Stiff Knee Gait Disorders as Neuromechanical Consequences of Spastic Hemiplegia in Chronic Stroke

被引:7
|
作者
Li, Sheng [1 ,2 ]
机构
[1] Univ Texas Hlth Sci Ctr Houston, McGovern Med Sch, Dept Phys Med & Rehabil, Houston, TX 77030 USA
[2] TIRR Mem Hermann Hosp, TIRR Mem Hermann Res Ctr, Houston, TX 77030 USA
关键词
spasticity; gait; stroke; botulinum toxin; nerve block; RECTUS-FEMORIS MUSCLE; LEGGED GAIT; SWING PERIOD; INJECTION; FLEXION; PATTERN; TOXIN;
D O I
10.3390/toxins15030204
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Stiff knee gait (SKG) is defined as decreased knee flexion during the swing phase. It is one of the most common gait disorders following stroke. Knee extensor spasticity is commonly accepted as the primary cause. Clinical management has focused on the reduction in knee extensor spasticity. Recent advances in understanding of post-stroke hemiplegic gait suggest that SKG can present as mechanical consequences between muscle spasticity, weakness, and their interactions with ground reactions during walking. Various underlying mechanisms are presented through sample cases in this article. They include ankle plantar flexor spasticity, knee extensor spasticity, knee flexor and extensor coactivation, and hip flexor spasticity. Careful and thorough clinical assessment is advised to determine the primary cause for each patient. Understanding of these various presentations of SKG is helpful to guide clinical assessment and select appropriate target muscles for interventions.
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页数:7
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