Kawamura Mitsuru, Sugimoto Azusa, Kobayakawa Mutsutaka, Tsuruya Natsuko
Department of Neurology, Showa University School of Medicine, Tokyo, Japan.
Brain Nerve. 2012 Jul;64(7):799-813.
To discuss the neurological basis of facial recognition, we present our case reports of impaired recognition and a review of previous literature. First, we present a case of infarction and discuss prosopagnosia, which has had a large impact on face recognition research. From a study of patient symptoms, we assume that prosopagnosia may be caused by unilateral right occipitotemporal lesion and right cerebral dominance of facial recognition. Further, circumscribed lesion and degenerative disease may also cause progressive prosopagnosia. Apperceptive prosopagnosia is observed in patients with posterior cortical atrophy (PCA), pathologically considered as Alzheimer's disease, and associative prosopagnosia in frontotemporal lobar degeneration (FTLD). Second, we discuss face recognition as part of communication. Patients with Parkinson disease show social cognitive impairments, such as difficulty in facial expression recognition and deficits in theory of mind as detected by the reading the mind in the eyes test. Pathological and functional imaging studies indicate that social cognitive impairment in Parkinson disease is possibly related to damages in the amygdalae and surrounding limbic system. The social cognitive deficits can be observed in the early stages of Parkinson disease, and even in the prodromal stage, for example, patients with rapid eye movement (REM) sleep behavior disorder (RBD) show impairment in facial expression recognition. Further, patients with myotonic dystrophy type 1 (DM 1), which is a multisystem disease that mainly affects the muscles, show social cognitive impairment similar to that of Parkinson disease. Our previous study showed that facial expression recognition impairment of DM 1 patients is associated with lesion in the amygdalae and insulae. Our study results indicate that behaviors and personality traits in DM 1 patients, which are revealed by social cognitive impairment, are attributable to dysfunction of the limbic system.
为探讨面部识别的神经学基础，我们展示了关于识别受损的病例报告以及对既往文献的综述。首先，我们介绍一例梗死病例并讨论人面失认症，其对面部识别研究产生了重大影响。通过对患者症状的研究，我们推测人面失认症可能由右侧枕颞叶单侧病变以及面部识别的右脑优势所致。此外，局限性病变和退行性疾病也可能导致进行性人面失认症。在病理上被认为是阿尔茨海默病的后皮质萎缩（PCA）患者中观察到知觉性人面失认症，而在额颞叶变性（FTLD）患者中观察到联想性人面失认症。其次，我们将面部识别作为交流的一部分进行讨论。帕金森病患者表现出社会认知障碍，例如面部表情识别困难以及通过眼睛解读心灵测试检测到的心理理论缺陷。病理和功能成像研究表明，帕金森病中的社会认知障碍可能与杏仁核及周围边缘系统的损伤有关。社会认知缺陷在帕金森病的早期甚至前驱期就可观察到，例如，快速眼动（REM）睡眠行为障碍（RBD）患者表现出面部表情识别受损。此外，1型强直性肌营养不良（DM 1）是一种主要影响肌肉的多系统疾病，其患者表现出与帕金森病类似的社会认知障碍。我们之前的研究表明，DM 1患者的面部表情识别受损与杏仁核和脑岛的病变有关。我们的研究结果表明，DM 1患者中由社会认知障碍所揭示的行为和人格特质可归因于边缘系统功能障碍。
