Emotional and neurocognitive deficits in fragile X
β Scribed by Sobesky, William E. ;Pennington, Bruce F. ;Porter, Deborah ;Hull, Claire E. ;Hagerman, Randi J.
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 889 KB
- Volume
- 51
- Category
- Article
- ISSN
- 0148-7299
No coin nor oath required. For personal study only.
β¦ Synopsis
We have studied the neurocognitive deficit in premutation and full mutation women as compared to control women and to explore the relationship between those deficits and the incidence of emotional problems. Four groups of women were examined two fragile X (fra(X)) negative control groups, one of which grew up in fra(X) families and one not; and two DNA positive groups, one with a premutation (CGG repeats 200). All women were assessed using the MMPI-2, the SADS-L, and a battery of neuropsychological tests.
Full mutation women had lower scores on composite measures of executive function and nonverbal function. There was no difference between the groups in terms of the lifetime incidence of depressive and anxiety disorders on the SADS-L. Full mutation women displayed Lie scales higher than the other groups on the MMPI-2. Neurocognitive measures were not related to SADS-L diagnoses but were related to the Lie scale on the MMPI-2. Finally, number of CGG repeats was related to the neuropsychological variables and the Lie scale.
π SIMILAR VOLUMES
We describe a follow-up of a study of behavior and emotional problems in a cohort of young people with Fragile X syndrome over 7 years. The study demonstrates that there is substantial persistence of the overall level of behavior and emotional problems. However, there are changes in certain types of
Fifteen postpubertal males with fragile X syndrome (FFWX)) and 15 non-FRA(X) males matched on I& and age were assessed for their ability to identify the facially expressed emotions of happiness, sadness, anger, fear, disgust, and surprise. Emotions of happiness and sadness were the easiest to identi
Although previous studies have documented a significant risk of intellectual loss after treatment for childhood medulloblastoma (MED), the pathophysiology underlying this process is poorly understood. The purpose of this study was to test the hypotheses that (1) patients treated for MED in childhood