Publications

STUDY DESIGN: Between-session reliability of a magnetic resonance imaging (MRI) based experimental technique to quantify lumbar inter-vertebral motion in humans. PURPOSE: We have developed a novel, dynamic, MRI-based approach for quantifying in vivo lumbar inter-vertebral motion. In this study, we present the protocol's reliability results to quantify inter-vertebral spine motion. OVERVIEW OF LITERATURE: Morphometric studies on intervertebral displacements using static, supine MRI and quantification of dynamic spine motion using different X-ray based radiography techniques are commonly found in the literature. However, reliability testing of techniques assessing real-time lumbar intervertebral motion using weight-bearing MRI has rarely been reported. METHODS: Ten adults without a history of back pain performed a side-bending task on two separate occasions, inside an open-MRI, in a weight-bearing, upright position. The images were acquired during the task using a dynamic magnetic resonance (MR) sequence. The MRI imaging space was externally calibrated before the study to recreate the imaging volume for subsequent use in an animation software. The dynamic MR images were processed to create side-bending movement animations in the virtual environment. Participant-specific three-dimensional models were manually superimposed over vertebral image silhouettes in a sequence of image frames, representing the motion trials. Inter-vertebral axes and translation and rotational displacements of vertebrae were quantified using the animation software. RESULTS: Quantification of inter-vertebral rotations and translations shows high reliability. Between-session reliability results yielded high values for the intra-class correlation coefficient (0.86-0.93), coefficient of variation (13.3%-16.04%), and Pearson's correlation coefficients (0.89-0.98). CONCLUSIONS: This technique may be developed further to improve its speed and accuracy for diagnostic applications, to study in vivo spine stability, and to assess outcomes of surgical and non-surgical interventions applied to manage pathological spine motion.

BACKGROUND: Motoric cognitive risk (MCR) syndrome is characterized by slow gait and memory complaints that could be used to predict an increased risk of dementia. This study aims to determine the MCR syndrome and its risk factors among low-income (B40) older adults in Malaysia. METHODS: Data from TUA cohort study involving 1366 older adults (aged 60 years and above) categorized as low-income were analysed, for risk of MCR syndrome based on defined criteria. Chi-square analysis and independent t test were employed to examine differences in socioeconomic, demographic, chronic diseases and lifestyle factors between MCR and non-MCR groups. Risk factors of MCR syndrome were determined using hierarchical logistic regression. RESULTS: A total of 3.4% of participants fulfilled the criteria of MCR syndrome. Majority of them were female (74.5%, p = 0.001), single/widow/widower/divorced (55.3%, p = 0.002), living in rural area (72.3%, p = 0.011), older age (72.74 +/- 7.08 year old, p 0.001) and had lower years of education (3.26 +/- 2.91 years, p = 0.001) than non-MCR group. After adjustment for age, gender and years of education, participants living in rural area (Adjusted OR = 2.19, 95% CI = 1.10-4.35, p = 0.026), with obesity (Adjusted OR = 3.82, 95% CI = 1.70-8.57, p = 0.001), diabetes (Adjusted OR = 2.04, 95% CI = 1.01-4.11, p = 0.046), heart disease (Adjusted OR = 2.50, 95% CI = 1.00-6.20, p = 0.049) and cancer (Adjusted OR = 6.57, 95% CI = 1.18-36.65, p = 0.032) were associated with increased risk of MCR syndrome. CONCLUSION: Only 3.4% of older adults from low-income group were identified as having MCR syndrome. Women, those living in rural areas, had obesity, diabetes, heart disease and cancer were more likely to have MCR syndrome. Further investigation on MCR as a predementia syndrome will help in development of preventive strategies and interventions to reduce the growing burden of dementia, especially among individuals with low socioeconomic status.

The capacity to move is essential for independence and declines with age. Limitations in mobility impact  35% of adults over 70 and the majority of adults over 85. These limitations are highly associated with disability, dependency, and survival. More than 25-years ago the term "sarcopenia" was coined to highlight the age-related loss of muscle mass and strength with the assumption being that sarcopenia led to limitations in mobility. However, contrary to expectations, recent findings clearly indicate these variables only modestly explain limitations in mobility. One likely reason the current sarcopenia variables of muscle mass and strength do not discriminate, or predict, mobility limitations well is because they are heavily influenced by musculoskeletal mechanisms and do not incorporate measures reflective of the central neural control of mobility. Unfortunately, the precise central neural changes associated with aging that lead to decreased mobility are poorly understood. This knowledge gap has hampered the development of effective interventions for mobility limitations and the subsequent reduction of major functional disability for older adults. Here, we discuss the potential role of the motor control circuit of the dorsal basal ganglia as well as dopaminergic function in age-related reductions in mobility.

This cross-sectional study compares voluntary neural activation of lower extremity muscles in clinically weak older adults vs stronger older adults.

