Spinal cord · 2026
Pathogenesis of pediatric acute hyperextension spinal cord injury based on clinical outcomes and early radiological characteristics.
СтатьяНаблюдательное исследованиеМногоцентровое исследованиеНазвание и аннотация: Перевод в очереди
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Lu Hongwei, Xue Peiran, Fan Qianqian, Sun Wenzhe, Zeng Lian, Zhang Pengqing, Ye Bing, Shen Xiantao, Wu Bin, Guo Xiaodong
Аннотация
STUDY DESIGN: Retrospective observational cohort study SETTING: Three hospitals in China.
OBJECTIVE: To elucidate the pathogenesis of pediatric acute hyperextension spinal cord injury (PAHSCI) through comprehensive analysis of acute-phase clinical outcomes and multimodal magnetic resonance imaging (MRI) characteristics.
METHODS: We retrospectively analyzed 49 persons with PAHSCI. Case data and MRI multimodal imaging such as MRI, magnetic resonance angiography (MRA), and diffusion tensor imaging (DTI) were collected. Pathogenesis was analyzed based on clinical outcomes, radiological characteristics, spinal anatomy, and biomechanics.
RESULTS: The primary cause of PAHSCI was back-bending training (45/49). The American Spinal Injury Association (ASIA) impairment scale distribution at admission was grade A (n = 29), B (n = 13), C (n = 4), D (n = 3). Final follow-up revealed grade A (n = 29), B (n = 4), C (n = 1), D (n = 10), E (n = 5). The level of spinal cord injury in most cases (48/49) was located at the Th9-L1 level, and intramedullary edema was observed on MRI in 48 persons at admission. Intramedullary hemorrhage was observed in 27 cases, and sequential MRI showed progressively increasing intramedullary edema. In 22 cases, atrophy or even disappearance of the middle and lower thoracic spinal cord occurred 2-6 months after spinal cord injury. MRI of 19 cases showed same radiological changes at the conus-cauda equina junction, which manifested as an arcuate depression on the anterior side of the conus medullaris. Seventeen persons with MRA examination did not have vascular malformations, vascular embolisms, or arteriovenous fistulas.
CONCLUSION: We believe that the possible pathogenesis of PAHSCI is: "axial traction (especially at conus) + transverse compression (especially at Th9-10)" of the spinal cord and the resulting microvascular damage ultimately resulting in spinal cord ischemia, edema, necrosis, and the formation of a vicious cycle, ultimately causing spinal cord atrophy.
OBJECTIVE: To elucidate the pathogenesis of pediatric acute hyperextension spinal cord injury (PAHSCI) through comprehensive analysis of acute-phase clinical outcomes and multimodal magnetic resonance imaging (MRI) characteristics.
METHODS: We retrospectively analyzed 49 persons with PAHSCI. Case data and MRI multimodal imaging such as MRI, magnetic resonance angiography (MRA), and diffusion tensor imaging (DTI) were collected. Pathogenesis was analyzed based on clinical outcomes, radiological characteristics, spinal anatomy, and biomechanics.
RESULTS: The primary cause of PAHSCI was back-bending training (45/49). The American Spinal Injury Association (ASIA) impairment scale distribution at admission was grade A (n = 29), B (n = 13), C (n = 4), D (n = 3). Final follow-up revealed grade A (n = 29), B (n = 4), C (n = 1), D (n = 10), E (n = 5). The level of spinal cord injury in most cases (48/49) was located at the Th9-L1 level, and intramedullary edema was observed on MRI in 48 persons at admission. Intramedullary hemorrhage was observed in 27 cases, and sequential MRI showed progressively increasing intramedullary edema. In 22 cases, atrophy or even disappearance of the middle and lower thoracic spinal cord occurred 2-6 months after spinal cord injury. MRI of 19 cases showed same radiological changes at the conus-cauda equina junction, which manifested as an arcuate depression on the anterior side of the conus medullaris. Seventeen persons with MRA examination did not have vascular malformations, vascular embolisms, or arteriovenous fistulas.
CONCLUSION: We believe that the possible pathogenesis of PAHSCI is: "axial traction (especially at conus) + transverse compression (especially at Th9-10)" of the spinal cord and the resulting microvascular damage ultimately resulting in spinal cord ischemia, edema, necrosis, and the formation of a vicious cycle, ultimately causing spinal cord atrophy.