Background
The 22q11.2 Deletion Syndrome (22q11.2DS) is regarded as an etiologically homogenous model for understanding neuroanatomic disruptions associated with a high risk for schizophrenia. This study utilized diffusion tensor imaging (DTI) to analyze white matter microstructure in individuals with 22q11.2DS. We focused on the cingulum bundle (CB), previously shown to be disrupted in patients with schizophrenia and associated with symptoms of psychosis.
Methods
White matter microstructure was assessed in the anterior, superior, and posterior CB using the tractography algorithm in DTIStudio. Neuropsychological function, presence of prodromal symptoms of psychosis, and medication history were assessed in all participants.
Results
Relative to controls, young adults with 22q11.2DS showed alterations in most DTI metrics of the CB. Alterations were associated with positive prodromal symptoms of psychosis. However, when individuals with 22q11.2DS were divided by usage of antipsychotics / mood stabilizers, the medicated and non-medicated groups differed significantly in axial diffusivity of the anterior CB and in fractional anisotropy of the superior CB. DTI metrics did not differ between the medicated group and the control group.
Conclusions
Results suggest that the microstructure of the CB is altered in individuals with 22q11.2DS, and that those alterations may underlie positive prodromal symptoms of psychosis. Our findings further provide preliminary evidence that antipsychotic / mood stabilizer usage may have a reparative effect on white matter microstructure in prodromal 22q11.2DS, independent of the potential effects of psychosis. Future studies of white matter pathology in individuals with 22q11.2DS should test for potential effects of medication on white matter microstructure.
Children with 22q11.2 deletion syndrome (22q11DS), a copy-number variation (CNV) genetic disorder, demonstrate a great deal of variability in IQ scores and are at particular risk for cognitive difficulties, with up to 45% experiencing intellectual disability. This study explored the IQ relationship between individuals with 22q11DS, their parents and their siblings. Participants included individuals with 22q11DS, unaffected siblings and community controls, who participated in a longitudinal study of 22q11DS. Significant associations between proband and relative (parent, sibling) IQ scores were found. Results suggest that the cognitive functioning of first-degree relatives could be a useful marker of general genetic background and/or environmental effects, and can explain some of the large phenotypic variability in 22q11DS. These findings underscore the importance of including siblings and parents in studies of 22q11DS whenever possible.
Aims: To determine whether baseline levels of self-reported sleep and sleep problems among obese adolescents referred to an outpatient multidisciplinary family-based weight management program predict reduction in BMI 3 months later. Methods: A retrospective medical chart review was conducted for 83 obese adolescents. The following baseline variables were extracted: self-reported sleep duration (weekdays and weekends), and presence of snoring, daytime fatigue, suspected sleep apnea, and physician-diagnosed sleep apnea. Anthropometric data at baseline and 3 months were also collected. Results: On average, adolescents reported significantly less sleeping on weeknights (7.7 ± 1.3 h) compared to weekend nights (10.0 ± 1.8 h), t(82) = 10.5, p = 0.0001. Reduction in BMI after 3 months of treatment was predicted by more weekly sleep at baseline (R2 = 0.113, F(1, 80) = 10.2, p = 0.002). Adolescents who reduced their BMI by ≥1 kg/m2 reported greater weekly sleep at baseline compared to adolescents who experienced <1 kg/m2 reduction (60.7 ± 7.5 h vs. 56.4 ± 8.6 h; F(1, 80) = 5.7, p = 0.02). Conclusion: Findings from this study, though correlational, raise the possibility that increased duration of sleep may be associated with weight loss among obese adolescents enrolled in a weight management program. Evidence-based behavioral techniques to improve sleep hygiene and increase sleep duration should be explored in pediatric weight management settings.
BackgroundGaze processing deficits are a seminal, early, and enduring behavioral deficit in autism spectrum disorder (ASD); however, a comprehensive characterization of the neural processes mediating abnormal gaze processing in ASD has yet to be conducted.MethodsThis study investigated whole-brain patterns of neural synchrony during passive viewing of direct and averted eye gaze in ASD adolescents and young adults (M
Age
= 16.6) compared to neurotypicals (NT) (M
Age
= 17.5) while undergoing magnetoencephalography. Coherence between each pair of 54 brain regions within each of three frequency bands (low frequency (0 to 15 Hz), beta (15 to 30 Hz), and low gamma (30 to 45 Hz)) was calculated.ResultsSignificantly higher coherence and synchronization in posterior brain regions (temporo-parietal-occipital) across all frequencies was evident in ASD, particularly within the low 0 to 15 Hz frequency range. Higher coherence in fronto-temporo-parietal regions was noted in NT. A significantly higher number of low frequency cross-hemispheric synchronous connections and a near absence of right intra-hemispheric coherence in the beta frequency band were noted in ASD. Significantly higher low frequency coherent activity in bilateral temporo-parieto-occipital cortical regions and higher gamma band coherence in right temporo-parieto-occipital brain regions during averted gaze was related to more severe symptomology as reported on the Autism Diagnostic Interview-Revised (ADI-R).ConclusionsThe preliminary results suggest a pattern of aberrant connectivity that includes higher low frequency synchronization in posterior cortical regions, lack of long-range right hemispheric beta and gamma coherence, and decreased coherence in fronto-temporo-parietal regions necessary for orienting to shifts in eye gaze in ASD; a critical behavior essential for social communication.
The results of this study have implications for developing cognitive-behavioral therapy interventions targeting relationship difficulties in young adults with ADHD.
This study investigates the functional connectivity of neuronal networks critical for working memory in individuals with dyslexia by means of magnetoenchephalographic (MEG) coherence imaging. Individuals with dyslexia showed an early onset of activation in anterior cortical regions (precentral gyrus and the superior frontal gyrus), which differed from controls where activation initiated in posterior cortical regions (supramarginal gyrus and superior temporal gyrus). Further, individuals with dyslexia showed lower brain activity in the right superior temporal gyrus and right middle temporal gyrus than controls during a spatial working memory (SWM) task. In contrast, during a verbal working memory (VWM) task, individuals with dyslexia showed lower activity in the right insular cortex and right superior temporal gyrus and higher, likely compensatory, activity in the right fusiform gyrus, left parahippocampal gyrus, and left precentral gyrus. When performing a SWM task, individuals with dyslexia showed significantly lower coherent activity and synchronization in 1) right frontal connectivity, 2) right fronto-temporal connectivity, 3) left and right frontal connectivity, 4) left temporal and right frontal connectivity, and 5) left occipital and right frontal connectivity. MEG coherence source imaging (CSI) by frequency bands showed lower * Corresponding author. A. Mansour et al. 1880 mean coherence values in individuals with dyslexia compared to controls for each frequency range during the SWM task. In contrast, during the VWM task, individuals with dyslexia showed higher coherent low frequency (3-15 Hz) and lower coherent high frequency (30-45 Hz) synchronization than control subjects. Logistic regression of coherent activity by group membership was significant, with an overall predictive success of 84.4% (88.9% for controls and 77.8% for dyslexia). Coherence between the right lateral orbitofrontal and middle orbitofrontal gyri pair substantially contributed to group membership. The results suggest a pattern of aberrant connectivity as evidenced by the early onset and reliance on prefrontal cortical areas, the differential activation of fronto-temporal brain systems, and an altered pattern of functional connectivity in the frontotemporal pathways mediating these behaviors.
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