Objective To generate a national multiple sclerosis (MS) prevalence estimate for the United States by applying a validated algorithm to multiple administrative health claims (AHC) datasets. Methods A validated algorithm was applied to private, military, and public AHC datasets to identify adult cases of MS between 2008 and 2010. In each dataset, we determined the 3-year cumulative prevalence overall and stratified by age, sex, and census region. We applied insurance-specific and stratum-specific estimates to the 2010 US Census data and pooled the findings to calculate the 2010 prevalence of MS in the United States cumulated over 3 years. We also estimated the 2010 prevalence cumulated over 10 years using 2 models and extrapolated our estimate to 2017. Results The estimated 2010 prevalence of MS in the US adult population cumulated over 10 years was 309.2 per 100,000 (95% confidence interval [CI] 308.1–310.1), representing 727,344 cases. During the same time period, the MS prevalence was 450.1 per 100,000 (95% CI 448.1–451.6) for women and 159.7 (95% CI 158.7–160.6) for men (female:male ratio 2.8). The estimated 2010 prevalence of MS was highest in the 55- to 64-year age group. A US north-south decreasing prevalence gradient was identified. The estimated MS prevalence is also presented for 2017. Conclusion The estimated US national MS prevalence for 2010 is the highest reported to date and provides evidence that the north-south gradient persists. Our rigorous algorithm-based approach to estimating prevalence is efficient and has the potential to be used for other chronic neurologic conditions.

OBJECTIVES: This study examined the relationship between child sexual abuse (CSA) and subsequent onset of psychiatric disorders, accounting for other childhood adversities, CSA type, and chronicity of the abuse. METHODS: Retrospective reports of CSA, other adversities, and psychiatric disorders were obtained by the National Comorbidity Survey, a nationally representative survey of the United States (n = 5877). Reports were analyzed by multivariate methods. RESULTS: CSA was reported by 13.5% of women and 2.5% of men. When other childhood adversities were controlled for, significant associations were found between CSA and subsequent onset of 14 mood, anxiety, and substance use disorders among women and 5 among men. In a subsample of respondents reporting no other adversities, odds of depression and substance problems associated with CSA were higher. Among women, rape (vs molestation), knowing the perpetrator (vs strangers), and chronicity of CSA (vs isolated incidents) were associated with higher odds of some disorders. CONCLUSIONS: CSA usually occurs as part of a larger syndrome of childhood adversities. Nonetheless, CSA, whether alone or in a larger adversity cluster, is associated with substantial increased risk of subsequent psychopathology.

Background: The aetiology of autism is unknown, although prenatal exposures have been the focus of epidemiological research for over 40 years.Aims: To provide the first quantitative review and meta-analysis of the association between maternal pregnancy complications and pregnancy-related factors and risk of autism.Method: PubMed, Embase and PsycINFO databases were searched for epidemiological studies that examined the association between pregnancy-related factors and autism. Forty studies were eligible for inclusion in the meta-analysis. Summary effect estimates were calculated for factors examined in multiple studies.Results: Over 50 prenatal factors have been examined. The factors associated with autism risk in the meta-analysis were advanced parental age at birth, maternal prenatal medication use, bleeding, gestational diabetes, being first born v. third or later, and having a mother born abroad. The factors with the strongest evidence against a role in autism risk included previous fetal loss and maternal hypertension, proteinuria, pre-eclampsia and swelling.Conclusions: There is insufficient evidence to implicate any one prenatal factor in autism aetiology, although there is some evidence to suggest that exposure to pregnancy complications may increase the risk.

BACKGROUND: The etiology of autism is unknown, although perinatal and neonatal exposures have been the focus of epidemiologic research for over 40 years.OBJECTIVE: To provide the first review and meta-analysis of the association between perinatal and neonatal factors and autism risk.METHODS: PubMed, Embase, and PsycInfo databases were searched for studies that examined the association between perinatal and neonatal factors and autism through March 2007. Forty studies were eligible for the meta-analysis. For each exposure, a summary effect estimate was calculated using a random-effects model. Heterogeneity in effect estimates across studies was examined, and, if found, a meta-regression was conducted to identify measured methodological factors that could explain between-study variability.RESULTS: Over 60 perinatal and neonatal factors were examined. Factors associated with autism risk in the meta-analysis were abnormal presentation, umbilical-cord complications, fetal distress, birth injury or trauma, multiple birth, maternal hemorrhage, summer birth, low birth weight, small for gestational age, congenital malformation, low 5-minute Apgar score, feeding difficulties, meconium aspiration, neonatal anemia, ABO or Rh incompatibility, and hyperbilirubinemia. Factors not associated with autism risk included anesthesia, assisted vaginal delivery, postterm birth, high birth weight, and head circumference.CONCLUSIONS: There is insufficient evidence to implicate any 1 perinatal or neonatal factor in autism etiology, although there is some evidence to suggest that exposure to a broad class of conditions reflecting general compromises to perinatal and neonatal health may increase the risk. Methodological variations were likely sources of heterogeneity of risk factor effects across studies.

SCHIZOPHRENIA AND related psychotic illnesses are a class of pervasive neuropsychiatric disorders of uncertain origin. Family, twin, and adoption studies have identified a genetic component to schizophrenia and other psychotic illnesses. However, specific genes have not as yet been identified.^1-5 Epidemiological studies have identified several environmental factors associated with these illnesses, many related to events that occur during pregnancy or during the birth process. These include winter and spring birth, birth in an urban area, prematurity, complications during labor and delivery, and extreme famine during pregnancy.^6-10 Studies have also suggested an association between exposure to infectious agents during pregnancy and the subsequent development of schizophrenia,^11-13 although findings in this area are equivocal^14,15 and with the occurrence of infections in early infancy.^16,17 This body of research suggests that prenatal and perinatal infections and other environmental insults that adversely affect infant brain development may result in schizophrenia in later life, most likely in genetically susceptible individuals.^4,18-20