Koskiniemi M
Acta Neurol Scand. 1975 Jan;51(1):12-20. doi: 10.1111/j.1600-0404.1975.tb01355.x.
Thirty-one patients suffering from progressive myoclonus epilepsy, (also called Unverricht-Lundborg's disease) without Lafora bodies, were examined to check the findings reported in literature and to chart out the main abnormalities in routine laboratory findings. Many alterations could be pointed out, but a high proportion of them were due to factors which are secondary to the syndrome of progressive myoclonus epilepsy: continuous anticonvulsive medication; immobilization; frequent infections; and the patient's poor nutritional condition. The most remarkable finding, and the only one which supported the abnormality reported earlier, was the raised excretion of indican which could not be explained by fermentation in the bowels. The urinary 5-hydroxyindoleacetic acid excretion was a little low, but still within the normal range. The tryptophan and 5-hydroxytryptamine metabolism deserves further investigation in attempting to discover the aetiology of progressive myoclonus epilepsy.
对31例患有进行性肌阵挛癫痫（也称为翁韦里希特-伦德伯格病）且无拉福拉小体的患者进行了检查，以核实文献报道的结果，并梳理出常规实验室检查结果中的主要异常情况。可以指出许多改变，但其中很大一部分是由进行性肌阵挛癫痫综合征的继发因素引起的：持续抗惊厥药物治疗；活动受限；频繁感染；以及患者营养不良状况。最显著的发现，也是唯一支持先前报道异常情况的发现，是吲哚苷排泄增加，这无法用肠道发酵来解释。尿5-羟吲哚乙酸排泄量略低，但仍在正常范围内。在试图发现进行性肌阵挛癫痫的病因时，色氨酸和5-羟色胺代谢值得进一步研究。
