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Sudden unexpected death in epilepsy (SUDEP) is a leading epilepsy-related cause of death. Researchers have highlighted the similarities between SUDEP and sudden infant death syndrome (SIDS), but perinatal risk factors such as those identified for SIDS have not been assessed previously for SUDEP. We conducted a population-based case-control study of 58 SUDEP individuals and 384 living epilepsy controls born after 1982, utilizing the Swedish Medical Birth Register together with other national health registers and individual medical records to examine if prenatal and perinatal factors are associated with SUDEP risk. We observed a 3-fold SUDEP risk increase for infants who were small for gestational age (SGA) (odds ratio [OR] 3.13; 95% confidence interval [CI] 1.05-9.30) and for those with an Apgar score of 0-6 compared to 9-10 at 10 min (OR 3.22; 95% CI 1.05-9.87). After adjusting for a number of known SUDEP risk factors, we observed that the Apgar score between 0 and 6 after 10 min had a 10-fold increased risk for SUDEP OR 10.37 (95% CI 1.49-72.01) and over a 2-fold risk for those born after the 40th gestational week (OR 2.42; 95% CI 1.03-5.65). The potential mechanisms linking low Apgar score, gestational age, and SGA to SUDEP risk remain to be explored.

Objective Population‐based data on epilepsy syndromes and etiologies in early onset epilepsy are scarce. The use of next‐generation sequencing (NGS) has hitherto not been reported in this context. The aim of this study is to describe children with epilepsy onset before 2 years of age, and to explore to what degree whole exome and whole genome sequencing (WES/WGS) can help reveal a molecular genetic diagnosis. Methods Children presenting with a first unprovoked epileptic seizure before age 2 years and registered in the Stockholm Incidence Registry of Epilepsy (SIRE) between September 1, 2001 and December 31, 2006, were retrieved and their medical records up to age 7 years reviewed. Children who met the epilepsy criteria were included in the study cohort. WES/WGS was offered in cases of suspected genetic etiology regardless of whether a structural or metabolic diagnosis had been established. Results One hundred sixteen children were included, of which 88 had seizure onset during the first year of life and 28 during the second, corresponding to incidences of 139 and 42/100 000 person‐years, respectively. An epilepsy syndrome could be diagnosed in 54% of cases, corresponding to a birth prevalence of 1/1100. Structural etiology was revealed in 34% of cases, a genetic cause in 20%, and altogether etiology was known in 65% of children. The highest diagnostic yield was seen in magnetic resonance imaging (MRI) with 65% revealing an etiology. WES/WGS was performed in 26/116 cases (22%), with a diagnostic yield of 58%. Significance Epilepsy syndromes can be diagnosed and etiologies revealed in a majority of early onset cases. NGS can identify a molecular diagnosis in a substantial number of children, and should be included in the work‐up, especially in cases of epileptic encephalopathy, cerebral malformation, or metabolic disease without molecular diagnosis. A genetic diagnosis is essential to genetic counselling, prenatal diagnostics, and precision therapy.

OBJECTIVE Given the increasing attention being paid to potential strategies for sudden unexpected death in epilepsy (SUDEP) prevention, we analyzed the circumstances of SUDEP and its incidence in relation to time of year, week, and day. METHODS Prospective case-series based on persons with an International Classification of Diseases (ICD-10) code for epilepsy in the Swedish Patient Registry 1998-2005, who were alive on June 30, 2006 (n = 60 952). Linkage to the National Cause-of-Death Registry identified all deaths from July 2006 through December 2011, with epilepsy mentioned on death certificate, together with all deaths during 2008 (n = 3166). Death certificates, medical charts, autopsy, and police reports were reviewed to identify SUDEP cases and related circumstances. Autopsied non-SUDEP deaths (n = 60) from the study population served as a reference. RESULTS There were 329 SUDEPs (63% men) of which 167 were definite, 89 probable, and 73 possible. SUDEP cases were younger at death (50.8 years) than non-SUDEP deaths (73.3 years) (P < .001) and more likely to be male (63% vs 55%, P = .0079). Most SUDEP cases died at night (58%), at home (91%), and 65% were found dead in bed. When documented, 70% were found in prone position. In 17%, death was witnessed and in 88% of these, a seizure was observed. Of the 329 SUDEP cases, 71% were living alone and 14% shared a bedroom. Compared to an autopsied non-SUDEP reference group, definite SUDEPs were more likely to die at home, during the night, unwitnessed, in the prone position, to live alone, and more often with a preceding seizure. SIGNIFICANCE SUDEP cases live alone, die unwitnessed at home at night, with indication of a preceding seizure, supporting the critical role of lack of supervision. These facts need to be considered in the development of preventive strategies.

