Summary Purpose:  Thalamofrontal abnormalities have been identified in chronic primary generalized epilepsy, specifically in juvenile myoclonic epilepsy (JME). These regions also underlie executive functioning, although their relationship has yet to be examined in JME. This study examined the relationship between thalamic and frontal volumes and executive function in recent‐onset JME compared to healthy control subjects and recent‐onset benign childhood epilepsy with centrotemporal spikes (BCECTS), a syndrome not typically associated with thalamocortical or executive dysfunction. Methods:  Twenty children with recent‐onset JME were compared to 51 healthy controls and 12 children with BCECTS using quantitative magnetic resonance imaging (MRI) and measures of executive abilities. Quantitative thalamic and frontal volumes were obtained through semi‐automated software. Subtests from the Delis–Kaplan Executive Function System (D‐KEFS) and the Behavior Rating Inventory of Executive Function (BRIEF) were used to measure executive function. Results:  Executive functions were impaired in JME subjects compared to control and BCECTS subjects. Subjects with JME had significantly smaller thalamic volumes and more frontal cerebrospinal fluid (CSF) than control and BCECTS subjects. Thalamic and frontal volumes were significantly related to executive functioning in the JME group, but not in the other two groups. Discussion:  Children with JME have significant executive dysfunction associated with significantly smaller thalami and more frontal CSF. Children with recent‐onset BCECTS do not display the same pattern. Frontal and thalamic volumes appear to mediate the relationship between executive functioning and brain structure in JME.

SUMMARYThe purpose of this investigation was to examine the diffusion properties of cerebral white matter in children with recent onset epilepsy (n=19) compared to healthy controls (n=11). Subjects underwent DTI with quantification of mean diffusion (MD), fractional anisotropy (FA), axial diffusivity (D ax ) and radial diffusivity (D rad ) for regions of interest including anterior and posterior corpus callosum, fornix, cingulum, and internal and external capsules. Quantitative volumetrics were also performed for the corpus callosum and its subregions (anterior, midbody and posterior) and total lobar white and gray matter for the frontal, parietal, temporal and occipital lobes. The results demonstrated no group differences in total lobar gray or white matter volumes or volume of the corpus callosum and its subregions, but did show reduced FA and increased D rad in the posterior corpus callosum and cingulum. These results provide the earliest indication of microstructural abnormality in cerebral white matter among children with idiopathic epilepsies. This abnormality occurs in the context of normal volumetrics and suggests disruption in myelination processes.

This study verified and compared the factor structures of two frequently used measures of small group climate, the Group Climate Questionnaire (GCQ-S; MacKenzie, 1983) and the Curative Climate Instrument (CCI; Fuhriman, Drescher, Hanson, Henrie, & Rybicki, 1986) at both group and individual levels. Data included third session assessments of 124 group members in 20 university counseling center groups. Confirmatory factor analyses partially supported the GCQ factor structure, but indicated that the Catharsis subscale of the CCI was not independent of the other two CCI subscales. Factor analysis of the six subscales from both measures yielded two higher order factors, representing positive (Engagement, Cohesion, Insight, and Catharsis) and negative (Conflict and Avoidance) group processes. Findings provide guidance for interpreting and comparing group processes using these measures.

Comorbid health conditions are common among people with epilepsy. Proposed explanations for this association include the possibility that first, epilepsy (including its treatment) causes the comorbid condition; second, the comorbid condition (including its treatment) causes epilepsy; or third, a common pathogenic mechanism mediates the co-occurrence of epilepsy and the comorbid condition. It is unlikely that a single explanation will suffice for all of the epilepsy comorbid conditions. Determining the basis of the association between epilepsy and its comorbid conditions has important implications for diagnosis and management. In this paper, we discuss this issue in the context of five common epilepsy comorbid conditions: bone health and fractures, stroke, depression, migraine and attention-deficit hyperactivity disorder. Current findings, research limitations and future directions of research efforts are discussed. KeywordsADHD; bone health; causal models; comorbidity; depression; epilepsy; migraine; risk factors; stroke Comorbidity refers to the co-occurrence of two conditions with a greater frequency than found in the general population [1,2]. Comorbid conditions are common in people with epilepsy, and their presence has important implications for diagnosis, treatment, medical costs and quality of life [3][4][5]. Comorbid conditions in epilepsy are found across the lifespan, and include medical, psychiatric and cognitive conditions alone or in combination. In 2003, Boro and Haut succinctly summarized the problem of comorbidity in epilepsy: "Nearly every patient with †Author for correspondence:

The issue of cognitive progression in people with epilepsy is of considerable interest and has important clinical and theoretical implications. In this paper, we review recent studies in both the adult and childhood epilepsy literature which have included a longitudinal test-retest design to examine this question. Several important methodological issues of this literature are highlighted and areas which require more investigation are identified.