BackgroundOver the last two decades, various measures of entropy have been used to examine the complexity of human postural control. In general, entropy measures provide information regarding the health, stability and adaptability of the postural system that is not captured when using more traditional analytical techniques. The purpose of this study was to examine how noise, sampling frequency and time series length influence various measures of entropy when applied to human center of pressure (CoP) data, as well as in synthetic signals with known properties. Such a comparison is necessary to interpret data between and within studies that use different entropy measures, equipment, sampling frequencies or data collection durations.Methods and FindingsThe complexity of synthetic signals with known properties and standing CoP data was calculated using Approximate Entropy (ApEn), Sample Entropy (SampEn) and Recurrence Quantification Analysis Entropy (RQAEn). All signals were examined at varying sampling frequencies and with varying amounts of added noise. Additionally, an increment time series of the original CoP data was examined to remove long-range correlations. Of the three measures examined, ApEn was the least robust to sampling frequency and noise manipulations. Additionally, increased noise led to an increase in SampEn, but a decrease in RQAEn. Thus, noise can yield inconsistent results between the various entropy measures. Finally, the differences between the entropy measures were minimized in the increment CoP data, suggesting that long-range correlations should be removed from CoP data prior to calculating entropy.ConclusionsThe various algorithms typically used to quantify the complexity (entropy) of CoP may yield very different results, particularly when sampling frequency and noise are different. The results of this study are discussed within the context of the neural noise and loss of complexity hypotheses.
Growing evidence demonstrates that aging not only leads to structural and functional alterations of individual components of the neuro-musculo-skeletal system (NMSS) but also results in a systemic re-organization of interactions within and between the different levels and functional domains. Understanding the principles that drive the dynamics of these re-organizations is an important challenge for aging research. The present Hypothesis and Theory paper is a contribution in this direction. We propose that age-related declines in brain and behavior that have been characterized in the literature as dedifferentiation and the loss of complexity (LOC) are: (i) synonymous; and (ii) integrated. We argue that a causal link between the aforementioned phenomena exists, evident in the dynamic changes occurring in the aging NMSS. Through models and methods provided by a dynamical systems approach to coordination processes in complex living systems, we: (i) formalize operational hypotheses about the general principles of changes in cross-level and cross-domain interactions during aging; and (ii) develop a theory of the aging NMSS based on the combination of the frameworks of coordination dynamics (CD), dedifferentiation, and LOC. Finally, we provide operational predictions in the study of aging at neural, muscular, and behavioral levels, which lead to testable hypotheses and an experimental agenda to explore the link between CD, LOC and dedifferentiation within and between these different levels.
Motor dysfunction is a consistently reported but understudied aspect of schizophrenia. Postural sway area was examined in individuals with schizophrenia under four conditions with different amounts of visual and proprioceptive feedback: eyes open or closed and feet together or shoulder width apart. The nonlinear complexity of postural sway was assessed by detrended fluctuation analysis (DFA). The schizophrenia group (n = 27) exhibited greater sway area compared to controls (n = 37). Participants with schizophrenia showed increased sway area following the removal of visual input, while this pattern was absent in controls. Examination of DFA revealed decreased complexity of postural sway and abnormal changes in complexity upon removal of visual input in individuals with schizophrenia. Additionally, less complex postural sway was associated with increased symptom severity in participants with schizophrenia. Given the critical involvement of the cerebellum and related circuits in postural stability and sensorimotor integration, these results are consistent with growing evidence of motor, cerebellar, and sensory integration dysfunction in the disorder, and with theoretical models that implicate cerebellar deficits and more general disconnection of function in schizophrenia.
This paper seeks to present a new perspective on the aging brain. Here, we make connections between two key phenomena of brain aging: (1) increased neural noise or random background activity; and (2) slowing of brain activity. Our perspective proposes the possibility that the slowing of neural processing due to decreasing nerve conduction velocities leads to a compensatory speeding of neuron firing rates. These increased firing rates lead to a broader distribution of power in the frequency spectrum of neural oscillations, which we propose, can just as easily be interpreted as neural noise. Compensatory speeding of neural activity, as we present, is constrained by the: (A) availability of metabolic energy sources; and (B) competition for frequency bandwidth needed for neural communication. We propose that these constraints lead to the eventual inability to compensate for age-related declines in neural function that are manifested clinically as deficits in cognition, affect, and motor behavior.
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