Striatal dopamine in bulimia nervosa: A pet imaging study
Allegra BroftRebecca M. ShingletonJenna KaufmanFei LiuDileep KumarMark SlifsteinAnissa Abi‐DarghamJanet SchebendachRonald Van HeertumEvelyn AttiaDiana MartínezB. Timothy Walsh
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Abstract:
Bulimia nervosa (BN) has been characterized as similar to an addiction, though the empirical support for this characterization is limited. This study utilized PET imaging to determine whether abnormalities in brain dopamine (DA) similar to those described in substance use disorders occur in BN.PET imaging with [(11) C]raclopride, pre/post methylphenidate administration, to assess dopamine type 2 (D(2)) receptor binding (BP(ND)) and striatal DA release (ΔBP(ND)).There was a trend toward lower D(2) receptor BP(ND) in two striatal subregions in the patient group when compared with the control group. DA release in the putamen in the patient group was significantly reduced and, overall, there was a trend toward a difference in striatal DA release. Striatal DA release was significantly associated with the frequency of binge eating.These data suggest that BN is characterized by abnormalities in brain DA that resemble, in some ways, those described in addictive disorders.Keywords:
Raclopride
Putamen
Binge eating
Cocaine dependence
Objective This study sought to examine the differences in the quantity and quality of binges between binge eating disorder (BED) and bulimia nervosa. Method Patients (N = 77) seeking treatment for eating disorders were assessed on binge content. Results Results suggest no differences in binge quantity with BED and bulimia, but there were differences in the binge quality. The binges of bulimics were higher in carbohydrates and sugar than those with BED. Discussion The higher levels of obesity of our BED individuals may account for the lack of differences between those with bulimia and BED. The importance of increasing our knowledge of the continuum of weight and binging is discussed. © 2000 by John Wiley & Sons, Inc. Int J Eat Disord 27: 238–243, 2000.
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Human post‐mortem and animal experimental results suggest a decline of the cerebral dopaminergic neuronal system with age. In this study, the radiotracer [ 11 C]raclopride (dopamine D2 antagonist) and positron emission tomography were applied to determine the effect of age on striatal dopamine D2 receptors in 32 healthy volunteer subjects (age range 21–68 years). Subjects were divided in two age groups on the basis of median age (31 years). An index for specific tracer uptake was calculated for caudate nucleus and putamen. Uptake indices in the older group of subjects were reduced on average 26% in putamen and 20% in caudate nucleus. The decline appeared to be steep until 30 years, but slower afterwards. After 30 years of age the decline of specific raclopride binding was found to be 0.6% per year. These results suggest that dopamine D2 receptor binding sites (mainly post‐synaptically located) decrease as a consequence of normal aging in parallel with the decline of the pre‐synaptic nigrostriatal dopa‐minergic system.
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While most individuals with bulimia nervosa begin dieting prior to the onset of binge eating, some individuals begin binge eating prior to dieting. The purpose of this study was to assess the differences between these two groups.Participants (N = 120) in a treatment study for bulimia nervosa were separated into two groups (Binge First vs. Diet First) based on the ages they reported for the onset of binge eating and of dieting and then compared across a number of variables.Individuals in the Binge First group reported higher weight, higher shape and weight concern, lower age of onset of eating disorder symptoms, and an altered relationship of binge eating to vomiting when compared to individuals in the Diet First group.The differences between the two groups suggest that there may be subgroups of individuals with purging bulimia nervosa and that individuals in the Binge First group more closely resemble individuals with binge eating disorder than do those in the Diet First group.
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Animal studies suggest that the dopaminergic system plays a role in central pain modulation. We have previously demonstrated with positron emission tomography (PET) that striatal dopaminergic hypofunction may be involved in the burning mouth syndrome. The aim of the present study was to evaluate the nigrostriatal dopaminergic system in patients with atypical facial pain using PET. In seven patients with atypical facial pain, striatal presynaptic dopaminergic function was assessed with [18F]FDOPA and dopamine D1 and D2 receptor availabilities with [11C]NNC 756 and [11C]raclopride, respectively. The results were compared with those of healthy controls. A quantitative region-of-interest analysis showed that the uptakes of [18F]FDOPA and [11C]NNC 756 did not differ between patients and controls. There was a tendency of increased D2 receptor availability in the left putamen (P=0.056), and the D1/D2 ratio in the putamen was decreased bilaterally by 7.7% (P=0.002) in patients when compared to controls. In a voxel-based analysis, the uptake of [11C]raclopride was increased in the left putamen (P=0.025). In conclusion, the increase in D2 receptor availability in the left putamen and the decrease in D1/D2 ratio imply that alterations in the striatal dopaminergic system as evaluated by PET may be involved in chronic orofacial pain conditions.
