Hantson Philippe, Grandin Cécile, Duprez Thierry, Nassogne Marie-Cécile, Guérit Jean-Michel
Department of Intensive Care, Cliniques Saint-Luc, Université catholique de Louvain, Avenue Hippocrate, 10, 1200 Brussels, Belgium.
Eur Radiol. 2005 Jan;15(1):59-64. doi: 10.1007/s00330-004-2338-9. Epub 2004 Apr 29.
Magnetic resonance (MR) multimodality evoked potentials (MEPs) and clinical findings were correlated in a 47-year-old epileptic man in whom parenteral valproic acid (VPA) therapy induced severe comatose hyperammonemic encephalopathy without biological signs of hepatotoxicity (or hepatocytic dysfunction). Although the plasma VPA level remained within a normal therapeutic range, the ammoniemia increased to a toxic peak level at 411 micromol/l 24 h after symptom onset, requiring VPA therapy discontinuation. Brain MR monitoring demonstrated early cytotoxic edema evolving into delayed vasogenic edema and final brain atrophy. Concomitantly to abnormalities within the brainstem on MR images, an increase in brainstem conduction at MEPs and clinical disturbance of brainstem reflexes were observed at the initial phase of the disease course. Later, the resolution of the MR and MEPs abnormalities paralleled the clinical recovery of the reflexes.
在一名47岁的癫痫男性患者中,对磁共振(MR)多模态诱发电位(MEP)与临床发现进行了相关性研究。该患者接受胃肠外丙戊酸(VPA)治疗后诱发了严重的昏迷性高氨血症性脑病,但无肝毒性(或肝细胞功能障碍)的生物学迹象。尽管血浆VPA水平仍在正常治疗范围内,但症状出现后24小时,氨血症升至411微摩尔/升的毒性峰值水平,需要停用VPA治疗。脑部MR监测显示早期细胞毒性水肿演变为迟发性血管源性水肿,最终导致脑萎缩。在病程初期,与MR图像上脑干的异常情况同时出现的是,MEP显示脑干传导增加,且临床出现脑干反射障碍。后来,MR和MEP异常的消退与反射的临床恢复情况平行。