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In This Issue

Developmental Pathways in Schizophrenia

Male infants of women with schizophrenia or schizoaffective disorder, compared to male infants of healthy mothers, had larger volumes of gray matter, cerebrospinal fluid, lateral ventricles, and total intracranial matter at 1 month of age. Gilmore et al. (p. Original article: 1083) did not find differences in female infants. Neither sex had abnormalities in white matter tracts at 1 month or in ultrasound measurements of lateral ventricle width and head circumference at two points during pregnancy. The findings of large brain volumes in the male high-risk infants, however, expand the evidence for the neurodevelopmental hypothesis of schizophrenia, described by Dr. Randal Ross in an editorial (p. Original article: 1017). Two periods are considered critical: the perinatal period, when vulnerability is established, and adolescence/young adulthood, when conversion from vulnerability to psychosis occurs. This latter transition is the focus of a 10-year study by Dominguez et al. (p. Original article: 1075), who tracked schizophrenia-like features in a random sample of the general population ages 14–24 years. Negative and disorganized symptoms (e.g., reduced speech, illogical thoughts) were associated with male sex, younger age, and future onset of psychotic experiences (figure). In contrast, psychotic experiences were not related to subsequent onset of negative/disorganized symptoms but were associated with three environmental factors: trauma, urbanicity, and cannabis use. The combination of negative and psychotic features raised the risk for psychosisrelated impairment. The editorial by Dr. William Carpenter (p. Original article: 1013) links these findings to current discussions about dimensions of psychopathology, diagnostic classification, and care for persons with attenuated psychotic symptoms.

Persistent negative symptoms in 14–24-year-olds predicted onset of psychosis, but not vice versa (Dominguez et al., p. 1075)

Clinical Guidance: Paraneoplastic Illness Presenting as Severely Deteriorating Mental Disorder

Thymomas and other tumors can induce the formation of antibodies to the NMDA glutamate receptor and other neuronal elements, which results in a limbic encephalitis, as described by Kayser et al. (p. Original article: 1039). Emergence of psychotic symptoms may be a first sign leading to psychiatric evaluation. A clinical course that includes marked deterioration in both cognitive abilities and neurological status should lead to consideration of this condition as part of a differential diagnosis. Identification of antineuronal antibodies in the serum and CSF is a key diagnostic test, along with discovery and excision of the primary tumor. Steroids, intravenous immunoglobulins, and plasma exchange are utilized in the treatment.

Other neoplasms that should be considered in the differential diagnosis of a severely deteriorating mental disorder include pineal tumors. The clinical course of a young man who was initially assessed to be in the prodrome of schizophrenia and subsequently was found to have a pineal tumor is presented by Mittal et al. (p. Original article: 1033). The tumor was identified by magnetic resonance imaging, undertaken because of a deteriorating clinical course. Treatment of the tumor with chemotherapy and autologous stem cell rescue resulted in improvement in what were thought to be emerging symptoms of schizophrenia.

Gene-Diet Interaction in ADHD

Variations in genes influencing histamine degradation influenced whether food additives had an adverse effect on symptoms of attention deficit hyperactivity disorder (ADHD) in 3- and 8/9-year-old children. Stevenson et al. (CME, p. Original article: 1108) discovered the interaction in a double-blind challenge trial that involved withdrawing food coloring additives from the children's diet and then adding them back. Genetic effects were also apparent in the 3-year-old children at baseline, when hyperactivity levels were related to one of the histamine-related polymorphisms and to one affecting dopamine neurotransmission. As noted by Dr. Bonnie Kaplan in an editorial (p. Original article: 1023), this research clarifies links between ADHD and diet by identifying possible mechanisms.