Ann E. Saunders
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Ann E. Saunders has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Elisabeth A. Wilde
Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, TX, USA
1 shared publication - Erin D. Bigler
Brigham Young University
1 shared publication - Eva Keatley
3109 Cathedral Ave, NW Washington DC 20008 United States
1 shared publication - Harvey S. Levin
Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas 77030, USA
1 shared publication - Jeffrey E. Max
Department of Psychiatry, University of California, San Diego, USA
1 shared publication - Linda Ewing-Cobbs
Department of Pediatrics and Children's Learning Institute, University of Texas Health Science Center at Houston, Houston, Texas
1 shared publication
Latest Publications
- 17 December 2011
- Published by Wiley in International Journal of Developmental Neuroscience
- Vol. 30 (3) , 239-245
Depression in children and adolescents in the first 6 months after traumatic brain injury
The objective was to assess the nature, rate, predictive factors, and neuroimaging correlates of novel (new‐onset) depressive disorders, both definite and subclinical, after traumatic brain injury (TBI). Children with TBI from consecutive admissions were enrolled and studied with psychiatric interviews soon after injury (baseline), and again 6 months post‐injury. Novel definite/subclinical depressive disorders at 6‐month follow up occurred in 11% (n = 15) of the children and subsets of children with non‐anxious depression (n = 9) and anxious depression (n = 6) were identified. Novel definite/subclinical depressive disorder was significantly associated with older age at the time of injury, family history of anxiety disorder, left inferior frontal gyrus (IFG) lesions, and right frontal white matter lesions. Non‐anxious depressions were associated with older age at injury, left IFG and left temporal pole lesions. Anxious depressions were associated with family history of anxiety disorder, Personality Change due to TBI, right frontal white matter lesions, and left parietal lesions. These findings, which are similar to those reported after adult TBI, identify both similarities and differences in non‐anxious and anxious depression following childhood TBI with respect to lesion laterality, genetic factors (in the form of family psychiatric history of anxiety disorder), age at injury, and more generalized affective dysregulation.
- 17 December 2011
- Published by Wiley in International Journal of Developmental Neuroscience
- Vol. 30 (3) , 239-245
Depression in children and adolescents in the first 6 months after traumatic brain injury
The objective was to assess the nature, rate, predictive factors, and neuroimaging correlates of novel (new‐onset) depressive disorders, both definite and subclinical, after traumatic brain injury (TBI). Children with TBI from consecutive admissions were enrolled and studied with psychiatric interviews soon after injury (baseline), and again 6 months post‐injury. Novel definite/subclinical depressive disorders at 6‐month follow up occurred in 11% (n = 15) of the children and subsets of children with non‐anxious depression (n = 9) and anxious depression (n = 6) were identified. Novel definite/subclinical depressive disorder was significantly associated with older age at the time of injury, family history of anxiety disorder, left inferior frontal gyrus (IFG) lesions, and right frontal white matter lesions. Non‐anxious depressions were associated with older age at injury, left IFG and left temporal pole lesions. Anxious depressions were associated with family history of anxiety disorder, Personality Change due to TBI, right frontal white matter lesions, and left parietal lesions. These findings, which are similar to those reported after adult TBI, identify both similarities and differences in non‐anxious and anxious depression following childhood TBI with respect to lesion laterality, genetic factors (in the form of family psychiatric history of anxiety disorder), age at injury, and more generalized affective dysregulation.