The Changes Of Brain Glucose Metabolism In Somatoform Disorder And Generalized Anxiety Disorder:a PET Study

PartⅠThe changes of brain glucose metabolism in patients with somatization disorder and undifferentiated somatoform disorder:a PET studyObjective:To explore the brain glucose metabolism in somatization disorder(SD) and undifferentiated somatoform disorder(USD) with18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) compared with health subjects,and the possible pathogenesis will be discussed.Methods:Screened and identified subjects who met the criterion for SD and USD according to the Diagnostic and Statistical Manual of Mental Disorders(DSM-Ⅳ) as the patients group.In this group,a self-designed general questionnaire was adopted to collect the demographic and clinical data,the Self-Rating Anxiety Scale(SAS) and Self-Rating Depression Scale(SDS) were used to assess the anxiety and depression symptoms respectively,the Somato Symptom Self-Rating Scale(SSS) together with the somatization subscale of the Symptom Checklist90(SCL-90) was employed to evaluate the somatization severity and a correlation was tested between them.Compared the total scores of SAS,SDS and the somatization subscale of SCL-90among the patients group with that in the Chinese norm respectively.The healthy volunteers were selected as control groups,matched with patients for age,gender and education.All the subjects were screened with the Mini-International Neuropsychiatric Interview(MINI) to exclude any axis I psychiatric disorders. Finally,25patients(8cases for SD and17for USD) and29health subjects were enrolled,and then they were performed a brain18F-FDG PET/CT scan. All18F-FDG PET images were spatially normalized using statistical parametric mapping(SPM2; http://www.fil.ion.ucl.ac.uk/spm/) with an original template of SPM. Then the study analyzed the differences between two groups to compare regarding respective FDG metabolism. The rate of cerebral glucose metabolism(rCMRG1c) in any abnormal areas in patients group was calculated and the correlation to the scores of rating scales was also analyzed. Results:1.The patients group showed no significant difference in the total scores for SAS(35.68±6.81)(P>0.05) and significantly reduced total scores for SDS(36.56±7.29)(P<0.01), compared with the Chinese norms.2. The patients group exhibited significantly higher socres (12.28±7.63) for the somatization subscale of SCL-90than that in the Chinese norm. The Somatization Severity Index(SSI) and the numbers of symptoms in the Somato Symptom Self-Rating Scale(SSS) were154.04±38.97and18±13respectively. The scatterplot and correlation analysis showed that the scores for somatization subscale of SCL-90had a tendency of positive correlation with SSI(r=0.750,.P<0.001) and numbers of sysmptoms(r=0.730,P<0.001).3. Voxel-wise comparison of FDG-PET images was conducted using SPM2to identify the brain regions showing glucose hypermetabolism in the right posterior cingulate gyrus(Z=4.20), right precuneate gyrus(Z=3.22), right middle(Z≥3.53) and inferior(Z=3.91) temporal gyrus, right middle frontal gyrus(Z≥3.44), right inferior parietal lobule(Z=3.51) and right supramarginal gyrus(Z=3.45)(P<0.001). In addition,glucose hypometabolism was found in the left superior temporal gyrus(Z=4.56), left supramarginal gyrus(Z=4.48), left(Z=4.45) and right(Z≥3.57) middle temporal gyrus,left middle frontal gyrus(Z=3.65)(P<0.001). The glucose hypermetabolism was mainly observed in the right posteromedial parietal lobe, right posterolateral parietal lobe, right lateral temporal lobe and right prefrontal lobe, whereas hypometabolism primarily appeared in the left posterolateral parietal lobe, left lateral temporal lobe and left prefrontal lobe. It suggested that the abnormal glucose metabolism in the bilateral hemispheres obviously showed functional asymmetry of brain.4.As the multiple linear regression showed,the rCMRG1c in the left supramarginal gyrus(-62-2038) had a correlation with the total scores for SAS(β=0.517,P=0.003) and the scores for somatization subscale of SCL-90(β=-0.375,P=0.028), and such a relationship was not observed in other brain areas(P>0.05).Conclusions:1.Both the SSI and numbers of symptoms in SSS can be used to evaluate the somatization symptom severity.2. The SD and USD patients were showed abnormal glucose metabolism in multiple regions of the brain, which suggest a functional asymmetry of brain.3.The functional cerebral asymmetry may exist as a compensation to the disorder itself,and also as the cause for the recurrent somatization symptoms.4. The central dysfunction in SD and USD may involve a process of emotional stimulation. Part