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急性脊髓損傷之藥物治療

Pharmacotherapy in Acute Spinal Cord Injury

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摘要


急性外傷性脊髓損傷是一悲慘事件,會造成病人及社會巨額負擔。目前處理多著重在一般性支持療法與穩定合併的脊柱傷害,以防止脊髓進一步受傷。大多數研究急性脊髓損傷後病理生理變化之實驗指出,損傷破壞脊髓為兩階段機轉,外傷造成的初發(直接)機械性傷害會引起脊髓續發(間接)進行性自體毀滅傷害。近年來,氧自由基生成與脂肪過氧化被認為需為續發傷害負責。 許多藥物在不同動物模型進行檢驗,雖然甲基脫氫皮質醇(methylprednisolone, MP)是主要的研究對象,但尚有不少藥物發展出來。在七十年代早期,脊損動物以類固醇治療的成果,提供美國國家急性脊髓損傷研究(NASCIS)之基礎。這主要是基於類固醇可以抑制脊髓損傷後脂肪過氧化,且透過抑制損傷引發之連鎖效應而促進恢復。在初次試驗,MP不能改善損傷結果。在NASCIS第二試驗,傷後八小時內先給MP每公斤體重30毫克劑量,再於後二十三小時續給每小時每公斤體重5.4毫克劑量。一年後追蹤結果顯示,該投藥法比安慰劑帶來更為顯著的神經改善現象。NASCIS第三試驗主要在探討MP投藥最佳時機,治療的最適期間,以及在首劑後改投tirilazad能否帶來好處。結果顯示,假使首劑MP在傷後三小時內投予,MP治療二十四小時就可,但首劑若在傷後三到八小時才投與,則MP治療應延長為四十八小時。近年來,投予高劑量MP已成為最佳治療脊髓損傷之標準,但傷後八小時則不應投藥。

關鍵字

脊髓損傷 類固醇 神經恢復

並列摘要


Acute traumatic spinal cord injury (SCI), a devastating event, results in huge costs to patients and society. Current management emphasizes general supportive care and stabilization of associated spinal columnar injury to prevent worsening of the cord lesions. Most of the numerous experimental studies to investigate pathophysiological changes following acute SCI suggest a two-step mechanism of damage to the spinal cord in which the primary (direct) or mechanical injury caused by trauma initiates secondary (indirect) or progressive autodestructive injury of the cord. During recent years, free oxygen radical generation and lipid peroxidation have been implicated in the secondary injury. Several pharmacological agents have been examined in a variety of animal models. Although methylprednisolone (MP) is the major agent currently being studied, other agents are also being developed. Animal models of SCI treated with steroids in the early 1970s served as the basis for the National Acute Spinal Cord Injury Study (NASCIS) in America. The leading theory is that steroids inhibit post-SCI lipid peroxidation and enhance recovery by inhibiting the injury-induced degenerative cascade that follows. In initial trails, MP was not effective in improving the outcome. In NASCIS II, MP was given in a dosage of 30 mg/kg body weight within 8 hours of injury, followed by the administration of MP, 5.4 mg/kg/hr, for 23 hours. This regimen produced a significant neurologic improvement in one-year follow-up when compared with placebo. The study of NASCIS III trial is intended to determine the best time for starting the MP regimen, the optimal duration of therapy, and the benefits, if any, of substituting tirilazad mesylate for MP after the initial dose. In conclusion, if the initial bolus is started within 3 hours of injury, 24-hour MP treatment is appropriate; if the bolus is not administered until 3-8 hours, treatment should be extended for 48 hours. Recently the administration of high-dose MP has become the standard care in the optimal management of SCI. The therapy should not be given more than 8 hours after injury.

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