Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After spinal cord injury, hyper-reflexia can lead to episodic hypertension, muscle spasticity and urinary bladder dyssynergia. This condition may be caused by primary afferent fiber sprouting providing new input to partially denervated spinal interneurons, autonomic neurons and motor neurons. However, conflicting reports concerning afferent neurite sprouting after cord injury do not provide adequate information to associate sprouting with hyper-reflexia. Therefore, we studied the effect of mid-thoracic spinal cord transection on central projections of sensory neurons, quantified by area measurements. The area of myelinated afferent arbors, immunolabeled by cholera toxin B, was greater in laminae I-V in lumbar, but not thoracic cord, by one week after cord transection. Changes in small sensory neurons and their unmyelinated fibers, immunolabeled for calcitonin gene-related peptide, were assessed in the cord and in dorsal root ganglia. The area of calcitonin gene-related peptide-immunoreactive fibers in laminae III-V increased in all cord segments at two weeks after cord transection, but not at one week. Numbers of sensory neurons immunoreactive for calcitonin gene-related peptide were unchanged, suggesting that the increased area of immunoreactivity reflected sprouting rather than peptide up-regulation. Immunoreactive fibers in the lateral horn increased only above the lesion and in lumbar segments at two weeks after cord transection. They were not continuous with dorsal horn fibers, suggesting that they were not primary afferent fibers. Using the fluorescent tracer DiI to label afferent fibers, an increase in area could be seen in Clarke's nucleus caudal to the injury two weeks after transection. In conclusion, site- and time-dependent sprouting of myelinated and unmyelinated primary afferent fibers, and possibly interneurons, occurred after spinal cord transection. Afferent fiber sprouting did not reach autonomic or motor neurons directly, but may cause hyper-reflexia by increasing inputs to interneurons.
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PMID:Sprouting of primary afferent fibers after spinal cord transection in the rat. 962 43

Following spinal cord injury (SCI), exaggerated reflexes and muscle tone emerge that contribute to a general spastic syndrome in humans. At present, the underlying mechanisms involved with the development of spasticity following traumatic spinal cord injury, especially with regard to axial musculature, remains unclear. The purpose of the present study was to examine the temporal changes in sacrocaudal motoneuronal morphology following complete transection of the sacral spinal cord and to correlate these changes with the onset and progression of spasticity within the tail musculature. The spinal cords of rats were transected at the upper sacral (S(2)) level. Animals were behaviorally tested for the onset and progression of spasticity in the tail and at 1, 2, 4, or 12 weeks postinjury were sacrificed. At these time points, the animals demonstrated stage 1, 2, 3, or 4 spastic behavior, respectively. Sacrocaudal motoneurons innervating selected flexor muscles within the tail were retrogradely labeled with cholera toxin beta-subunit and neuronal morphology was analyzed using a combination of immunocytochemistry and standard microscopy. Initially over the first 2 weeks postinjury, a transient increase in the lengths of primary and secondary dendrites occurred. However, a progressive decrease in the overall number of dendritic branches was observed between 2 and 12 weeks postinjury, which parallels the time frame for the progressive increase in spastic behavior in the tail musculature. Following spinal cord injury, there is an alteration in the morphology of tail flexor motoneurons, which may be relevant to the development of spasticity within the tail.
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PMID:Alteration in axial motoneuronal morphology in the spinal cord injured spastic rat. 1569 23

Spasticity of the midline (axial) musculature may hinder (1) performing transfers, (2) efficient extremity and head movements, and (3) efficient respiration. Currently, gaps exist in our knowledge of the pathophysiology involved in spasticity development within the axial musculature. The goals of this study were (1) to study the effects of S(2) transection on the number and distribution of glutamatergic inputs, arising from primary afferents, and glycinergic inputs to sacrocaudal motoneurons; and (2) to correlate changes in these synaptic inputs with the development of spasticity within the tail musculature, which are the caudal counterparts to the trunk axial musculature. Animals with S(2) spinal transection were tested behaviorally using our established system. At 1, 2, 4, and 12 weeks post-injury, sacrocaudal motoneurons were retrogradely labeled with cholera toxin beta-subunit (CTB), and temporal changes in vesicular glutamate transporter 1 (VGLUT1) and glycine transporter 2 (GlyT2) inputs to CTB-labeled motoneurons were visualized using antibodies specific for each synaptic type and confocal microscopy. These time points correspond to each of 4 stages of spasticity development. There was no significant change in either VGLUT1 or GlyT2 labeling of sacrocaudal motoneurons at any of the time points examined. Spinal cord injury-induced spasticity, in the tail musculature, does not appear to involve either an increase in monosynaptic glutamatergic inputs from myelinated afferents or a decrease in glycinergic inputs to sacrocaudal motoneurons.
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PMID:VGLUT1 and GLYT2 labeling of sacrocaudal motoneurons in the spinal cord injured spastic rat. 1713 99

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.
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PMID:Hindlimb spasticity after unilateral motor cortex lesion in rats is reduced by contralateral nerve root transfer. 2787 56