偏执型精神分裂症康复期患者自杀意念与认知损害状况

目的探讨伴有自杀意念的偏执型精神分裂症康复期患者的认知功能状况以及自杀意念与认知损害的关系。方法使用重复性成套神经心理状态测验(RBANS)对40例伴自杀意念的偏执型精神分裂症康复期患者和40例不伴自杀意念的偏执型精神分裂症康复期患者进行认知功能检测。结果①有无自杀意念偏执型精神分裂症康复期患者两组间年龄、性别、教育程度、婚姻状态、抑郁量表评分比较差异无统计学意义;②伴自杀意念偏执型精神分裂症康复期患者患者RBANS总分(t=3.230,P=0.002)、视觉广度分值(t=5.190,P=0.000)、即刻记忆分值(t=9.255,P=0.000)、言语功能分值(t=11.840,P=0.000)均低于不伴自杀意念患者;③Logistic回归分析结果显示,视觉广度分值(OR=1.205,P0.05)、即刻记忆分值(OR=2.237,P0.05)、言语功能分值(OR=1.193,P0.05)是偏执型精神分裂症康复期患者自杀意念的危险因素。结论伴自杀意念偏执型精神分裂症康复期患者存在明显认知功能缺陷,认知功能缺陷者可能存在更高的自杀意念发生率。     

精神分裂症伴2型糖尿病抗氧化酶与空腹血糖的分析

目的:探讨伴有2型糖尿病的精神分裂症患者抗氧化酶与空腹血糖的关系。方法:收集精神分裂症伴2型糖尿病患者67例(受试组),健康对照组59例(正常对照组),两组性别、年龄的差异无统计学意义。检测空腹血糖(FBG)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH)水平,及空腹血糖(FBG)与过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH)的相关性。结果:1受试组空腹血糖(FBG)较正常对照组升高(t=18.92,P=0.000),受试组过氧化氢酶(CAT)较正常对照组降低(t=-3.54,P=0.000);受试组谷胱甘肽过氧化物酶(GSH)较正常对照组降低(t=-4.28,P=0.000);2Pearson相关分析表明,受试组过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH)与空腹血糖(FBG)存在负相关(r=-0.66,-0.74;P=0.000)。结论:精神分裂症伴2型糖尿病患者抗氧化酶降低,存在氧化应激;抗氧化酶的水平与空腹血糖存在负相关,氧化应激可能参与抗精神病药物引起糖代谢异常的中间机制。     

精神分裂症患者亲属心理健康状况调查

目的了解精神分裂症患者亲属心理健康状况。方法采用症状自评量表(SCL-90),对开滦精神卫生中心精神分裂患者75名亲属进行调查。结果①精神分裂症患者亲属与常模相比,在躯体化(t=9.959,P=0.000)、焦虑(t=7.225,P=0.000)、抑郁(t=4.418,P=0.000)及偏执(t=5.505,P=0.000)因子分差异有统计学意义;②女性亲属较男性亲属总分(t=2.04,P=0.045)和敌对(t=2.59,P=0.012)因子分差异有统计学意义;③未完成九年义务教育和完成九年义务教育的患者亲属总分(t=2.92,P=0.005)、躯体化(t=3.53,P=0.001)、抑郁(t=3.56,P=0.001)、焦虑(t=2.29,P=0.025)、恐怖(t=-2.18,P=0.035)因子分差异有统计学意义;④一级亲属和二级亲属相比总分(t=4.04,P=0.000)、强迫(t=2.22,P=0.029)、抑郁(t=3.88,P=0.000)、焦虑(t=3.58,P=0.001)、恐怖(t=2.50,P=0.015)和精神病性(t=2.04,P=0.045)因子分差异有统计学意义。结论精神分裂症患者亲属存在较明显的心理问题。     

帕利哌酮对首发精神分裂症的疗效和认知功能的影响

目的探讨帕利哌酮对首发精神分裂症患者的疗效及认知功能的影响。方法对42例首发精神分裂症患者给予帕利哌酮治疗12周,治疗前后进行修订韦氏成人记忆量表(WMS-RC)记忆广度(MS)、威斯康星卡片分类测验(WCST)和阳性与阴性症状量表(PANSS)等评定,并与45例正常人对照。结果研究组治疗12周后,PANSS量表各项指标分值均较治疗前有显著下降(P<0.01)。研究组治疗前后WCST卡片总数(t=3.93,P=0.000)、持续错误(t=2.09,P=0.039)、随机错误(t=3.78,P=0.000)、WMS-RC总分(t=2.37,P=0.020)、记忆商数(t=4.20,P=0.000)均有显著性差异。研究组治疗后在上述WCST、MS数字广度与对照组比较仍有显著性差异(P均<0.05)。治疗前WCST卡片总数、持续错误、随机错误与PANSS总分呈正相关,而WMS-RC总分、记忆商数与阴性症状因子分呈负相关。结论帕利哌酮对精神分裂症有良好的疗效,并能改善认知功能障碍。     