Aim: It has been suggested that experiencing serious life events may promote Type 1 diabetes in children. Studies in adults are lacking, as are studies on the interaction of life events with genetic factors. We aimed to investigate life events and the risk of latent autoimmune diabetes in adults (LADA) and Type 2 diabetes while taking into account HLA genotype. Methods: Analysis was based on 425 incident cases of LADA, 1417 incident cases of Type 2 diabetes and 1702 population-based controls recruited in Sweden between 2010 and 2016. Self-reported information on life events including conflicts, divorce, illness/accidents, death and financial problems experienced during the 5 years preceding diagnosis/index year was used. Odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated by logistic regression and adjusted for age, sex, BMI, family history of diabetes, smoking, physical activity and education. Results: Overall there was no association between experience of any life event and either LADA (OR 0.86, 95% CI 0.68-1.08) or Type 2 diabetes (OR 1.00, 95% CI 0.83-1.21). The results were similar for individual events as well as in separate analysis of men and women. Similar results were seen in more autoimmune LADA (glutamic acid decarboxylase antibodies > median) [OR (any life event) 0.88, 95% CI 0.64-1.21] and in LADA carriers of the high-risk HLADR4-DQ8 genotype (OR 0.89, 95% CI 0.61-1.29). Conclusions: Our findings indicate that experience of a serious life event, including the death of a family member, divorce or financial problems, is not associated with an increased risk of LADA, overall or in genetically susceptible individuals.

Summary Objective To quantify the risk of unprovoked seizures after traumatic brain injury (TBI) Methods We used the Stockholm Incidence Registry on Epilepsy to carry out a population-based case–control study, including 1,885 cases with incident unprovoked seizures from September 1, 2000 through August 31, 2008, together with 15,080 matched controls. Information of prior hospitalizations for TBI was obtained through record linkage with the Swedish National Inpatient Registry for the period 1980–2008. Relative risks (RRs) for unprovoked seizures were estimated after various TBI diagnoses, and influences of TBI severity and time since trauma were studied in detail. Results After hospitalization for mild TBI, the RR was 2.0 (95% confidence interval [CI] 1.5–2.7). The RR was higher after brain contusion (5.9, 95% CI 2.4–15.0) or intracranial hemorrhage (ICH) (4.5, 95% CI 2.2–9.0), whereas a combination of both diagnoses led to a further sevenfold increase in RR (42.6, 95% CI 12.2–148.5). The risk was greatest during the first 6 months after severe TBI (RR 48.9, 95% CI 10.9–218.9) or mild TBI (RR 8.1, 95% CI 3.1–21.7), but was still elevated >10 years after any TBI. Significance Herein we present a large population-based case–control study on TBI as a risk factor for unprovoked epileptic seizures, including cases of all ages with individually validated seizure diagnoses. The risk for epileptic seizures was substantially increased after TBI, especially during the first 6 months after the injury and in patients with a combination of ICH and brain contusion.

Aims and objectives To describe patients' expectations before and experiences during a head-first magnetic resonance imaging scan. Background Previous studies have reported that patients experience fear and anxiety leading to discomfort before, during and after magnetic resonance imaging scans. Frequent problems persist in producing high-quality images due to motion artefacts. These results imply a need for improvement of patient conditions to allow for the added benefit of better diagnostic quality. Provision of extended written information has not appeared to reduce patients' stress, while interaction with staff has been described as the most important factor for reducing such feelings. Design and methods A qualitative, phenomenological approach. Semi-structured interviews were conducted, and data were analysed with systematic text condensation. Results The experiences of the ten participants were encapsulated by the main theme: ‘The situation and the uncertainty about the coming result scared me but interaction with the radiographers helped me through’. Subthemes were ‘Prescan preparation’, ‘Mastering threats to self-control’ and ‘Personal achievements by completing the scan’. Conclusions Our study has provided a deeper understanding of the expectations before, and experiences during, a head-first magnetic resonance imaging scan. Valuable insight into patients' apprehension about written and verbal information was obtained. The patients reported how they coped with the unfamiliar and stressful magnetic resonance imaging scanning procedure. A trustful dialogue with the radiographer was described as being crucial for patients' ability to manage fear, discomfort and feelings of loss of self-control. We suggest a need for individualised information based on patient participation. Relevance to clinical practice Radiographers, as well as nurses caring for patients who will undergo magnetic resonance imaging examinations, should recognise the difficulties inherent in written information. It is also of importance to adjust the patient–radiographer interaction to address patients' expressions of worries about the scanning procedure or the following result.

