Shenton Martha E, Whitford Thomas J, Kubicki Marek
Psychiatry Neuroimaging Laboratory, Department of Psychiatry, Brigham and Women's Hospital, 1249 Boylston Street Boston, MA 02215, USA.
Dialogues Clin Neurosci. 2010;12(3):317-32. doi: 10.31887/DCNS.2010.12.3/mshenton.
Historically, Kraepelin speculated that dementia praecox resulted from damage to the cerebral cortex, most notably the frontal and temporal cortices. It is only recently, however, that tools have been available to test this hypothesis. Now, more than a century later, we know that schizophrenia is a brain disorder. This knowledge comes from critical advances in imaging technology--including computerized axial tomography, magnetic resonance imaging, and diffusion imaging--all of which provide an unprecedented view of neuroanatomical structures, in vivo. Here, we review evidence for structural neuroimaging abnormalities, beginning with evidence for focal brain abnormalities, primarily in gray matter, and proceeding to the quest to identify abnormalities in brain systems and circuits by focusing on damage to white matter connections in the brain. We then review future prospects that need to be explored and pursued in order to translate our current knowledge into an understanding of the neurobiology of schizophrenia, which can then be translated into novel treatments.
从历史上看,克雷佩林推测早发性痴呆是由大脑皮层受损引起的,最明显的是额叶和颞叶皮层。然而,直到最近才有工具来检验这一假设。现在,一个多世纪过去了,我们知道精神分裂症是一种脑部疾病。这一认识源于成像技术的重大进展,包括计算机断层扫描、磁共振成像和扩散成像,所有这些技术都能在活体状态下以前所未有的视角呈现神经解剖结构。在此,我们回顾结构性神经成像异常的证据,首先是局灶性脑异常的证据,主要存在于灰质中,然后通过关注大脑白质连接的损伤来探寻大脑系统和回路中的异常。接着,我们回顾为将我们目前的知识转化为对精神分裂症神经生物学的理解进而转化为新疗法而需要探索和追求的未来前景。