精神分裂症患者血清同型半胱氨酸水平及其影响因素

目的:探讨精神分裂症患者血清同型半胱氨酸(Homocystein,Hcy)水平及其影响因素。方法:采用病例对照研究方法,对住院精神分裂症患者(患者组)412例和健康对照者(对照组)110例进行一般情况调查和代谢相关指标、血清Hcy水平的测量。结果:患者组血清Hcy水平[(22.61±18.98)μmol/L]显著高于对照组[(11.65±5.74)μmol/L],差异具有统计学意义(Z=7.157,P0.01),且男性患者血清Hcy水平显著高于女性患者(Z=3.075,P0.01)。患者组高同型半胱氨酸血症发生率(57.28%)显著高于对照组(16.36%)(χ~2=58.186,P0.01)。相关分析显示,性别、病程和年龄与血清Hcy水平呈正相关(r=0.152,P0.01;r=0.206,P0.01;r=0.112,P0.01),高密度脂蛋白(HDL)水平与血清Hcy水平呈负相关(r=-0.106,P0.05)。逐步多元回归分析显示,病程和性别对血清Hcy水平有显著影响(t=2.819,P0.01;t=3.360,P0.01)。结论:精神分裂症患者血清Hcy水平升高,并与病程和性别有关。     

Survivin在MPP~+诱导的SH-SY5Y细胞凋亡过程中的作用

目的探讨存活素(Survivin)能否抑制(1-甲基-4-苯基-吡啶离子(1-methyl-4-phenylpyridinium,MPP~+)诱导的神经元(SH-SY5Y细胞)的凋亡过程。方法运用1 mmol/L MPP~+处理SH-SY5Y细胞,诱导其发生凋亡,建立帕金森病的细胞模型,采用不同浓度的Survivin进行预处理,使用倒置显微镜观察细胞形态,采用MTT法、Real-time PCR、Western blot检测相关指标,进而评价Survivin对SH-SY5Y凋亡的作用。结果 1 mmol/L MPP~+作用24 h可诱导SH-SY5Y的凋亡,显著降低细胞存活率(F=13.32,P=0.000)。MPP~+作用前,预先经Survivin处理2 h的SH-SY5Y细胞的存活率显著提高(F=13.32,P=0.000,P=0.000,P=0.000),并呈剂量依赖性关系。Real-time PCR结果显示Survivin能够显著抑制SH-SY5Y细胞中凋亡蛋白Caspase 3和Caspase 9的表达水平(F=61.57,P=0.000,P=0.000,P=0.000;F=54.26,P=0.001,P=0.000,P=0.000);Western blot结果亦显示Survivin能够显著抑制SH-SY5Y细胞中凋亡蛋白Caspase 3和Caspase 9的表达水平。结论 Survivin能够剂量依赖性地抑制MPP~+诱导的SH-SY5Y细胞凋亡,其机制可能与阻断Caspase信号通路相关。     

孤立型肺结节术前良恶性预测模型的建立

目的联合多项检查指标,发现促进肺癌形成的危险因素,制定孤立型肺结节(SPN)良恶性预测模型,以期为临床鉴别提供参考依据,监测SPN恶变,以及改善SPN预后提供帮助。方法回顾性分析2015年10月至2017年12月于上海市第一人民医院就诊的395例肺结节患者的临床资料,运用t检验、χ2检验进行单因素分析,运用Logistic对肺癌危险因素进行多因素分析并建立肺部结节诊断预测模型,ROC曲线对该模型的预测效力进行验证。结果单因素分析中,性别(P=0.000),结节最大直径(P=0.000),血管征(P=0.000),NSE(P=0.001),分叶征(P=0.000),左下叶(P=0.047),CEA(P=0.003),在诊断肺癌方面有显著统计学意义。多因素分析中,性别(P=0.018),结节最大直径(P=0.001),血管征(P=0.001),NSE(P=0.043),分叶征(P=0.000)在预测肺癌方面有显著统计学意义。SPN良恶性预测模型为Y=1/[1+EXP(0.626×女性+0.082×结节最大直径+0.091×NSE+0.896×血管征+1.231×分叶征-1.977)],ROC曲线检测该模型预测效力,曲线下面积为0.752。结论结节直径、性别、血管征、分叶征、NSE与肺癌密切相关,建立孤立型肺结节术前良恶性预测模型可以帮助临床医生诊断肺结节良恶性。     

