David R. Dolbow

Emanating from several decades of study into the effects of the aging process after spinal cord injury (SCI), “accelerated aging” has become a common expression as the SCI accelerates the onset of age-related pathologies. However, the aging process follows a distinct trajectory, characterized by unique patterns of decline that differ from those observed in the general population without SCI. Aging brings significant changes to muscles, bones, and hormones, impacting overall physical function. Muscle mass and strength begin to decrease with a reduction in muscle fibers and impaired repair mechanisms. Bones become susceptible to fractures as bone density decreases. Hormonal changes combined with decreased physical activity accelerate the reduction of muscle mass and increase in body fat. Muscle atrophy and skeletal muscle fiber type transformation occur rapidly and in a unique pattern after SCI. Bone loss develops more rapidly and results in an increased risk of fractures in body regions unique to individuals with SCI. Other factors, such as excessive adiposity, decreased testosterone and human growth hormone, and increased systemic inflammation, contribute to a higher risk of neuropathically driven obesity, dyslipidemia, glucose intolerance, insulin resistance, and increasing cardiovascular disease risk. Cardiorespiratory changes after SCI result in lower exercise heart rates, decreased oxygenation, and mitochondrial dysfunction. While it is important to acknowledge the accelerated aging processes after SCI, it is essential to recognize the distinct differences in the aging process between individuals without physical disabilities and those with SCI. These differences, influenced by neuropathology, indicate that it may be more accurate to describe the aging process in individuals with chronic SCI as neurogenic accelerated aging (NAA). Research should continue to address conditions associated with NAA and how to ameliorate the accelerated rate of premature age-related conditions. This review focuses on the NAA processes and the differences between them and the aging process in those without SCI. Recommendations are provided to help slow the development of premature aging conditions.

Background: Patellofemoral pain is one of the most common injuries in recreational runners, with significant implications for dynamic knee valgus. The knee valgus angle can be corrected surgically or with a more conservative non-operative approach. Increasing running cadence may be an effective biomechanical gait retraining intervention to reduce knee valgus and thus patellofemoral pain. The primary purpose of this study was to examine if an increase in cadence could change the knee valgus angle. Methods: Ten asymptomatic recreational runners were recorded running on a treadmill during control and experimental intervals. Each interval lasted five minutes, and participants ran at 100% and 110% of their baseline cadence. Peak angles of knee valgus were compared between both intervals using the video analysis software application Dartfish Express. A paired sample, a two-tailed t-test, was used to determine the significant difference between bilateral frontal plane knee angle measurements during both intervals. Results: The average decrease in knee valgus measured in control versus experimental intervals was 2.23° for the right leg and 2.05° for the left leg, with a significance of p < 0.001 and p < 0.001, respectively. Conclusion: The results indicated a statistically significant decrease in angles of dynamic knee valgus, attributable to increased cadence. These changes in knee valgus angle are likely to have a positive impact on preventing and reducing pain associated with PFP.

Emanating from several decades of study into the effects of the aging process after spinal cord injury (SCI), "accelerated aging" has become a common expression as the SCI accelerates the onset of age-related pathologies. However, the aging process follows a distinct trajectory, characterized by unique patterns of decline that differ from those observed in the general population without SCI. Aging brings significant changes to muscles, bones, and hormones, impacting overall physical function. Muscle mass and strength begin to decrease with a reduction in muscle fibers and impaired repair mechanisms. Bones become susceptible to fractures as bone density decreases. Hormonal changes combined with decreased physical activity accelerate the reduction of muscle mass and increase in body fat. Muscle atrophy and skeletal muscle fiber type transformation occur rapidly and in a unique pattern after SCI. Bone loss develops more rapidly and results in an increased risk of fractures in body regions unique to individuals with SCI. Other factors, such as excessive adiposity, decreased testosterone and human growth hormone, and increased systemic inflammation, contribute to a higher risk of neuropathically driven obesity, dyslipidemia, glucose intolerance, insulin resistance, and increasing cardiovascular disease risk. Cardiorespiratory changes after SCI result in lower exercise heart rates, decreased oxygenation, and mitochondrial dysfunction. While it is important to acknowledge the accelerated aging processes after SCI, it is essential to recognize the distinct differences in the aging process between individuals without physical disabilities and those with SCI. These differences, influenced by neuropathology, indicate that it may be more accurate to describe the aging process in individuals with chronic SCI as neurogenic accelerated aging (NAA). Research should continue to address conditions associated with NAA and how to ameliorate the accelerated rate of premature age-related conditions. This review focuses on the processes of NAA and the differences compared to the aging process in those without SCI. Recommendations are provided to help slow the development of premature aging conditions.

