轻度认知功能障碍患者动态脑电图的定量分析

探讨轻度认知功能障碍患者动态脑电图的量化指标,为认知功能障碍早期诊断预防提供依据。选取30例轻度认知功能障碍患者和30例正常老年人作为病例组和对照组,进行MMSE测试和动态脑电图监测,比较两组观察对象α、β、和慢波功率。病例组和对照组的双侧顶枕α功率及大脑各位点的θ和δ功率差别有统计学意义（P＜0．05）。病例组及对照组在睡眠2期纺锤波的时限、频率及密度差别有统计学意义（P＜0．05））。脑电图α功率下降,θ和δ功率增加可以提示认知功能下降,睡眠2期纺锤波的时限、频率及密度可以作为认知功能水平脑电图测试的参考指标。     

老年人人格特征与认知功能

目的：了解老年人人格特征与认知功能的关系。方法：采用整群随机抽样的方法调查山西省太原市两个社区的老人109人，进行算术、数字广度、填图、木块图、数字符号、情节记忆、短时视觉记忆、空间推理8项认知功能测验．应用卡氏16项人格因素测验进行人格特征的测查。结果：所调查的老年群体的人格特征主要表现为“谦逊顺从”和“沉着自信”。各人格因素中，聪慧、有恒对算术、幻想对数字广度、聪慧对木块图、恃强对数字符号、敏感对空间推理、忧虑、实验对短期视觉记忆的影响具有统计学显著性。结论：年龄是影响老年人认知水平的主要因素。高的受教育水平对认知下降有保护作用。不同的人格因素影响不同的认知功能，人格特征与认知功能的互动作用可能为老年人认知功能下降的干预提供重要线索．     

老年慢性精神分裂症患者脑电地形图初步研究

目的：为探讨老年慢性精神分裂症患者（SCS）与正常老人在脑电地形图（BEAM）检查中的各自特点。方法：使用16道地形图仪，对39例正常老人和24例SCS患者的BEAM作了检测。结果：在头颅模式图中，SCS患者的BEAM趋向凹字形低密度带。在前颞区θ频域及枕区和中央区δ频域均右侧高于左侧（P＜0．05）。与正常老人相比，SCS患者δ与θ波功率在主要记录点均增高（P＜0．05或P＜0．01）。α波功率在F3、F4、P3、P4以及Fp1、F7记录点下降（P＜0．01或P＜0．05）。β波功率在主要记录点（Fp1、Fp2、T3、T4、T5、T6、O1、O2、F3、F4）上降低也有显著性差异（P＜0．05）。SCS患者BEAM－EEG比EEG提高阳性检出率12．5％。结论：SCS患者的BEAM－EEG具有不同于正常衰老的改变。     

阿尔茨海默病患者定量脑电图特点

目的 探讨阿尔茨海默病（AD）患者定量脑电图（QEEG）的特点,慢波与快波比例与阿尔茨海默病认知能力的关系.方法 将30例AD患者与30例正常老人行QEEG功率谱分析及视觉脑电图（EEG）评分.功率谱按频率分：δ（0.8 ～4.0Hz）、θ（4.0～7.8Hz）、α（7.8～ 12.8Hz）、β（13.0～20.0Hz）,以δ＋θ/α＋β值作为观察评估指标进行比较.对两组全脑、额叶、颞叶、顶叶、枕叶δ＋θ/α＋β值及视觉EEG评分进行比较.将30例AD患者的简易智力状态评定量表（MMSE）评分和δ＋θ/α＋β值行Spearman相关分析.结果 AD组在全脑、额叶、颞叶、顶叶及枕叶的δ＋θ/α＋β值显著高于对照组,差异有统计学意义（t=3.11δ,2.694,3.051,3.657,4.167;P均＜0.01）.AD组的视觉EEG评分显著高于对照组,差异有统计学意义（t=4.052,P＜0.01）.30例AD患者的MMSE评分和全脑、额叶、颞叶、顶叶、枕叶δ＋θ/α＋β值呈负相关（r=-0.646-0.728,P均＜0.01）.结论 定量脑电图作为一种客观、量化的脑功能检测手段,有助于AD诊断,对AD患者认知能力评估有重要的价值.     

城市老年人认知功能的相关因素分析

目的探讨影响城市老年人认知功能的相关危险因素.方法对来自同一调查样本的2485名65岁及以上城市老人,以简明精神状态检查(MMSE)、韦氏成人智力量表(WAIS)中的数字广度测验(DST)得分的"均数-标准差”(M-SD)值划界,将认知功能分为下降/正常,"认知功能”可转变为二项分类变量,作为因变量,同时将作为自变量的相关因素也转变为二项分类变量,进行非条件Logistic回归分析.结果MMSE得分,男性高于女性(25.6±5.2/22.0±6.4,t=15.4,P<0.01).高龄、文盲、农民或无正式职业、日常生活能力障碍、社会支持不佳、离婚丧偶等后独居是影响老年认知功能的危险因素.结论城市老年人认知功能的与生物、心理、社会等多种因素的影响有关.     