Sarcopenia was originally conceptualized as the age-related loss of skeletal muscle mass. Over the ensuing decades, the conceptual definition of sarcopenia has changed to represent a condition in older adults that is characterized by declining muscle mass and function, with "function" most commonly conceived as muscle weakness and/or impaired physical performance (e.g., slow gait speed). Findings over the past 15-years, however, have demonstrated that changes in grip and leg extensor strength are not primarily due to muscle atrophy per se, and that to a large extent, are reflective of declines in the integrity of the nervous system. This article briefly summarizes findings relating to the complex neuromuscular mechanisms that contribute to reductions in muscle function associated with advancing age, and the implications of these findings on the development of effective therapies.

PURPOSE: The goal of this trial was to determine whether low-load blood flow-restricted (BFR) exercise of appendicular muscles induces a cross-transfer of effect to the trunk extensor (TE) muscles, such that low-load TE exercise would enhance TE size and function to a greater extent than standard low-load exercise in people with recurrent low back pain (LBP). We also investigated the direct effects of BFR exercise in the appendicular muscles. METHODS: Thirty-two adults with recurrent, nonspecific LBP were randomized into two groups: Appendicular BFR exercise (BFR exercise) or control exercise (CON exercise). All participants trained (two times per week) for 10 wk, with a 12-wk follow-up. Participants performed three sets of leg extension (LE), plantar flexion (PF), and elbow flexion (EF) exercises followed by low-load TE exercise without BFR. Outcome measures included magnetic resonance imaging-derived muscle size (quadriceps and TE), strength (LE, PF, EF, and TE), and endurance (LE and TE). RESULTS: There was no evidence for a cross-transfer of effect to the TE. There was also no statistically significant enhancement of limb skeletal muscle size or function of BFR relative to CON exercise at any time point; though, moderate effect sizes for BFR exercise were observed for enhanced muscle size and strength in the leg extensors. CONCLUSIONS: Low-load BFR exercise of the appendicular muscles did not result in a cross-transfer of effect to the TE musculature. There was also no significant benefit of low-load BFR exercise on the appendicular muscle size and function, suggesting no benefit from low-load BFR exercise in adults with recurrent, nonspecific LBP.

To reduce disability and dependence in older adults, frailty may represent an appropriate target for intervention. While preventing frailty through lifestyle interventions may be the optimal public health approach for many population groups, pharmacological approaches will likely be needed for individuals who meet frailty criteria or who have comorbid conditions that contribute to and complicate the frailty syndrome, and for those who are not compliant with lifestyle interventions. Barriers to successful development of drug treatments for frailty include variability in how the frailty syndrome is defined, lack of agreement on the best diagnostic tools and outcome measures, and the paucity of sensitive, reliable, and validated biomarkers. The International Conference on Frailty and Sarcopenia Research Task Force met in Miami, Florida, on February 28, 2018, to consider the status of treatments under development for frailty and discuss potential strategies for advancing the field. They concluded that at the present time, there may be a more productive regulatory pathway for adjuvant treatments or trials targeting specific functional outcomes such as gait speed. They also expressed optimism that several studies currently underway may provide the insight needed to advance drug development for frailty.

Research suggests that poor nutrition is an underlying cause of sarcopenia and frailty, and that dietary interventions may prevent or treat age-related loss of muscle mass and strength. In February 2018, the International Conference on Frailty and Sarcopenia Research Task Force explored the current status of research on nutritional interventions for sarcopenia as well as gaps in knowledge, including whether nutritional supplements must be combined with physical activity, and the role of nutritional intervention in sarcopenic obese individuals. The lack of consistency across trials in terms of target populations, assessments, health-care settings, control groups, and choice of outcomes has made it difficult to draw meaningful conclusions from recent studies. The Task Force recommended large randomized controlled trials in heterogeneous, real-world populations to enable sub-group analysis. The field also needs to reach consensus on what outcomes are most meaningful and what represents clinically meaningful change.

OBJECTIVES: Sarcopenia, defined as an age-associated loss of skeletal muscle function and muscle mass, occurs in approximately 6 - 22 % of older adults. This paper presents evidence-based clinical practice guidelines for screening, diagnosis and management of sarcopenia from the task force of the International Conference on Sarcopenia and Frailty Research (ICSFR). METHODS: To develop the guidelines, we drew upon the best available evidence from two systematic reviews paired with consensus statements by international working groups on sarcopenia. Eight topics were selected for the recommendations: (i) defining sarcopenia; (ii) screening and diagnosis; (iii) physical activity prescription; (iv) protein supplementation; (v) vitamin D supplementation; (vi) anabolic hormone prescription; (vii) medications under development; and (viii) research. The ICSFR task force evaluated the evidence behind each topic including the quality of evidence, the benefit-harm balance of treatment, patient preferences/values, and cost-effectiveness. Recommendations were graded as either strong or conditional (weak) as per the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. Consensus was achieved via one face-to-face workshop and a modified Delphi process. RECOMMENDATIONS: We make a conditional recommendation for the use of an internationally accepted measurement tool for the diagnosis of sarcopenia including the EWGSOP and FNIH definitions, and advocate for rapid screening using gait speed or the SARC-F. To treat sarcopenia, we strongly recommend the prescription of resistance-based physical activity, and conditionally recommend protein supplementation/a protein-rich diet. No recommendation is given for Vitamin D supplementation or for anabolic hormone prescription. There is a lack of robust evidence to assess the strength of other treatment options.