62例).收集患者的临床资料,检测其血同型半胱氨酸(Hcy)及血脂水平.采用Essen卒中风险评分量表(ESRS)对患者进行评分.采用多元Logistic回归分析大动脉狭窄性脑梗死的相关因素.结果 狭窄组有高血压、高Hcy血症、高血压伴高Hcy血症及ESRS评分高危的比率均显著高于无狭窄组(均P＜0.05).多元Logistic回归分析显示,ESRS评分高危及高血压伴高Hcy血症是大动脉狭窄性脑梗死的独立危险因素(Wald值8.60、5.73;P＜0.05 ～0.005).结论 ESRS评分高危、高血压伴高Hcy血症是大动脉粥样硬化狭窄性脑梗死的独立危险因素.     

血浆同型半胱氨酸及MTHFR基因多态性与颅内动脉粥样硬化的相关性研究

目的评价血浆半胱氨酸(Hcy)及亚甲基四氢叶酸还原酶(MTHFR)C677T基因多态性与非心源性脑梗死患者颅内动脉粥样硬化性大血管病变(LVD)的关系。方法共纳入非心源性脑梗死患者552例,测定血浆同型半胱氨酸浓度、MTHFR C677T基因型、脑核磁共振及核磁共振脑血管成像造影,以评价颅内动脉狭窄-闭塞程度和数目积分(LVD积分)。结果纳入552例脑梗死患者中,MTHFR C677T基因型中CC基因型148例(26.8%),CT基因型293例(53.1%),TT基因型111例(20.1%),基因型分布符合Hardy-Weinberg遗传平衡(χ~2=2.371,P0.250);合并颅内动脉狭窄342例,无颅内动脉狭窄210例,颅内动脉狭窄组血浆Hcy浓度显著高于无颅内动脉狭窄组(t=10.502,P=0.032),组间MTHFR C677T基因型分布有显著性差异(χ~2=7.066,P=0.039),多元回归分析显示,高Hcy血症为急性脑梗死患者存在颅内动脉狭窄的独立危险因素(OR1.650,95%CI 1.123～3.021,P=0.034),MTHFR C677T的TT基因型并非为颅内动脉狭窄的独立危险因素(OR1.015,95%CI 1.010～2.532,P=0.079);MTHFR C677T不同基因型组间血浆Hcy浓度有显著性差异(F=7.283,P 0.001),LVD积分无显著性差异(F=2.993,P=0.067),血浆Hcy浓度与颅内血管LVD积分呈正相关关系(r=0.365,P=0.009),高Hcy血症与颅内动脉LVD积分相关(OR1.531,95%CI 1.172～1.463,P=0.040)。结论高同型半胱氨酸血症与颅内动脉LVD具有相关性,MTHFR C677T基因多态性与高同型半胱氨酸血症有相关性,但与颅内动脉动脉粥样硬化无相关性。     

高同型半胱氨酸血症型高血压患者脑血管病变特点

目的比较脑梗死合并高同型半胱氨酸血症(HHcy)型高血压(H型高血压)及原发性高血压患者脑血管病变特点。方法检测258例脑梗死合并高血压患者的同型半胱氨酸(Hcy)水平,根据Hcy水平分为H型高血压组及高血压组。采用DSA检查患者的脑血管病变情况。结果 H型高血压组112例,高血压组146例。两组间性别、年龄、收缩压、舒张压,以及吸烟、饮酒史比率差异均无统计学意义(均P0.05)。两组均以颈内动脉(ICA)及大脑中动脉(MCA)受累多,以颅内血管狭窄病变为主。与高血压组比较,H型高血压组颅内血管病变及重度脑血管狭窄发生率显著增高,侧支循环比率显著降低(均P0.05)。结论脑梗死合并H型高血压患者血管狭窄较多,程度较重,且侧支代偿较少。     

