Abstract
Lower extremity spasticity is a common sequela among patients with acquired brain injury. The optimum treatment remains controversial. The aim of our study was to test the feasibility and effectiveness of contralateral nerve root transfer in reducing post stroke spasticity of the affected hindlimb muscles in rats. In our study, we for the first time created a novel animal hindlimb spastic hemiplegia model in rats with photothrombotic lesion of unilateral motor cortex and we established a novel surgical procedure in reducing motor cortex lesion-induced hindlimb spastic hemiplegia in rats. Thirty six rats were randomized into three groups. In group A, rats received sham operation. In group B, rats underwent unilateral hindlimb motor cortex lesion. In group C, rats underwent unilateral hindlimb cortex lesion followed by contralateral L4 ventral root transfer to L5 ventral root of the affected side. Footprint analysis, Hoffmann reflex (H-reflex), cholera toxin subunit B (CTB) retrograde tracing of gastrocnemius muscle (GM) motoneurons and immunofluorescent staining of vesicle glutamate transporter 1 (VGLUT1) on CTB-labelled motoneurons were used to assess spasticity of the affected hindlimb. Sixteen weeks postoperatively, toe spread and stride length recovered significantly in group C compared with group B (P<0.001). Hmax (H-wave maximum amplitude)/Mmax (M-wave maximum amplitude) ratio of gastrocnemius and plantaris muscles (PMs) significantly reduced in group C (P<0.01). Average VGLUT1 positive boutons per CTB-labelled motoneurons significantly reduced in group C (P<0.001). We demonstrated for the first time that contralateral L4 ventral root transfer to L5 ventral root of the affected side was effective in relieving unilateral motor cortex lesion-induced hindlimb spasticity in rats. Our data indicated that this could be an alternative treatment for unilateral lower extremity spasticity after brain injury. Therefore, contralateral neurotization may exert a potential therapeutic candidate to improve the function of lower extremity in patients with spastic hemiplegia.
Highlights
Acquired brain injury is a major cause of long-term disability in adults
Quantification of vesicle glutamate transporter 1 (VGLUT1) boutons on cholera toxin subunit B (CTB)-labelled motorneurons The CTB retrograde labelled motoneurons were identified in each spinal cord segment from the right ventral horn in groups A and B
In group C, the labelled motoneurons were found on both sides of L4 ventral horn and the right side of L6 ventral horn, but not in the L5 spinal cord segment (Figure 3)
Summary
Acquired brain injury is a major cause of long-term disability in adults. Spasticity is one of the most common sequelae to stroke or traumatic brain injury survivors. 30% patients develop spasticity few weeks after stroke [1]. Patients with spasticity showed a lower quality of life compared with patients without this symptom [2]. The direct cost of stroke survivors with spasticity increased 4-fold compared with that of patients without spasticity up to 1 year after stroke [3]. A variety of therapeutic methods have been introduced to manage spasticity of the lower extremities. Conservative treatments such as oral medications, selective nerve blocks, botulinum toxin
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