Background and Purpose-To prevent new cardiovascular events after stroke, prescribed preventive drugs should be used continuously. This study measures persistent use of preventive drugs after stroke and identifies factors associated with persistence. Methods-A 1-year cohort (21 077 survivors) from Riks-Stroke, the Swedish Stroke Register, was linked to the Swedish Prescribed Drug Register. Results-The proportion of patients who were persistent users of drugs prescribed at discharge from hospital declined progressively over the first 2 years to reach 74.2% for antihypertensive drugs, 56.1% for statins, 63.7% for antiplatelet drugs, and 45.0% for warfarin. For most drugs, advanced age, comorbidity, good self-perceived health, absence of low mood, acute treatment in a stroke unit, and institutional living at follow-up were independently associated with persistent medication use. Conclusion-Persistent secondary prevention treatment declines rapidly during the first 2 years after stroke, particularly for statins and warfarin. Effective interventions to improve persistent secondary prevention after stroke need to be developed. (Stroke. 2010;41:397-401.)

In a record-linkage study in Stockholm, Sweden, the year 2011 prevalence of diagnosed autism spectrum disorders (ASD) was found to be 0.40, 1.74, 2.46, and 1.76% among 0-5, 6-12, 13-17, and 18-27 year olds, respectively. The corresponding proportion of cases with a recorded diagnosis of intellectual disability was 17.4, 22.1, 26.1 and 29.4%. Between 2001 and 2011, ASD prevalence increased almost 3.5 fold among children aged 2-17 years. The increase was mainly accounted for by an eightfold increase of ASD without intellectual disability (from 0.14 to 1.10 %), while the prevalence of ASD with intellectual disability increased only slightly (from 0.28 to 0.34%). The increase in ASD prevalence is likely contributed to by extrinsic factors such as increased awareness and diagnostics.

BackgroundMigration has been implicated as a risk factor for autism, but evidence is limited and inconsistent.AimsTo investigate the relationship between parental migration status and risk of autism spectrum disorder, taking into consideration the importance of region of origin, timing of migration and possible discrepancies in associations between autism subtypes.MethodRecord-linkage study within the total child population of Stockholm County between 2001 and 2007. Individuals with high- and low-functioning autism were defined as having autism spectrum disorder with and without comorbid intellectual disability, and ascertained via health and habilitation service registers.ResultsIn total, 4952 individuals with autism spectrum disorder were identified, comprising 2855 children with high-functioning autism and 2097 children with low-functioning autism. Children of migrant parents were at increased risk of low-functioning autism (odds ratio (OR) = 1.5, 95% CI 1.3–1.7); this risk was highest when parents migrated from regions with a low human development index, and peaked when migration occurred around pregnancy (OR = 2.3, 95% CI 1.7–3.0). A decreased risk of high-functioning autism was observed in children of migrant parents, regardless of area of origin or timing of migration. Parental age, income or obstetric complications did not fully explain any of these associations.ConclusionsEnvironmental factors associated with migration may contribute to the development of autism presenting with comorbid intellectual disability, especially when actingin utero.High- and low-functioning autism may have partly different aetiologies, and should be studied separately.

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Chronic pain is a leading cause of disability globally and associated with enormous health-care costs. The discrepancy between the extent of tissue damage and the magnitude of pain, disability, and associated symptoms represents a diagnostic challenge for rheumatology specialists. Central sensitisation, defined as an amplification of neural signalling within the CNS that elicits pain hypersensitivity, has been investigated as a reason for this discrepancy. Features of central sensitisation have been documented in various pain conditions common in rheumatology practice, including fibromyalgia, osteoarthritis, rheumatoid arthritis, Ehlers-Danlos syndrome, upper extremity tendinopathies, headache, and spinal pain. Within individual pain conditions, there is substantial variation among patients in terms of presence and magnitude of central sensitisation, stressing the importance of individual assessment. Central sensitisation predicts poor treatment outcomes in multiple patient populations. The available evidence supports various pharmacological and non-pharmacological strategies to reduce central sensitisation and to improve patient outcomes in several conditions commonly seen in rheumatology practice. These data open up new treatment perspectives, with the possibility for precision pain medicine treatment according to pain phenotyping as a logical next step. With this view, studies suggest the possibility of matching non-pharmacological approaches, or medications, or both to the central sensitisation pain phenotypes.

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Objectives: In regards to pain-related fear, this study aimed to: (1) identify existing measures and review their measurement properties, and (2) identify the optimum measure for specific constructs of fear-avoidance, pain-related fear, fear of movement, and kinesiophobia. Design: Systematic literature search for instruments designed to measure fear of pain in patients with persistent musculoskeletal pain. Psychometric properties were evaluated by adjusted Wind criteria. Results: Five questionnaires (Fear-Avoidance Beliefs Questionnaire (FABQ), Fear-Avoidance of Pain Scale (FAPS), Fear of Pain Questionnaire (FPQ), Pain and Anxiety Symptoms Scale (PASS), and the Tampa Scale for Kinesiophobia (TSK)) were included in the review. The main findings were that for most questionnaires, there was no underlying conceptual model to support the questionnaire's construct. Psychometric properties were evaluated by diverse methods, which complicated comparisons of different versions of the same questionnaires. Construct validity and responsiveness was generally not supported and/or untested. Conclusion: The weak construct validity implies that no measure can currently identify who is fearful. The lack of evidence for responsiveness restricts the current use of the instruments to identify clinically relevant change from treatment. Finally, more theoretically driven research is needed to support the construct and thus the measurement of pain-related fear.

Background The clinical and etiological relation between autism spectrum disorders (ASD) and schizophrenia is unclear. The degree to which these disorders share a basis in etiology has important implications for clinicians, researchers, and those affected. Our objective was to determine if a family history of schizophrenia and/or bipolar disorder was a risk factor for ASD. We conducted a case-control evaluation of histories of schizophrenia or bipolar disorder in first-degree relatives of probands in three samples, population registers in Sweden, Stockholm County, and Israel. Probands met criteria for ASD, and affection status of parents and siblings for schizophrenia and bipolar disorder were established. Findings The presence of schizophrenia in parents was associated with an increased risk for ASD in a Swedish national cohort (odds ratio 2.9, 95% CI 2.5–3.4) and in a Stockholm County cohort (odds ratio 2.9, 95% CI 2.0–4.1). Similarly, schizophrenia in a sibling was associated with an increased risk for ASD in a Swedish national cohort (odds ratio 2.6, 95% CI 2.0–3.2) and in an Israeli conscription cohort (odds ratio 12.1, 95% CI 4.5–32). Bipolar disorder showed a similar pattern of associations but of lesser magnitude. Interpretation Findings from these three registers along with consistent findings from a similar study in Denmark suggest that ASD, schizophrenia, and bipolar disorder share common etiological factors. Funding Swedish Council for Working Life and Social Research, the Swedish Research Council, and the Beatrice and Samuel A. Seaver Foundation.