轻度认知功能障碍和不同程度Alzheimer病患者认知功能与内颞叶结构体积的关系

目的：研究轻度认知功能障碍（mild cognitive impairment，MCI）和不同程度阿尔茨海默病（Alzheimer disease，AD）患者的认知功能与内颞叶结构体积的相关关系。方法：16例MCI、20例轻度AD和19例中重度AD患者分别接受临床评估、神经心理学检查和头颅核磁共振（MR）扫描，在重建的图像上测量杏仁核、海马、内嗅皮质及颞角的体积并行标准化处理，然后对神经心理学指标与内颞叶结构MR指标进行相关性分析。其中神经心理学检查包括简易精神状态检查量表（mini mental state examination，MMSE）和无意义图形再认、逻辑记忆、数字广度、延迟回忆、画钟测验、词语流畅性测验及日常生活行为量表。结果：三组间各结构MR标化体积除左、右颞角外差异均无统计学意义（P〉0．05）。在MCI组中，注意力计算力、数字广度测验得分与左侧杏仁核体积负相关（r=-0．51～-0．57，P〈0．05），无意义图形再认得分与右侧海马体积正相关（r=0．77，P〈0．001）；在轻度AD组中，MMSE总分、无意义图形再认得分与杏仁核体积正相关（r=0．46～0．55，P〈0．05）；在中重度AD组中，定向力得分与右侧内嗅皮质体积正相关（r=0．47，P=0．041）。结论：无意义图形再认和数字广度测验等与内颞叶结构MR体积之间存在中度相关关系；杏仁核在AD的发展过程中可能起着更萤要的作用。     

动脉瘤性蛛网膜下腔出血后认知功能检查及损害特点

目的：检测动脉瘤性蛛网膜下腔出血后认知功能损害的发生率及损害程度。分析SAH对认知功能的影响。方法：对37例动脉瘤性蛛网膜下腔出血病人手术前进行了认知功能检查。检查内容包括算术、数字广度、数字符号、图画填充、视觉再生、词语流畅性测验、连线测验、简易精神状态检查等内容。结果：表现有认知功能损害者26人，总的发生率为70．3％。有一项损害者14人(37．8％)，二项损害及以上者12人(32．4％)。在所测验项目中．算术发生损害率为2．7％、数字广度为5．4％、数字符号为2．7％、填图项目为2．7％、视觉再生为48．6％、词语流畅性测验为(食品名称)27％和(日用品)18．9％、连线测验为(A)18．9％和(B)21．6％、MMSE为18．9％。结论：动脉瘤性蛛网膜下腔出血本身可引起认知功能损害，以图形记忆力、注意力、额叶功能损害为主。     

定量脑电图在帕金森病认知功能障碍中的应用

目的:探讨定量脑电图在帕金森病(PD)认知功能障碍中的应用价值.方法:选择2017年1月至2018年6月江门市中心医院收治的80例PD患者,按照简易智力状态检查量表(MMSE)进行分组,将37例认知功能正常者纳入对照组,将43例认知功能障碍者纳入观察组.对两组患者进行脑电图检查,将两组的MMSE评分、功率谱、(δ+θ)...     

药物定量脑电图对短暂性脑缺血发作病人疗效判断的研究

目的 :采用药物定量脑电图检测观察静脉滴注尼莫通对短暂性脑缺血发作 (TIA)病人脑功能的改善作用。方法 :对 30例TIA病人用静滴尼莫通 5 0ml治疗 ,比较治疗前后定量脑电图主频、θ、δ频段相对功率值的动态变化 ,并设置年龄匹配的对照组 2 5例进行比较。结果 :对照组与治疗组治疗前及治疗后主频、θ、δ相对功率值有显著性差异。治疗组治疗前与对照组比较 ,主频呈现慢波化 (后移 ) ,θ、δ相对功率值明显升高 ,治疗后与治疗前比较主频大部分前移 ,θ、δ相对功率值明显下降。结论 :TIA病人定量脑电图显示慢波化趋势 ,存在明显的脑电生理功能障碍。用定量脑电图的指标可以客观判断尼莫通对TIA病人有明确的疗效。     

不同行为状态下大鼠脑电时频变化特性的直方图分析

结合应用多分辨率小波分解方法和直方图参数统计方法 ,分析大鼠脑电信号 (Electroencephalogram,EEG)在不同行为状态下的非稳态时频动态变化特性。利用埋植电极记录自由活动大鼠在清醒期、慢波睡眠期和快动眼睡眠期的皮层 EEG,应用小波变换将 EEG分解成 δ、θ、α和 β四个分量 ,求各分量功率对数值直方图和功率百分比值直方图的均值、方差、偏斜度和峭度。结果表明 :EEG功率对数值的分布比较接近正态分布 ,而多数功率百分比值的分布与正态分布差别显著。单因素方差分析结果显示这些直方图统计参数在不同行为状态之间和不同分解分量之间具有显著差别。 EEG在不同时期的某些特征波 (例如 :慢波睡眠期的 δ波、清醒期和快动眼睡眠期的 θ波等 )使功率对数值分布具有较大的偏斜度值和峭度值。由此可见 ,EEG小波分解分量的直方图参数是一种新的描述EEG动态时频变化特性的定量分析指标     

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.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.