MR导向丘脑,苍白球毁损治疗锥体外系疾病

从１９９５年１０月－１９９６年５月，我们使用Ｌｅｋｓｅｌｌ－Ｇ型定向仪，１．０ｔｓｌａ超导磁共振导向，对３４例，锥体外系疾病，进行靶点毁损术，通过临床效果和术前，后ＭＲ复查，证实ＭＲ民向三维误差〈１ｍｍ，ＭＲＩ导向的功能性神经外科疾病治疗，几何图像失真小，清晰靶点易辨认，术后反应小，若在电生理监测下更安全，有效。     

微电极导向同期双侧腹后苍白球 毁损术治疗帕金森病

目的介绍微电极导向同期双侧腹后苍白球毁损术治疗帕金森病的方法与效果。方法应用微电极电生理记录技术术对毁损靶点进行确认定位,对３１例难治性帕金森病患者行同期双侧腹后内侧苍白球毁损治疗,术前及术后于开状态、关状态分别行改良Ｗｅｂｓｔｅｒ记分,计算改善率,评价其疗效。结果经微电极确认后的电生理靶点与ＣＴ定位靶点存在明显差异,靶点调整率８０６％。３１例手术均有效,其中治愈７例,明显进步２４例。Ｗｅｂｓｔｅｒ计分术后１周开状态改善率为７４２％±９５％,关状态改善率为８９１％±８９％。无永久性并发症。结论微电极导向同期双侧腹后苍白球毁损术安全、有效,具有明显临床治疗优势,微电极记录技术可使术中定位精确度大大提高。     

帕金森氏病主要症状的内外科治疗长期效果研究

本研究将帕金森氏病人随机分成三组：（１）单纯服用Ｌ－ＤＡ和／或美多巴治疗组；（２）丘脑腹外侧核，苍白球腹后外侧部脑立体定向术后规律性服用抗震颤药物组；（３）术后不规律服药组。治疗前一周停药物观测基本症状，治疗后１月，６月及１年对ＰＤ主要症状进行ＨＹＰＤＳ评估并进行统计学分析。立体定向术后规律性服用抗震颤药物是治疗ＰＤ病人最佳途径。所有治疗不能阻断其自然进展     

颅内肿瘤术后合并大面积脑梗塞

颅内肿瘤术后合并大面积脑梗塞杨富成赵长坡颅内肿瘤术后合并大面积脑梗塞临床并不多见。我院３年来利用磁共振血管成像（ＭＲＡ）连续发现３例，现报告如下。例１女，６０岁，主诉记忆力减退伴呕吐２个月。ＣＴ及ＭＲＩ示左蝶骨嵴脑膜瘤。高血压病史１年。入院检查：血压...     

磁共振血管成像诊断脑血管疾病(10例MRA和DSA对照)

０例做ＭＲＡ的患者与其中同时做ＤＳＡ（９例）及手术（１例）的患者进行对照分析，５例ＭＲＡ结果与ＤＳＡ一致，包括２例大脑中动脉起始部闭塞，１例大脑中动脉主干狭窄，２例血管畸形。另５例中，１例ＭＲＡ检查结果显示大脑中动脉主干闭塞，但ＤＳＡ仅显示该段动脉狭窄，２例ＭＲＡ显示两侧颈内动脉虹吸部闭塞，ＤＳＡ除有上述发现外，还检出脑底部异常血管网，１例ＭＲＡ显示左侧颈内血流来自前、后交通动脉，ＤＳＡ检查结果为左侧主动脉弓颈总动脉起始部的闭塞，１例ＭＲＡ显示前交通动脉的动脉瘤，瘤腔大小为１．０ｃｍ×０．９ｃｍ，手术中证实为２．０ｃｍ×１．０ｃｍ，部分瘤腔内有血栓样物质充填。本组资料说明ＭＲＡ能较清晰地显示颅内血管畸形、动脉瘤、Ｗｉｌｉｓ动脉环和大动脉的闭塞和狭窄病变，不足之处为（１）ＭＲＡ可因血管闭塞或动脉瘤腔内有血栓样物质不能准确反映瘤腔大小。（２）目前ＭＲＡ仅能检出大动脉及其一、二级分枝。（３）ＭＲＡ显示动脉狭窄可有病变“夸大现象”。     

脊髓肿瘤337例的临床及磁共振诊断

脊髓肿瘤３３７例的临床及磁共振诊断林翔，李明磁共振（ＭＲ）是近年来发展起来的新技术，我院自１９８６年１１月至１９９２年１月用ＭＲ检查诊断脊髓肿瘤３３７例，经手术病理证实，现将临床应用结果分析报告如下。临床资料一、一般资料本组男２１６例（６４％），女１...     

