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A PET STUDY OF BULIMIA NERVOSA

 

 

SOCIETY OF BIOLOGICAL PSYCHIATRY

ANNUAL MEETING - 1996

A PET STUDY OF BULIMIA NERVOSA REVEALS CAUDATE HYPERMETABOLISM

EA, KLEIN; BJ BLINDER; JC, WU; JO, HAGMAN; MS, BUCHSBAUM

Brain Imaging Center, Department of Psychiatry
University of California at Irvine
Irvine, CA 92717

PURPOSE:
To reassess the brain metabolism of bulimic subjects studied in prior research1 using statistical parametric mapping with Monte Carlo simulation thresholding.

METHODS:
The brain metabolism of eight women with a history of bulimia nervosa (28.62+/- 6.5 years) and twenty-nine age and sex matched controls (28.57+/- 6.42 years) was measured with positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) as the radio-tracer during a continuous performance uptake task. Group relative average images were generated and subjected to a pixel by pixel Student's test procedure to yield statistical paramentric p-maps. These p-maps were then thresholded using a Monte Carlo simulation. This analysis tool used a normal control pool to generate a continuous cluster size frequency distribution. P-map clusters smaller than the critical size were discarded from analysis.

RESULTS:
Analysis revealed that bulimic individuals had higher caudate metabolism across three PET slices at a significance level of p<.01. Paradoxically, caudate metabolism correlated inversely with the clinical pathology, measured by EAT scores (p<.05). This finding is consistent with the hypotheses that heightened alimentary ideation is a compensatory mechanism which somehow counteracts caudate hypermetabolism. Limbic metabolism in bulimic groups was lower in deep orbital cortex and anterior paracingulate (both p<.05) and higher in amygdala and left anterior cingulate (both p<.01). These findings suggest involvement of the caudate-orbitofrontal-cingulate "worry circuit" in manner analogous to and yet distinct from that seen in obsessive compulsive disorder.

1 Wu, JC, Hagman, J, Buchsbaum, MS, et al. Greater Left Cerebral Hemispheric Metabolism in bulimia Assessed by Positron Emission Tomography.American Journal of Psychiatry 1990; 147:309-312.

A PET STUDY OF BULIMIA NERVOSA REVEALS CAUDATE HYPERMETABOLISM

The purpose of this study was to reassess the brain metabolism of bulimic subjects studied in prior research (JC Wu et al Amer. Journ. Psychiatry 1990 147:309-312) using statistical parametric mapping with Monte Carlo simulation thresholding. The brain metabolism of eight women with a history of bulimia nervosa (28.62+/- 6.5 years) and twenty-nine age and sex matched controls (28.57+/- 6.42 years) was measured with positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) as the radio-tracer during a continuous performance uptake task. Group relative average images were generated and subjected to a pixel by pixel Student's test procedure to yield statistical paramentric p-maps. These p-maps were then thresholded using a Monte Carlo simulation. This analysis tool used a normal control pool to generate a continuous cluster size frequency distribution. P-map clusters smaller than the critical size were discarded from analysis. Analysis revealed that bulimic individuals had higher caudate metabolism across three PET slices at a significance level of p<.01. Paradoxically, caudate metabolism correlated inversely with the clinical pathology measured by EAT scores (p<.05). This finding is consistent with the hypotheses that heightened alimentary ideation is a compensatory mechanism which somehow counteracts caudate hypermetabolism. Limbic metabolism in bulimic groups was lower in deep orbital cortex and anterior paracingulate (both p<.05) and higher in the amygdala and left anterior cingulate (both p<.01). These findings suggest involvement of the caudate-orbitofrontal cingulate "worry circuit" in a manner analogous to and yet distinct from than seen in obsessive compulsive disorder.


 

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