原发性甲状腺功能减退致垂体增生的诊断与治疗

目的探讨原发性甲状腺功能减退致垂体增生的诊断和治疗原则。方法回顾性分析3例原发性甲状腺功能减退致垂体增生患者的临床资料。对3例原发性甲状腺功能减退患者行垂体及靶腺功能和影像学检查,并在左旋甲状腺素替代治疗l～3个月后行内分泌功能及MRI复查。结果3例均为原发性甲状腺功能减退症,MRI示垂体明显增大,信号强化均匀。左旋甲状腺素替代治疗3个月后甲状腺功能减退症状消失;MRI示垂体大小恢复正常2例,明显缩小1例;血浆甲状腺素、促甲状腺素和泌乳素水平恢复正常。结论原发性甲状腺功能减退病人可以伴有垂体增生;努力提高对其垂体增生MRI表现的认识,及时诊断,并首选甲状腺素替代治疗效果好。     

重症肌无力患者甲状腺功能和甲状腺抗体情况的临床分析

目的　了解重症肌无力 ( MG)患者甲状腺功能及甲状腺抗体的情况。方法　回顾性分析了 2 67例临床确诊 MG患者的甲状腺素水平 ,对其中 2 64例患者检测了甲状腺球蛋白抗体 ( TGAb)和甲状腺过氧化物酶抗体( TPOAb)或甲状腺微粒体抗体 ( TMAb)。结果　 5 5例 ( 2 0 .6% )患者有甲状腺功能异常 ,48例 ( 1 8.2 % )至少有 1项上述抗体阳性。甲状腺功能异常的 MG患者中 , 、 、 型抗体阳性者较多 ( P <0 .0 1 )。甲状腺抗体阳性者较抗体阴性者 MG发病晚 ( P <0 .0 5 ) ;甲状腺抗体阴性 MG患者有甲状腺功能障碍者 MG发病早于功能正常组 ( P <0 .0 5 )。甲状腺功能异常、抗体阳性的 MG患者病程较抗体阴性者长 ( P <0 .0 5 ) ;甲状腺抗体阳性者伴发胸腺增生或胸腺瘤的几率明显增高 ( P <0 .0 5 )。结论　MG合并甲状腺功能异常并不少见 ,甲状腺抗体阳性、功能异常的 MG患者病程长 ,伴发胸腺增生或胸腺瘤的几率高 ,临床应予以重视。     

难治性抑郁症患者甲状腺激素水平的分析

目的 探讨难治性抑郁症患者的甲状腺激素水平。方法 按性别、年龄1：1匹配选取难治性抑郁症患者和健康对照各30例,采用放射免疫法测定患者组治疗前和对照组血清TSH、T3、T4、FT3、FT4水平。结果 患者组异常者17例,占56．7％,对照组异常者2例,占6．7％,两组比较,患者组甲状腺激素水平出现异常的比率明显高于对照组,主要表现为TSH升高、T3降低、FT4降低,差异均有统计学意义（P〈0．05）。结论 难治性抑郁症患者中有56．7％的患者存在亚临床型甲状腺功能的减退。     

伴甲状腺疾病重症肌无力患者的临床特点

目的 研究伴甲状腺疾病的重症肌无力(MG)患者的临床特点.方法 同期住院及门诊MG患者88例(均排除其他自身免疫性疾病),分为甲状腺正常组(61例)和伴甲状腺疾病组(27例),回顾性分析其资料,比较两组患者的一般情况、首发症状、临床分型、实验室检查、治疗及疗效等临床特点.结果 伴甲状腺疾病MG组中女性比例明显高于甲状腺...     

原发性甲状腺功能减退致垂体增生的诊断和治疗(附3例报告)

目的探讨原发性甲状腺功能减退致垂体增生的诊断和治疗。方法回顾性总结3例原发性甲状腺功能减退患者的临床表现、影像学表现、内分泌检查资料。结果根据临床表现、影像学表现、内分泌检查可明确诊断原发性甲状腺功能减退合并垂体增生;甲状腺素替代治疗5～8个月,甲状腺功能减退症状消失,血清促甲状腺激素和三碘甲状腺原氨酸、四碘甲状腺原氨酸、泌乳素水平正常,垂体大小恢复正常。结论原发性甲状腺功能减退导致的垂体增生,不应该简单考虑垂体瘤予以手术治疗。甲状腺素替代治疗是治疗原发性甲状腺功能减退致垂体增生的有效手段。     

重症肌无力合并甲状腺功能亢进一例

目的探讨重症肌无力(MG)合并甲状腺功能亢进临床特点及诊治,增进对此类疾病的认识。方法报道1例MG合并甲状腺功能亢进的临床资料,结合文献进行分析。结果 MG合并甲状腺功能亢进同时治疗效果更好。结论 MG和甲状腺功能亢进的关联是自身免疫性疾病在人体不同组织系统中针对相同抗原决定簇的损伤,临床医生应该注意到两种疾病同时存在的可能性。     

原发性甲状腺功能减退致垂体增生的诊断和治疗

目的 探讨原发性甲状腺功能减退致垂体增生的诊断和治疗.方法 回顾性总结3例原发性甲状腺功能减退患者的临床表现、影像学表现、内分泌检查资料.结果 根据临床表现、影像学表现、内分泌检查可明确诊断原发性甲状腺功能减退合并垂体增生;甲状腺素替代治疗5～8个月,甲状腺功能减退症状消失,血清促甲状腺激素和三碘甲状腺原氨酸、四碘甲状腺原氨酸、泌乳素水平正常,垂体大小恢复正常.结论 原发性甲状腺功能减退导致的垂体增生,不应该简单考虑垂体瘤予以手术治疗.甲状腺素替代治疗是治疗原发性甲状腺功能减退致垂体增生的有效手段.     

