Tatemichi T K, Desmond D W, Prohovnik I
Department of Neurology, Columbia-Presbyterian Medical Center, New York, NY, USA.
Arzneimittelforschung. 1995 Mar;45(3A):371-85.
The mechanisms of dementia resulting from small deep infarctions are incompletely understood. The thesis underlying the concept of "multi-infarct dementia" is that multiple lesions have a synergistic effect on mental functions, resulting in dementia irrespective of specific location or volume. In this report, we summarize our experience with six patients reported previously along with additional patients examined subsequently, whose clinical features and brain imaging findings allow an alternative formulation for dementia resulting from lacunar stroke. The six initial patients presented with an abrupt change in behavior after acute infarction involving the inferior genu of the internal capsule documented by computed tomography (CT) and magnetic resonance imaging (MRI). The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia were evident in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients using 133xenon regional cerebral blood flow (rCBF) and single photon emission computed tomography (SPECT) showed focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. Perfusion was also defective in the medial and laterial temporal cortex. Important pathways of the limbic system traverse the inferior capsule in the region of the genu. Corticothalamic and thalamocortical fibers form the thalamic peduncles which detach from the internal capsule and enter the thalamus at its rostral and caudal poles and along its dorsal surface. The anterior thalamic peduncle, conveys reciprocal connections between the dorsomedial nucleus and the cingulate gyrus, as well as the prefrontal and orbitofrontal cortex. The inferior thalamic peduncle carries fibers which connect the thalamus with orbitofrontal, insular, and temporal cortex, as well as the amygdala via the ansa peduncularis to the ventral amygdalofugal pathway. Thus, damage to one or both white-matter tracts may occur with infarctions in the region of the inferior genu, causing striking frontal behavioral effects and memory loss in our patients associated with functional deactivation of the ipsilateral frontal and temporal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
小的深部梗死导致痴呆的机制尚未完全明了。“多发梗死性痴呆”概念的基本论点是，多个病灶对心理功能具有协同作用，无论其具体位置或大小如何，均可导致痴呆。在本报告中，我们总结了之前报道的6例患者以及随后检查的其他患者的经验，这些患者的临床特征和脑影像学表现为腔隙性卒中所致痴呆提供了另一种解释。最初的6例患者在急性梗死累及内囊膝部后出现行为突然改变，这已通过计算机断层扫描（CT）和磁共振成像（MRI）得以证实。急性综合征的特征为警觉性波动、注意力不集中、记忆力减退、淡漠、意志缺失和精神运动迟缓，提示额叶功能障碍。对侧偏瘫和构音障碍通常较轻，除非梗死扩展至后肢。对5例左侧梗死患者进行的神经心理学测试显示存在严重的言语记忆丧失。另外4例患者存在与痴呆相符的其他认知缺陷。右侧梗死导致视觉空间记忆短暂受损。3例患者采用133氙区域脑血流（rCBF）和单光子发射计算机断层扫描（SPECT）进行的功能性脑成像显示，半球灌注局部减少，在同侧额叶下部和内侧皮质最为明显。内侧和外侧颞叶皮质的灌注也存在缺陷。边缘系统的重要通路在膝部区域穿过内囊。皮质丘脑纤维和丘脑皮质纤维形成丘脑脚，它们从内囊分离，在丘脑的头端和尾端以及背表面进入丘脑。前丘脑脚传递背内侧核与扣带回以及前额叶和眶额叶皮质之间的相互连接。丘脑下脚携带的纤维将丘脑与眶额叶、岛叶和颞叶皮质相连，还通过脚间袢与杏仁核相连，进而与腹侧杏仁体传出通路相连。因此，在下膝部区域发生梗死时，一条或两条白质束可能受损，导致我们的患者出现明显的额叶行为效应和记忆丧失，并伴有同侧额叶和颞叶皮质的功能失活。（摘要截选至400字）
