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Published on: September 12, 2020
The cholinergic system is involved in cervical dystonia - An [18F]FEOBV PET study
S A J E A Lagerweij1, J R Dalenberg2, M Smit2
1Department of Neurology, University Medical Center Groningen (UMCG), University of Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands; UMCG Expertise Center Movement Disorders Groningen, University Medical Center Groningen (UMCG), Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Background:
Cervical dystonia (CD) is a movement disorder characterized by involuntary muscle contractions that result in abnormal head postures and movements. In addition to motor symptoms, CD patients frequently experience non-motor symptoms such as cognitive impairment, anxiety, depression, and reduced quality of life (QoL). The cholinergic system is believed to contribute to dystonia pathophysiology, as supported by the clinical effectiveness of anticholinergic treatments. However, in vivo evidence of cholinergic dysfunction in CD is limited.
Objectives:
This study aimed to assess presynaptic cholinergic activity in CD patients using [18F]FEOBV PET imaging and to explore associations between cholinergic binding and motor and non-motor symptoms.
Methods:
Thirteen CD patients and thirteen matched controls underwent [18F]FEOBV PET scans. Clinical evaluations included the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS), neuropsychological testing (assessing memory, information processing speed, and executive functioning), and validated questionnaires measuring depression, anxiety, and QoL. Group differences in [18F]FEOBV binding were analyzed using volume of interest (VOI) and voxel-based approaches. Correlation analyses explored relationships between regional binding and clinical measures.
Results:
CD patients showed poorer cognitive performance, higher anxiety and depression levels, and lower QoL compared to controls. VOI and voxel-based analyses demonstrated increased [18F]FEOBV binding in the right cerebellar lobes III and IV-V in CD patients. No correlations were found between binding and motor severity, but modest associations emerged with non-motor symptoms.
Conclusions:
These results suggest altered cerebellar cholinergic function in CD, potentially contributing to non-motor symptomatology. Further studies are needed to clarify cholinergic mechanisms in CD.
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