Jablensky Assen
Centre for Clinical Research in Neuropsychiatry, School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Perth, Australia.
Dialogues Clin Neurosci. 2010;12(3):271-87. doi: 10.31887/DCNS.2010.12.3/ajablensky.
More than a century since the delineation of dementia praecox by Kraepelin, the etiology, neuropathology, and pathophysiology of schizophrenia remain elusive. Despite the availability of criteria allowing reliable diagnostic identification, schizophrenia essentially remains a broad clinical syndrome defined by reported subjective experiences (symptoms), loss of function (behavioral impairments), and variable patterns of course. Research has identified a number of putative biological markers associated with the disorder, including neurocognitive dysfunction, brain dysmorphology, and neurochemical abnormalities. Yet none of these variables has to date been definitively proven to possess the sensitivity and specificity expected of a diagnostic test. Genetic linkage and association studies have targeted multiple candidate loci and genes, but failed to demonstrate that any specific gene variant, or a combination of genes, is either necessary or sufficient to cause schizophrenia. Thus, the existence of a specific brain disease underlying schizophrenia remains a hypothesis. Against a background of an ever-increasing volume of research data, the inconclusiveness of the search for causes of the disorder fuels doubts about the validity of the schizophrenia construct as presently defined. Given the protean nature of the symptoms of schizophrenia and the poor coherence of the clinical and biological findings, such doubts are not without reason. However, simply dismantling the concept is unlikely to result in an alternative model that would account for the host of clinical phenomena and research data consistent with a disease hypothesis of schizophrenia. For the time being, the clinical concept of schizophrenia is supported by empirical evidence that its multiple facets form a broad syndrome with non-negligible internal cohesion and a characteristic evolution over time. The dissection of the syndrome with the aid of endophenotypes is beginning to be perceived as a promising approach in schizophrenia genetics.
自克雷佩林(Kraepelin)界定早发性痴呆以来,已过去一个多世纪,但精神分裂症的病因、神经病理学和病理生理学仍然难以捉摸。尽管有了能够进行可靠诊断识别的标准,但精神分裂症本质上仍然是一种宽泛的临床综合征,由所报告的主观体验(症状)、功能丧失(行为障碍)以及不同的病程模式所定义。研究已经确定了一些与该疾病相关的假定生物标志物,包括神经认知功能障碍、脑形态异常和神经化学异常。然而,迄今为止,这些变量中没有一个被明确证明具有诊断测试所期望的敏感性和特异性。基因连锁和关联研究针对了多个候选基因座和基因,但未能证明任何特定的基因变体或基因组合是导致精神分裂症的必要或充分条件。因此,精神分裂症背后存在特定脑部疾病这一观点仍然只是一个假说。在研究数据量不断增加的背景下,对该疾病病因的探索尚无定论,这引发了人们对当前所定义的精神分裂症概念有效性的质疑。鉴于精神分裂症症状的多变性以及临床和生物学发现缺乏连贯性,这种质疑并非毫无道理。然而,简单地摒弃这一概念不太可能产生一个能够解释与精神分裂症疾病假说相符的一系列临床现象和研究数据的替代模型。目前,精神分裂症的临床概念得到了经验证据的支持,即其多个方面构成了一个具有不可忽视的内部凝聚力和随时间变化的特征性演变的宽泛综合征。借助内表型对该综合征进行剖析,正开始被视为精神分裂症遗传学中一种有前景的方法。