Spasticity is a well-known symptom seen in patients of all ages with a broad range of neurological disorders. Spasticity occurs at a variable rate and the highest incidences are found in patients with cerebral palsy, traumatic brain injury, spinal cord injury and stroke. Recent studies have highlighted that while the etiology of spasticity is neurological in origin, secondary, non-neurological component impairments are difficult to differentiate from neurological components in clinical settings. The neurological component is believed to be caused by an exaggerated spinal reflex in response to muscle spindle firing and the non-neurological component consists of secondary impairments as a result of muscular adaptations to the neural dysregulation. Despite a large amount of research effort, the mechanisms that underlie spasticity and the influences of spasticity on functional movement are not well understood. Management of spasticity is challenging as it is important to evaluate the advantages and disadvantages that the patients gain from their spasticity so that treatment strategies and goals can be better identified.
The most common clinical examination of spasticity includes assessment of exaggerated tendon tap reflexes and the velocity-dependent resistance by passive muscle stretch. Several laboratories have custom-built instruments to quantitatively examine joint resistance to passive stretch; these provide a more reliable description of spasticity than using clinical scores. However, the relationship between spasticity assessed during passive stretching and functional movement are still under debate. During functional movements, direct measurement and differentiation of neural and non-neural muscular impairments is a very challenging task. Although clinical neurophysiological approaches such as Hoffmann’s reflex (H-reflex) and F-waves can provide direct measurement of the neural component in spasticity, the reliability and sensitivity are relatively low. Neuromusculoskeletal models and simulation maybe a feasible approach to relate the neural and non-neural responses to muscle stretch and their influences on functional movement. Commonly seen neuromusculoskeletal models and simulations compute the mechanical output without considering sensory organs such as muscle spindles and Golgi tendon organs, which are essential for understanding neurophysiological characteristics of spasticity.
We welcome researchers to contribute original work of theoretical, computational or experimental studies focusing on understanding neuromechanical properties of spastic muscles and their effects on function. The scope of this Research Topic includes, but is not limited to:
(1) Innovation of joint and/or muscle assessment e.g., instruments and other imaging modalities that contribute to better understanding of neuromechanical properties of the spastic muscle
(2) New experimental, e.g., electrophysiological, and theoretic approaches to better understand the influences of neural and non-neural impairments during functional movement in subjects with neurological disorders
(3) Development of neuromusculoskeletal models with sensory organ integration and evaluation its fidelity in simulating the neuromechanical properties of spastic muscle
(4) Quantitative evaluation of current and new interventions and therapies aimed at altering the neuromechanical properties of spastic muscles in a broad range of neurological disorders
Spasticity is a well-known symptom seen in patients of all ages with a broad range of neurological disorders. Spasticity occurs at a variable rate and the highest incidences are found in patients with cerebral palsy, traumatic brain injury, spinal cord injury and stroke. Recent studies have highlighted that while the etiology of spasticity is neurological in origin, secondary, non-neurological component impairments are difficult to differentiate from neurological components in clinical settings. The neurological component is believed to be caused by an exaggerated spinal reflex in response to muscle spindle firing and the non-neurological component consists of secondary impairments as a result of muscular adaptations to the neural dysregulation. Despite a large amount of research effort, the mechanisms that underlie spasticity and the influences of spasticity on functional movement are not well understood. Management of spasticity is challenging as it is important to evaluate the advantages and disadvantages that the patients gain from their spasticity so that treatment strategies and goals can be better identified.
The most common clinical examination of spasticity includes assessment of exaggerated tendon tap reflexes and the velocity-dependent resistance by passive muscle stretch. Several laboratories have custom-built instruments to quantitatively examine joint resistance to passive stretch; these provide a more reliable description of spasticity than using clinical scores. However, the relationship between spasticity assessed during passive stretching and functional movement are still under debate. During functional movements, direct measurement and differentiation of neural and non-neural muscular impairments is a very challenging task. Although clinical neurophysiological approaches such as Hoffmann’s reflex (H-reflex) and F-waves can provide direct measurement of the neural component in spasticity, the reliability and sensitivity are relatively low. Neuromusculoskeletal models and simulation maybe a feasible approach to relate the neural and non-neural responses to muscle stretch and their influences on functional movement. Commonly seen neuromusculoskeletal models and simulations compute the mechanical output without considering sensory organs such as muscle spindles and Golgi tendon organs, which are essential for understanding neurophysiological characteristics of spasticity.
We welcome researchers to contribute original work of theoretical, computational or experimental studies focusing on understanding neuromechanical properties of spastic muscles and their effects on function. The scope of this Research Topic includes, but is not limited to:
(1) Innovation of joint and/or muscle assessment e.g., instruments and other imaging modalities that contribute to better understanding of neuromechanical properties of the spastic muscle
(2) New experimental, e.g., electrophysiological, and theoretic approaches to better understand the influences of neural and non-neural impairments during functional movement in subjects with neurological disorders
(3) Development of neuromusculoskeletal models with sensory organ integration and evaluation its fidelity in simulating the neuromechanical properties of spastic muscle
(4) Quantitative evaluation of current and new interventions and therapies aimed at altering the neuromechanical properties of spastic muscles in a broad range of neurological disorders
