Abstract
Objective: To evaluate metabolite concentration differences in PD subtypes: tremor-dominant and rigid-akinetic.
Background The mechanisms involved in the pathogenesis of Parkinson's disease (PD) are multiple and poorly understood, however changes in mitochondrial function seem to play a major role. Cerebellar involvement in PD is mostly correlated with tremor-dominant subtype. Magnetic resonance spectroscopy (MRS) allows measurement of specific biochemical compounds in anatomic structures, involved in different biochemical processes within cerebral metabolism.
Design/Methods: We prospectively evaluated 14 PD patients (10 tremor-dominant and 4 rigid-akinetic) and 14 age-matched healthy controls. The patients were submitted to a standard clinical evaluation using cognitive and motor scales. Mean age of PD patients was 57.1 years (41-74; SD= 9.75) and controls was 53.42 years (40-68; SD=8.41). Mean duration of disease was 7.76 years (0.6-15; SD=4.37). We acquired 1H-MR spectra from a 1.5x1.5x1.5 cm3 voxel located at the cerebellum, using a 3.0T scanner (Achieva, Philips) with a PRESS sequence (TR/TE=2000/144ms,128scans, 2kHz bandwidth, 1024 data points), and performed quantification using LCModel. Only metabolites quantified with Cramer-Rao bounds < 30% were used in the statistical analysis. We used Mann-Whitney U test for comparison between groups and Spearman correlation matrix for clinical-MRS correlations.
Results: We found increased cerebellar N-acetylaspartate+acetylaspartylglutamate (NAA)/creatine+phosphocreatine ratios in PD patients compared to controls (1.282 +/- 0.27 versus 1.109 +/- 0.21; p=0.041) and also increased cerebellar glutamate+glycine/ creatine+phosphocreatine ratio (0.513 +/- 0.11 versus 0.434 +/- 0.10; p= 0.045). We did not find significant differences in metabolite concentrations in both subtypes or a significant correlation between metabolite concentration and clinical markers.
Conclusions: Increases in NAA compounds are observed during brain development and maturation, which may suggest increased cerebellar plasticity in PD. Increases in glutamate points to excitotoxicity and energetic failure. The lack of difference between subtypes are probably due to the small sample size.
Disclosure: Dr.Campos has received personal compensation for activities with Ipsen. Dr. Landim has nothing to disclose. Dr. Mineli has nothing to disclose. Dr. Castellano has nothing to disclose. Dr. Amato-Filho has nothing to disclose. Dr. Piovesana has nothing to disclose. Dr. Cendes has nothing to disclose. Dr. D'Abreu has received research support from Roche.
Background The mechanisms involved in the pathogenesis of Parkinson's disease (PD) are multiple and poorly understood, however changes in mitochondrial function seem to play a major role. Cerebellar involvement in PD is mostly correlated with tremor-dominant subtype. Magnetic resonance spectroscopy (MRS) allows measurement of specific biochemical compounds in anatomic structures, involved in different biochemical processes within cerebral metabolism.
Design/Methods: We prospectively evaluated 14 PD patients (10 tremor-dominant and 4 rigid-akinetic) and 14 age-matched healthy controls. The patients were submitted to a standard clinical evaluation using cognitive and motor scales. Mean age of PD patients was 57.1 years (41-74; SD= 9.75) and controls was 53.42 years (40-68; SD=8.41). Mean duration of disease was 7.76 years (0.6-15; SD=4.37). We acquired 1H-MR spectra from a 1.5x1.5x1.5 cm3 voxel located at the cerebellum, using a 3.0T scanner (Achieva, Philips) with a PRESS sequence (TR/TE=2000/144ms,128scans, 2kHz bandwidth, 1024 data points), and performed quantification using LCModel. Only metabolites quantified with Cramer-Rao bounds < 30% were used in the statistical analysis. We used Mann-Whitney U test for comparison between groups and Spearman correlation matrix for clinical-MRS correlations.
Results: We found increased cerebellar N-acetylaspartate+acetylaspartylglutamate (NAA)/creatine+phosphocreatine ratios in PD patients compared to controls (1.282 +/- 0.27 versus 1.109 +/- 0.21; p=0.041) and also increased cerebellar glutamate+glycine/ creatine+phosphocreatine ratio (0.513 +/- 0.11 versus 0.434 +/- 0.10; p= 0.045). We did not find significant differences in metabolite concentrations in both subtypes or a significant correlation between metabolite concentration and clinical markers.
Conclusions: Increases in NAA compounds are observed during brain development and maturation, which may suggest increased cerebellar plasticity in PD. Increases in glutamate points to excitotoxicity and energetic failure. The lack of difference between subtypes are probably due to the small sample size.
Disclosure: Dr.Campos has received personal compensation for activities with Ipsen. Dr. Landim has nothing to disclose. Dr. Mineli has nothing to disclose. Dr. Castellano has nothing to disclose. Dr. Amato-Filho has nothing to disclose. Dr. Piovesana has nothing to disclose. Dr. Cendes has nothing to disclose. Dr. D'Abreu has received research support from Roche.
| Original language | English |
|---|---|
| Number of pages | 3 |
| Journal | Neurology |
| Volume | 78 |
| Issue number | 1 Supplement |
| Publication status | Published - 23 Apr 2012 |
| Event | American Academy of Neurology (AAN) 64th Annual Meeting - New Orleans, United States Duration: 21 Apr 2012 → 28 Apr 2012 |