Department of Medicine, University of Virginia Health System, Charlottesville, 22908, USA.
Am J Med Sci. 2010 Jun;339(6):561-7. doi: 10.1097/MAJ.0b013e3181d3cd78.
The osmotic demyelination syndrome (ODS) has been a recognized complication of the rapid correction of hyponatremia for decades. However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium. This finding suggests that the pathogenesis of ODS may be more complex and involve the inability of brain cells to respond to rapid changes in osmolality of the interstitial (extracellular) compartment of the brain, leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas. Features of the syndrome include quadriparesis and neurocognitive changes in the presence of characteristic lesions found on magnetic resonance imaging of the brain. Although slow correction of hyponatremia seems to be the best way to prevent development of the syndrome, there are new data that suggest reintroduction of hyponatremia in those patients who have undergone inadvertent rapid correction of the serum sodium and corticosteroids may play a role in prevention of ODS.
渗透性脱髓鞘综合征（ODS）几十年来一直被认为是纠正低钠血症过快的并发症。然而，近年来，多种其他医学病症与 ODS 的发生相关，与血清钠的变化无关。这一发现表明，ODS 的发病机制可能更为复杂，涉及脑细胞无法对大脑细胞外间质（细胞外）渗透压的快速变化做出反应，导致能量耗尽的细胞脱水，随后发生在特征性区域的轴突损伤。该综合征的特征包括在大脑磁共振成像上发现的特征性病变存在时出现四肢瘫痪和神经认知变化。尽管缓慢纠正低钠血症似乎是预防该综合征发生的最佳方法，但有新数据表明，对于那些血清钠已被意外快速纠正的患者，重新引入低钠血症，皮质类固醇可能在预防 ODS 中发挥作用。