H型高血压与脑动脉狭窄的相关性研究

目的研究H型高血压与脑动脉狭窄的相关性。方法随机选取2013-05—2015-05我院神经内科收治的缺血性脑血管病患者80例,依伴血浆同型半胱氨酸升高情况将患者分为2组,即H型高血压组(n=40)和单纯高血压组(n=40)。对2组患者的血管狭窄发生情况及其危险因素进行统计分析。结果 H型高血压组患者的血管狭窄发生率85.0%(34/40)显著高于单纯高血压组67.5%(27/40)(P0.05),其中颅内外同时病变发生率50.0%(20/40)显著高于单纯高血压组32.5%(13/40)(P0.05),但2组患者单纯颅内病变、单纯颅外病变发生率间差异无统计学意义(P0.05);应用单因素Logistic回归分析,将应变量设定为血管狭窄,将自变量设定为年龄、性别、吸烟、酗酒、高血压、H型高血压、高血糖、甘油三酯、低密度脂蛋白,结果表明,脑动脉狭窄的危险因素包括年龄、吸烟、高血压、H型高血压、甘油三酯(P0.05)。结论 H型高血压与脑动脉狭窄呈显著的正相关关系,值得临床重视。     

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。     

代谢综合征与颅内外动脉粥样硬化性狭窄的相关性研究

目的:探讨代谢综合征(Metabolic syndrome,MS)与颅内外动脉粥样硬化性病变的相关性。方法:连续收集579例因急性脑梗塞或血管性危险因素入院的患者,借助经颅多普勒超声和/或核磁共振血管成像明确有无颅内外动脉粥样硬化性狭窄,分为狭窄组和非狭窄组;采用IDF的MS诊断标准,明确两组MS的发生率;分析颅内外动脉粥样硬化性狭窄的危险因素,并探讨MS与颅内、颅外动脉粥样硬化性狭窄的相关性。结果:1、狭窄组和非狭窄组MS的发生率分别为71.26%,58.43%,两组比较有统计学差异(P=0.0015)。2、与脑动脉粥样硬化性狭窄相关的危险因素依次为:脑梗塞病史、高血糖、高胆固醇血症、高血压、低HDL血症,年龄,MS并非脑动脉粥样硬化性狭窄的独立危险因素,OR0.798。3、MS与颅内动脉粥样硬化性狭窄相关,OR1.736,但其风险依赖于其组分中的高血糖、高血压及低HDL血症;MS与颅外动脉粥样硬化性狭窄不相关,OR1.466。结论:MS不是脑动脉粥样硬化性狭窄的独立危险因素,MS与颅内动脉粥样硬化性狭窄相关,但这种危险性依赖于MS各组分,MS与颅外动脉粥样硬化性狭窄无相关性。     

高同型半胱氨酸血症与颅内外血管狭窄的相关性研究

目的 探讨缺血性脑血管病患者高同型半胱氨酸(Hcy)血症与颅内外血管狭窄的关系.方法 应用全自动生化分析仪,用循环酶法检测405例缺血性脑血管病患者血清Hcy水平,同时检测血清叶酸、维生素B12水平,应用经颅多普勒(TCD)检测所有患者的颅内血管,应用双功能彩色多普勒检测颅外血管.根据检测结果将颈内动脉(ICA)分为:正常、轻度狭窄(＜50%)、中度狭窄(50%～69%)、重度狭窄(70%～99%)、闭塞;大脑中动脉(MCA)分为:正常、中度狭窄(50%～69%)、重度狭窄(70%～95%)、极度狭窄(＞95%).结果 有颅内外血管狭窄组血清Hcy水平显著高于无颅内外血管狭窄组(P<0.01),血清叶酸水平显著低于无颅内外血管狭窄组(P<0.05),血清维生素B12水平两组间差异无统计学意义(P>0.05);ICA、MCA不同程度狭窄患者间血清Hcy水平差异有统计学意义(均P<0.01),血清叶酸水平差异有统计学意义(均P<0.05),维生素B12水平差异无统计学意义(均P>0.05);Hcy水平与ICA、MCA狭窄程度呈正相关(r=0.356 ,P<0.01;r=0.345 ,P<0.01);血清叶酸水平与ICA、MCA狭窄程度呈负相关(r=-0.272 ,P<0.05;r=-0.265,P<0.05).结论 高Hcy血症与颅内外血管狭窄程度密切相关,高Hcy血症可能是缺血性脑血管病新的危险因素.     

