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Understanding that young patients with first-episode psychosis have many continuities with the characteristics of older patients was a step forward in the field and led to the development of initiating first-episode psychosis programs and reducing the duration of untreated psychosis. As programs have developed, so have strategies to develop initial evaluations to clarify the health of the young patient with psychosis. The next steps of treatment include medication, talk therapy, family therapy, and team work. Beyond starting treatment, there are significant emerging issues such as use of long-acting injectable medication and strategies for patients who do not respond to first-line treatments, such as using clozapine. The integration of cognitive-behavioral therapy, cognitive remediation, and a day treatment center for the first-episode psychosis program are integral. [Psychiatr Ann. 2015;45(11):561-568.] [ABSTRACT FROM AUTHOR]

Background: Air pollution has been associated with adverse neurological and behavioral health effects in children and adults. Recent studies link air pollutant exposure to adverse neurodevelopmental outcomes, including increased risk for autism, cognitive decline, ischemic stroke, schizophrenia, and depression. Objectives: We sought to investigate the mechanism(s) by which exposure to ultrafine concentrated ambient particles (CAPs) adversely influences central nervous system (CNS) development. Methods: We exposed C57BL6/J mice to ultrafine (< 100 nm) CAPs using the Harvard University Concentrated Ambient Particle System or to filtered air on postnatal days (PNDs) 4–7 and 10–13, and the animals were euthanized either 24 hr or 40 days after cessation of exposure. Another group of males was exposed at PND270, and lateral ventricle area, glial activation, CNS cytokines, and monoamine and amino acid neurotransmitters were quantified. Results: We observed ventriculomegaly (i.e., lateral ventricle dilation) preferentially in male mice exposed to CAPs, and it persisted through young adulthood. In addition, CAPs-exposed males generally showed decreases in developmentally important CNS cytokines, whereas in CAPs-exposed females, we observed a neuroinflammatory response as indicated by increases in CNS cytokines. We also saw changes in CNS neurotransmitters and glial activation across multiple brain regions in a sex-dependent manner and increased hippocampal glutamate in CAPs-exposed males. Conclusions: We observed brain region– and sex-dependent alterations in cytokines and neurotransmitters in both male and female CAPs-exposed mice. Lateral ventricle dilation (i.e., ventriculomegaly) was observed only in CAPs-exposed male mice. Ventriculomegaly is a neuropathology that has been associated with poor neurodevelopmental outcome, autism, and schizophrenia. Our findings suggest alteration of developmentally important neurochemicals and lateral ventricle dilation may be mechanistically related to observations linking ambient air pollutant exposure and adverse neurological/ neurodevelopmental outcomes in humans. [ABSTRACT FROM AUTHOR]

Objective: Factors underlying progressive brain volume changes in schizophrenia remain poorly understood. The authors investigated whether a gene polymorphism influencing neuroplasticity may contribute to longitudinal brain volume alterations. Method: High-resolution magnetic resonance (MR) images of the whole brain were obtained for 119 patients with recent-onset schizophrenia spectrum disorders. Changes in brain volumes over an average of 3 years were compared between brain-derived neurotrophic factor (BDNF) val66met genotype groupings. Exploratory analyses were conducted to examine relationships between antipsychotic treatment and brain volume changes as well as the effects of BDNF genotype on changes in cognition and symptoms. Results: Significant genotype effects were observed on within-subject changes in volumes of frontal lobe gray matter, lateral ventricles, and sulcal CSF. Met allele carriers had significantly greater reductions in frontal gray matter volume, with reciprocal volume increases in the lateral ventricles and sulcal (especially frontal and temporal) CSF than Val homozygous patients. Independent of BDNF genotype, more antipsychotic exposure between MRI scans correlated with greater volume reductions in frontal gray matter, particularly among patients who were initially treatment naive. There were no statistically significant genotype effects on within-subject changes in cognition or symptoms. Conclusions: BDNFMet variant may be one of several factors affecting progressive brain volume changes in schizophrenia. [ABSTRACT FROM AUTHOR]

The article reports on the nature of schizophrenic prodrome with emphasis on its symptoms and development. It is indicated that researchers and clinicians examined cases of adolescents who possess unspecific behavioral and cognitive alterations. Furthermore, diagnosis of such illness may be provided with certain treatments.

Summary. This review discusses functional and structural brain abnormalities in childhood-onset schizophrenia identified by neuroimaging techniques. Published literature regarding both morphological and functional neuroimaging is discussed, regarding also the diversity of neuroimaging findings which partly reduces their reliability. The findings in early onset schizophrenia are compared with those of adult patients. The results of long-term investigations of structural abnormalities in early onset schizophrenia are given particular attention. The most consistent findings are ventricular enlargement and reduced total brain volume. Further, volumetric changes in the temporal and frontal cortex, thalamus, basal ganglia and limbic system are reported, as are hemispheric asymmetries and, conversely, reduction of normal differences. Findings regarding the corpus callosum and cerebellum are less consistent. In patients whose schizophrenia commenced in early childhood, the differences were generally more marked than in adolescence- or adult-onset schizophrenia. Atrophy of total brain volume was progressive throughout the course of the disorder. It is probable that neuroanatomical cerebral abnormalities present prior to disease onset play an etiopathogenic role in the development of schizophrenia. [ABSTRACT FROM AUTHOR]

Summary. The cranial computer-assisted tomograms of 19 patients suffering from schizophrenic psychoses with onset by age of 14 were examined. The emphasis was on the extent of the inner liquor spaces. Compared to healthy controls, at the beginning of illness a significant enlargement was revealed only in the patient group with very early onset schizophrenia (VEOS, onset prior to the age of 12), whereas children with early onset (EOS, 12 to 14 years of age) showed no significant brain pathology. As a second result, an increase in the extent of the inner liquor spaces seems to correlate with the duration of illness. It is therefore concluded that psychoses interfere with neurodevelopmental processes and cause more severe brain pathology in very young children, already detectable at the onset of the illness. EOS, on the other hand, induces progressive morphological abnormalities over the course of the illness. [ABSTRACT FROM AUTHOR]