颅内不同靶点定向毁损术后的小脑症状与手术灶的关系

目的：评价并探讨立体定向毁损颅内不同靶点治疗帕金森病（PD）术后出现小脑体征与手术灶关系。方法：随机抽出颅内3个不同靶点毁损治疗PD共90例进行回顾性分析。所有病例均采用Leksell定向仪,选择常规靶点。结果：丘脑外侧苍白球（VpLp）毁损术后一周以上出现小脑体征者占3．3％,在丘脑腹测中间校（Vim）毁损出现小脑体征者占6．6％。而毁损丘脑腹外侧核（VL）出现率最高。结论：毁损灶越靠近丘脑脑底部,术后出现小脑症状的发生率越高,说明走向毁损灶的位置与小脑症状的出现有着很大的关系。     

糖皮质激素对重症肌无力患者周围血IL－2活性及sIL－2R水平的影响

检测了４２例重症肌无力（ＭＧ）患者周围血单个核细胞（ＰＢＭＣ）白细胞介素－２（ＩＬ－２）活性及血清可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）水平，重点观察了１４例ＭＧ患者在糖皮质激素（ＧＣ）治疗后ＩＬ－２活性及ｓＩＬ－２Ｒ水平变化。结果显示，ＭＧ患者ＰＢＭＣＩＬ－２活性显著低于正常对照组，而血清ｓＩＬ－２Ｒ水平显著高于正常对照组，且ＭＧ患者ＩＬ－２活性与ｓＩＬ－２Ｒ水平之间呈显著负相关；应用ＧＣ治疗后，ＩＬ－２活性显著升高，ｓＩＬ－２Ｒ水平显著下降。提示ＭＧ患者ＩＬ－２活性变化与ｓＩＬ－２Ｒ水平密切相关，ＧＣ可通过影响ＩＬ－２活性及ｓＩＬ－２Ｒ水平而发挥免疫治疗作用。     

SHR大鼠延髓腹外侧头端区血管紧张素Ⅱ的作用研究

探讨ＳＨＲ及ＷＫＹ大鼠延髓腹外侧头端区（ｒｏｓｔｒａｌｖｅｎｔｒｏｌａｔｅｒａｌｍ ｅｄｕｌｌａ， ＲＶＬＭ）内微量注射血管紧张素Ⅱ（Ａｎｇ Ⅱ）和血管紧张素Ⅱ受体阻滞剂［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ对心血管活动的影响。在ＳＨＲ及ＷＫＹ 大鼠，ＲＶＬＭ 微量注射人工脑脊液，不引起明显的心血管效应。ＲＶＬＭ 内微量注射递增剂量的Ａｎｇ Ⅱ（ｐｍ ｏｌ：０１，１０，１０，１００），引起血压升高，心率增加。两组实验动物血压、心率的变化无统计学差别。Ａｎｇ Ⅱ的效应可被预先注射［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ所阻断。相反，ＲＶＬＭ 微量注射剂量递增的［Ｓａｒ１，Ｔｈｒ８］Ａｎｇ Ⅱ（ｐｍ ｏｌ：０１，１０，１０，１００），引起血压下降，心率减慢。在ＳＨＲ大鼠，血压下降的幅度明显大于ＷＫＹ大鼠，而心率的变化在两组动物中无显著差别。实验结果提示大鼠ＲＶＬＭ 内Ａｎｇ Ⅱ具有升高血压和增加心率的作用。Ａｎｇ Ⅱ的作用与Ａｎｇ Ⅱ受体介导有关。ＳＨＲ大鼠ＲＶＬＭ 内神经元对内源性Ａｎｇ Ⅱ的敏感性增高。ＳＨＲ大鼠高血压的形成与ＲＶＬＭ 内Ａｎｇ Ⅱ的升压作用增强有关。     

顽固性癫痫伽玛刀放射外科治疗

目的：采用伽玛刀对脑内某些靶点结构行立体定向放射毁损术治疗顽固性癫痫，探讨治疗癫痫的方法。方法：选择癫痫诊断明确，术前ＥＥＧ、ＢＥＡＭ、ＭＲ、ＳＰＥＣＴ检查，病程３年以上，频繁发作的不同类型的癫痫病人，均经抗癫痫药物（ＡＥＤ）系统治疗不能控制。按外科治疗癫痫适应证原则，１．５Ｔ磁共振扫描，确定靶区，计算机Ｇａｍｍａ－Ｐｌａｎ软件定位，γ－刀治疗。结果：伽玛刀治疗顽固性癫痫病人３６例，其中２３例随访期１２～４８个月（平均１９个月）。其优良率ＥｎｇｅｌＩ）７３．９％（１７例），有效率（ＥｎｇｅｌⅠ和Ⅱ）８６．９５％（２０例）。４例伽玛刀术后３～９个月靶点周围脑水肿（２例自然消退，另２例经激素和脱水治疗后消退）。发作无改变３例病人的病态性格和异常行为有改善。无病情恶化和死亡病例。结论：短、中期的随访结果证明伽玛刀放射外科是一种无创伤性治疗顽固性癫痫的有效和安全的治疗方法，长期效果有待进一步观察。     

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.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

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.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.