胰岛素强化治疗重型颅脑损伤合并糖尿病

目的探讨胰岛素强化治疗对重型颅脑损伤(STBI)合并糖尿病患者的临床疗效及预后的影响。方法选择入住重症监护病房(ICU)既往有糖尿病史的重型颅脑损伤患者80例,随机分为治疗组和对照组,每组40例,治疗组给予7 d胰岛素强化治疗,随后给予常规血糖控制,对照组全程常规血糖控制。强化胰岛素治疗组血糖控制目标为4.4~8.3 mmol/L,常规血糖控制目标为4.4~11.1 mmol/L。结果伤后随访6月按(GOS)评分评价疗效,治疗组恢复良好率较对照组组提高15%,死亡率下降17%(P0.05),ICU住院时间、机械通气时间、院内感染发生率均低于对照组(P0.05)。结论短期胰岛素强化治疗能有效改善重型颅脑损伤合并糖尿病患者的预后,降低ICU内并发症的发生率。     

即刻血糖水平检测对颅脑损伤患者病情及预后判断的意义

目的探讨院前接诊即刻血糖水平检测在评估颅脑损伤患者病情及预后中的价值。方法选取颅脑创伤患者76例为研究对象,根据格拉斯哥昏迷评分(GCS)分为3组,轻型组(13~15分)20例、中型组(9~12分)27例和重型组(3~8分)29例,探讨患者入院时即刻血糖水平与患者病情严重程度及预后的关系。结果轻型组患者即刻血糖为(5.16±1.30)mmol/L,显著低于中型组(7.92±1.63)mmol/L、重型组(8.82±1.91)mmol/L,两两对比差异均具有统计学意义(P0.05);轻型组不同血糖水平对预后无影响(P0.05);中型组、重型组血糖11.1mmol患者的预后良好率高于血糖≥11.1mmol患者,差异具有统计学意义(P0.05);轻型组不良预后的发生率为0,显著低于中型组、重型组,差异具有统计学意义(P0.05)。结论即刻血糖水平与颅脑损伤患者预后显著相关。     

急性颅脑损伤患者血糖水平与预后的关系探讨

目的探讨急性颅脑损伤患者血糖水平的变化与颅脑损伤程度及预后的关系。方法 118例急性颅脑损伤患者入院后检测血糖,并在第1周内隔天检测血糖,2～4周每周检测血糖一次,取入院时和1个月血糖水平,分析血糖水平与GCS评分、病死率、预后之间的关系。结果 GCS评分与预后存在相关性：入院时正常血糖组（3.6～6.4mmol/L）GCS评分较高,较高血糖水平组（〉6.4～11.0mmol/L）GCS评分较低,高血糖水平组（〉11.0mmol/L）GCS评分最低,三者比较差异有统计学意义（P〈0.05）;入院时正常血糖组病死率为0（0/34）,较高血糖水平组病死率3.5%（2/57）,高血糖水平组病死率最高,为22.2%（6/27）,三者之间差异有统计学意义（P〈0.05）;经过控制血糖1个月后,大部分患者血糖水平均下降,正常血糖组病死率为0（0/80）,较高血糖水平组病死率13.0%（3/23）,高血糖水平组病死率最高,为33.3%（5/15）,三者之间差异有统计学意义（P〈0.05）。结论急性颅脑损伤后血糖水平可作为判断颅脑损伤严重程度及预后的一个指标,患者血糖水平越高,预后愈差。     

应激性高血糖对急性重型颅脑损伤预后的评估

目的探讨血糖在急性重型颅脑损伤病情评估及预后判断的临床价值。方法对150例既往无糖尿病的急性颅脑损伤患者均于入院时进行GCS评分,根据GCS评分分为轻中度颅脑外伤组(GCS 9~15分)和重度颅脑外伤组(GCS 3~8分),并对患者48h内的血糖变化进行检测,探讨伤后血糖水平与患者伤情、预后的关系。结果重度颅脑损伤组患者的平均血糖水平高于轻中度组(P<0.05),血糖>11.1 mmol/L颅脑损伤患者的病死率明显高于血糖<11.1 mmol/L者(P<0.05),死亡患者的血糖水平明显高于存活患者(P<0.05)。结论重度颅脑外伤患者急性期的血糖浓度是判断颅脑损伤的严重程度及近期预后的参考指标,可作为GCS评分外的辅助指标。     

血糖变化对急性严重颅脑损伤程度及预后评估的价值

目的探讨急性严重颅脑损伤患者血糖变化与预后的关系,为颅脑损伤患者伤情及预后判断提供理论依据。方法根据发病与否分为颅脑创伤组和对照组;以入院时GCS评分判定病情分成3~4分组(10例),5~6分组(15例),7~8分组(23例);按照预后分为存活和死亡2组。结果急性颅脑创伤患者的血糖含量明显高于对照组(P<0.01);GCS评分3组间血糖值有显著性差异(P<0.01);血糖水平与GCS评分呈显著负相关(r=-0.721,P<0.01);死亡组的血糖含量明显高于非死亡组(P<0.01)。结论颅脑损伤后血糖值可作为判断伤情的指标,应重视颅脑损伤患者血糖监测,努力控制高血糖,提高急性严重颅脑创伤患者的治愈率。     

