Chris Vriend1, Premika S W Boedhoe2, Sonja Rutten3, Henk W Berendse4, Ysbrand D van der Werf5, Odile A van den Heuvel2. 1. Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands Neuroscience Campus Amsterdam, VU/VUMC, Amsterdam, The Netherlands Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands. 2. Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands Neuroscience Campus Amsterdam, VU/VUMC, Amsterdam, The Netherlands. 3. Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands. 4. Neuroscience Campus Amsterdam, VU/VUMC, Amsterdam, The Netherlands Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands. 5. Department of Anatomy & Neurosciences, VU University Medical Center, Amsterdam, The Netherlands Neuroscience Campus Amsterdam, VU/VUMC, Amsterdam, The Netherlands Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.
Abstract
BACKGROUND: Up to 50% of all patients with Parkinson's disease (PD) suffer from anxiety symptoms, a much higher percentage than in the general population. This suggests that PD associated pathological alterations partly underlie these symptoms, although empirical evidence is limited. METHODS: Here we investigated the association between anxiety symptoms measured with the Beck Anxiety Inventory (BAI) and hippocampal and amygdalar volume in 110 early-stage patients with PD. Measures of anxiety in PD are often obscured by overlap with the somatic symptoms. We therefore also used a subscale of the BAI, established by our recent factor analysis, that reflects 'psychological' anxiety symptoms and is independent of the severity of PD-related motor and autonomic symptoms. We used FreeSurfer and voxel-based morphometry for the volumetric analyses. RESULTS: Both software packages showed a negative correlation between the 'psychological' subscale of the BAI, but not total BAI and volume of the left amygdala, independent of the severity of motor symptoms, autonomic dysfunction and dopaminergic or anxiolytic medication status. CONCLUSIONS: These results confirm studies in non-PD samples showing lower left amygdalar volume in anxious patients. The results also indicate that the 'psychological' BAI subscale is a better reflection of neural correlates of anxiety in PD. Whether the left amygdalar volume decrease constitutes a premorbid trait, a PD-associated neurobiological susceptibility to anxiety or arises as a consequence of chronic anxiety symptoms remains to be determined by future prospective longitudinal studies. Nonetheless, we speculate that the Parkinson pathology is responsible for the reduction in amygdalar volume and the concomitant development of anxiety symptoms. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
BACKGROUND: Up to 50% of all patients with Parkinson's disease (PD) suffer from anxiety symptoms, a much higher percentage than in the general population. This suggests that PD associated pathological alterations partly underlie these symptoms, although empirical evidence is limited. METHODS: Here we investigated the association between anxiety symptoms measured with the Beck Anxiety Inventory (BAI) and hippocampal and amygdalar volume in 110 early-stage patients with PD. Measures of anxiety in PD are often obscured by overlap with the somatic symptoms. We therefore also used a subscale of the BAI, established by our recent factor analysis, that reflects 'psychological' anxiety symptoms and is independent of the severity of PD-related motor and autonomic symptoms. We used FreeSurfer and voxel-based morphometry for the volumetric analyses. RESULTS: Both software packages showed a negative correlation between the 'psychological' subscale of the BAI, but not total BAI and volume of the left amygdala, independent of the severity of motor symptoms, autonomic dysfunction and dopaminergic or anxiolytic medication status. CONCLUSIONS: These results confirm studies in non-PD samples showing lower left amygdalar volume in anxiouspatients. The results also indicate that the 'psychological' BAI subscale is a better reflection of neural correlates of anxiety in PD. Whether the left amygdalar volume decrease constitutes a premorbid trait, a PD-associated neurobiological susceptibility to anxiety or arises as a consequence of chronic anxiety symptoms remains to be determined by future prospective longitudinal studies. Nonetheless, we speculate that the Parkinson pathology is responsible for the reduction in amygdalar volume and the concomitant development of anxiety symptoms. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
Authors: Silvia Mangia; Alena Svatkova; Daniele Mascali; Mikko J Nissi; Philip C Burton; Petr Bednarik; Edward J Auerbach; Federico Giove; Lynn E Eberly; Michael J Howell; Igor Nestrasil; Paul J Tuite; Shalom Michaeli Journal: Front Neurosci Date: 2017-12-19 Impact factor: 4.677
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