RESUMO
Parkinson's disease is a neurodegenerative condition associated with motor and cognitive impairments. While the execution of dual cognitive-motor tasks imposes a cost on gait velocity, it has been barely determined if the gait deterioration depends on the specific cognitive domain involved in the dual-task. Twenty-four subjects (12 patients with Parkinson's disease and 12 healthy subjects) carried out a single task (gait alone) and several dual tasks where the concurrent second task was the Trail Making Test (Part A) and the six tasks of the Frontal Assessment Battery. Gait variables were measured by accelerometry via smartphone. Data analysis included analysis of variance (ANOVA) and exploratory factorial analysis. Both groups showed a similar gait performance, except for velocity, where patients exhibited a bradykinetic profile. The dual-task during the Trail Making Test showed the highest motor cost. Frontal Assessment Battery's tasks as conceptualization, mental flexibility and motor programming showed a higher motor cost than the other tasks (sensibility to interference, inhibitory control and environmental autonomy). The factorial analysis applied to the motor costs confirmed two profiles, grouping those related to the dorsolateral prefrontal cortex (mental flexibility and motor programming tasks) in an independent factor. Among cognitive functions, attention is critical for gait control in Parkinson's disease and healthy elderly people. The interference posed by several executive operations suggests a specific competition in prefrontal regions that support dual tasks. Moreover, the higher cost for patients with Parkinson's disease patients emphasizes the cognitive decline and compensatory cognitive strategy for gait control related to attention and executive functions.
Assuntos
Doença de Parkinson , Idoso , Cognição , Função Executiva , Marcha , Humanos , Doença de Parkinson/complicaçõesRESUMO
Stroke is a neurological condition that impacts activity performance and quality of life for survivors. While neurological impairments after the event explain the performance of patients in specific activities, the origin of such impairments has traditionally been explained as a consequence of structural and functional damage to the nervous system. However, there are important mechanisms related to energy efficiency (trade-off between biological functions and energy consumption) at different levels that can be related to these impairments and restrictions: first, at the neuronal level, where the availability of energy resources is the initial cause of the event, as well as determines the possibilities of spontaneous recovery. Second, at the level of neural networks, where the "small world" operation of the network is compromised after the stroke, implicating a high energetic cost and inefficiency in the information transfer, which is related to the neurological recovery and clinical status. Finally, at the behavioral level, the performance limitations are related to the highest cost of energy or augmented energy expenditure during the tasks to maintain the stability of the segment, system, body, and finally, the behavior of the patients. In other words, the postural homeostasis. In this way, we intend to provide a synthetic vision of the energy impact of stroke, from the particularities of the operation of the nervous system, its implications, as one of the determinant factors in the possibilities of neurological, functional, and behavioral recovery of our patients.
RESUMO
Surface electromyography (sEMG) has long been used in research, health care, and other fields such as ergonomics and brain-machine interfaces. In health care, sEMG has been employed to diagnose as well as to treat musculoskeletal disorders, pelvic floor dysfunction, and post-stroke motor deficits, among others. Despite the extensive literature on sEMG, the clinical community has not widely adopted it. We believe that in developing countries, such as Chile, this phenomenon may be explained by several interacting barriers. First, the socioeconomics of the country creates an environment where only high cost-effective treatments are routinely applied. Second, the majority of the sEMG literature on clinical applications has not extensively translated into decisive outcomes, which interferes with its applicability in low-income contexts. Third, clinical training on rehabilitation provides inadequate instruction on sEMG. And fourth, accessibility to equipment (i.e., affordability, availability, portability) may constitute another barrier, especially among developing countries. Here, we analyze socio-economic indicators of health care in Chile and comment on current literature about the use of sEMG in rehabilitation. Then we analyze the curricula of several physical therapy schools in Chile and report some estimations of the training on sEMG. Finally, we analyze the accessibility of some available sEMG devices and show that several match predefined criteria. We conclude that in developing countries, the insufficient use of sEMG in health might be explained by a shortage of evidence showing a crucial role in specific outcomes and the lack of training in rehabilitation-related careers, which interact with local socioeconomic factors that limit the application of these techniques.
RESUMO
Fibrotic disorders are typically characterised by excessive connective tissue and extracellular matrix (ECM) deposition that preclude the normal healing of different tissues. Several skeletal muscle dystrophies are characterised by extensive fibrosis. Among the factors involved in skeletal muscle fibrosis is angiotensin II (Ang-II), a key protein of the renin-angiotensin system (RAS). We previously demonstrated that myoblasts responded to Ang-II by increasing the ECM protein levels mediated by AT-1 receptors, implicating an Ang-II-induced reactive oxygen species (ROS) by a NAD(P)H oxidase-dependent mechanism. In this paper, we show that in myoblasts, Ang-II induced the increase of transforming growth factor beta 1 (TGF-ß1) and connective tissue growth factor (CTGF) expression through its AT-1 receptor. This effect is dependent of the NAD(P)H oxidase (NOX)-induced ROS, as indicated by a decrease of the expression of both pro-fibrotic factors when the ROS production was inhibited via the NOX inhibitor apocynin. The increase in pro-fibrotic factors levels was paralleled by enhanced p38MAPK and ERK1/2 phosphorylation in response to Ang-II. However, only the p38MAPK activity was critical for the Ang-II-induced fibrotic effects, as indicated by the decrease in the Ang-II-induced TGF-ß1 and CTGF expression and fibronectin levels by SB-203580, an inhibitor of the p38MAPK, but not by U0126, an inhibitor of ERK1/2 phosphorylation. Furthermore, we showed that the Ang-II-dependent p38MAPK activation, but not the ERK1/2 phosphorylation, was necessary for the NOX-derived ROS. In addition, we demonstrated that TGF-ß1 expression was required for the Ang-II-induced pro-fibrotic effects evaluated by using SB-431542, an inhibitor of TGF-ßRI kinase activity, and by knocking down TGF-ß1 levels by shRNA technique. These results strongly suggest that the fibrotic response to Ang-II is mediated by the AT-1 receptor and requires the p38MAPK phosphorylation, NOX-induced ROS, and TGF-ß1 expression increase mediated by Ang-II in skeletal muscle cells.