Isolating the energetic and mechanical consequences of imposed reductions in ankle and knee flexion during gait

 I can tell you precisely why my gait is screwed up. SPASTICITY. Solve that and I will easily be able to recover even with the massive dead area in my motor and pre-motor cortex. Of course the infamous Dr. William M. Landau

thinks spasticity is not worth treating. 

Do you believe in to do nothingism of Dr. William M. Landau on spasticity?  

His statement from here:

Spasticity After Stroke: Why Bother? Aug. 2004

Wonder if he will be singing the same tune after he becomes the 1 in 4 per WHO that has a stroke will he be satisfied with not getting recovered?

The latest here:

Isolating the energetic and mechanical consequences of imposed reductions in ankle and knee flexion during gait

• Emily M. McCain,
• Theresa L. Libera,
• Matthew E. Berno,
• Gregory S. Sawicki,
• Katherine R. Saul &
• Michael D. Lewek 

Journal of NeuroEngineering and Rehabilitation volume 18, Article number: 21 (2021) Cite this article

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Abstract

Background

Weakness of ankle and knee musculature following injury or disorder results in reduced joint motion associated with metabolically expensive gait compensations to enable limb support and advancement. However, neuromechanical coupling between the ankle and knee make it difficult to discern independent roles of these restrictions in joint motion on compensatory mechanics and metabolic penalties.

Methods

We sought to determine relative impacts of ankle and knee impairment on compensatory gait strategies and energetic outcomes using an unimpaired cohort (N = 15) with imposed unilateral joint range of motion restrictions as a surrogate for reduced motion resulting from gait pathology. Participants walked on a dual-belt instrumented treadmill at 0.8 m s⁻¹ using a 3D printed ankle stay and a knee brace to systematically limit ankle motion (restricted-ank), knee motion (restricted-knee), and ankle and knee motion (restricted-a + k) simultaneously. In addition, participants walked without any ankle or knee bracing (control) and with knee bracing worn but unrestricted (braced).

Results

When ankle motion was restricted (restricted-ank, restricted-a + k) we observed decreased peak propulsion relative to the braced condition on the restricted limb. Reduced knee motion (restricted-knee, restricted-a + k) increased restricted limb circumduction relative to the restricted-ank condition through ipsilateral hip hiking. Interestingly, restricted limb average positive hip power increased in the restricted-ank condition but decreased in the restricted-a + k and restricted-knee conditions, suggesting that locking the knee impeded hip compensation. As expected, reduced ankle motion, either without (restricted-ank) or in addition to knee restriction (restricted-a + k) yielded significant increase in net metabolic rate when compared with the braced condition. Furthermore, the relative increase in metabolic cost was significantly larger with restricted-a + k when compared to restricted-knee condition.

Conclusions

Our methods allowed for the reproduction of asymmetric gait characteristics including reduced propulsive symmetry and increased circumduction. The metabolic consequences bolster the potential energetic benefit of targeting ankle function during rehabilitation.

Trial registration

N/A.

Background

Acute or chronic injuries or diseases including amputations [1, 2], osteoarthritis [3,4,5], or stroke [6,7,8,9] can result in unilateral lower limb impairment and lead to walking that is asymmetric [10, 11], requires more positive joint work [12, 13], and is metabolically expensive [14]. Increased metabolic cost may be driven by changes in mechanical work requirements resulting from compensations for impairment of the ankle and knee [12]. For example, reduced ankle function following a stroke limits propulsion [15] which may impact swing phase mechanics [16] and correlate with decreased long-term walking function [17, 18]. Alternatively, reduced knee flexion—the cornerstone of “stiff-knee gait”—results in compensatory mechanisms including hip hiking and circumduction [19], which can lead to reduced walking speeds and altered joint power distribution [20, 21]. Perhaps most importantly, induced weakness at both the ankle [22] and knee [23] is reported to increase the energetic cost of walking.

