Konishi Y, Yasujima M, Kuriyama M, Konishi K, Hayakawa K, Fujii Y, Ishii Y, Sudo M
Department of Pediatrics, Fukui Medical School, Japan.
Epilepsia. 1992 Mar-Apr;33(2):304-9. doi: 10.1111/j.1528-1157.1992.tb02320.x.
Magnetic resonance imaging (MRI) was performed on five patients with infantile spasms who were treated with relatively low doses of adrenocorticotrophic hormone (ACTH) to study the extent of brain shrinkage induced by ACTH therapy. MRI prior to ACTH therapy revealed periventricular hyperintensity (PVH) areas and poor myelination in four patients. In one case, MRI performed 2 days after initiation of ACTH therapy also showed PVH and poor myelination. Brain shrinkage was observed 2 weeks after initiation of ACTH therapy. The most impressive follow-up finding upon MRI was the decrease in PVH found in four patients. The differentiation between myelinated white matter and surrounding cortex became poorer in three cases. Cortical atrophy progressed in all patients but ventricular dilation progressed in only one patient. At the end of ACTH therapy, ventricular dilation progressed in all cases. These findings suggest that loss of water not only from periventricular white matter but also from cortex is the main etiological factor of brain shrinkage induced by ACTH.
对五名接受相对低剂量促肾上腺皮质激素（ACTH）治疗的婴儿痉挛症患者进行了磁共振成像（MRI）检查，以研究ACTH治疗引起的脑萎缩程度。ACTH治疗前的MRI显示，四名患者存在脑室周围高信号（PVH）区域和髓鞘形成不良。在一例患者中，ACTH治疗开始2天后进行的MRI也显示有PVH和髓鞘形成不良。ACTH治疗开始2周后观察到脑萎缩。MRI最显著的随访结果是四名患者的PVH减少。在三例患者中，有髓鞘的白质与周围皮质之间的区分变得更差。所有患者均出现皮质萎缩，但仅一名患者出现脑室扩张。在ACTH治疗结束时，所有病例均出现脑室扩张。这些发现表明，不仅脑室周围白质，而且皮质中的水分流失是ACTH引起脑萎缩的主要病因。
