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• W3120485718 abstract "The cause of surfer myelopathy remains enigmatic and long-term follow-up outcomes are not well documented. In the present study, the mechanisms underlying surfer myelopathy in children are analyzed and the long-term follow-up outcomes are reported. Clinical data from 3 institutions were retrospectively analyzed. Patients were assessed using the American Spinal Injury Association Impairment Scale (AIS) on admission and at follow-up. The mechanisms were studied by analyzing patients' medical history, magnetic resonance imaging, and magnetic resonance angiography . The prognosis of long-term follow-up was summarized. Thirty-one children were diagnosed with surfer myelopathy. Intramedullary high-intensity T2 signal from mid to lower thoracic level to conus was found during the acute stage. Follow-up magnetic resonance imaging in the subacute stage showed cranial progression of the T2 hyperintensity up to 1–10 vertebral segments, and no neurologic deterioration was found. Intramedullary lesion length between the complete and incomplete injury was significantly different ( P < 0.01) in the subacute phase. Flow voids around nerve roots and in the epidural space were detected in 18 patients and 15 patients, respectively, on axial T2-weighted imaging. Enlarged tortuous veins were found in 3 of 6 patients who underwent spinal magnetic resonance angiography, which were discontinuous around nerve root. During long-term follow-up, no patients with AIS grade A recovered, and atrophic cord was observed in the later stage in 14 patients. Patients with incomplete injury had different recoveries. Surfer myelopathy in children is caused by spinal venous hypertension. The AIS grade on admission is a predictor of prognosis." @default.
• W3120485718 created "2021-01-18" @default.
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• W3120485718 date "2021-04-01" @default.
• W3120485718 modified "2023-10-18" @default.
• W3120485718 title "Surfer Myelopathy in Children: A Case Series Study" @default.
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• W3120485718 doi "https://doi.org/10.1016/j.wneu.2020.12.135" @default.
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