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Several antidepressants raise striatal dopamine, but the role of striatal dopamine during major depressive episodes is unclear. Striatal [(11)C]raclopride binding potential measured with positron emission tomography is an index of D(2) type receptors and is sensitive to extracellular dopamine levels (higher D(2) binding potential occurs when dopamine is lower). It was hypothesized that putamen D(2) binding potential would be higher during major depressive episodes featuring motor retardation.Drug-free, nonsmoking subjects experiencing a major depressive episode (N=21) underwent [(11)C]raclopride PET imaging as did 21 healthy age-matched comparison subjects. Motor retardation was measured with the finger tapping test.The depressed subjects exhibiting motor retardation had significantly higher D(2) binding potential in both the left and right putamen than did healthy subjects, and putamen D(2) binding potential correlated significantly with motor speed in the depressed subjects.The results argue that extracellular dopamine is lower in subjects experiencing a major depressive episode that features motor retardation. This depression subtype should preferentially benefit from dopamine-increasing medications and should be targeted in future clinical trials of dopamine reuptake inhibitors.
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• Human postmortem and animal experimental results suggest a decline of the cerebral dopaminergic neuronal system with age. In this study, the radiotracer carbon 11-labeled-raclopride and positron emission tomography were applied to determine the effect of age on striatal D2dopamine receptors in 32 healthy volunteer subjects (age range, 21 to 68 years; median, 31 years). An index of specific11C-raclopride binding was calculated for putamen, caudate nucleus, and other brain regions in each subject. A significant decrease with age of the index for specific tracer uptake was found in putamen and caudate nucleus. The decrease was steep until 30 years, but slower afterward. After approximately 30 years of age, the decline of specific11C-raclopride binding in putamen was found to be 0.6% per year. Our results suggest that D2dopamine receptor binding sites (mainly postsynaptically located) decrease as a consequence of normal aging in parallel with the decline of the presynaptic nigrostriatal dopaminergic neuronal system.
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We studied cerebral dopamine D2-receptor binding using [11C]raclopride and PET in 18 previously untreated patients with Parkinson9s disease (PD) and 14 healthy volunteer subjects. Sixteen patients were scanned before and after 3 to 4 months of stable oral therapy with either L-dopa (300 mg/d) (n = 7) or lisuride (0.8 to 1.2 mg/d) (n = 9). Two additional patients were investigated before and after a continuous IV infusion of L-dopa. In addition, we studied the effect of acute IV L-dopa and lisuride administration on [11C]raclopride binding in a healthy rhesus monkey. At baseline, PD patients showed higher uptake values in the putamen than did healthy subjects (p < 0.0001). Oral lisuride treatment lowered [11C]raclopride uptake in the putamen (-19%) and in the caudate nucleus (-15%) compared with baseline, but the difference did not reach significance upon Bonferroni correction for multiple comparisons. However, putamen tracer uptake returned to baseline in two patients when we repeated [11C]raclopride scans 4 days after lisuride withdrawal. Oral L-dopa treatment did not induce changes in the putamen or caudate nucleus indices. Acute lisuride (25 μg) administration in a healthy monkey reduced striatal uptake values, but acute injection of L-dopa (300 mg) did not. The results suggest that lisuride blocks [nC]raclopride binding at dopamine D2-receptor sites and demonstrate that 3 to 4 months9 oral therapy with L-dopa or lisuride does not change striatal dopamine D2-receptor density in PD patients.
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We investigated in vivo D2 receptor binding using 11C-raclopride and PET in the striatum of 17 subjects with the narcoleptic syndrome. Putamen and caudate nucleus 11C-raclopride uptake was comparable in the total patient group and controls, and the tracer uptake was similar in the HLA-DR2-positive (n = 12) and HLA-DR2-negative (n = 5) narcoleptic subjects. There was a significant increase in 11C-raclopride uptake in the putamen of narcoleptic subjects older than 31 years (n = 11) when compared with age-matched controls (n = 15). There was no evidence of involvement of the striatal D2 dopaminergic neurotransmitter system in the basic pathophysiology of the narcoleptic syndrome despite an age-related increase in putaminal 11C-raclopride uptake.
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Caudate nucleus
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Objective This study sought to examine the differences in the quantity and quality of binges between binge eating disorder (BED) and bulimia nervosa. Method Patients (N = 77) seeking treatment for eating disorders were assessed on binge content. Results Results suggest no differences in binge quantity with BED and bulimia, but there were differences in the binge quality. The binges of bulimics were higher in carbohydrates and sugar than those with BED. Discussion The higher levels of obesity of our BED individuals may account for the lack of differences between those with bulimia and BED. The importance of increasing our knowledge of the continuum of weight and binging is discussed. © 2000 by John Wiley & Sons, Inc. Int J Eat Disord 27: 238–243, 2000.
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Twenty women with bulimia nervosa (binge-eating and vomiting) recorded all food consumption for one week and identified eating episodes that they considered to be a binge. A content analysis including the type and amount of food consumed was performed on 199 binge-eating and 440 nonbinge-eating episodes. The average binge-eating episode was much higher in calories; however, most of these eating episodes involved small amounts of food. The distinguishing characteristic of binge-eating episodes was relatively more snacks and desserts and less fruits and vegetables. The size of binge-eating episodes in bulimia nervosa appears to be much smaller, on average, than previous reports of typical binge eating.
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