Neural Constraints Affect the Ability to Generate Hip Abduction Torques When Combined With Hip Extension or Ankle Plantarflexion in Chronic Hemiparetic Stroke

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https://www.frontiersin.org/articles/10.3389/fneur.2018.00564/full?

Natalia Sánchez¹, Ana M. Acosta², Roberto López-Rosado² and Julius P. A. Dewald^2,3,4*

• ¹Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, United States
• ²Department of Physical Therapy and Human Movement Sciences, Northwestern University, Chicago, IL, United States
• ³Department of Biomedical Engineering, Northwestern University, Chicago, IL, United States
• ⁴Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, IL, United States

Stroke lesions interrupt descending corticofugal fibers that provide the volitional control of the upper and lower extremities. Despite the evident manifestation of movement impairments post-stroke during standing and gait, neural constraints in the ability to generate joint torque combinations in the lower extremities are not yet well determined. Twelve chronic hemiparetic participants and 8 age-matched control individuals participated in the present study. In an isometric setup, participants were instructed to combine submaximal hip extension or ankle plantarflexion torques with maximal hip abduction torques. Statistical analyses were run using linear mixed effects models. Results for the protocol combining hip extension and abduction indicate that participants post-stroke have severe limitations in the amount of hip abduction torque they can generate, dependent upon hip extension torque magnitude. These effects are manifested in the paretic extremity by the appearance of hip adduction torques instead of hip abduction at higher levels of hip extension. In the non-paretic extremity, significant reductions of hip abduction were also observed. In contrast, healthy control individuals were capable of combining varied levels of hip extension with maximal hip abduction. When combining ankle plantarflexion and hip abduction, only the paretic extremity showed reductions in the ability to generate hip abduction torques at increased levels of ankle plantarflexion. Our results provide insight into the neural mechanisms controlling the lower extremity post-stroke, supporting previously hypothesized increased reliance on postural brainstem motor pathways. These pathways have a greater dominance in the control of proximal joints (hip) compared to distal joints (ankle) and lead to synergistic activation of musculature due to their diffuse, bilateral connections at multiple spinal cord levels. We measured, for the first time, bilateral constraints in hip extension/abduction coupling in hemiparetic stroke, again in agreement with the expected increased reliance on bilateral brainstem motor pathways. Understanding of these neural constraints in the post-stroke lower extremities is key in the development of more effective rehabilitation interventions that target abnormal joint torque coupling patterns.

Introduction

Stroke affects 6.6 million people in the United States with about 800,000 new and recurring strokes occurring every year (1). Stroke-induced brain injury interrupts descending motor pathways affecting motor commands from the cortex to motor neurons innervating the extremities. Despite the disruption of motor commands to the lower extremity, over 80% of stroke survivors regain the ability to stand and walk (2). However, stance, balance and gait post-stroke differ significantly from healthy individuals: upright stance is asymmetrical and biased toward the non-paretic leg (3, 4). Likewise, post-stroke gait is asymmetric (5–9), slow (7, 10–12) and prone to falls (13–16). These differences may be in part due to changes in the voluntary control of the lower extremity which may constrain joint torque combinations, leading individuals to over-rely on their non-paretic leg. Nonetheless, existence of constraints in the voluntary control of lower extremities after stroke and their potential impact during upright function are yet to be fully understood.

After stroke, interruption of corticofugal pathways has been hypothesized to result in an increased reliance on diffuse brainstem pathways that branch across multiple spinal segments (17–19). These diffuse pathways activate multiple motor neuron pools and consequently, multiple muscles simultaneously, which in the upper extremity, leads to abnormal muscle coactivation (20) and loss of independent joint control due to an increased dependence on contralesional corticoreticulospinal pathways (20–24). Similarly, in the lower extremity, previous studies have shown that independent joint control might be affected when generating maximal and submaximal voluntary torques in either hip extension or ankle plantarflexion (25). Generation of maximal ankle plantarflexion and maximal hip extension in individuals post-stroke leads to coupled extension/adduction torques across the hip, knee and ankle joints (25–27). These results are in agreement with what is referred clinically as the extensor synergy: coupling of hip extension and hip adduction with knee extension and ankle plantarflexion (28, 29). Despite the apparent dominance of the extensor synergy, research has yet to demonstrate whether individuals post-stroke can generate lower extremity joint torque combination patterns away from this synergy.

In this study, we probed the ability of participants to generate joint torque couples outside of the extensor synergy, by assessing their capacity to concurrently generate hip abduction torques with hip extension or ankle plantarflexion torques. We also investigated whether instructing participants to couple hip flexion with hip abduction, i.e., coupling inside the flexor synergy, facilitated the generation of hip abduction torque, which is significantly weakened after stroke (25), thus providing insight into the potential functional importance of the flexor synergy (28). We hypothesized that given the changes in the neural control of the lower extremity post-stroke, attributed to increased reliance on bilateral brainstem pathways that control proximal and postural hip muscles (30–32), the capacity to generate hip abduction with both the paretic and non-paretic extremities would be constrained by hip extension but would possibly benefit from hip flexion. In contrast, in control participants, we expected that the magnitude of hip abduction torques would be independent from the torques generated in the hip flexion/extension degree of freedom. The present characterization is of critical importance because it may help explain the impairments seen during upright posture both in quiet standing (3, 33) and in gait (10, 11, 34). For instance, the inability to couple hip extension with abduction may explain the failure to stabilize the pelvis leading to pelvic drop during single leg stance (11). Also, restrictions in hip abduction torque generation may hinder frontal plane displacement of the center of mass (35), compromising the ability to generate adequate responses to medio-lateral perturbations during standing (15). A better understanding of constraints in the ability to generate hip abduction during hip extension or ankle plantarflexion in the lower extremity after stroke may lead to the development of more targeted rehabilitation interventions that seek to restore individual joint control and coordination and are expected to improve standing posture and balance in people post-stroke.

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