Larry Burd
University of North Dakota
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Developmental Medicine & Child Neurology | 2000
Roger D. Freeman; Diane K. Fast; Larry Burd; Jacob Kerbeshian; Mary M. Robertson; Paul Sandor
We have established a multisite, international database of 3500 individuals diagnosed with Tourette syndrome (TS). The male:female ratio is 4.3:1 for the total sample, with wide variation among sites; the male excess occurs at every site. Anger control problems, sleep difficulties, coprolalia, and self‐injurious behavior only reach impressive levels in individuals with comorbidity. Anger control problems are strongly correlated with comorbidity, regardless of site, region, or whether assessed by neurologists or psychiatrists. The mean age at onset of tics is 6.4 years. At all ages, about 12% of individuals with TS have no reported comorbidity. The most common reported comorbidity is attention‐deficit‐hyperactivity disorder. Males are more likely to have comorbid disorders than females. The earlier the age at onset, the greater the likelihood of a positive family history of tics. An understanding of the factors producing these and other variations might assist in better subtyping of TS. Because behavioral problems are associated with comorbidity, their presence should dictate a high index of suspicion of the latter, whose treatment may be at least as important as tic reduction. The established database can be used as the entry point for further research when large samples are studied and generalizability of results is important.
American Journal of Medical Genetics Part C-seminars in Medical Genetics | 2004
Chuck Lupton; Larry Burd; Rick Harwood
Fetal alcohol syndrome (FAS) is a common identifiable teratogenic cause of mental retardation, neurological deficit, mental disorders, and developmental disabilities. Accurate estimates of the cost of care for persons with FAS are essential for appropriate funding of health care, developmental disabilities services, special education, and other service systems, as well as prioritizing funding of public health prevention efforts. The cost of care for individuals with FAS can be conceptualized as the annual cost of care for one person or a population, or as the lifetime cost of care for an individual. Annual cost estimates for the United States range from
Journal of the American Academy of Child and Adolescent Psychiatry | 1987
Larry Burd; Wayne Fisher; Jacob Kerbeshian
75 million in 1984 to
Journal of Perinatal Medicine | 1999
Larry Burd; Robin Severud; Jacob Kerbeshian; Marilyn G. Klug
4.0 billion in 1998. Estimates of lifetime cost vary from
Journal of Maternal-fetal & Neonatal Medicine | 2007
Larry Burd; Drucilla J. Roberts; Meredith Olson; Hein J. Odendaal
596,000 in 1980 to
Congenital Heart Disease | 2007
Larry Burd; Eric Deal; Rodrigo Rios; Edward Adickes; Joshua Wynne; Marilyn G. Klug
1.4 million in 1988. After adjustments for changes in inflation and population, 2002 estimates of total annual cost and lifetime cost are higher. FAS is increasingly being recognized as a large public health problem with high potential for the prevention of future cases and for the prevention of excess disability and premature mortality in persons who are affected. Each day, from 6–22 infants with FAS are born in the United States, and as many as 87–103 more are born with other impairments resulting from prenatal alcohol exposure. Updated and improved cost data on FAS should be a research priority.
Developmental Medicine & Child Neurology | 2009
Roger D. Freeman; Samuel H. Zinner; Kirsten Müller-Vahl; Diane K. Fast; Larry Burd; Yukiko Kano; Aribert Rothenberger; Veit Roessner; Jacob Kerbeshian; Jeremy S. Stern
To determine prevalence rates for the pervasive developmental disorders (PDD) in North Dakota, all relevant health and service providers were asked to provide names and records of all patients who had autistic symptoms. All identified patients were seen by the authors for a comprehensive evaluation. Of North Dakotas 180,986 children, ages 2 through 18, 21 met DSM-III criteria for infantile autism (IA), two met criteria for childhood onset pervasive developmental disorder (COPDD), and 36 were diagnosed as having atypical pervasive developmental disorder (APDD) because they met behavioral criteria for COPDD before age 30 months but never met criteria for IA. The prevalence rates were estimated at 1.16 per 10,000 for IA, 0.11 per 10,000 for COPDD, and 1.99 per 10,000 for APDD. The combined rate for all PDD was 3.26 per 10,000 with a male to female ratio of 2.7 to 1. Results are discussed in relation to previous prevalence studies using other diagnostic criteria.
BMC Pediatrics | 2005
Larry Burd; Roger D. Freeman; Marilyn G. Klug; Jacob Kerbeshian
Abstract Aim: To identify pre- and perinatal risk factors for autism. Method: Case control study. We matched names of patients from North Dakota who met DSM criteria for autism, a pervasive developmental disorder, and autisticdisorder with their birth certificates. Five matched controls were selected for each case. Results: Univariate analysis of the 78 cases and 390 controls identified seven risk factors. Logistic modeling to control for confounding produced a five variable model. The model parameters were χ2 = 36.6 and p <0.001. The five variables in the model were decreased birth weight, low maternal education, later start of prenatal care, and having a previous termination of pregnancy. Increasing fathers age was associated with increased risk of autism. Conclusion: This methodology may provide an inexpensive method for clinics and public health providers to identify risk factors and to identify maternal characteristics of patients with mental illness and developmental disorders.
Journal of Child Neurology | 2003
Larry Burd; Marilyn G. Klug; Matthew J. Coumbe; Jacob Kerbeshian
Objective. In this paper we review published studies of alcohol exposure on placentation, placenta growth and function. Methods. We searched PubMed using the MeSH terms: placenta, ethanol, fetal alcohol syndrome and prenatal exposure with delayed effects. We searched the years 1996–2006 and used the references from other articles to expand our search. We limited the search to English only and human only. We excluded studies using choriocarcinoma and animal studies. We grouped the 66 papers into seven topic areas for ease of review. Results. Alcohol exposure is associated with placental dysfunction, decreased placental size, impaired blood flow and nutrient transport, endocrine changes, increased rates of stillbirth and abruption, umbilical cord vasoconstriction, and low birth weight. Conclusions. Prenatal alcohol exposure has a broad range of adverse effects on placental development and function. Additional research on placental development from populations with heavy alcohol exposure should be encouraged. A tissue bank of placentas with detailed assessment of exposure to alcohol, smoking and other relevant data should be considered as a repository to support additional research.
Journal of Child Neurology | 2001
Larry Burd; Jacob Kerbeshian; Amy Barth; Marilyn G. Klug; Karilyn Avery; Becky Benz
OBJECTIVE Review of the prevalence of congenital heart defects (CHD) and fetal alcohol spectrum disorder (FASD). DESIGN We conducted a search of the Medline and Pubmed databases to identify papers reporting the association. We then searched the reference lists of the papers and reference books for additional sources. RESULTS We found 29 studies that met our inclusion criteria. In the 12 case series studies of subjects with FASD, the proportion of cases with a CHD (atrial [ASD] and ventricular [VSD] septal defects, other defects, or unspecified CHD) ranged from 33% to 100%. From the 14 retrospective studies, the rate of septal defects was 21%, other structural defects 6% and unspecified defects was 12%. For the 2 case-control studies, the odds of CHD ranged from 1.0 (subjects with fetal alcohol effect) to 18.0 (subjects with fetal alcohol syndrome). In the 1 prospective study of CHD the OR for a child to have CHD and FASD was 1.0. KEY CONCLUSION Pediatric cardiologists may have frequent contact with children with FASD and increased levels of attention to prenatal alcohol exposure as a potential etiology of CHD is indicated.