36例手足口病合并急性弛缓性麻痹患儿的肌电图分析

目的：探讨神经电生理检查在手足口病（HFMD）合并急性迟缓性麻痹（AFP）患儿的特点及应用价值。方法：对36例手足口病合并急性迟缓性麻痹患儿进行运动神经传导速度（MCV）、感觉神经传导速度（SCV）、F波及肌电图（EMG）检查,共检测176条运动神经、88条感觉冲经、98条神经的F波及285块肌肉,并对结果进行分析。结果：运动神经传导异常率为52．8％,其中运动传导波幅下降占81％,未引出反应波者为15％,MCV减慢或潜伏期延长者为4％,感觉传导异常牢为6％,F波异常率为10％,EMG出现自发电位者为28．4％,出现高大运动单位电位（MUP）者为48．1％,募集相减少63.9％。结论：HFMD合并AFP患儿有神经原性损害,以轴突损害电生理改变为主,多累及近端神经,以运动神经受累为主。神经电生理检查对HFMD合并AFP患儿的诊断治疗及判断预后有重要价值。     

吉兰-巴雷综合征患者神经电生理检测结果分析

目的：探讨吉兰-巴雷综合征（GBS）患者的神经电生理特点。方法：对30例GBS患者进行运动神经传导速度（MCV）、感觉神经传导速度（SCV）、肌电图（MMG）及F波检测，共检测运动神经180条，感觉神经180条，肌肉60块，F波40条神经，并对结果进行分析。结果：在被检测的180条运动和感觉神经中，MCV、SCV减慢分别为70．0％和51．6％，潜伏期（Lat）延长分别为49．4％和44．4％，波幅（Amp）下降或引不出波形分别为58．3％、13．9％和14．4％、27．8％。EMG提示神经源性损害。F波潜伏期（Lat）延长为47．5％，出现率下降为57．5％，未引出波形为15．0％。结论：GBS为广泛的周围神经损害，存在以脱髓鞘为主伴有轴索变性的电生理改变。神经电生理检测对GBS的诊断是极为重要的诊断手段。     

吉兰-巴雷综合征患者肌电图及神经传导速度检测

目的：探讨吉兰-巴雷综合征（GBS）的电生理改变特点。方法：对32例GBS患者进行肌电图（EMG）、神经电图及F波检测。测定运动神经传导速度（MCV）、感觉神经传导速度（SCV）及末端潜伏期（Lat）和波幅（Amp）;测定F波最短潜伏期、出现率。结果：肢体神经远端潜伏期延长占53．7％,MCV减慢占68．7％。F波异常占91．8％,SCV减慢占64．4％,EMG提示神经源性改变占71．9％。结论：GBS为广泛的周围神经损害,神经肌电图电生理检测在GBS诊断中起着重要的作用,对于吉兰一巴雷综合征的诊断及预后具有重要价值。     

60例慢性酒精中毒患者的临床与神经电生理特征分析

目的：分析慢性酒精中毒患者的临床与神经电生理特征,企为相关临床研究与治疗提供借鉴。方法：对60例慢性酒精中毒患者与健康人的正中神经、腓总神经、胫神经的运动神经传导速度（MCV）和F波以及正中神经、胫神经和尺神经的感觉神经传导速度（SCV）及F波进行比较分析。结果：与正常对照组相比,慢性酒精中毒患者的MCV及SCV明显减慢,差异有统计学意义（P〈0．01）,且SCV比MCV受累重。同时,慢性酒精中毒患者的电生理变化比临床症状更早。结论：神经电生理特征可以作为慢性酒精中毒的早期诊断指标,具有重要的临床意义。     

肌电图、神经电图在格林—巴利综合征中的应用

目的:探讨肌电图(EMG)、神经电图在格林-巴利综合征(GBS)中的特点。方法:对31例GBS患者进行运动神经124条、感觉神经93条及128块肌肉进行EMG;运动神经传导速度(MCV);远端潜伏期;F波的出现率、潜伏期、波形;感觉神经传导速度(SCV)及一过性离散(TD)测定。结果:每例均有3条以上神经受累;远端潜伏期延长58％;MCV减慢70％;SCV减慢50％;F波异常率73％;TD异常55％。EMG出现自发电位占32％。结论:GBS为广泛的周围神经远端,近端损害,感觉运动均受累,存在以脱髓鞘为主伴有轴索变性的特点。EMG、神经电图的无创性,简便及可重复性使其成为GBS极为重要的诊断手段。     

吉兰-巴雷综合征患者神经电生理检测结果分析

目的：探讨吉兰-巴雷综合征(GBS)患者的神经电生理特点。方法：对25例GBS患者进行肌电图(EMG)、运动神经传导速度(MCV)、F波及感觉神经传导速度(SCV)检测，共检测126条运动神经、89条感觉神经及57块肌肉，并对结果进行分析。结果：上、下肢神经远端潜伏期延长占53．2％，MCV减慢占70．6％，F波异常占92．0％，SCV减慢占64．0％，EMG提示神经源性改变占68．4％。结论：GBS为广泛的周围神经损害，存在以脱髓鞘为主伴有轴索变性的神经电生理改变。神经电生理检测对GBS的诊断是极为重要的诊断手段。     