慢性阻塞性肺疾病患者心理痛苦及相关影响因素

目的:调查慢性阻塞性肺疾病(Chronic Obstructive Pulmonary Disease,COPD)患者心理痛苦水平,并分析其相关影响因素。方法:选取我院2016年4月-2017年9月收治的COPD患者220例为研究对象,采用一般人口学调查问卷、心理痛苦温度计(Distress Thermometer,DT)以及问题列表(problem list,PL)进行调查,并分析COPD患者心理痛苦的影响因素。结果:发放220份调查问卷,回收率为100%;COPD患者DT评分为(6.00±1.59)分,PL调查显示引起痛苦的原因主要为情感问题(77.73%),依次为实际问题(55.91%)、交往问题(43.64%)、身体问题(25.45%);DT得分与性别(t=2.979,P=0.004)、年龄(t=4.806,P=0.000)、受教育程度(t=4.666,P=0.000)、职业(F=5.413,P=0.001)、收入水平(t=3.164,P=0.002)、家庭关系(F=8.733,P=0.000)、疾病程度(F=8.852,P=0.000)相关;经多因素分析结果显示,女性(OR=2.102,P=0.019)、年龄高(OR=1.379,P=0.030)、疾病程度严重(OR=1.373,P=0.020)是心理痛苦的危险因素,收入水平高(OR=0.485,P=0.000)、家庭关系好(OR=0.277,P=0.000)是心理痛苦的保护因素。结论:COPD患者心理痛苦水平较高,性别、年龄、收入水平、家庭关系以及疾病程度是影响患者心理痛苦水平的关键因素。     

住院精神分裂症患者高血糖发生率及其相关因素

目的:对住院精神分裂症患者高血糖发生率及其相关因素进行调查.方法:采用 自制的调查表对287例住院精神分裂症患者进行了调查,分别收集了患者的性别、年龄、受教育年限、病程、精神疾病家族史、既往病史(高血压、高脂血症)、服用抗精神病药物等相关资料,同时测了体质量、身高、血糖、甘油三酯、总胆固醇、高密度脂蛋白及低密度脂蛋白等相关指标.结果:287例住院精神分裂症患者中,存有高血糖65例,发生率为22.6％.住院精神分裂症患者中,高血糖组年龄明显大于非高血糖组(t=-2.310,P＜0.05);高血糖组甘油三酯明显高于非高血糖组(t=-2.512,P＜0.05);高血糖组高密度脂蛋白明显低于非高血糖组(t=2.687,P＜0.01).≥50岁的住院精神分裂症患者伴有高血糖比率明显高于＜50岁的患者(x2=6.609,P＜0.05);≥50岁的住院精神分裂症患者空腹血糖明显高于＜50岁的患者(t=-2.978,P＜0.01).Logistic回归分析显示,年龄、家族史、甘油三酯与高血糖的发生有关(P＜0.05).结论:住院精神分裂症患者高血糖发生率较高,年龄越大、有精神疾病家族史、甘油三酯值越高的患者,发生高血糖的风险越大.     

有无宗教信仰的慢性疼痛患者疼痛、依恋和应对方式差异

目的探讨有无宗教信仰的慢性疼痛患者疼痛、依恋和应对方式的差异。方法 2012年9月-2013年1月住院的110例患者中,有22例信仰宗教,根据性别、年龄、受教育程度均衡的原则,按1:4的比例匹配不信仰宗教组88例。采用简化McGill疼痛问卷、亲密关系体验问卷和应对方式量表进行测量。结果独立样本t检验显示两组疼痛总分,疼痛感觉项,依恋回避,应对方式的祈祷维度有统计学差异(t=2.280,P=0.025;t=2.719,P=0.008;t=2.522,P=0.013;t=6.088,P=0.000);Logistic回归模型显示祈祷是慢性疼痛患者是否信仰宗教的影响因素(OR=0.788,P=0.000)。结论宗教信仰在慢性疼痛患者应对疼痛、与他人建立安全依恋关系的过程中发挥重要作用,应进一步研究宗教信仰在慢性疼痛患者心理干预中的作用。     

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.