Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, July 23, 2019

Alterations of Elastic Property of Spastic Muscle With Its Joint Resistance Evaluated From Shear Wave Elastography and Biomechanical Model

I saw nothing in here that will help survivors recover from spasticity. The whole fucking point of stroke research is to get survivors recovered. WHOM is going to inform stroke researchers that that is the only goal in stroke. 100% recovery, not prediction, prevention or descriptions. 

Alterations of Elastic Property of Spastic Muscle With Its Joint Resistance Evaluated From Shear Wave Elastography and Biomechanical Model

Yan Leng1, Zhu Wang2, Ruihao Bian1, Wai Leung Ambrose Lo1, Xiaoyan Xie2, Ruoli Wang3,4,5, Dongfeng Huang1,6* and Le Li1*
  • 1Department of Rehabilitation Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
  • 2Department of Medical Ultrasonics, Institute of Diagnostic and Interventional Ultrasound, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
  • 3Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden
  • 4Department of Mechanics, Royal Institute of Technology, Stockholm, Sweden
  • 5KTH BioMEx Center, Royal Institute of Technology, Stockholm, Sweden
  • 6Department of Rehabilitation Medicine, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China
This study aims to quantify passive muscle stiffness of spastic wrist flexors in stroke survivors using shear wave elastography (SWE) and to correlate with neural and non-neural contributors estimated from a biomechanical model to hyper-resistance measured during passive wrist extension. Fifteen hemiplegic individuals after stroke with Modified Ashworth Scale (MAS) score larger than one were recruited. SWE were used to measure Young's modulus of flexor carpi radialis muscle with joint from 0° (at rest) to 50° flexion (passive stretch condition), with 10° interval. The neural (NC) and non-neural components i.e., elasticity component (EC) and viscosity component (VC) of the wrist joint were analyzed from a motorized mechanical device NeuroFlexor® (NF). Combining with a validated biomechanical model, the neural reflex and muscle stiffness contribution to the increased resistance can be estimated. MAS and Fugl-Meyer upper limb score were also measured to evaluate the spasticity and motor function of paretic upper limb. Young's modulus was significantly higher in the paretic side of flexor carpi radialis than that of the non-paretic side (p < 0.001) and it increased significantly from 0° to 50° of the paretic side (p < 0.001). NC, EC, and VC on the paretic side were higher than the non-paretic side (p < 0.05). There was moderate significant positive correlation between the Young's Modulus and EC (r = 0.565, p = 0.028) and VC (r = 0.645, p = 0.009) of the paretic forearm flexor muscle. Fugl-Meyer of the paretic forearm flexor has a moderate significant negative correlation with NC (r = −0.578, p = 0.024). No significant correlation between MAS and shear elastic modulus or NF components was observed. This study demonstrated the feasibility of combining SWE and NF as a non-invasive approach to assess spasticity of paretic muscle and joint in stroke clinics. The neural and non-neural components analysis as well as correlation findings of muscle stiffness of SWE might provide understanding of mechanism behind the neuromuscular alterations in stroke survivors and facilitate the design of suitable intervention for them.