重症肌无力与甲状腺抗体异常的相关性

目的 研究重症肌无力(MG)与甲状腺异常在抗体方面的相关性.方法 比较100例MG患者和100名健康对照在甲状腺功能、甲状腺抗体异常率方面的差异.随机选取其中32例MG患者,探讨其血清乙酰胆碱受体(AChR)抗体与促甲状腺激素受体抗体(TRAb)、甲状腺球蛋白抗体(TGAb)和甲状腺微粒体抗体(TMAb)的相关性及临床特点.结果 100例MG中,甲状腺功能亢进(甲亢)和甲状腺功能减退(甲减)者共16例(16%),甲状腺抗体检查阳性者71例(71%),甲状腺抗体阳性率高于甲状腺功能阳性率(χ2=4.788,P<0.05).32例MG血清AChR抗体与TRAb浓度存在线性相关(r=0.609,P=0.O002).结论 MG患者出现甲状腺抗体异常比出现甲亢或甲减更多见.MG血清AChR抗体与TRAb浓度存在线性相关.     

儿童及青少年原发性甲状腺功能减退导致垂体增生的诊断与治疗

目的探讨原发性甲状腺功能减退所致垂体增生患者的临床特征、影像学特征、诊断及治疗。方法回顾性分析14例18岁以下儿童及青少年原发性甲状腺功能减退所致垂体增生患者的临床资料,包括内分泌学检查、影像学检查及治疗结果。结果头部MRI检查显示14患者垂体均存在不同程度增大,信号均匀,增强后均匀强化。14例患者血清三碘甲状腺原氨酸和四碘甲状腺原氨酸水平均正常,14例患者血清促甲状腺激素水平均升高,9例患者血清催乳素水平升高。14例患者经甲状腺素替代治疗后随访12个月,头部MRI显示增大的垂体均恢复到正常范围内,内分泌学检查均恢复正常。结论MRI检查可有效诊断原发性甲状腺功能减退导致的垂体增生,确诊应结合临床表现、内分泌检查以及甲状腺素替代治疗结果,正确诊断可避免不必要手术治疗。     

原发性甲状腺功能减退致垂体增生四例报告及文献复习

目的 探讨原发性甲状腺功能减退致垂体增生的诊断和处理原则.方法 结合文献回顾性分析4例原发性甲状腺功能减退致垂体增生的临床资料.结果 4例均表现为促甲状腺激素(TSH)及催乳素(PRL)增高,FT3及FT4减少,MRI示垂体增大,甲状腺素替代治疗2-4个月后,垂体恢复正常,TSH及PRL水平亦恢复正常.结论 原发性甲状腺功能减退致垂体增生具有影像学特征,结合临床可明确诊断.治疗首选甲状腺素实验性替代治疗,而不宜行手术治疗.     

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.     

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.     

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.     

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.     

Neonatal Seizures: Problems in Diagnosis and Classification

Summary: The clinical identification of neonatal seizures is critical for the recognition of brain dysfunction; however, diagnosis is often difficult because of the poorly organized and varied nature of these behaviors. Current classification systems are limited in their ability to communicate motor, autonomic, and electroencephalo-graphic features of seizures precisely and to provide a basis for uniform effective diagnosis, therapy, and determination of prognosis. Recent investigations of neonates, utilizing bedside electroencephalographic/polygraphic/ video monitoring techniques, have provided the basis for improved diagnosis and classification of seizures in the newborn. These studies have demonstrated that not all clinical phenomena currently considered to be seizures require electrocortical epileptiform activity for their initiation or elaboration. In addition, the specific clinical character of the phenomena considered to be seizures, the clinical state of the infant, and the character of the EEG indicate the probable pathophysiological mechanisms involved and suggest probable etiologies, prognosis, and therapy. Similarities between animal models that demonstrate reflex physiology and neonates with motor automatisms and tonic posturing suggest that these clinical behaviors may not be epileptic in origin but, rather, primitive movements of progression and posture mediated by brainstem mechanisms. Although not all clinical behaviors currently considered to be neonatal seizures may have similar pathophysiological mechanisms, they are clinically significant because they all indicate brain dysfunction.     

Valproate Monotherapy in the Management of Generalized and Partial Seizures

Summary: For decades, therapeutic tradition has promoted the concept of polypharmacy in the management of epilepsy. In recent years, however, studies have shown that, for most patients, monotherapy can provide comparable or better seizure control than administration of multiple anticonvulsants, while diminishing the potential for adverse reactions, drug interactions, and poor compliance. Valproate is an important monotherapeutic agent that is highly effective in the control of idiopathic primary and secondarily generalized epilepsies, and partial seizures that do not generalize. Comparative studies have found that valproate is at least as effective as phenytoin and carbamazepine in the treatment of generalized and partial seizures. Given the similar efficacy, other factors such as pharmacokinetics and side effects may therefore determine anticonvulsant selection for monotherapy.     

Un nouveau cadre conceptuel de travail pour la psychiatrie

In an attempt to place psychiatric thinking and the training of future psychiatrists more centrally into the context of modern biology, the author outlines the beginnings of a new intellectual framework for psychiatry that derives from current biological thinking about the relationship of mind to brain. The purpose of this framework is twofold. First, it is designed to emphasize that the professional requirements for future psychiatrists will demand a greater knowledge of the structure and functioning of the brain than is currently available in most training programs. Second, it is designed to illustrate that the unique domain which psychiatry occupies within academic medicine, the analysis of the interaction between social and biological determinants of behavior, can best be studied by also having a full understanding of the biological components of behavior.