Framework for understanding balance dysfunction in Parkinson's disease

Bernadette Schoneburg, Martina Mancini, Fay Horak, John G Nutt, Bernadette Schoneburg, Martina Mancini, Fay Horak, John G Nutt

Abstract

People with Parkinson's disease (PD) suffer from progressive impairment in their mobility. Locomotor and balance dysfunction that impairs mobility in PD is an important cause of physical and psychosocial disability. The recognition and evaluation of balance dysfunction by the clinician are an essential component of managing PD. In this review, we describe a framework for understanding balance dysfunction in PD to help clinicians recognize patients who are at risk for falling and impaired mobility.

Keywords: Parkinson's disease; balance; gait; posture.

Conflict of interest statement

Relevant conflicts of interest/financial disclosures:

  1. Fay Horak and OHSU have significant financial interests in APDM, a company that might have a commercial interest in the results of this research and technology. This potential conflict of interest has been reviewed and managed by OHSU and the Integrity Oversight Council.

  2. John Nutt serves as a consultant for Neuroderm Ltd, Merck, Elan Pharmaceuticals, Lundbeck Inc, ONO Pharma, SynAgile Crop, Prexa Inc and US World Med. He has received honoraria from the American Academy of Neurology.

© 2013 Movement Disorder Society.

Figures

Figure 1
Figure 1
Framework for balance dysfunction. Summarized here are the four domains that contribute to postural stability including quiet stance, reactive postural adjustments, anticipatory postural adjustments and dynamic balance.
Figure 2
Figure 2
Postural sway during quiet stance. A. Subject standing on a foreceplate that measures fluctuations of CoP (postural sway), B. Health Control subject, C. Subject with early PD with large sway area prior to initiation of treatment, D. Subject before and after DBS in the GPi, demonstrating a reduction in sway area following surgery, E. Subject before and after DBS in the STN, showing no significant change following surgery. (St George, et al, 2011).
Figure 3
Figure 3
Reactive (Automatic) Postural Adjustment. Although the latency is normal, maximum force is reduced and reached more slowly in subjects with PD, especially when OFF. A. Subject standing on forceplate that is translated forward, resulting in backwards body displacement. B. Center of pressure (CoP) displacement associated with dorsiflexion torque in a healthy control subject. C. CoP displacement in a subject with DBS in the GPi illustrates how levodopa and DBS surgery decrease postural response. D. CoP displacement in subject with DBS in STN shows how postural response decreases significantly following surgery.
Figure 4
Figure 4
Lateral anticipatory Postural Adjustments (APA) in preparation for a voluntary step. A. Subject standing on a forceplate stepping forward. B. Healthy control subject. C. Early, untreated PD shows smaller APA and longer latency before stepping foot leaves the ground. D. Example of APA in subject with DBS in the GPi illustrates how levodopa increases APA but after DBS surgery APA decreases, even with levodopa. E. Example of subject with DBS in STN shows how levodopa increases APA, but APA decreases following surgery.
Figure 5
Figure 5
Swing time (as a % of gait cycle) series in a healthy control and in a PD patient under usual walking condition and dual task condition (subtracting backward by 7s). Coefficient of variation (CV=SD/mean) is reported for each condition. (Adapted from Yogev G. et al., European Journal of Neuroscience, 2005)

Source: PubMed

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