Robert R. Althoff

Amnesia is a Deficit in Relational Memory

Eye movements were monitored to assess memory for scenes indirectly (implicitly). Two eye movement—based memory phenomena were observed: (a) the repetition effect, a decrease in sampling of previously viewed scenes compared with new scenes, reflecting memory for those scenes, and (b) the relational manipulation effect, an increase in viewing of the regions where manipulations of relations among scene elements had occurred. In normal control subjects, the relational manipulation effect was expressed only in the absence of explicit awareness of the scene manipulations. Thus, memory representations of scenes contain information about relations among elements of the scenes, at least some of which is not accessible to verbal report. But amnesic patients with severe memory impairment failed to show the relational manipulation effect. Their failure to show any demonstrable memory for relations among the constituent elements of scenes suggests that amnesia involves a fundamental deficit in relational (declarative) memory processing.

Prevalence and Genetic Architecture of Child Behavior Checklist-Juvenile Bipolar Disorder

BACKGROUND No consensus has been reached yet on how best to characterize children with juvenile bipolar disorder (JBD). Several groups have shown that children on the attention problems (AP), aggressive behavior (AGG), and anxious-depressed (AD) syndromes of the Child Behavior Checklist (CBCL) are likely to meet criteria for DSM-JBD. We aimed to use a large population-based twin sample to evaluate the prevalence and genetic architecture of the CBCL-JBD (deviant on AP, AGG, and AD) phenotype and compare these data to children who are deviant on just the CBCL-AP syndrome. METHODS Structural equation modeling (SEM) was applied to CBCL data from 5418, 3562, and 1971 Dutch twin pairs at ages 7, 10, and 12 years. RESULTS The CBCL-JBD phenotype occurs in approximately 1% of children at each age. Among the children who meet criteria for the CBCL-AP phenotype ( approximately 5%), between 13 and 20% also meet criteria for CBCL-JBD. The best SEM for CBCL-JBD includes additive genetic, shared and unique environmental factors. The best SEM for CBCL-AP includes dominant and additive genetic and unique environmental factors. CONCLUSIONS These data suggest that CBCL-JBD is common, and even more common among children who have severe attention problems. CBCL-JBD shows familial aggregation due to both genetic and shared environmental factors.

Longitudinal Stability of the CBCL-Juvenile Bipolar Disorder Phenotype: A Study in Dutch Twins

BACKGROUND The Child Behavior Checklist-juvenile bipolar disorder phenotype (CBCL-JBD) is a quantitative phenotype that is based on parental ratings of the behavior of the child. The phenotype is predictive of DSM-IV characterizations of BD and has been shown to be sensitive and specific. Its genetic architecture differs from that for inattentive, aggressive, or anxious-depressed syndromes. The purpose of this study is to assess the developmental stability of the CBCL-JBD phenotype across ages 7, 10, and 12 years in a large population-based twin sample and to examine its genetic architecture. METHODS Longitudinal data on Dutch mono- and dizygotic twin pairs (N = 8013 pairs) are analyzed to decompose the stability of the CBCL-JBD phenotype into genetic and environmental contributions. RESULTS Heritability of the CBCL-JBD increases with age (from 63% to 75%), whereas the effects of shared environment decrease (from 20% to 8%). The stability of the CBCL-JBD phenotype is high, with correlations between .66 and .77 across ages 7, 10, and 12 years. Genetic factors account for the majority of the stability of this phenotype. There were no sex differences in genetic architecture. CONCLUSIONS Roughly 80% of the stability in childhood CBCL-JBD is a result of additive genetic effects.

Lethal obesity associated with sodium valproate in a brain-injured patient.

A 34-year-old man developed posttraumatic epilepsy and a disinhibited orbitofrontal syndrome following severe head trauma at age 22. After an 11-year prison term marked by repeated impulsive aggression, he was transferred to a state psychiatric hospital. Replacement of phenytoin by valproic acid resulted in a 100-lb weight gain, exacerbation of sleep apnea, and right heart failure. Despite replacement of valproate with topiramate, he died of a cardiorespiratory arrest during a seizure. This case illustrates the potential risks associated with valproate therapy in the obese brain-damaged population.