Amygdala volumes in childhood absence epilepsy

Department of Psychiatry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Epilepsy & Behavior (Impact Factor: 2.26). 09/2009; 16(3):436-41. DOI: 10.1016/j.yebeh.2009.08.009
Source: PubMed


Abnormal amygdala volumes in pediatric mood-anxiety disorders and attention deficit hyperactivity disorder (ADHD), as well as high rates of these diagnoses in childhood absence epilepsy (CAE), prompted this study of amygdala volume in CAE. Twenty-six children with CAE and 23 normal children, aged 6.6-15.8 years, underwent MRI at 1.5 T. The tissue imaged with MRI was segmented, and amygdala volumes were obtained by manual tracings. There were no significant amygdala volume differences between the CAE and normal groups. Within the CAE group, however, the children with ADHD had significantly smaller amygdala volumes than the subjects with CAE with no psychopathology and those with mood/anxiety diagnoses. There was also a significant relationship between higher seizure frequency and greater amygdala asymmetry in the epilepsy group. Given ongoing development of the amygdala during late childhood and adolescence, despite the lack of significant group differences in amygdala volumes, the association of amygdala volume abnormalities with ADHD and seizure frequency implies a possible impact of the disorder on amygdala development and CAE-associated comorbidities, such as ADHD.

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    • "FULL-LENGTH ORIGINAL RESEARCH 1997, 1998, 2000; Cormack et al., 2005; Daley et al., 2006, 2007, 2008; Guimaraes et al., 2007; Caplan et al., 2008). Similar cross-sectional investigations of children with idiopathic generalized epilepsies, including childhood absence and juvenile myoclonic epilepsy, have revealed distributed patterns of abnormality predominantly affecting thalamus and frontal lobe (Betting et al., 2006a– c; Pardoe et al., 2008; Pulsipher et al., 2009), but also with reports of abnormal volumes of the amygdala and regions of the temporal and frontal lobes (Caplan et al., 2009; Schreibman Cohen et al., 2009). Collectively, these studies clearly indicate a neurodevelopmental contribution to anatomic abnormalities that have been observed in adults with these syndromes of epilepsy (c.f., Hermann et al., 2008), but the onset and course of their emergence remains uncertain. "
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