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Genetic Disorders of Attention
Can you name the Genetic Disorders of Attention?
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Sig correlation between LVL PRFC activation an task performance in inhibition task for FXS. Prominent dysfunction in the R fronto-striatal network.
20 subjects with FXS, both high and low MA DS pps showed evidence of reflecive orienting. Low MA FXS showed no evidence of reflexive orienting.
Affects 1/730 children and involves 3 rather than 2 copies of c21.
COMT gene has recieved large emphasis in schizophrenia involved with 22q11DS.
Thinner superior and right partietal and ventro-medial cortices found in 22q11DS.
% of those with Fragile X who meet the ADHD criteria.
N=100. Found no correlation between selective attention and increased MA with children with DS. Sig. correlation between C and MA for sustained attention in FXS but not DS. Inhibit
Main deficit of FXS is inhibitory control, impletmented by the R VL PFC.
Subjects with either FXS, DS, WS performed attention tasks (N=36). Toddlers with FXS had difficulties in inhibiting cue looking behaviour. WS experienced greater difficulties in di
Greater activation of LParietal regions in inhibition tasks in 22q11DS.
Affects 1/2500 children on the FMR1 gene with over 200 repeats. Results in loss of FMR protein and underdevelopment of dendritic spines.
% of those with 22q11 syndrome that meet ADHD criteria.
affects 1/1400 children and also known as velo-cardio-facial syndrome. Results in loss of the COMT gene. High comorbidity of schizophrenia and ADHD.
Affects 1/10,000 people involving mutation on chromosome 12, which codes for the enzyme PAH, which converts phenylalanine into tyrosine in the dopamine production cycle.
% of those with WS who meet critera.
Affects 1/7500 and is not hereditary. Caused by deletion of 26 genes on long arm of c7. Symptoms include MD, heart defects and unusual facial features.
59pps with 22q11DS. Several clusters of thicker cortex compared to age matched controls. Minimal thickness changes in younger patients, sig thicker in preadolescence and no changes
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