12例椎-基底动脉串联病变的血管内治疗探讨

目的探讨经皮血管内支架成形术(PTAS)治疗椎-基底动脉重度狭窄串联病变的有效性、安全性及可行性。方法对12例(26处)经药物治疗无效的症状性椎-基底动脉串联病变患者采用经皮血管内支架成形术治疗。术前DSA示动脉直径狭窄率为65～100%,平均84.62±8.24%。结果本组支架置放成功率92.6%,术后平均狭窄率为16.92±14.84%;术后用mRS量表(改良RANKIN量表)评分,7例0分,3例1分,2例3分。发生2例围手术期并发症,年卒中率为6.2%;随访期间2例发生支架内再狭窄。结论血管内支架成形术治疗椎-基底动脉串联病变,在技术上可行,远期疗效良好。     

支架成形术治疗椎-基底动脉狭窄的疗效观察

目的 评价支架成形术治疗椎-基底动脉狭窄的疗效.方法 对34例经数字减影血管造影(DSA)确诊的椎-基底动脉狭窄的患者,采用球囊扩张支架对椎-基底动脉狭窄段进行支架成形术.结果 34例患者共放置36枚支架,手术成功率为100%,术后DSA示狭窄段全部成形良好,无并发症发生,椎-基底动脉狭窄段狭窄程度从术前的(78.3±6.2)%降至(3.6±4.2)%.随访6～38个月,患者临床症状消失31例,明显改善2例,复发1例.未见椎-基底动脉系统短暂性脑缺血发作(TIA)及新发后循环供血系统脑梗死等并发症.结论 支架成形术治疗椎-基底动脉狭窄是一种安全有效的方法.     

基底动脉狭窄的支架成形术治疗

目的探讨支架成形术治疗基底动脉狭窄的疗效和安全性。方法回顾性分析2016~2018年采用支架成形术治疗的73例基底动脉狭窄的临床资料。结果围手术期血管不良事件发生率为9.6%;术后1年支架再狭窄率为5.5%。术后6~12个月复查DSA发现63例(86.3%)支架良好;4例(5.5%)支架内再狭窄,但无后循环缺血症状。结论支架成形术治疗基底动脉狭窄效果良好;术前对血管及斑块的评估、术中球囊及支架的选择、术后血压的控制及术者的经验等保证疗效至关重要。     

经皮血管内支架成形术治疗椎基底动脉狭窄的中短期疗效及安全性评价

目的观察经皮血管内支架成形术治疗椎基底动脉狭窄的中短期疗效,并评价其安全性。方法回顾性分析沧州市中心医院2012-01-2013-01收治的50例行经皮血管内支架成形术治疗椎基底动脉狭窄患者的临床资料和术后随访资料,评价治疗方法的中短期疗效及安全性。结果所有患者手术均一次成功,手术成功率100%;手术前后DSA狭窄率差异具有统计学意义(P0.05);42例患者术前症状消失或明显缓解,好转8例,均未见神经功能恶化和死亡病例;随访3~24个月,复查结果显示未见管腔再狭窄、支架移位、塌陷等问题。结论经皮血管内支架成形术治疗椎基底动脉狭窄的手术成功率高、并发症发生风险低,中短期疗效显著,是一种有效且安全的治疗方法。     

支架成形术治疗椎动脉颅内段和基底动脉狭窄17例临床观察

目的评估症状性椎动脉颅内段、基底动脉狭窄患者经皮血管内支架成形术(PTAS)治疗的安全性和有效性。方法17例症状性椎动脉颅内段及基底动脉狭窄患者,狭窄程度在50%以上且规范的内科药物治疗无效,给予PTAS治疗,术后常规给予抗凝、抗血小板聚集、降脂药物。结果17例患者20处狭窄行PTAS,所有的病例手术均取得成功,没有严重并发症,术后即刻造影残存狭窄平均在10%以下,病人平均随访6.8个月(3～10个月),有1例患者出现再狭窄(狭窄程度>50%),所有患者均无缺血症状发作。结论PTAS治疗椎动脉颅内段及基底动脉狭窄是安全和有效的。     

经血管内成形治疗高龄颈动脉颅外段狭窄的风险分析

目的总结经皮腔内血管成形支架置入(PTAS)治疗高龄颈动脉颅外段狭窄的手术方法、风险性及并发症的预防。方法回顾性分析20例(22处狭窄)高龄颈动脉颅外段狭窄病人经数字减影血管造影(DSA)确诊后进行经皮腔内PTAS。结果PTAS成功率100%,术后平均狭窄率由术前(73.9±15.7)%降至(13.0±7.2)%,差异具有统计学意义,术后临床缺血症状及体征均有明显改善。并发症:术后2d支架内血栓形成1例经溶栓后再通,1例发生消化道出血,1例发生脑出血(约2￣3ml),经保守治疗后治愈。随访2～36个月均无脑缺血发作。DSA复查2例,均经Doppler超声复查均未发现再狭窄。结论PTAS是治疗高龄颈动脉狭窄病人的一种简便、安全、有效的方法;围手术期应采取综合措施以降低PTA手术风险及并发症的发生。     