脑梗死患者血浆同型半胱氨酸水平与颈动脉粥样硬化的相关性分析

目的探讨脑梗死患者血浆同型半胱氨酸(Hcy)水平与颈动脉粥样硬化程度的关系。方法选择住院确诊为脑梗死患者136例,应用颈动脉多普勒彩色超声检查患者颈动脉内膜中层厚度(intimal-medial wall thickness,IMT),根据颈动脉彩超检查的结果分为颈动脉中-重度狭窄组、颈动脉轻度狭窄组、颈动脉内膜正常组,应用微粒子酶联免疫分析法(MEIA)测定Hcy并进行组间比较。结果颈动脉中-重度狭窄组的Hcy水平为(32.69±17.54)μmol/L,高于颈动脉内膜正常组(17.15±4.97)μmol/L和颈动脉轻度狭窄组(24.74±10.51)μmol/L,差异具有统计学意义(P0.01)。颈动脉轻度狭窄组和颈动脉内膜正常组Hcy水平有显著性差异(P0.05)。直线相关分析显示血浆Hcy水平与IMT呈正相关(r=0.689,P0.05)。结论高Hcy血症可能通过加速动脉粥样硬化而导致脑梗死,血浆Hcy水平与动脉粥样硬化程度呈正相关,将二者结合起来,对脑梗死的预防、治疗及判断预后有重要意义。     

缺血性脑血管病患者脑动脉狭窄与血压变异性的相关性

目的 探讨缺血性脑血管病患者脑动脉粥样硬化性狭窄与血压变异性的关系. 方法 选择自2006年11月至2010年6月在淮南市第一人民医院神经内科住院的206例缺血性脑血管病患者为研究对象,对患者进行连续主动脉弓+全脑血管造影检查,并作动脉血压监测.根据造影结果分组,并对其临床资料进行回顾性分析. 结果 (1)206例患者中75例颅内外动脉无狭窄,131例存在脑动脉狭窄,其中42例仅有颅外动脉狭窄,38例仅有颅内动脉狭窄,51例颅内外狭窄并存;颅外动脉狭窄的发生率(71.0％,93例)高于颅内动脉(67.9％,89例).(2)与颅内外动脉无狭窄组比较.单纯颅外动脉狭窄组、单纯颅内动脉狭窄组、颅内外动脉狭窄并存组24h平均收缩压、舒张压标准差,白昼平均收缩压、舒张压标准差,夜间平均收缩压、舒张压标准差均明显增大,差异有统计学意义(P＜0.05).(3)收缩压变异系数与脑动脉狭窄患病率成正相关(r=0.918,P=0.002),而舒张压变异系数与脑动脉狭窄发患病率无明显相关性(P＞0.05);24 h平均收缩压与脑动脉狭窄患病率成正相关(r=0.936,P=0.001),而24 h平均舒张压与脑动脉狭窄患病率无明显相关性(P＞0.05).(4)多元回归分析显示:24h平均收缩压、收缩压变异系数与颅内外动脉狭窄患病率呈明显正相关.(5)血脂异常是单纯颅内动脉狭窄的独立危险因素;高龄是单纯颅外动脉狭窄的独立危险因素;吸烟是单纯颅内动脉狭窄及单纯颅外动脉狭窄的独立危险因素;高血压是单纯颅外动脉狭窄及颅内外动脉狭窄并存的独立危险因素. 结论 在缺血性脑血管病患者中,脑动脉狭窄与平均血压标准差、收缩压变异系数独立相关.高血压、高脂血症、冠心病、吸烟、高龄、糖尿病和高同型半胱氨酸血症等危险因素与脑动脉狭窄的分布模式有一定关系.动脉血压变异性是缺血性脑血管病患者颅内外狭窄的独立危险因素,但与狭窄的分布模式无相关性.     

同型半胱氨酸血症与脑卒中的关系分析

目的 探讨高同型半胱氨酸血症或伴高血压的高同型半胱氨酸血症人群与脑卒中发生的关系.方法 采用高压液相色谱技术（HPLC）检测266例脑卒中患者（204例脑梗死,62例脑出血）和140非卒中患者血同型半胱氨酸（Hcy）水平.结果 脑卒中组Hcy平均值和高Hcy血症检出率明显高于对照组（P〈0.05）;脑卒中组Hcy水平中度以上升高比例明显高于对照组（P〈0.05）,脑卒中组高Hcy伴高血压比例相对单纯高血压或单纯高Hcy成倍数增加.结论 高同型半胱氨酸或伴高血压的同型半胱氨酸血症是脑卒中的重要风险因子之一,伴高血压的同型半胱氨酸血症患脑卒中的风险更大.     

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”.