Brain Metabolic Abnormalities For Freezing Of Gait In Parkinson’s Disease

Objective: The aim of this study is to investigate the cerebral glucose metabolism characteristics for freezing of gait in Parkinson’s disease using 18F-FDG PET/CT and Statistical Parametric Mapping,in order to detect the mechanism under freezing of gait and provide guidance to cure the disease.Methods: Our study consisted of 31 PD patients with FDG-PET.These patients(15 women and 16 men)with a diagnosis of PD according to the clinical diagnostic criteria of the United Kingdom Parkinson’s disease Society Brain Bank by a trained movement disorder specialist.Patients were classified with FOG based on both the following two conditions:(1)score>0 to item 3 of the FOG questionnaire,(2)patients showed at least once FOG phenomenon to the specialist.Patients who inconformity anyone of the above conditions were classified as FOG-.The motor state in PD patients was assessed using the Hoehn and Yahr scale(H&Y)and the motor section of the Unified Parkinson’s Disease Rating Scale(UPDRS-Ⅲ)in the “off”(minimum of 12 h without anti-parkinsonian medication and not more than 2 h before the PET scan).All patients underwent MMSE and MOCA testing.All subjects were scanned with FDG-PET.Imaging data was processed by Statistical Parametric Mapping(SPM8)software(Welcome Department of Neurology,London,UK)running in Matlab 8.0.1(Mathworks Inc,Sherborn,MA).Changes in metabolism were assessed by analysis of the preprocessed images using two-sample t tests to analysis the variance.The coordinates were reported in the standard anatomical space developed at the Montreal Neurological Institute.The cytoarchitectonic localization of each reported hypometabolism region was confirmed using the Talairach space.Statistical analyzes of clinical data variables were carried out using the statistical SPSS17.0.Student t tests were used to assess group differences between PD-FOG+ and PD-FOGgroups and Chi-square test was applied to assess group differences in categorical variables.A value of P<0.05 was considered to indicate statistical significance.Results: 1.There was no statistically significant differences(P > 0.05)between the PD-FOG + and PD-FOG-groups in gender,age,course of the disease,H-Y in installment,the UPDRS-Ⅲ(close)score,MMSE,MOCA scores at P = 0.05 level lines of two independent samples t test and chi-square test.2 SPM analysis showed that,PD-FOG + group’s main features are: the superior frontal gyrus(BA11),inferior frontal gyrus(BA10),near the central back,caudate nucleus and putamen,midbrain,anterior cingulate,reduce the cerebellum metabolism when compared with PD group-FOG-.3.Compared the indivisual MOCA score between the PD-FOG+ and PD-FOG-: The study found that visual space/executive function,naming,memory,language,abstract distinction had no statistical significance(P > 0.05);but the executive function correlation analysis found that visual space and FOGQ into negative correlation,the correlation coefficient is-0.417(was significantly associated with both at the 0.05 level).Thus the worse the visual space/executive function was,the higher the FOGQ score was,the more serious the freezing gait clinical syndrome was.4.The attention between PD-FOG+ group and PD-FOG-group was statistically significant,then the Pearson correlation coefficient test between attention and freezing gait is negative,the correlation coefficient is-0.577(was significantly associated with both at the 0.01 level).The worse the attention,the higher of the FOGQ score was,the more serious the freezing gait clinical syndrome was.Conclusion: 1.Freezing gait in patients with Parkinson’s disease showed reduced cerebellum metabolism in the superior frontal gyrus(BA11),inferior frontal gyrus(BA10),near the central back,caudate nucleus and putamen,midbrain,anterior cingulate when compared with PD-FOG-group.2.Attention has close reality to freezing of gait,the worse the attention,the more serious the freezing gait clinical severity was.3.The worse the visual space/executive function was,the more serious the freezing of gait clinical syndrome was.