Therefore, a common objective of gait interventions is to alter the underlying mechanics and reduce additional work that may be associated with metabolic penalties [24,25,26]. Unilateral impairments following a stroke are particularly challenging to treat because the impairment due to joint contractures and reduced muscle flexibility limit joint motion across multiple joints [27,28,29,30]. Thus, the independent roles of ankle and knee motion on compensatory mechanics and energetic cost are difficult to discern because ankle and knee motion are interrelated. For example, persons with stiff-knee gait also present with reductions in ankle excursion and ankle power during push-off [20] that limit knee joint velocity at toe-off and knee flexion during swing [31, 32]. Additionally, impaired limb advancement could result from either ankle or knee weakness post-stroke and lead to compensatory circumduction of the foot [33,34,35].

Understanding the metabolic penalties resulting from reduced motion at individual joints would provide insight into which rehabilitation or therapeutic interventions are likely to be metabolically advantageous. Changes in coordination patterns in persons post-stroke [36] make coaching a participant with hemiparesis to walk with ‘improved’ function of a joint impossible. Additionally, isolating the metabolic consequence of reduced joint function in persons post-stroke is further complicated because the changes in motor control and muscle weakness that result in joint impairment are difficult to manipulate. Instead, previous research has applied an ankle [37,38,39] or knee [19, 40] brace in unimpaired participants to target reductions in a single joint’s range of motion (ROM) to experimentally isolate the specific impacts of reduced ankle versus knee function. Bracing at the ankle resulted in the redistribution of power from the braced ankle to the ipsilateral and contralateral hips and an increase in metabolic cost [37]. Those authors postulated that the increase in metabolic cost resulted from the transfer of power away from the ankle joint which is suited for efficient energy storage and return through the Achilles tendon [41]. Similarly, research investigating unilateral knee bracing to simulate stiff-knee gait found increases in limb circumduction achieved through hip hiking and increased whole-body metabolic energy cost [19, 40].

Individually limiting ankle or knee ROM is known to be metabolically costly, but it is not clear which restriction is more detrimental, or how these restrictions interact. A synthesis of the literature suggests that restricting the ankle may be more metabolically costly than restricting the knee for several reasons. First, the ankle is responsible for more positive joint power than the knee during unimpaired walking [41, 42], and therefore limitations at the ankle are likely to require larger increases in positive joint power elsewhere. Second, in contrast to the ankle, during the stance phase the knee is primarily responsible for power absorption which is accomplished through negative muscle work. Because negative muscle work has a higher efficiency than positive muscle work, it is unlikely that compensations for reduced power absorptions will be as metabolically detrimental [43]. During swing, we expect impaired ankle and knee motion will both result in the inability to flex the limb and induce similar compensations and penalties. Finally, due in part to the elastic energy storage of the Achilles tendon, the ankle is a more efficient producer of positive power when compared to the knee or hip [41, 44]. Therefore, redistributing power away from the ankle to other joints is likely to increase the total cost of positive power more than redistribution from the knee to other joints [37]. Overall, with ample research suggesting the importance of the ankle in energetic efficiency, it is reasonable to hypothesize a restriction of the ankle should result in larger increases in metabolic cost than a restriction of the knee. Though previous research has begun to address metabolic impacts of restricting joints individually, no research has examined the isolated versus combined effects of reduced unilateral ankle and knee ROM on mechanical or metabolic outcomes.

The purpose of this study is to provide insight into the individual and combined effects of reduced ankle and knee ROM on gait adaptations and metabolic consequences. We used a custom 3D printed ankle stay and knee brace to isolate the impacts of reduced unilateral ankle, knee, and ankle + knee ROM on joint and limb-level compensations and the resulting metabolic consequences. Based on findings from previous literature, we hypothesized that: (h1) Limiting ankle ROM would attenuate peak ankle power at pushoff, reduce peak limb propulsion and require bilateral increases in sagittal hip power to compensate, (h2) Limiting knee ROM would decrease knee flexion velocity at toe off, impair swing limb advancement and require increased circumduction via ipsilateral increases in frontal plane hip power, and (h3) the metabolic cost of compensatory mechanics resulting from restricting ankle ROM would be larger than the cost of compensations from restricting knee ROM.