Satomi K, Terashima Y, Goto K, Arakawa M, Ito H
Second Department of Internal Medicine, Gifu University School of Medicine.
Rinsho Shinkeigaku. 1990 Mar;30(3):299-303.
A patient of mutism with pseudobulbar palsy and frontal lobe syndrome resulting from lacunar state was reported. The patient, a 64-year-old man, was admitted to Gifu University Hospital because of a decrease in spontaneous activity, lack of volition and anorexia. The CT scan, performed on July 29, 1987, demonstrated lacune in the right internal capsule (IC), periventricular lucency especially around the anterior horn of lateral ventricles, and ventricular dilatation. He was transferred to a medical ward because of repeated aspiration pneumonia. Neurological examination revealed mutism, pseudobulbar palsy, and frontal lobe signs. The CT scan, performed on March 30 1988, demonstrated the newly developed lacune in the left IC. The MRI also showed two coinciding lacunes, one in the genu of the right IC and the other in the anterior limb of the left IC. The SPECT with 123I iodoamphetamine showed decreased blood supply predominantly to the frontal lobes. A mechanism by which the mutism occurs is discussed from two points of view, pseudobulbar palsy and frontal lobe syndrome. He developed initially frontal lobe syndrome in which paucity of spontaneous speech was noted. The CT scan at that time demonstrated lacune in the right IC. About eight months later when he became mute, the CT scan showed lacunes in bilateral ICs without any other low density areas in frontal language areas such as Broca's area, subcortical area and supplementary motor area. As the MRI showed that the right lacune was in the genu but the left lacune was in the anterior limb of IC, the left cortico-bulbar tract was thought to be not directly involved. The SPECT showed decreased blood supply predominantly to the frontal lobes. Although dysphagia improved, mutism did not improve at all. Therefore it is postulated that both pseudobulbar palsy and frontal lobe dysfunction might play a role in producing the mutism of this patient.
报告了一例因腔隙状态导致缄默症伴假性球麻痹和额叶综合征的患者。该患者为64岁男性，因自发活动减少、意志缺乏和厌食入住岐阜大学医院。1987年7月29日进行的CT扫描显示右侧内囊有腔隙、脑室周围透亮区，尤其是侧脑室前角周围，以及脑室扩张。由于反复发生吸入性肺炎，他被转到内科病房。神经系统检查发现缄默症、假性球麻痹和额叶体征。1988年3月30日进行的CT扫描显示左侧内囊出现新的腔隙。MRI也显示两个重合的腔隙，一个在右侧内囊膝部，另一个在左侧内囊前肢。用123I 碘安非他明进行的单光子发射计算机断层扫描（SPECT）显示主要是额叶的血液供应减少。从假性球麻痹和额叶综合征两个角度讨论了缄默症发生的机制。他最初出现额叶综合征，表现为自发言语减少。当时的CT扫描显示右侧内囊有腔隙。大约八个月后他变得缄默时，CT扫描显示双侧内囊有腔隙，而额叶语言区如布洛卡区、皮质下区和辅助运动区没有任何其他低密度区。由于MRI显示右侧腔隙在膝部，而左侧腔隙在内囊前肢，因此认为左侧皮质延髓束未直接受累。SPECT显示主要是额叶的血液供应减少。尽管吞咽困难有所改善，但缄默症完全没有改善。因此推测假性球麻痹和额叶功能障碍可能都在该患者缄默症的产生中起作用。
