Visual deprivation elicits subclinical postural inflexibilities in early Parkinson's disease

Panyakaew, Pattamon; Anan, Chanawat; Bhidayasiri, Roongroj

doi:10.1016/j.jns.2015.01.022

Cited by 21 publications

(21 citation statements)

References 44 publications

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“…However, many studies emphasized the emergence of postural instability in PD especially in the frontal plane [12, 40]. Some even believe in the assessment of mediolateral direction as an early detector of PD [1, 47]. Furthermore, our model lacks passive stiffness and damping of the ankle joint.…”

Section: Discussionmentioning

confidence: 99%

Disentangling stability and flexibility degrees in Parkinson’s disease using a computational postural control model

Rahmati

Schouten

Behzadipour

et al. 2019

J NeuroEngineering Rehabil

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Background Impaired postural control in Parkinson’s disease (PD) seriously compromises life quality. Although balance training improves mobility and postural stability, lack of quantitative studies on the neurophysiological mechanisms of balance training in PD impedes the development of patient-specific therapies. We evaluated the effects of a balance-training program using functional balance and mobility tests, posturography, and a postural control model. Methods Center-of-pressure (COP) data of 40 PD patients before and after a 12-session balance-training program, and 20 healthy control subjects were recorded in four conditions with two tasks on a rigid surface (R-tasks) and two on foam. A postural control model was fitted to describe the posturography data. The model comprises a neuromuscular controller, a time delay, and a gain scaling the internal disturbance torque. Results Patients’ axial rigidity before training resulted in slower COP velocity in R-tasks; which was reflected as lower internal torque gain. Furthermore, patients exhibited poor stability on foam, remarked by abnormal higher sway amplitude. Lower control parameters as well as higher time delay were responsible for patients’ abnormal high sway amplitude. Balance training improved all clinical scores on functional balance and mobility. Consistently, improved ‘flexibility’ appeared as enhanced sway velocity (increased internal torque gain). Balance training also helped patients to develop the ‘stability degree’ (increase control parameters), and to respond more quickly in unstable condition of stance on foam. Conclusions Projection of the common posturography measures on a postural control model provided a quantitative framework for unraveling the neurophysiological factors and different recovery mechanisms in impaired postural control in PD. Electronic supplementary material The online version of this article (10.1186/s12984-019-0574-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Disentangling stability and flexibility degrees in Parkinson’s disease using a computational postural control model

Rahmati

Schouten

Behzadipour

et al. 2019

J NeuroEngineering Rehabil

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“…Bronstein et al [23] also demonstrated that patients with PD exhibited a larger body sway magnitude response when exposed to displacements of the visual environment than other patients, suggesting that patients with PD have an abnormal reliance on visual information for postural control. Following these studies, several reports have suggested that patients with PD are more dependent on visual information, which leads to difficulties in performing certain motor tasks [26–29], most likely to compensate for poor and less informative somatosensory cues [30]. Conversely, visual cues have been used to improve motor performance, particularly gait, as a typical therapeutic approach to minimize the lack of automatic control [31].…”

Section: Introductionmentioning

confidence: 99%

Parkinson’s disease does not alter automatic visual-motor coupling in postural control

Cruz

Piemonte

Okai-Nóbrega

et al. 2018

Neuroscience Letters

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This study examined the coupling between visual information and body sway in patients with Parkinson's disease (PD) compared with healthy controls. Postural control performance was compared between 14 patients with PD (age: 69.6 ± 8.8 years - stages 1-3 of the Hoehn and Yahr scale) and 14 healthy control participants (age: 68.6 ± 3.0 years). Participants stood upright in a moving room that remained motionless or continuously oscillated in the anterior-posterior direction. Ten trials were performed in the following conditions: no movement of the room (1 trial) and with the room moving at frequencies of 0.1, 0.17, and 0.5 Hz (3 trials each frequency). Body sway and moving room displacement were recorded. The results indicated that patients with PD displayed larger body sway magnitude in the stationary room condition. Body sway of patients with PD was induced by visual manipulation in all three visual stimulus frequencies, but body sway of patients with PD was less coherent compared to that of the control participants. However, no difference was observed in the visual-body sway coupling structure. These results indicate that patients with PD can unconsciously couple body sway to visual information in order to control postural sway in a similar manner to healthy participants with intact visual-motor coupling for posture control. However, this coupling is marked by greater variability, indicating that people with PD have a motor system with greater inherent noise leading to a more varied behavior.

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“…Gait and postural disturbances are present but can be subtle, which will eventually affect all PD patients as the disease progresses [35,36]. In addition, visual dependency exists in early PD, which can help identify subclinical postural instability [37]. During later stages of PD, notable clinical challenges, such as levodopa-induced dyskinesias, rigidity, tremor, and medication on-off phenomena, become more prevalent [38].…”

Section: Discussionmentioning

confidence: 99%

Human Basic Fibroblast Growth Factor Inhibits Tau Phosphorylation via the PI3K/Akt-GSK3β Signaling Pathway in a 6-Hydroxydopamine-Induced Model of Parkinson's Disease

Yang¹,

Zhu²,

Huang³

et al. 2016

Neurodegener Dis

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Background: Basic fibroblast growth factor (bFGF) has been increasingly investigated due to its neuroprotection in neurodegenerative disorders. Because there are still no cures for any of these disorders, it is crucial to identify new therapeutic targets and screen potential drugs. The increased phosphorylation of tau at Ser³⁹⁶ leads to intracellular tau accumulation, which forms neurofibrillary tangles in Parkinson's disease (PD). In this study, neuroprotection by bFGF was observed, and the mechanisms related to its regulation of phosphorylated tau were investigated. Methods: bFGF-loaded liposome carriers were intranasally administered to rats. The neuroprotective effects of bFGF were assessed in a PD model induced by 6-hydroxydopamine (6-OHDA) in vivo and in vitro. The phosphorylation of tau was measured, and the PI3K/Akt-GSK3β signaling pathway was investigated. Results: Our study demonstrated that liposomes markedly assisted in the delivery of bFGF to the striatum and substantia nigra of rats and enhanced the neuroprotective effects of bFGF on dopaminergic neurons. bFGF treatment significantly ameliorated the behavioral deficits induced by 6-OHDA, rescued the loss of tyrosine hydroxylase-positive neurons and increased the number of Nissl bodies. bFGF reduced the phosphorylation of tau and GSK3β and increased the phosphorylation of PI3K/Akt. Conclusion: Liposomes markedly assisted in the delivery of bFGF to the brain and enhanced the neuroprotective effects of bFGF by inhibiting the phosphorylation of tau. bFGF down-regulated the phosphorylation of tau by increasing the phosphorylation of GSK3β via the PI3K/Akt signaling pathway. These findings provide a new vision of bFGF as a potential therapy for PD.

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Visual deprivation elicits subclinical postural inflexibilities in early Parkinson's disease

Cited by 21 publications

References 44 publications

Disentangling stability and flexibility degrees in Parkinson’s disease using a computational postural control model

Disentangling stability and flexibility degrees in Parkinson’s disease using a computational postural control model

Parkinson’s disease does not alter automatic visual-motor coupling in postural control

Human Basic Fibroblast Growth Factor Inhibits Tau Phosphorylation via the PI3K/Akt-GSK3β Signaling Pathway in a 6-Hydroxydopamine-Induced Model of Parkinson's Disease

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