经皮血管内支架成形术治疗椎-基底动脉狭窄疗效观察

目的 评价经皮血管内支架成形术治疗椎-基底动脉狭窄的安全性、有效性和中短期疗效.方法 23例椎-基底动脉狭窄患者施行经皮血管内支架成形术,共检出25个狭窄病变,其中22个位于椎动脉起始段(左侧13个,右侧9个),1个位于椎动脉颅内段,2个位于基底动脉.共成功植入26枚球囊支架,金属裸支架15枚,药物洗脱支架11枚;基底动脉植入2枚,椎动脉植入24枚.其中1例基底动脉急性闭塞患者采用尿激酶动脉溶栓辅助药物洗脱支架治疗.结果 23例患者施行经皮血管内支架成形术后血管平均狭窄率从治疗前的81.40%(50%～95%)降至6.30%(0～15%).20例患者平均持续随访21个月,17例(85%)症状明显缓解或消失,3例(15%)部分缓解;2例复发患者中1例再次血管内植入药物洗脱支架后血管开通良好,1例拒绝接受再次治疗.结论 经皮血管内支架成形术治疗椎-基底动脉狭窄安全、有效,中短期疗效满意.药物洗脱支架对手术后支架内再狭窄具有一定的预防作用且优于金属裸支架,若手术后积极辅以抗血小板治疗可进一步提高药物洗脱支架治疗椎-基底动脉狭窄的有效性.     

椎-基底动脉重度狭窄的血管内治疗

目的回顾性分析椎-基底动脉重度狭窄患者临床诊断与治疗经过,以评价血管内支架成形术的可行性和临床疗效。方法16例椎-基底动脉重度狭窄患者均施行血管内支架成形术,观察其技术成功率、围手术期并发症发生率及远期疗效。结果16例患者经脑血管造影检查共发现27个狭窄病变,共成功植入36枚球囊扩张式支架,技术成功率达100%(16/16)。1例于手术后24h发生支架内急性血栓形成,围手术期并发症发生率为6.25%(1/16)。随访期间,3例(18.75%)发生支架内再狭窄而致卒中再发。结论血管内支架成形术治疗椎-基底动脉重度狭窄,在技术上可行,远期疗效良好。     

血管内支架成形术治疗颅内动脉狭窄

目的分析血管内支架成形术治疗症状性颅内动脉狭窄的有效性及安全性。方法回顾性分析103例症状性颅内动脉狭窄病人的临床资料,共103处狭窄,其中基底动脉狭窄29处,椎动脉颅内段狭窄23处,颈内动脉颅内段狭窄3处,大脑中动脉狭窄48处。均行血管内支架成形术,并通过临床症状、改良Rankin量表评分评价其疗效。结果手术成功101例,植入支架101枚,平均动脉狭窄程度从术前的82.84%±8.14%降为术后的10.61%±5.09%;手术失败2例(支架无法到位1例,刺破动脉1例)。术后临床症状消失28例,好转51例,无明显变化19例,因并发症加重5例。67例DSA随访6～14个月,出现再狭窄27例,其中再狭窄率50%21例,再狭窄率≥50%6例。临床随访12个月,新发TIA 4例,小面积脑梗死4例,少量脑室出血1例。结论血管内支架成形术是治疗症状性颅内动脉粥样硬化性狭窄的安全、有效手段。     

前后循环动脉重度狭窄Ⅰ期支架成形术体会

目的探讨前后循环动脉狭窄同期行血管内支架成形术的手术方法、疗效及安全性。方法对2006-06—2011-02我院16例症状性颈内动脉狭窄同时合并椎基底动脉系统狭窄的患者Ⅰ期行颈动脉及椎基底动脉血管内支架成形术,总结手术经验,观察围手术期并发症,分析临床效果。结果 16例患者共置入34枚支架(其中1例患者同时合并锁骨下动脉狭窄,Ⅰ期行颈动脉、锁骨下动脉、椎动脉支架植入术),术后即刻造影残余狭窄<18%,颈动脉支架置入后9例出现心率下降,11例出现心率、血压同时下降,围手术期未出现动脉夹层、支架内血栓形成以及术后过度灌注脑出血等并发症。术后9例临床症状完全消失,7例明显改善,随访5～24个月,1例术后1a复出现缺血症状,复查DSA提示椎动脉支架内再狭窄,再次给予支架内成形术,症状消失。结论前后循环动脉狭窄同期行血管内支架成形术是一种安全有效的方法,能够降低医疗费用,避免二次手术创伤,但远期效果尚需进一步探讨。     

Hepatic Considerations in the Use of Antiepileptic Drugs

Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.     

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.     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Carbamazepine Efficacy and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

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.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.