Tarhan N Cagla, Agildere A Muhtesem, Benli U Sibel, Ozdemir F Nurhan, Aytekin Cuneyt, Can Ufuk
Department of Radiology, Baskent University Faculty of Medicine, Fevzi Cakmak Cad. 10. Sok No. 45, 06490 Bahçelievler, Ankara, Turkey.
AJR Am J Roentgenol. 2004 Mar;182(3):809-16. doi: 10.2214/ajr.182.3.1820809.
Osmotic demyelination syndrome has been reported in patients with end-stage renal disease, but the specific MRI findings in this patient group have not been documented in detail. Our aims were to present the brain MRI findings during an episode after hemodialysis and at follow-up, and to identify possible factors that may contribute to lesion development.
Seventeen patients with osmotic demyelination syndrome who had undergone hemodialysis at least once and had brain MRI examinations were retrospectively reviewed. Neurologic and MRI examinations were performed during a clinical episode. Serum levels of sodium, creatinine, blood urea nitrogen, and glucose were assessed, and serum osmolality and the ratio of blood urea nitrogen to creatinine (BUN:Cr) were calculated. Follow-up MRI was performed in nine cases. Laboratory and imaging findings were evaluated.
An altered level of consciousness and convulsions were the most common neurologic symptoms. The pons was involved in 11 patients (65%) and extrapontine sites in 12 (71%). Four patients had dysequilibrium syndrome. Follow-up MRI showed complete resolution in six patients and lesion reduction in three within a short time. The most common biochemical changes at the time of MRI were hyponatremia and low BUN:Cr in the blood. Only one patient showed rapid correction of hyponatremia and a rapid change in osmolality during the acute stage.
In patients who develop osmotic demyelination syndrome after hemodialysis, the lesions may involve the pons or the pons and extrapontine sites. Most lesions that were followed up resolved rapidly and almost completely, favoring transient edema rather than demyelination. Blood chemistries suggested underlying changes in osmolality, particularly as a result of urea shift from the extracellular fluid.
终末期肾病患者中已报道有渗透性脱髓鞘综合征，但该患者群体的具体MRI表现尚未有详细记录。我们的目的是展示血液透析后发作期及随访时的脑部MRI表现，并确定可能导致病变发展的因素。
回顾性分析17例至少接受过一次血液透析且进行过脑部MRI检查的渗透性脱髓鞘综合征患者。在临床发作期进行神经学和MRI检查。评估血清钠、肌酐、血尿素氮和葡萄糖水平，并计算血清渗透压以及血尿素氮与肌酐的比值（BUN:Cr）。9例患者进行了随访MRI检查。对实验室和影像学检查结果进行评估。
意识水平改变和惊厥是最常见的神经学症状。11例患者（65%）脑桥受累，12例患者（71%）脑桥外部位受累。4例患者出现失衡综合征。随访MRI显示6例患者病变完全消退，3例患者短期内病变减轻。MRI检查时最常见的生化改变是低钠血症和血液中BUN:Cr降低。仅1例患者在急性期出现低钠血症迅速纠正和渗透压快速变化。
血液透析后发生渗透性脱髓鞘综合征的患者，病变可能累及脑桥或脑桥及脑桥外部位。大多数接受随访的病变迅速且几乎完全消退，提示为短暂性水肿而非脱髓鞘。血液化学指标提示渗透压存在潜在变化，尤其是由于尿素从细胞外液转移所致。