Introduction

Stroke is one of the major causes of long-term disability worldwide and leads to motor and sensory impairments on upper and lower extremity of survivors (1, 2). Spasticity, a neurological problem secondary to stroke, has a significant effect on skeletal muscle and affects motor function and quality of life (3, 4). Despite the high prevalence of spasticity in people with stroke, the underlying mechanism remains poorly understood due to the confusion in concept of spasticity. Alterations of spastic muscle might not simply due to chronic stimulation or disuse, and literatures showed that exaggerated reflexes and secondary changes in mechanical muscle properties may have a major role in spastic movement disorder (5). Understanding the mechanical and neurophysiological characteristics of spasticity may provide important clues to its intervention.
Previous studies involving a variety of methods studying joint and tissue mechanics as well as muscle morphology offered clear evidence to suggest that skeletal muscle tissue itself is altered under spastic conditions (6). The mechanical property of spastic muscle could be assessed by imaging technique such as ultrasound. Architectural parameters such as pennation angles, fascicle lengths, and muscle thickness assessed by ultrasound could quantitatively evaluate the morphological characteristics of the muscle tendon complex (79). Shortened muscle fascicle length and smaller physiological cross section area were observed in patients with stroke (7). However, muscle function is not only related to its morphology parameters but also the mechanical properties. Shear wave elastography (SWE) tracks the propagation of the shear wave through the muscle tissue using ultra-fast ultrasonic imaging and shear wave travels faster through stiffer tissues (10). It is a new approach to provide a real-time quantitative metrics of tissue material properties, including mechanical properties such as stiffness of skeletal muscles in upper and lower limbs (1115). Koo and coworkers found SWE was significantly correlated with passive muscle stiffness in both animal models (16) and healthy subjects (17). Bouillard applied SWE and electromyography (EMG) to estimate individual muscle force of healthy subjects and found a significant linear correlation between shear elastic modulus and muscle force (18). These findings suggest that SWE may be a feasible way to quantify the inherent strain-stress behavior of muscle after neuromuscular disease. Published studies showed that shear wave speed and echo intensity were higher in the relaxed paretic limb than in the relaxed non-paretic limb of stroke survivors (1921), multiple sclerosis (22), cerebral palsy (2325), and Duchanne muscular dystrophin (26). However, previous studies of SWE on spastic muscle mainly focused on investigating relaxed muscles with a specific posture (1921). A systematic assessment of muscle stiffness in relation to joint angle is needed to provide comprehensive information on muscle properties alterations after pathology and how they relate to the ability to conduct activities of daily living (ADL) such as feeding and dressing.
In clinics, physicians often examine the alterations in muscle stiffness by passively stretching the spastic limbs and palpating the spastic muscle. The outcomes of the assessments are subjected to the experience of the clinicians. The sub-optimal evaluation method adopted in clinics may due to the fact that quantitative assessment of spastic muscle-tendon-joint is rare. Spasticity, defined as hyper-resistance measured during passive rotation of a joint, is related to neural and non-neural factors (2729). To separate and analyze individual components of this hyper-resistance would lead to better understanding of spasticity and further assist the selection of appropriate intervention (28). The NeuroFlexor (Aggro MedTech AB, Solna, Sweden) is a recently developed motorized instrument which can passively extend the wrist joint at controlled velocities (30). Based on the biomechanical modeling method, the recorded resistant force can be separated into three contributors to the measured resistant force: neural component (NC), elasticity component (EC), and viscosity component (VC) (31, 32). It was found that the NC and EC increased in paretic side compared to that from non-paretic side in stroke survivors (28.30). In addition, it was reported that the NC decreased significantly after injections of Botulinum toxin type A, but the passive components of EC and VC did not change overtime (31). The NeuroFlexor (NF) has been also used to evaluate neural and non-neural contributions to the wrist resistance in patients with Parkinson's disease and cerebral palsy (3033). The validity of the NF-method has been demonstrated through the strong correlation between the NC and the EMG activity of flexor carpi radialis, both across all subjects and between-subject during the nerve block test in the stroke survivors (31, 34). However, there is still controversial opinion on whether the neural factor from central nervous system or the mechanical factor of musculotendon system is a primary contributor to spasticity (35). In addition, there is limited information on whether the non-neural components of resistance measured by the NF-method are clinically relevant. For instance, it is unclear that whether non-neural components are associated with intrinsic muscle mechanical properties.
The aim of the present study was to investigate the feasibility and applications of combining SWE and NF to quantitatively assess musculoskeletal properties alterations in spastic muscle joint post-stroke. Understanding the delicate variations of muscles properties during passive movement, and the neural and non-neural components that contribute to joint resistance might facilitate the development of targeted therapeutic regime to address spasticity for motor function improvement.

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