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Olsen, Richard D.

Mayo Clinic

Mayo Clinic

Citations 2

Maternal Parenting Stress in Physicians' Families
Olsen, Richard D., Sande, Jonathan R., Olsen, Gayle

Clinical Pediatrics | November 26, 2007 | Volume: 30 | Issue: 10 | Pages: 586-590

10.1177/000992289103001003 Get It

The families of 16 male staff physicians and 26 male residents were studied. All spouses completed the Abidin Parenting Stress Index (PSI) prior to a well-child visit. Home interviews were conducted to identify factors contributing to stress. PSI scores were similar in both groups. The interviews suggested that physician fathers had limited time and energy for parenting. Resident fathers were twice as likely as staff fathers to participate in child care when home. Parenting stress tended to stay the same in 25% of families or increased in 50% of families after residency training.
Screening for Biotinidase Deficiency in Children with Unexplained Neurologic or Developmental Abnormalities
Sutherland, Steven J., Olsen, Richard D., Michels, Virginia V., Schmidt, Michael A. , O’Brien, John F.

Clinical Pediatrics | November 26, 2007 | Volume: 30 | Issue: 2 | Pages: 81-84

10.1177/000992289103000203 Get It

To test the hypothesis that the frequency of biotinidase deficiency is greater in children with unexplained developmental delay or neurologic abnormalities than in the general population, we studied children seen at a large outpatient clinic over a four-year period who had one or more of these neurologic abnormalities and for whom no specific cause for their abnormalities could be found. The group totaled 274 children (163 boys; 111 girls) whose ages ranged from 2 weeks to 17 years. Characteristics were IQ/DQ, 30 to 70 in the 115 for whom scores were available; 41% had seizures; 15% had sensorineural hearing loss; 54% showed gross motor delay or ataxia; and 27% had decreased muscle tone. One patient with a classical clinical picture of biotinidase deficiency was diagnosed during the study period and was not included in the study. None of the patients with nonclassic findings had a deficiency of biotinidase activity. Our results suggest that biotinidase deficiency does not account for a large proportion of children with unexplained neurologic abnormalities or developmental delay. This does not negate the importance of biotinidase testing in children with clinical patterns specifically suggestive of the deficiency.