糖尿病性神经病变的SEP临床研究

目的：探讨SEP与MCV、SCV检测在糖尿病伴有周围神经症状中的诊断应用价值。方法：对61例糖尿病伴有神经症状施行了胫神经感觉诱发电位(SEP)，腓总神经运动传导速度(MCV)，正中神经感觉传导速度(SCV)，并进行了比较分析。结果：总异常率为75．41％。SEP异常率最高(65．57％)；SCV次之(50．82％)；MCV最低(26．23％)。大多数(80％)SCV减慢患均有SEP延长，而1／3SCV正常的病人，SEP潜伏期是延长的。结论：SEP与SCV、MCV合并检测对糖尿病患神经系统损害程度的判断是有益的。     

糖尿病患者周围神经传导速度及其临床意义

目的探讨糖尿病患者周围神经传导速度的变化及其临床意义。方法应用日本光电MEB-2200型肌电／诱发电位仪，对56例临床上确诊为糖尿病的患者和30例健康人，进行了周围运动神经传导速度（MCV）及感觉神经传导速度（SCV）检查及研究。并进行对照分析。结果56例患者中MCV或SCV至少有一项异常者37例，占66％（37／56例）。其中正中神经异常率为35．7％（40／112侧），尺神经异常率为26．8％（30／112侧），腓总神经异常率为61．6％（69／112侧）。而临床上确诊有周围神经病变者仅为17．9％（10／56）。病程大于10年的糖尿病患者组MCV、SCV与健康人比较有统计学意义（P〈0．01）。异常率下肢高于上肢，且传导速度的改变呈双侧对称性并与病程有关。结论神经传导速度的测定对早期诊断糖尿病性周围神经病变（DPN）是有价值的。     

吉兰-巴雷综合征早期电生理变化特点分析

目的：分析吉兰-巴雷综合征（GBS）早期（1～7d）的电生理改变特点,探讨其对GBS的早期诊断价值。方法：采用回顾性分析方法对69例GBS患者的电生理检测结果与临床特点进行分析,比较发病7d之内和大于7d的神经电生理变化特点。结果：运动神经传导速度（MCV）的异常率为55％,发病7d内为45％,发病7d后为55％;F波异常率为77％,发病7d内为52％,发病7d后为48％,感觉神经传导速度（SCV）异常率为52％,发病7d内及7d后均为50％;运动神经复合肌肉动作电位（CMAP）波幅降低异常率为64％,发病7d内为52％,发病7d后为48％;上肢感觉神经动作电位（SNAP）异常同时伴有腓肠神经SNAP正常者占39％,发病7d内占44％,发病7d后为56％。结论：GBS患者早期（7d之内）即可出现神经传导速度、F波、运动及感觉神经传导的改变,以F波更为明显,因此神经电生理检查在GBS中的早期诊断具有重要的作用。     

慢性炎症性脱髓鞘性多发神经病的临床及电生理研究

目的 探讨慢性炎症性脱髓鞘性多神经病(CIDP)的临床及电生理特征.方法 对16例CIDP的患者进行肌电图(EMG)、运动神经传导速度(MCV)、F波、H反射及感觉神经传导速度(SCV)检测,共检测64条运动神经、48条感觉神经及96块肌肉,并对结果进行分析.结果 全部患者均缓慢进行上、下肢神经远端潜伏期延长占56.25%,MCV减慢占60.46%,F波异常占95.83%,H反射异常率占75%,SCV减慢占77.08%,EMG提示神经源性损害占39.58%.结论 CIDP为广泛的周围神经损害,存在以多灶性脱髓鞘为主伴有不同数量的轴索退变.神经电生理检测对CIDP的诊断具有重要的诊断价值.     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

Class II HLA in Georgia Caucasus Tbilisi Georgians and their Mediterranean ancestry: The Usko Mediterranean languages

Georgia (or Sakartvelo in its own language) is a South Caucasus Mts. country with its easternmost part is enigmatically named Iberia, like the Iberian Peninsula, which may refer to rivers “Kura” and “Ebro” or their valleys respectively. Most of their inhabitants speak Georgian which is included within Dene-Caucasian group and Usko-Mediterranean subgroup of languages. The latter includes Basque, Berber, ancient Iberian-Tartessian, Etruscan, Hittite, Minoan Lineal A and others. In the present paper, HLA class II -DRB1 and -DQB1 alleles has been studied and extended haplotypes calculated. Most frequent haplotypes are also of Mediterranean origin (i. e.: (A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*51)-DRB1*13:01-DQB1*06:03, or (A*24-B*35)-DRB1*01:01-DQB1*05:01) and DA genetic distances show that closest world populations to Georgians are Mediterraneans. Georgians also show common extended haplotypes ((A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*13)-DRB1*07:01-DQB1*02:01 and (A*03-B*35)-DRB1*11:01-DQB1*03:01) with Svan people, a secluded population in North Georgia mountains. We can conclude that Georgians belong to a very old Mediterranean substratum according to both linguistics (Usko Mediterranean languages) and HLA genetics.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.