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.

Thursday, September 9, 2021

Coupling of shoulder joint torques in individuals with chronic stroke mirrors controls, with additional non-load-dependent negative effects in a combined-torque task

Maybe something is useful in here but I don't see it.  Obviously not written so survivors can understand and bring to their doctor's attention for 100% recovery

Coupling of shoulder joint torques in individuals with chronic stroke mirrors controls, with additional non-load-dependent negative effects in a combined-torque task

Abstract

Background

After stroke, motor control is often negatively affected, leaving survivors with less muscle strength and coordination, increased tone, and abnormal synergies (coupled joint movements) in their affected upper extremity. Humeral internal and external rotation have been included in definitions of abnormal synergy but have yet to be studied in-depth.

Objective

Determine the ability to generate internal and external rotation torque under different shoulder abduction and adduction loads in persons with chronic stroke (paretic and non-paretic arm) and uninjured controls.

Methods

24 participants, 12 with impairments after stroke and 12 controls, completed this study. A robotic device controlled abduction and adduction loading to 0, 25, and 50% of maximum strength in each direction. Once established against the vertical load, each participant generated maximum internal and external rotation torque in a dual-task paradigm. Four linear mixed-effects models tested the effect of group (control, non-paretic, and paretic), load (0, 25, 50% adduction or abduction), and their interaction on task performance; one model was created for each combination of dual-task directions (external or internal rotation during abduction or adduction). The protocol was then modeled using OpenSim to understand and explain the role of biomechanical (muscle action) constraints on task performance.

Results

Group was significant in all task combinations. Paretic arms were less able to generate internal and external rotation during abduction and adduction, respectively. There was a significant effect of load in three of four load/task combinations for all groups. Load-level and group interactions were not significant, indicating that abduction and adduction loading affected each group in a similar manner. OpenSim musculoskeletal modeling mirrored the experimental results of control and non-paretic arms and also, when adjusted for weakness, paretic arm performance. Simulations incorporating increased co-activation mirrored the drop in performance observed across all dual-tasks in paretic arms.

Conclusion

Common biomechanical constraints (muscle actions) explain limitations in external and internal rotation strength during adduction and abduction dual-tasks, respectively. Additional non-load-dependent effects such as increased antagonist co-activation (hypertonia) may cause the observed decreased performance in individuals with stroke. The inclusion of external rotation in flexion synergy and of internal rotation in extension synergy may be over-simplifications.

Background

Approximately 610,000 new strokes occur each year in the US and 16.9 million occur worldwide [1]. Currently, 6.6 million Americans are living post stroke, approximately 30–60% of whom have chronic upper extremity motor impairments [2, 3], including weakness, loss of multi-joint coordination, hypertonia, and spasticity. Weakness and loss of multi-joint coordination involving the upper extremity may affect activities of daily living that require control of arm position, stiffness, damping, and inertia [4] to enable the individual to accomplish tasks such as feeding themselves, dressing, preparing food, carrying objects, or opening doors.

One factor that contributes to the loss of multi-joint coordination after stroke is an unintentional co-contraction of muscles throughout a limb, described as an abnormal synergy, and loss of independent joint control [5,6,7]. Shoulder abduction is reported as being accompanied by shoulder external rotation, elbow flexion, supination, and wrist and finger flexion, while shoulder adduction is often accompanied by shoulder internal rotation, elbow extension, and wrist and finger flexion [8].

Using an isometric task in single directions, Dewald et al. compared control, non-paretic, and paretic internal and external rotation torques generated during shoulder abduction and found inconsistencies with the expectations of the abnormal synergy hypothesis [9]. Specifically, the paretic and control arms had similar secondary torque generation patterns in internal and external rotation that were different from the non-paretic arms. This result was not investigated further, the focus of subsequent work being on the more robust effects of abductor drive on distal joints, including elbow, wrist, and fingers [10].

We have also moved away from analyzing secondary torques (torques generated in directions that participants are not instructed to control or do not have feedback from) during single direction tasks because of the difficulty in determining if those torques are pathological (mandatory), normal, or just how these individuals chose (consciously or unconsciously) to perform the task [7, 11]. We have instead moved towards multi-degree of freedom (DOF) tasks that test ability in two or more directions simultaneously [12, 13]. At the cost of minimally increasing cognitive load [14], these tasks allow us to better test movement capacity after stroke, and to determine whether it is limited by neural or mechanical constraints. Importantly, this dual-task paradigm has been completed for multi-joint combinations of shoulder abduction, elbow extension, and wrist/finger extension [9, 11, 15] but not for within-shoulder movements such as internal and external rotation during abduction or adduction. Furthermore, our recent work has suggested that internal/external rotation and abduction/adduction joint torque coupling may be present in individuals without stroke. These results warrant an in-depth analysis of shoulder DOF coupling in individuals with and without stroke.

Minimal work has been published on attempts to quantify torque generation capacity at the shoulder (glenohumeral joint) during multi-DOF tasks. Baillargeon et al. recently published a study examining feasible torque space of the shoulder in young healthy adults [16]. They noted that external rotation during adduction and internal rotation during abduction were the weakest directions of the shoulder. Although these data are from unimpaired individuals, these torque combinations are considered to be out-of-synergy in individuals with stroke. Beer et. al confirmed that hemiparetic external rotation weakness was profound (33%); however, this weakness was unrelated to reaching performance against gravity (movement out of synergy) [17]. Nonetheless, internal/external rotation capacity after stroke has largely been assumed to be constrained by abnormal neural drive.

This study attempts to better understand and quantify longstanding observations going back to the work of Twitchell et al. [18] that included external/internal rotation in flexion/extension synergies, respectively. The nature of external/internal rotation capacity is of special relevance because technically sophisticated devices and associated protocols are being designed for rehabilitation of the upper extremity [19]. This study examines internal and external rotation torque generation capacity (strength) during abduction and adduction using a robotic device—a paradigm similar to that first described by Beer et al. to investigate task-dependent weakness in elbow flexion/extension during abduction/adduction [20]. In line with the described clinical presentation and laboratory-based findings of multi-joint synergistic movement and posturing following a stroke, we hypothesized that, compared to individuals without stroke, the paretic arm would reflect abnormal synergy within the DOFs of the glenohumeral joint, such that external rotation would be weaker during adduction and stronger during abduction, and conversely that internal rotation would be stronger during adduction and weaker during abduction.

 

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