Developmental Mental Disorders Research Articles

Altered gray matter volume and structural co-variance in adolescents with social anxiety disorder: evidence for a delayed and unsynchronized development of the fronto-limbic system.

Social anxiety disorder (SAD) is a prevalent mental disorder diagnosed in childhood and adolescence. Theories regarding brain development and SAD suggest a close link between neurodevelopmental dysfunction at the adolescent juncture and SAD, but direct evidence is rare. This study aims to examine brain structural abnormalities in adolescents with SAD. High-resolution T1-weighted images were obtained from 31 adolescents with SAD (15-17 years) and 42 matching healthy controls (HC). We evaluated symptom severity with the Social Anxiety Scale for Children (SASC) and the Screen for Child Anxiety Related Emotional Disorders (SCARED). We used voxel-based morphometry analysis to detect regional gray matter volume abnormalities and structural co-variance analysis to investigate inter-regional coordination patterns. We found significantly higher gray matter volume in the orbitofrontal cortex (OFC) and the insula in adolescents with SAD compared to HC. We also observed significant co-variance of the gray matter volume between the OFC and amygdala, and the OFC and insula in HC, but these co-variance relationships diminished in SAD. These findings provide the first evidence that the brain structural deficits in adolescents with SAD are not only in the core regions of the fronto-limbic system, but also represented by the diminished coordination in the development of these regions. The delayed and unsynchronized development pattern of the fronto-limbic system supports SAD as an adolescent-sensitive developmental mental disorder.

Infection during childhood and the risk of violent criminal behavior in adulthood

Infections during brain development appear to contribute to cognitive impairment and aggressive behavior, as well as to a number of developmental mental disorders closely associated with violent criminal behavior. Yet, no study has thus far ever investigated whether infections during brain development increases the risk of violent criminality later in life.In this population-based cohort study, about 2.2 million individuals born in Sweden between the years 1973 and 1995 were included in an effort to estimate the association between infections during childhood (registered ICD-10 diagnoses of infections incurred before the age of 14 years) and violent criminal behavior (registered convictions for a violent crime between the ages of 15 and 38 years, prior to December 31, 2011). After inclusion of several sociodemographic parameters, risks of violent criminal behavior conferred by childhood infections – expressed as hazard ratios (HRs) and 95% confidence intervals (CIs) – were calculated by means of Cox regression. Mediation analyses were performed to explore the effect of psychiatric disorders on the association between infections during childhood and violent criminality. Results revealed a modest, yet significant, association between an infection during childhood and violent criminality later in life (adjusted HR 1.14, 95% CI 1.12–1.16). Infections during the first year of life and infections in the central nervous system were associated with the highest risks of subsequent violent criminality (adjusted HR 1.20, 95% CI 1.18–1.23, and adjusted HR 1.17, 95% CI 1.08–1.26, respectively). The association was partly mediated by the presence of a psychiatric disorder.In summary, independent of a wide range of covariates, our results suggest that infections during brain development could be part of the genesis of violent criminal behavior.

Parenting stress of mothers of children with developmental mental disorder and influencing factors

Objective To explore the parenting stress of mothers of children with developmental mental disorder and influencing factors. Methods A total of 106 mothers of children with developmental mental disorder were included in study group, and 106 mothers of normal children were included in control group between January 2013 and December 2014 in our hospital. The parenting stress of mothers in two groups was compared and influencing factors of parenting stress were analyzed. Results The score of parenting stress in study group and control group were (109.83±17.89) and (85.57±16.79) respectively. The difference between the two groups was statistically significant (t=10.180, P<0.01). The risk factors of parenting stress of mothers were family income and the severity of mental disorder in children. Conclusions Mothers of children with developmental mental disorder have more parenting stress. We should pay more attention to decrease the parenting stress of mothers by improving children′s symptoms and providing more social supports. Key words: Developmental mental disorder; Parenting stress; Family income; Influencing factors

Effects of SPAK knockout on sensorimotor gating, novelty exploration, and brain area-dependent expressions of NKCC1 and KCC2 in a mouse model of schizophrenia.

SPAK (Sterile 20/SPS1-related proline/alanine-rich kinase) is a protein kinase belonging to the mitogen-activated protein kinase (MAPK) superfamily that has been found to be extensively distributed across the body. The SPAK downstream substrates NKCC1 and KCC2 in the central nervous system are important in the interpretation of developmental mental disorders. The present study aimed to clarify the role of SPAK-NKCC1/KCC2 using a rodent schizophrenia-like model. The mouse paradigm of isolation rearing (IR) was employed, as it simulates the sensorimotor gating abnormalities of schizophrenia. SPAK transgenic mice were used and were divided into four groups: social-wild type, social-SPAK(-/-), isolation-wild type, and isolation-SPAK(-/-). The prepulse inhibition (PPI) test and the novel object recognition test (NORT) were used to measure schizophrenia-associated dysfunctions in gating ability and the novelty recognition, respectively. Finally, the protein expressions of NKCC1/KCC2 in the prefrontal cortex and hippocampus were detected to determine correlations with the behavioral data. Our results demonstrated that SPAK-null mice had superior PPI and novelty recognition relative to wild type controls, with a concomitant increase in KCC2 in the prefrontal cortex. IR disrupted PPI and NORT performances with an associated increase in KCC2. Furthermore, rearing environment and gene manipulation had mutually interactive effects, as the IR-induced effects on PPI and NORT were reversed by SPAK knockout, and the increase in KCC2 and the decreased in the NKCC1/KCC2 ratio in the prefrontal cortex induced by SPAK knockout were reversed by IR. Our data supported the gene-environment hypothesis and demonstrated the potential value of SPAK manipulation in future schizophrenia studies.