Uhlhaas Peter J, Mishara Aaron L
Department of Neurophysiology, Max-Planck Institute for Brain Research, Deutschordenstrasse 46, Frankfurt am Main 60528, Germany.
Schizophr Bull. 2007 Jan;33(1):142-56. doi: 10.1093/schbul/sbl047. Epub 2006 Nov 21.
From phenomenological and experimental perspectives, research in schizophrenia has emphasized deficits in "higher" cognitive functions, including attention, executive function, as well as memory. In contrast, general consensus has viewed dysfunctions in basic perceptual processes to be relatively unimportant in the explanation of more complex aspects of the disorder, including changes in self-experience and the development of symptoms such as delusions. We present evidence from phenomenology and cognitive neuroscience that changes in the perceptual field in schizophrenia may represent a core impairment. After introducing the phenomenological approach to perception (Husserl, the Gestalt School), we discuss the views of Paul Matussek, Klaus Conrad, Ludwig Binswanger, and Wolfgang Blankenburg on perception in schizophrenia. These 4 psychiatrists describe changes in perception and automatic processes that are related to the altered experience of self. The altered self-experience, in turn, may be responsible for the emergence of delusions. The phenomenological data are compatible with current research that conceptualizes dysfunctions in perceptual processing as a deficit in the ability to combine stimulus elements into coherent object representations. Relationships of deficits in perceptual organization to cognitive and social dysfunction as well as the possible neurobiological mechanisms are discussed.
从现象学和实验的角度来看，对精神分裂症的研究一直强调“高级”认知功能的缺陷，包括注意力、执行功能以及记忆。相比之下，普遍的共识认为，在解释该疾病更复杂的方面，包括自我体验的变化和妄想等症状的发展时，基本感知过程的功能障碍相对不重要。我们从现象学和认知神经科学方面提供证据表明，精神分裂症患者感知领域的变化可能代表一种核心损伤。在介绍了感知的现象学方法（胡塞尔、格式塔学派）之后，我们讨论了保罗·马图塞克、克劳斯·康拉德、路德维希·宾斯万格和沃尔夫冈·布兰肯伯格对精神分裂症患者感知的看法。这四位精神病学家描述了与自我体验改变相关的感知和自动过程的变化。反过来，自我体验的改变可能是妄想产生的原因。这些现象学数据与当前的研究结果相符，当前研究将感知处理功能障碍概念化为将刺激元素组合成连贯物体表征的能力缺陷。本文还讨论了感知组织缺陷与认知和社会功能障碍的关系以及可能的神经生物学机制。