急性脑损害早期血糖变化临床分析

目的探讨急性脑损害后早期血糖变化与病情严重程度及预后的关系。方法对2008-01~2010-12收治的113例急性脑损害病人早期(24 h内)血糖值按GCS、GOS及年龄分别进行分组统计,并与GCS、GOS的关系进行统计学分析。当血糖值≥10.1 mmol/L时采用胰岛素治疗进行干预。结果血糖值高低与病情严重程度(GSC)、预后(GOS)及年龄呈正相关,早期血糖与GCS及GOS具有相关性。结论急性脑损害后早期血糖值可作为判断脑损害严重程度的一项指标,并间接影响预后。血糖值≥10.1 mmol/L可作为药物干预的阈值。     

控制重型颅脑损伤急性期高血糖对预后的影响

目的 对比观察不同程度的血糖控制对重型颅脑损伤伴高血糖患者预后的影响及应控制的血糖阈值。方法 将重型颅脑损伤患者随机分为三组，N1组血糖控制于3．9—5．6mmol/L，N2组控制于5．7--11．1mmol/L，N3组不进行血糖控制，对比三组入院时GCS评分及病死率。结果 N1及N2组预后优于N3组，但N1与N2组间无统计学差异。结论 颅脑损伤伴高血糖患者血糖控制于11．1mmol/L以下可显著改善预后，但不必将血糖控制于正常范围。     

高血糖对原发性脑干损伤患者预后的影响

目的探讨高血糖对原发性脑干损伤患者预后的影响。方法将108例原发性脑干损伤患者分为正常血糖组和高血糖组,高血糖组又按空腹血糖值分为血糖6.1～12.0 mmol/L和12.0 mmol/L组,按有无糖尿病史分为A、B两组,分析正常血糖组和高血糖组、血糖浓度高低组及A、B组的预后,并进一步分析高血糖对并发症的影响。结果①与血糖正常组比较,高血糖组死亡率明显升高,且与血糖值的高低有显著相关性(P0.01),而与既往有无糖尿病无显著相关性(P0.05)。②与血糖正常组比较,高血糖组的并发症发生率明显增高(P0.05)。结论原发性脑干损伤患者的血糖水平升高是影响预后的一个重要因素,高血糖者死亡率高,预后差。     

重型颅脑损伤急性期高血糖、伤情和预后的临床分析

目的 探讨重型颅脑损伤后高血糖形成机制与伤情和预后的关系.方法 48例重型颅脑损伤患者于入院当时、第3d和第7d检测空腹血糖,根据预后将患者分为死亡组和存活组,同时与对照组(轻、中型颅脑损伤者)进行对比分析.结果 重型颅脑损伤患者血糖均有不同程度增高,死亡组血糖明显高于存活组(P＜0.01);重型颅脑损伤组血糖显著高于对照组(P＜0.01);入院时血糖与 GCS 和预后显著相关(P＜0.01),且入院时血糖≥10mmol/L者,病死率显著增高.结论 重型颅脑损伤患者急性期血糖均有不同程度升高,血糖升高程度越明显,脑损伤程度越重、预后越差;动态检测重型颅脑损伤患者血糖对了解病情、判断预后具有重要的意义.     

重型颅脑创伤患者血清COR、ACTH及血糖的变化

目的评估重型颅脑创伤患者伤后不同时期的血清皮质醇(COR)、促肾上腺皮质激素(ACTH)及血糖水平的变化,及其在伤情判断与预后中的作用。方法前瞻性选择重型颅脑创伤患者56例,正常对照组23例,重型颅脑创伤患者按入院时GCS评分分为重型组(6～8分)、特重型组(3～5分)两个亚组,治疗4个月后对比预后评分(GOS评分),测定不同时期血清COR、ACTH及血糖浓度。结果 GCS 3～5分与6～8分组血清COR、ACTH及血糖浓度入院后5 d内均显著增高,与对照组比较差异有显著性(P<0.01),GCS 3～5分组血清COR、ACTH、血糖浓度高于GCS 6～8分组(P<0.05)。GCS 3～5分组死亡率明显高于6～8分组,颅脑损伤组第1 d血清COR、ACTH、血糖浓度均显著高于对照组(P<0.01)。结论重型颅脑创伤患者伤后血清COR、ACTH及血糖均有不同程度的增高,监测血清COR、ACTH及血糖浓度可作为判断患者病情轻重、治疗效果和预后的一项重要指标。     

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”.