Altered Achilles tendon morphology in individuals with chronic post-stroke hemiparesis: a case report

Stroke is a leading cause of adult long-term disabilities worldwide. While majority of individuals with post-stroke hemiparesis are able to regain walking function, there often remains the hallmark impairment of slow walking speed. Slower walking speed has been reported to increase fall risks in people post-stroke [1]. Insufficient propulsive forces has been identified as the major cause underlying slower walking speed [2]. As a critical component for successful execution of appropriate propulsive forces, the muscle-tendon unit has yet to be examined.

Abnormal forces applied to tendon tissues have been found to cause morphological changes similar to those observed in degenerative tendon. These changes include collagen fiber disorganization, increased water content, increased glycosaminoglycan content, thinner collagen fibers, reduced overall collagen content, increased type II collagen, and reduced tendon stiffness [3]. Using sonographic imaging, a number of previous studies have reported morphological changes (i.e. increased tendon thickness [4] and cross-sectional area [5]) in diseased tendons. Thus, although there is reason to believe the aforementioned abnormalities of the Achilles tendon can develop in individuals post-stroke due persistent increases in muscle tone, no data has been published to support this. In this case report, we examined muscle tone of the ankle plantarflexors, propulsive forces during walking, and thickness of the Achilles tendon in the paretic and non-paretic legs of individuals with chronic post-stroke hemiparesis compared with non-neurologically impaired controls.

Two individuals with chronic post-stroke hemiparesis are presented. The first case (Stroke 1) is a 50-year old male who survived a left hemorrhagic cortical cerebral vascular accident 5.2 years ago. The second case (Stroke 2) is a 62-year old male who survived a right ischemic cortical cerebral vascular accident 5.6 years ago. Both individuals with chronic post-stroke hemiparesis have since regained independent community ambulatory function without the use of assistive devices, but reported slow walking speed despite considerable effort to propel forward. Two non-neurologically impaired individuals are presented as controls (Table 1).

In this report, we sought to explore the association between muscle tone of the ankle plantarflexors, propulsive forces during walking, and gross morphology of the Achilles tendon in persons with chronic post-stroke hemiparesis. As none of the individuals with post-stroke hemiparesis reported in this study reported any past or current symptoms/injuries of the Achilles tendon, the increased insertional thickness of the Achilles tendon is likely associated with chronic increases of the muscle tone of ankle plantarflexors in the paretic limb. Our observations suggest that altered morphology of the Achilles tendon in the paretic limb might contribute to the insufficient propulsive forces during gait, and thus the slow walking speed in an individual chronically post-stroke.

One factor that may have been overlooked in patients with post-stroke hemiparesis is altered muscle-tendon unit output force as a result of altered mechanical properties of the Achilles tendon. Post-stroke, due to altered descending input, increased muscle tone, particularly in the paretic ankle plantarflexors, is common, and negatively impacts locomotor control. In the cases presented, it is speculated that chronic muscle tone maladaptations in paretic ankle plantarflexors resulted in altered tendon morphology and composition, thereby leading to altered mechanical properties. Specifically, it has been found that focal tendon thickening and collagen fiber disorganization are related to reduced stiffness and elastic modulus of the tendon [6]. The more compliant tendon as a result of collagen fiber disorganization might compromise force transmission during gait [7], thereby leading to insufficient propulsive forces generated during gait, observed in these cases.

One limitation of this study is that the stroke participants presented in this case series were all chronically post-stroke, where morphological adaptations have already occurred. It would be important to explore the time course of adaptations. Additionally, future studies should address multi-level adaptations by examining the contribution of the altered neural circuitry post-stroke [8, 9].

Our findings can significantly impact physical therapy interventions for people post-stroke. Current rehabilitative efforts to improve walking speed should consider examining tendon integrity in individuals post-stroke who demonstrate excessive muscle tone and insufficient propulsive forces during gait. Since tendon adaptations contribute to altered walking mechanics, a treatment strategy aiming at improving the neuromuscular control should be employed. For instance, a treatment plan focusing on improving tendon health (e.g., eccentric exercises) [10] may be included in their rehabilitation program to improve walking.