Biology subjects

Akbas, T.

Publications and source records attributed to Akbas, T..

3 recordsLinked to original sources

bioRxiv2019

Rectus femoris hyperreflexia predicts knee flexion angle in post-stroke Stiff-Knee gait

Stiff-knee gait (SKG) after stroke is often accompanied by decreased knee flexion angle during the swing phase. The decreased knee flexion has been hypothesized to originate from excessive quadriceps activation. However, it is unclear whether this activation is due to poor timing or hyperreflexia, both common post-stroke impairments. The goal of this study was to investigate the relation between quadriceps hyperreflexia in post-stroke SKG with knee flexion angle during walking. The rectus femoris (RF) H-reflex was recorded in eleven participants with post-stroke SKG and ten healthy controls during standing and walking during toe-off. In order to separate the effects of poorly timed quadriceps muscle activation from hyperreflexia, healthy individuals voluntarily increased quadriceps activity using RF electromyographic (EMG) biofeedback during standing and pre-swing upon H-reflex stimulation. We observed a negative correlation (R = -0.92, p=0.001) between knee flexion angle and RF H-reflexes in post-stroke SKG. In contrast, H-reflex amplitude in healthy individuals in presence (R = 0.47, p = 0.23) or absence (R = -0.17, p = 0.46) of increased RF activity had no correlation with knee flexion angle. The RF H-reflex amplitude differed between standing and walking in healthy individuals, including when RF activity was increased voluntarily (d = 2.86, p = 0.007), but was not observed post-stroke (d =0.73, p = 0.296). Thus, RF reflex modulation is impaired in post-stroke SKG. Further, RF hyperreflexia, as opposed to overactivity, may play a role in knee flexion kinematics in post-stroke SKG. Interventions targeting self-regulated quadriceps hyperreflexia may be effective in promoting better neural control of the knee joint and thus better quality of walking post-stroke.

bioengineering↗

bioRxiv2019

Hip circumduction is not a compensation for reduced knee flexion angle during gait

It has long been held that hip abduction compensates for reduced swing-phase knee flexion angle, especially in those after stroke. However, there are other compensatory motions such as pelvic obliquity (hip hiking) that could also be used to facilitate foot clearance with greater energy efficiency. Our previous work suggested that hip abduction may not be a compensation for reduced knee flexion after stroke. Previous study applied robotic knee flexion assistance in people with post-stroke Stiff-Knee Gait (SKG) during pre-swing, finding increased abduction despite improved knee flexion and toe clearance. Thus, our hypothesis was that hip abduction is not a compensation for reduced knee flexion. We simulated the kinematics of post-stroke SKG on unimpaired individuals with three factors: a knee orthosis to reduce knee flexion, an ankle-foot orthosis commonly worn by those post-stroke, and matching gait speeds. We compared spatiotemporal measures and kinematics between experimental factors within healthy controls and with a previously recorded cohort of people with post-stroke SKG. We focused on frontal plane motions of hip and pelvis as possible compensatory mechanisms. We observed that regardless of gait speed, knee flexion restriction significantly increased pelvic obliquity (2.79{degrees}, p<0.01) compared to unrestricted walking (1.5{degrees}, p<0.01), but similar to post-stroke SKG (3.4{degrees}). However, those with post-stroke SKG had significantly greater hip abduction (8.2{degrees}) compared to unimpaired individuals with restricted knee flexion (4.2{degrees}, p<0.05). These results show that pelvic obliquity, not hip abduction, compensates for reduced knee flexion angle. Thus, other factors, possibly neural, facilitate exaggerated hip abduction observed in post-stroke SKG.

bioengineering↗

bioRxiv2018

Neuromusculoskeletal simulation reveals abnormal rectus femoris-gluteus medius reflex coupling in post-stroke gait

Post-stroke gait is often accompanied by muscle impairments that result in adaptations such as hip circumduction to compensate for lack of knee flexion. Our previous work robotically enhanced knee flexion in individuals post-stroke with Stiff-Knee Gait (SKG), however, this resulted in greater circumduction, suggesting the existence of abnormal coordination in SKG. The purpose of this work is to investigate two possible mechanisms of the abnormal coordination: 1) an involuntary coupling between stretched quadriceps and abductors, and 2) a coupling between volitionally activated knee flexors and abductors. We used previously collected kinematic, kinetic and EMG measures from nine participants with chronic stroke and five healthy controls during walking with and without the applied knee flexion torque perturbations in the pre-swing phase of gait in the neuromusculoskeletal simulation. The measured muscle activity was supplemented by simulated muscle activations to estimate the muscle states of the quadriceps, hamstrings and hip abductors. We used linear mixed models to investigate two hypotheses: H1) association between quadriceps and abductor activation during an involuntary period (reflex latency) following the perturbation and H2) association between hamstrings and abductor activation after the perturbation was removed. We observed significantly higher rectus femoris (RF) activation in stroke participants compared to healthy controls within the reflex latency period following the perturbation based on both measured (H1, p < 0.001) and simulated (H1, p = 0.022) activity. Simulated RF and gluteus medius (GMed) activations were correlated only in those with SKG, which was significantly higher compared to healthy controls (H1, p = 0.030). There was no evidence of voluntary synergistic coupling between any combination of hamstrings and hip abductors (H2, p > 0.05) when the perturbation was removed. The RF-GMed coupling suggests an underlying abnormal reflex coordination pattern in post-stroke SKG. These results challenge earlier assumptions that hip circumduction in stroke is simply a kinematic adaptation due to reduced toe clearance. Instead, abnormal coordination may underlie circumduction, illustrating the deleterious role of abnormal coordination in post-stroke gait.

bioengineering↗