Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/19360
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dc.contributor.authorPerera, Thushara-
dc.contributor.authorTan, Joy L-
dc.contributor.authorCole, Michael H-
dc.contributor.authorYohanandan, Shivy A C-
dc.contributor.authorSilberstein, Paul-
dc.contributor.authorCook, Raymond-
dc.contributor.authorPeppard, Richard-
dc.contributor.authorAziz, Tipu-
dc.contributor.authorCoyne, Terry-
dc.contributor.authorBrown, Peter-
dc.contributor.authorSilburn, Peter A-
dc.contributor.authorThevathasan, Wesley-
dc.date2018-08-24-
dc.date.accessioned2018-09-17T01:47:01Z-
dc.date.available2018-09-17T01:47:01Z-
dc.date.issued2018-08-24-
dc.identifier.citationBrain : a journal of neurology 2018; 141(10): 3009-3022-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/19360-
dc.description.abstractImpaired balance is a major contributor to falls and diminished quality of life in Parkinson's disease, yet the pathophysiology is poorly understood. Here, we assessed if patients with Parkinson's disease and severe clinical balance impairment have deficits in the intermittent and continuous control systems proposed to maintain upright stance, and furthermore, whether such deficits are potentially reversible, with the experimental therapy of pedunculopontine nucleus deep brain stimulation. Two subject groups were assessed: (i) 13 patients with Parkinson's disease and severe clinical balance impairment, implanted with pedunculopontine nucleus deep brain stimulators; and (ii) 13 healthy control subjects. Patients were assessed in the OFF medication state and blinded to two conditions; off and on pedunculopontine nucleus stimulation. Postural sway data (deviations in centre of pressure) were collected during quiet stance using posturography. Intermittent control of sway was assessed by calculating the frequency of intermittent switching behaviour (discontinuities), derived using a wavelet-based transformation of the sway time series. Continuous control of sway was assessed with a proportional-integral-derivative (PID) controller model using ballistic reaction time as a measure of feedback delay. Clinical balance impairment was assessed using the 'pull test' to rate postural reflexes and by rating attempts to arise from sitting to standing. Patients with Parkinson's disease demonstrated reduced intermittent switching of postural sway compared with healthy controls. Patients also had abnormal feedback gains in postural sway according to the PID model. Pedunculopontine nucleus stimulation improved intermittent switching of postural sway, feedback gains in the PID model and clinical balance impairment. Clinical balance impairment correlated with intermittent switching of postural sway (rho = - 0.705, P < 0.001) and feedback gains in the PID model (rho = 0.619, P = 0.011). These results suggest that dysfunctional intermittent and continuous control systems may contribute to the pathophysiology of clinical balance impairment in Parkinson's disease. Clinical balance impairment and their related control system deficits are potentially reversible, as demonstrated by their improvement with pedunculopontine nucleus deep brain stimulation.-
dc.language.isoeng-
dc.titleBalance control systems in Parkinson's disease and the impact of pedunculopontine area stimulation.-
dc.typeJournal Article-
dc.identifier.journaltitleBrain : a journal of neurology-
dc.identifier.affiliationDepartment of Medicine, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationMedical Research Council Brain Network Dynamics Unit, University of Oxford, Oxford OX1 3TH, UKen
dc.identifier.affiliationDepartment of Neurology, The Royal Melbourne Hospital, Victoria, Australiaen
dc.identifier.affiliationThe Bionics Institute, East Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medical Bionics, The University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationSchool of Exercise Science, Australian Catholic University, Brisbane, Queensland, Australiaen
dc.identifier.affiliationRoyal North Shore and North Shore Private Hospitals, Sydney, New South Wales, Australiaen
dc.identifier.affiliationClinical Neurosciences, St Vincent's Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationNuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford OX1 3TH, UKen
dc.identifier.affiliationAsia-Pacific Centre for Neuromodulation, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australiaen
dc.identifier.affiliationDepartment of Neurology, Austin Health, Heidelberg, Victoria, Australia-
dc.identifier.doi10.1093/brain/awy216-
dc.identifier.pubmedid30165427-
dc.type.austinJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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