Diabet. Med. 30, 56–64 (2013) Abstract Aims We investigated the influence of different aspects of alcohol consumption on the risk of Type 2 diabetes and autoimmune diabetes in adults. Methods We used data from the Nord-Trondelag Health Survey (HUNT) study, in which all adults aged ≥ 20 years from Nord-Trondelag County were invited to participate in three surveys in 1984–1986, 1995–1997 and 2006–2008. Patients with diabetes were identified using self-reports, and participants with onset age ≥ 35 years were classified as having Type 2 diabetes if they were negative for anti-glutamic acid decarboxylase (n = 1841) and as having autoimmune diabetes if they were positive for anti-glutamic acid decarboxylase (n = 140). Hazard ratios of amount and frequency of alcohol use, alcoholic beverage choice, and binge drinking and alcohol use disorders were estimated. Results Moderate alcohol consumption (adjusted for confounders) was associated with a reduced risk of Type 2 diabetes in men, but not in women (hazard ratio for men 10–15 g/day 0.48, 95% CI 0.28–0.77; hazard ratio for women ≥ 10 g/day 0.81, 95% CI 0.33–1.96). The reduced risk was primarily linked to consumption of wine [hazard ratio 0.93, 95% CI 0.87–0.99 (per g/day)]. No increased risk was seen in participants reporting binge drinking or in problem drinkers. The results were also compatible with a reduced risk of autoimmune diabetes associated with alcohol consumption [hazard ratio 0.70, 95% CI 0.45–1.08 (frequent consumption) and hazard ratio 0.36, 95% CI 0.13–0.97 (2–7 g/day)]. Conclusions Moderate alcohol consumption associates with reduced risk of both Type 2 diabetes and autoimmune diabetes. A protective effect of alcohol intake may be limited to men. High alcohol consumption does not seem to carry an increased risk of diabetes.

Agardh EE, Carlsson S. Ahlbom A, Efendic S, Grill V, Hammar N, Hilding A & Ostenson C-G (Karolinska Institutet, Stockholm; Stockholm Center of Public Health, Stockholm; and AstraZeneca RD Sweden). Coffee consumption, type 2 diabetes and impaired glucose tolerance in Swedish men and women. J Intern Med 2004; 255: 645-652. Objectives. The association between coffee consumption, type 2 diabetes and impaired glucose tolerance was examined. In addition, indicators of insulin sensitivity and β-cell function according to homeostasis model assessment were studied in relation to coffee consumption. Design. Population-based cross-sectional study. Setting and subjects. The study comprised 7949 healthy Swedish subjects aged 35-56 years residing within five municipalities of Stockholm. An oral glucose tolerance test identified 55 men and 52 women with previously undiagnosed type 2 diabetes and 172 men and 167 women with impaired glucose tolerance. Information about coffee consumption and other factors was obtained by questionnaire. Results. The relative risks (adjusted for potential confounders) of type 2 diabetes and impaired glucose tolerance when drinking >5 cups of coffee per day compared with 5 cups day -1 ) was inversely associated with insulin resistance. In addition, in those with type 2 diabetes and in women (not in men) with impaired glucose tolerance high coffee consumption was inversely associated with low β-cell function. In women, but not obviously in men, with normal glucose tolerance, coffee consumption was associated with a reduced risk of insulin resistance. Conclusions. The results of this study indicated that high consumers of coffee have a reduced risk of type 2 diabetes and impaired glucose tolerance. The beneficial effects may involve both improved insulin sensitivity and enhanced insulin response.