Objective: Understanding the differences in brain glucose metabolism between hyperkinetic movement disorders.

Background: The Next Move in Movement Disorders (NEMO) study is a research initiative dedicated to improving hyperkinetic movement disorder classification and to better understand underlying pathophysiologies of these disorders. In the NEMO study, we measure patients during movement registrations¹ and neuroimaging scans. Here, we investigated differences in brain glucose metabolism between healthy volunteers (HV) and myoclonus, myoclonus-dystonia, and tremor patients.

Method: [18F] FDG PET scans were compared across 13 cortical myoclonus, 21 myoclonus-dystonia (10 SGCE² positive), and 21 essential tremor patients. Groups were matched with healthy volunteers. All participants were right-handed. Age, Montreal Cognitive Assessment³, and Hospital Anxiety and Depression⁴ scales were considered as covariates. Group comparisons were performed using mass univariate two-sample T-tests in Nilearn (v0.10.3)⁵. Statistical thresholds were set at p<0.001 uncorrected, and p<0.05 FDR corrected for multiple comparisons.

Results: When comparing essential tremor patients with HV, we found increased glucose uptake in the right cerebellum and decreased uptake in medial and lateral parietal areas (p(fdr)<0.05). Compared to myoclonus-dystonia, we found reduced uptake in the same parietal areas while glucose uptake was higher in the thalamus (p(fdr)<0.05). Between cortical myoclonus and HV, we found increased uptake in the bilateral amygdala and parahippocampal gyri, and decreased uptake in the dmPFC (p(fdr)<0.05). We also found increased bilateral amygdala and parahippocampal glucose uptake when comparing myoclonus with tremor and myoclonus-dystonia (p<0.001). For myoclonus-dystonia, glucose uptake was increased in the premotor cortex (p(fdr)<0.05) while glucose uptake was lower in the visual cortex (p<0.001) compared to HV. Compared to both myoclonus and tremor, myoclonus-dystonia patients had higher glucose uptake in lateral parietal cortex.

Conclusion: We found clear differences in brain metabolism between (1) hyperkinetic movement disorder patients and matched HV, and (2) across different hyperkinetic movement disorders. These results provide a starting point in classifying hyperkinetic movement disorders based on differences in brain metabolism measured with [18F] FDG PET.

References: 1. Van Der Stouwe AMM, Tuitert I, Giotis I, et al. Next move in movement disorders (NEMO): Developing a computer-aided classification tool for hyperkinetic movement disorders. BMJ Open. 2021;11(10):1-7. doi:10.1136/bmjopen-2021-055068
2. Zimprich A, Grabowski M, Asmus F, et al. Mutations in the gene encoding ε-sarcoglycan cause myoclonus-dystonia syndrome. Nat Genet. 2001;29(1):66-69. doi:10.1038/ng709
3. Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: A brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695-699. doi:10.1111/j.1532-5415.2005.53221.x
4. Herrero MJ, Blanch J, Peri JM, De Pablo J, Pintor L, Bulbena A. A validation study of the hospital anxiety and depression scale (HADS) in a Spanish population. Gen Hosp Psychiatry. 2003;25(4):277-283. doi:10.1016/S0163-8343(03)00043-4
5. Abraham A, Pedregosa F, Eickenberg M, et al. Machine learning for neuroimaging with scikit-learn. Front Neuroinform. 2014;8(FEB):1-10. doi:10.3389/fninf.2014.00014

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MDS Abstracts - https://www.mdsabstracts.org/abstract/the-next-move-in-movement-disorders-differentiating-between-hyperkinetic-movement-disorders-using-18f-fdg-pet/