Background: People with spinal cord injuries (SCIs) often have trouble remaining active because of paralysis. In the past, exercise recommendations focused on the non-paralyzed muscles in the arms, which provides limited benefits. However, recent studies show that electrical stimulation can help engage the paralyzed extremities, expanding the available muscle mass for exercise. Methods: The authors provide an evidence-based approach using expertise from diverse fields, supplemented by evidence from key studies toward the management of electrical stimulation therapies in individuals with SCIs. Literature searches were performed separately using the PubMed, Medline, and Google Scholar search engines. The keywords used for the searches included functional electrical stimulation cycling, hybrid cycling, neuromuscular electrical stimulation exercise, spinal cord injury, cardiovascular health, metabolic health, muscle strength, muscle mass, bone mass, upper limb treatment, diagnostic and prognostic use of functional electrical stimulation, tetraplegic hands, and hand deformities after SCI. The authors recently presented this information in a workshop at a major rehabilitation conference. Additional information beyond what was presented at the workshop was added for the writing of this paper. Results: Functional electrical stimulation (FES) cycling can improve aerobic fitness and reduce the risk of cardiovascular and metabolic diseases. The evidence indicates that while both FES leg cycling and neuromuscular electrical stimulation (NMES) resistance training can increase muscle strength and mass, NMES resistance training has been shown to be more effective for producing muscle hypertrophy in individual muscle groups. The response to the electrical stimulation of muscles can also help in the diagnosis and prognosis of hand dysfunction after tetraplegia. Conclusions: Electrical stimulation activities are safe and effective methods for exercise and testing for motor neuron lesions in individuals with SCIs and other paralytic or paretic conditions. They should be considered part of a comprehensive rehabilitation program in diagnosing, prognosing, and treating individuals with SCIs to improve function, physical activity, and overall health.

Electrical stimulation exercise has become an important modality to help improve the mobility and health of individuals with spinal cord injury (SCI). Electrical stimulation is used to stimulate peripheral nerves in the extremities to assist with muscle strengthening or functional activities such as cycling, rowing, and walking. Electrical stimulation of the peripheral nerves in the upper extremities has become a valuable tool for predicting the risk of hand deformities and rehabilitating functional grasping activities. The purpose of this paper is to provide healthcare providers perspective regarding the many rehabilitation uses of electrical stimulation in diagnosing and treating individuals with SCI. Electrical stimulation has been shown to improve functional mobility and overall health, decrease spasticity, decrease the risk of cardiometabolic conditions associated with inactivity, and assist in the diagnosis/prognosis of hand deformities in those with tetraplegia. Studies involving non-invasive stimulation of the spinal nerves via external electrodes aligned with the spinal cord and more invasive stimulation of electrodes implanted in the epidural lining of the spinal cord have demonstrated improvements in the ability to stand and enhanced the stepping pattern during ambulation. Evidence is also available to educate healthcare professionals in using functional electrical stimulation to reduce muscle spasticity and to recognize limitations and barriers to exercise compliance in those with SCI. Further investigation is required to optimize the dose-response relationship between electrical stimulation activities and the mobility and healthcare goals of those with SCI and their healthcare providers.

Arm crank ergometry (ACE), functional electrical stimulation leg cycling exercise (FES-LCE), and the combination of the two (FES hybrid exercise) have all been used as activities to help improve th...

The purpose of this screening and diagnostic study was to examine the accord among indices of glucose metabolism, including the Homeostatic Model Assessment for Insulin Resistance (HOMA), HOMA2, Matsuda Index, Quantitative Insulin-sensitivity Check Index (QUICKI), hemoglobin A1C (HbA1C), and fasting plasma glucose (FPG) against intravenous glucose tolerance test-measured insulin sensitivity (Si) in individuals with chronic motor complete SCI. Persons with chronic (≥12-months post-injury) SCI (n = 29; 79% men; age 42.2 ± 11.4; body mass index 28.6 ± 6.4 kg/m²; C4-T10) were included. Measures were compared using adjusted R² from linear regression models with Akaike information criterion (AIC, a measure of error). QUICKI had the greatest agreement with Si (adjusted R² = 0.463, AIC = 91.1, p = 0.0001), followed by HOMA (adjusted R² = 0.378, AIC = 95.4, p = 0.0008), HOMA2 (adjusted R² = 0.256, AIC = 99.7, p = 0.0030), and the Matsuda Index (adjusted R² = 0.356, AIC = 95.5, p = 0.0004). FPG (adjusted R² = 0.056, AIC = 107.5, p = 0.1799) and HbA1C (adjusted R² = 0.1, AIC = 106.1, p = 0.0975) had poor agreement with Si. While HbA1C and FPG are commonly used for evaluating disorders of glucose metabolism, QUICKI demonstrates the best accord with Si compared to the other measures.