## Abstract The 22q11 chromosomal deletion syndrome (22q11DS) is associated with a heterogeneous physical phenotype, neurocognitive deficits, and increased risk of later psychiatric illness. Sporadic clinical reports suggested motor differences, but quantitative studies of movement in children with
Schizophrenic-like neurocognitive deficits in children and adolescents with 22q11 deletion syndrome
✍ Scribed by Kathryn Eve Lewandowski; Vandana Shashi; Peggy M. Berry; Thomas R. Kwapil
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 109 KB
- Volume
- 144B
- Category
- Article
- ISSN
- 1552-4841
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
22q11.2 Deletion Syndrome (22q11DS) is the most common genetic microdeletion syndrome affecting humans. The syndrome is associated with general cognitive impairments and specific deficits in visual‐spatial ability, non‐verbal reasoning, and planning skills. 22q11DS is also associated with behavioral and psychiatric abnormalities, including a markedly elevated risk for schizophrenia. Research findings indicate that people with schizophrenia, as well as those identified as schizoptypic, show specific cognitive deficits in the areas of sustained attention, executive functioning, and verbal working memory. The present study examined such schizophrenic‐like cognitive deficits in children and adolescents with 22q11DS (n = 26) and controls (n = 25) using a cross‐sectional design. As hypothesized, 22q11DS participants exhibited deficits in intelligence, achievement, sustained attention, executive functioning, and verbal working memory compared to controls. Furthermore, deficits in attention and executive functioning were more pronounced in the 22q11DS sample relative to general cognitive impairment. These findings suggest that the same pattern of neuropsychological impairment seen in patients with schizophrenia is present in non‐psychotic children identified as at‐risk for the development of schizophrenia based on a known genetic risk marker. © 2006 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract In this article, I present an updated account that attempts to explain, in cognitive processing and neural terms, the nonverbal intellectual impairments experienced by most children with deletions of chromosome 22q11.2. Specifically, I propose that this genetic syndrome leads to early d