Comparison of Thalamic GABA and Glx Levels in Patients with Essential Tremor and Parkinson's Disease
Ruoyun Ma1,2, Johnathan P Dyke3, Shalmali Dharmadhikari4, Nora Hernandez5, Elizabath Zauber6, Elan Louis5,7,8, and Ulrike Dydak1,2

1School of Health Sciences, Purdue University, West Lafayette, IN, United States, 2Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, United States, 3Department of Radiology, Weill Cornell Medical College, New York, NY, United States, 4Radiology and Imaging Sciences, Emory University, Atlanta, GA, United States, 5Department of Neurology, Yale School of Medicine, New Heaven, CT, United States, 6Department of Neurology, Indianapolis University School of Medicine, Indianapolis, IN, United States, 7Department of Chronic Disease Epidemiology, Yale School of Public Health, New Heaven, CT, United States, 8Center for Neuroepidemiology and Clinical Neurological Research, Yale School of Medicine, New Heaven, CT, United States

Synopsis

Essential tremor (ET) and Parkinson’s disease (PD) are two most prevalent movement disorders. It was suggested that tremors in both diseases, though of different types, may be modulated by neuropathways involving the thalamus. We found a significant trend of elevated thalamic GABA levels from controls to ET patients to PD patients, which may be related to the increased risk of ET patients to develop PD, and thus suggesting thalamic GABA as imaging marker of preclinical parkinsonism. However, thalamic GABA is not associated with tremor of either type.

Purpose

Essential tremor (ET) and Parkinson’s Disease (PD) are two distinct, yet common movement disorders1. One of the differences lies in the tremor type, which is kinetic tremor for ET and resting tremor for PD. It was suggested that tremor in both conditions may be modulated by thalamic pathways1,2,3. A previous study found an increase of thalamic γ-aminobutyric acid (GABA) levels in PD patients4. Therefore, this study aims at comparing the levels of thalamic GABA and Glx (glutamate and glutamine), the main inhibitory and excitatory neurotransmitters, between PD and ET patients.

Methods

17 PD patients (63±10 yrs), 10 ET patients (73±6 yrs) and 17 healthy controls (58±10yrs) have been recruited to the study. Tremor levels of PD and ET patients were estimated using the tremor scores from the Unified Parkinson’s Disease Rating Scale (UPDRS) III5 and the Washington Heights-Inwood Genetic Study of ET (WHIGET) tremor rating scale6, respectively. MRI examinations were performed on a 3T Siemens Tim Trio scanner, equipped with a 32 channel head coil. Thalamic GABA and Glx levels were measured using MEGA-PRESS7 (TR/TE=2000ms/68ms, 256 averages with editing pulses at 1.9 and 7.5 ppm, voxel size 25mm×30mm×25mm) and quantified using LCModel8 V6.2-0R. Basis sets were generated from density matrix simulation of the pulse sequence using values for chemical shifts and J-couplings from Kaiser et al9. Water-unsuppressed scans on the same voxels were acquired for eddy current correction and water scaling. MPRAGE 3D T1-weighted images were acquired for segmentation. Cerebrospinal fluid (CSF) correction was performed using statistical parametric mapping (SPM8, Wellcome Department of Imaging Neuroscience, London, UK) for tissue segmentation and an in-house MATLAB program (MathWorks Inc., Natick, MA, USA) for partial volume correction. GABA and Glx levels, corrected for CSF, were obtained using the method described by Chowdhury et al10. The voxel placement overlaid on T1-weighted images and segmented gray matter images, as well as a typical MEGA-edited spectrum are shown in Fig. 1. Group difference analysis of the GABA and Glx levels across the three groups were performed using a multiple linear regression model in SAS 9.3. Age and gender were included in the regression model (Eq.1) as potential confounds11,12. Separate age-controlled correlations between tremor scores and GABA, as well as Glx levels, were performed for PD patients (using tremor scores from UPDRS III) and for ET patients (using tremor scores from WHIGET).

Eq. 1 $$$GABA=a×age+b×group+c×gender+d$$$

Results

Results: Thalamic GABA levels were found to be highest in PD patients, followed by ET patients and controls (controls: 1.74±0.30, ET patients: 1.89±0.36, PD patients: 2.06±0.36), as shown in Figure 2. The multiple regression model with GABA as dependent variable was estimated by setting the group variable to 0 for controls, 1 for ET cases and 2 for PD patients, according to the distribution of the mean value of each group. A significant group effect was found in the regression equation (F(2,42)=3.99,p=0.058,R2=0.16). The estimated parameters for each variable with the p values are listed in Eq. 2.

Eq. 2 $$$GABA=0.002(p=0.72)×age+0.160(p=0.01)×group-0.050(p=0.61)×gender+1.641$$$

The thalamic Glx levels were highest in ET patients, followed by similar values in PD patients and controls (controls: 6.54±1.58, ET patients: 7.41±1.63, PD patients: 6.19±1.57). However, by setting the group variable to be 0 for controls, 1 for PD patients and 2 for ET patients, it was found that the difference in Glx levels was driven by age, not by group, as shown in Eq. 3.

Eq. 3 $$$GABA=0.054(p=0.03)×age+0.004(p=0.98)×group-0.049(p=0.91)×gender+3.180$$$

No significant correlation between tremor scores from 1) UPDRS and GABA levels in PD patients (r=-0.29,p=0.26) or 2) WHIGET scores and GABA levels in ET patients (r=-0.09,p=0.86) or 3) UPDRS and Glx levels in PD patients (r=-0.29,p=0.26) or 4) WHIGET scores and GABA levels in ET patients (r=0.34,p=0.49) was found.

Conclusion and discussion

The significant positive group effect on GABA levels shows a trend that thalamic GABA levels of ET patients lies in-between the significantly increased levels of PD patients4 and the lower control values. Increased thalamic GABA leads to an over-inhibition of the thalamo-cortical loop and consequently to reduced neuronal excitation of the cortex, explaining the hypokinetic symptoms in PD13. Yet, as our data shows, there seems to be no association between thalamic GABA and tremor. ET has been identified to significantly increase the risk factor to develop PD14. Therefore, the trend of increased thalamic GABA levels in ET might possibly be interpreted as imaging marker of preclinical parkinsonism. This would be in line with findings of increased thalamic GABA in non-symptomatic welders and metal workers exposed to Mn15,16, an exposure that may lead to Mn-induced parkinsonism. A current limitation of our study is the small number of ET patients.

Acknowledgements

This study was supported by NIH/NIEHS R01 ES020529 and NINDS R01 NS085136 from the National Institutes of Health.

References

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Figures

Fig. 1 Voxel placement on axial (A) and sagittal (B) view of T1-weighted images and segmented gray matter images (C,D), as well as a MEGA-edited spectrum.

Fig. 2 Comparison of GABA and Glx levels in healthy controls, ET patients and PD patients.



Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)
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