Session Time: 1:45pm-3:15pm
Location: Hall 3FG
Objective: To explore the neuroanatomical correlates of the oculomotor abnormalities in Huntington’s disease (HD) through a 18-FDG PET study
Background: Alterations of the oculomotor function in HD are very common and may be the first manifestation of the disease. The increase of the latency in the saccade initiation, the alteration of the persecution and the decrease of the speed are the more common disturbances and their progression leads to a supranuclear paralysis of the gaze. The neuroanatomical correlates of the oculomotor alterations in HD have not been previously evaluated through a 18-FDG PET study
Methods: Cross-sectional, prospective study of HD-patients in early stage (UHDRS ≥4, TFC 8-13, DCL = 4). The oculomotor function was evaluated through the UHDRS (items: ocular pursuit, saccade initiation, saccade velocity). PET/CT was performed 50 minutes after i.v. injection of 18-FDG on a Philips Gemini TF PET/CT. Brain glucose metabolism analysis, as measured by 18-FDG PET relative standardized uptake value (SUVr), was achieved using the SPM8 and biological parametric mapping (BPM) toolbox. We established correlations between the different items of the oculomotricity and brain metabolism. Results showing p<0.005 (uncorrected) and a minimum extent of k=50 voxels were considered significant.
Results: Forty patients were included, mean age 47±12 years, 26 men, mean CAG 43±3. Total UHDRS 31±15; oculomotricity items 6.3±3. Hypometabolism was observed in relation to the alterations of the oculomotricity in the motor (MA), supplementary motor (SMA) and oculomotor areas (OA), dorsolateral prefrontal cortex (DLPC), anterior and posterior cingulate cortex (ACC, PCC) and cortical visuomotor area (VMA) (areas 4,6,7,8,23,24, Brodmann 46). Saccade initiation was highly associated with DLPC, OA, MA, ACC, PCC and VMA. Ocular pursuit with DLPC, OA and ACC. Velocity decrease was associated with hypometabolism in brain stem nuclei.
Conclusions: The metabolic alterations observed through the study with PET-18FDG draw the circuit that is responsible for the regulation of oculomotor movements, from planning and development to the motivational processes that influence its correct execution.
To cite this abstract in AMA style:J. Perez, S. Martinez Horta, F. Sampedro, J. Pagonabarraga, A. Horta, D. Lopez Mora, A. Lozano, V. Camacho, B. Gomez-Anson, J. Kulisevsky. Neuronal correlates of oculomotor alterations in Huntington’s disease. A 18-FDG PET study [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/neuronal-correlates-of-oculomotor-alterations-in-huntingtons-disease-a-18-fdg-pet-study/. Accessed December 5, 2023.
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MDS Abstracts - https://www.mdsabstracts.org/abstract/neuronal-correlates-of-oculomotor-alterations-in-huntingtons-disease-a-18-fdg-pet-study/