Murdoch University Research Repository

Welcome to the Murdoch University Research Repository

The Murdoch University Research Repository is an open access digital collection of research
created by Murdoch University staff, researchers and postgraduate students.

Learn more

Cholinergic deficits contribute to impaired postural control in early Parkinson's disease

Yarnall, A.J., Del Din, S., David, R., Galna, B.ORCID: 0000-0002-5890-1894, Baker, M.R., Burn, D.J. and Rochester, L. (2014) Cholinergic deficits contribute to impaired postural control in early Parkinson's disease. In: 18th International Congress of Parkinson's Disease and Movement Disorders, 8-12 June 2014, Stockholm, Sweden.

Abstract

[Poster]

Objective: To determine whether impaired postural control is associated with cholinergic dysfunction in early Parkinson's disease (PD).

Background: Impaired postural control is present even in early PD, and is an important determinant of impaired mobility and falls risk. Postural impairment is underpinned by complex, multisystem pathophysiology. While basal ganglia pathology and associated dopaminergic denervation are key contributors, recent work also implicates cholinergic degeneration in impaired postural control.

Methods: Short latency afferent inhibition (SAI), a proxy measure of cholinergic activity, and postural control were measured in 42 subjects with early PD (mean age 70.1 ± 9.9 years) and 38 age-matched controls (68.7 ± 8.4 years) as part of the ICICLE-PD study. SAI was determined by conditioning motor evoked potentials, elicited by transcranial magnetic stimulation of the motor cortex, with electrical stimuli delivered to the contralateral median nerve at intervals ranging from N20 (predetermined) to N20+4ms. Postural control was measured during two minutes of quiet standing with eyes open. Force plates were used to quantify sway, from which mean speed of the centre of pressure (CoP) in the anterior-posterior (AP) and medio-lateral (ML) direction were determined. Partial correlations, controlling for age and cognition, were used to explore relationships between SAI and postural control.

Results: SAI was significantly reduced in PD participants compared to controls (76.7 + 28.8% vs. 58.5 + 22.4%), indicating greater cholinergic dysfunction. There was no difference in postural control outcomes between the groups. In PD but not control participants, increased speed of movement of the CoP in the AP and ML direction (impaired postural control) was significantly associated with reduced SAI (cholinergic dysfunction), and this remained significant after controlling for age and cognition (r=0.565, p=0.008; r=0.632, p=0.002, respectively).

Conclusions: Our findings suggest that in PD cholinergic dysfunction contributes to postural impairment even in early disease. This study provides insights into non-dopaminergic mechanisms and suggests that therapies targeting acetylcholine may be useful for the treatment of impaired postural control in PD.

Item Type: Conference Item
Conference Website: https://www.mdscongress.org/Congress-2014.htm
Other Information: Part of: Movement Disorders (2015), Volume: 29, Issue: Suppl 1, S332, ISSN: 1531-8257. https://doi.org/10.1002/mds.25914
URI: http://researchrepository.murdoch.edu.au/id/eprint/63021
Item Control Page Item Control Page