ⅡThe changes of brain glucose metabolism in patients with hypochondriasis:a PET studyObjective:To investigate the brain glucose metabolism in hypochondriasis with18F-fluorodeoxyglucose positron emission tomography (FDG-PET) compared with healthy subjects.Methods:Eleven patients diagnosed as hypochondriasis according to CCMD-3and23age and sex-matched healthy subjects were performed FDG PET/CT scan. All FDG-PET images were spatially normalized using statistical parametric mapping (SPM8; http://www.fil.ion.ucl.ac.uk/spm/) with an original template of SPM. Then the study analyzed the differences between two groups to compare regarding respective FDG metabolism.Results:Voxel-wise comparison of FDG-PET images was conducted using SPM8to identify the brain regions showing glucose hypermetabolism in the right angular gyrus and inferior parietal lobule(Z=4.72), right insula(Z=4.19), right precentral gyrus(Z=4.15) and paracentral lobule(Z=3.52)., right precuneate gyrus(Z=4.09), right middle(Z=3.39) and inferior frontal gyrus(Z=3.79), left posterior cingulate(Z=3.95),left precuneate gyrus(Z=3.98), left precentral gyrus(Z=3.72), bilateral thalamus, mesencephalon and lentiform nucleus(Z≥3.94)(P<0.001). In addition,glucose hypometabolism was found in the right superior temporal gyrus(Z=4.05), right gyrusrectus(Z=3.93), right superior frontal gyrus(Z=3.14) and left gyrusrectus(Z=3.59) in comparison with that of the normal subjects(P<0.001). Conclusions:Hypochondriasis patients were showed abnormal glucose metabolism in multiple regions of brain, which may involve the regulation of the pathophysiology in the central nervous system. Part ⅢThe changes of brain glucose metabolism in patients with generalized anxiety disorder:a PET studyObjective:To explore the brain glucose metabolism in generalized anxiety disorder(GAD) with F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) compared with health subjects,and the possible pathogenesis will be discussed.Methods:Screened and identified subjects who met the criterion for generalized anxiety disorder according to the Diagnostic and Statistical Manual of Mental Disorders(DSM-Ⅳ) as the patients group.In this group,a self-designed general questionnaire was adopted to collect the demographic data,the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale(HAMD) were used to assess the anxiety and depression symptoms respectively.The healthy volunteers were selected as control groups,matched with patients for age and gender. All the subjects were screened with the Mini-International Neuropsychiatric Interview(MINI) to exclude any axis I psychiatric disorders.Finally,10patients and22health subjects were enrolled,and then they were performed a brain18F-FDG PET/CT scan. All18F-FDG PET images were spatially normalized using statistical parametric mapping(SPM2; http://www.fil.ion.ucl.ac.uk/spm/) with an original template of SPM. Then the study analyzed the differences between two groups to compare regarding respective FDG metabolism. The rate of cerebral glucose metabolism(rCMRGlc) in any abnormal areas in patients group was calculated and the correlation to the scores of HAMA and HAMD was also analyzed.Results:Voxel-wise comparison of FDG-PET images was conducted using SPM2to identify the brain regions showing glucose hypermetabolism in the left supramarginal gyrus(Z=5.56), right middle frontal gyrus(Z=4.78), left anterior and middle cingulate gyrus(Z=4.21), left inferior frontal gyrus(Z=4.07), left precentral gyrus(Z=3.24), left cerebellum(Z=4.02) and right cerebellum(Z=4.25)(P<0.001). In addition,glucose hypometabolism was found in the right inferior parietal lobule (Z=4.04), rigth fusiform gyrus(Z=4.13), right occipital lobe(Z=3.83), left cuneus gyrus(Z=3.58) and left occipital lobe(Z=4.39)(P<0.001). No correlation was observed between the HAMA scores and the rCMRG1c in any brain areas mentioned above.Conclusions:In our study, the patients with GAD showed abnormal glucose metabolism in multiple regions of brain, which may involve the regulation of the pathophysiology in the central nervous system.Glucose hypermetabolism was mainly observed in the medial prefrontal cortex(MFC), anterior cingulate cortex(ACC) and bilateral cerebella, whereas hypometabolism primarily appeared in the right inferior parietal lobule and bilateral occipital lobe. The results suggest patients with GAD have a dysfunction in the central circuit responsible for visual attention; whereas glucose hypermetabolism in the MFC and ACC perhaps play a role in the inhibition of subcortex regions such as amygdala and in the cognitive compensation for visual attention, which gradually resulted in an adaptive state.