Zyluk A
Kliniki Chirurgii Ogólnej i Chirurgii Reki Pomorskiej Akademii Medycznej w Szczecinie.
Chir Narzadow Ruchu Ortop Pol. 1996;61(5):493-8.
Algodystrophy (reflex sympathetic dystrophy, Sudeckłs atrophy) is the condition of still unclear pathogenesis. Paul Sudeck, who described the syndrome was convinced of its inflammatory nature; later research established the inducing role of the sympathetic nervous system for many years. This view has been questioned in the last decade. This paper presents some evidence of inflammatory explanation of the disorder: increased uptake of the immunoglobulin IgM labeled In111 in affected area, followed by increased vascular permeability for macromolecules, and impaired metabolism of the high energy phosphates following the impaired oxygen extraction in the affected extremity. Free oxygen and hydroxyl radicals injurious role in the course of algodystrophy is also established by beneficial treatment with the use of free radicals scavengers (mannitol, dimethyl sulfoxide, N-acetylcysteine) and by pathologic ultrastructural changes in muscle cells due to oxidative stress. The view of the inflammatory nature of acute stage of algodystrophy does not preclude a role of sympathetic nervous system but it better explains some clinical aspects of this phase of the condition and increases recognition of its complicated nature.
痛性营养不良（反射性交感神经营养不良、施戴克萎缩）是一种发病机制仍不清楚的病症。描述该综合征的保罗·施戴克确信其具有炎症性质；后来的研究确立了交感神经系统多年来的诱发作用。在过去十年中，这种观点受到了质疑。本文提供了一些对该病症进行炎症解释的证据：受累区域中标记有铟111的免疫球蛋白IgM摄取增加，随后大分子的血管通透性增加，以及受累肢体氧摄取受损后高能磷酸盐代谢受损。通过使用自由基清除剂（甘露醇、二甲基亚砜、N - 乙酰半胱氨酸）进行有益治疗以及氧化应激导致肌肉细胞出现病理性超微结构变化，也证实了游离氧和羟基自由基在痛性营养不良病程中的有害作用。痛性营养不良急性期具有炎症性质的观点并不排除交感神经系统的作用，但它能更好地解释该病症这一阶段的一些临床方面，并提高对其复杂性质的认识。
