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Bilateral medial prefrontal and temporal neocortical hypometabolism in children with epilepsy and aggression
1Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan, USA.
Insights
Children with intractable epilepsy and aggression show reduced brain glucose metabolism in prefrontal and temporal regions. This brain dysfunction may explain aggressive behavior by impairing inhibitory control.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Medical Imaging
Background:
- Intractable partial epilepsy in children can be associated with behavioral issues, including aggression.
- Understanding the neurobiological underpinnings of aggression in pediatric epilepsy is crucial for effective management.
Purpose of the Study:
- To investigate brain function abnormalities in children with intractable partial epilepsy and aggressive behavior using 2-deoxy-2-[18F]fluoro-D-glucose (FDG) positron emission tomography (PET).
Main Methods:
- Six children with intractable partial epilepsy and aggression underwent psychodevelopmental assessment and FDG-PET scans.
- Statistical parametric mapping (SPM) and region-of-interest (ROI) analyses compared glucose metabolism with normal adults and non-aggressive epilepsy patients.
- Correlations between aggression severity and metabolic activity were examined.
Main Results:
- Aggressive children exhibited developmental delay and autistic symptoms.
- Extensive bilateral glucose hypometabolism in the temporal and prefrontal cortex was observed in aggressive children compared to controls.
- Medial prefrontal hypometabolism was a key finding differentiating aggressive from non-aggressive pediatric epilepsy patients.
Conclusions:
- Widespread glucose hypometabolism in the prefrontal and temporal neocortex of children with epilepsy and aggression suggests impaired cortical inhibitory control over aggressive impulses.
- FDG-PET imaging can help elucidate the neurobiology of aggressive behavior in pediatric epilepsy.
Purpose:
To identify brain regions with abnormal function in children with intractable partial epilepsy and aggressive behavior by using 2-deoxy-2-[18F]fluoro-D-glucose (FDG) positron emission tomography (PET).
Methods:
Six children (mean age, 9.9 years) with intractable partial epilepsy and aggressive behavior underwent detailed psychodevelopmental assessment and FDG-PET scanning. The objective technique of statistical parametric mapping (SPM) was applied to define focal abnormalities of glucose metabolism, and compared those with those of a group of normal adult subjects (n = 17) as well as age-matched children with epilepsy with similar seizure characteristics but without aggression (n = 7). The findings were analyzed further by using a region-of-interest (ROI) approach.
Results:
The aggressive children all showed developmental delay, and four of them also manifested autistic symptoms. SPM analysis demonstrated extensive glucose hypometabolism in the aggressive group bilaterally in the temporal and prefrontal cortex compared with that in normal adult controls. A focal area of medial prefrontal glucose hypometabolism was defined in the aggressive children as compared with the nonaggressive pediatric group with SPM, whereas ROI comparison of these groups confirmed prefrontal hypometabolism and also showed glucose hypometabolism of the temporal neocortex in the aggressive children. Severity of aggression correlated inversely with glucose metabolism of the left temporal as well as bilateral medial prefrontal cortex.
Conclusions:
Bilateral prefrontal and temporal neocortical brain glucose hypometabolism in children with epilepsy and aggressive behavior may indicate a widespread dysfunction of cortical regions, which normally exert an inhibitory effect on subcortical aggressive impulses. PET studies may be used to elucidate the neurobiologic basis of aggressive behavior in children.