Henn F A
Zentralinstitat für Seelische Gesundheit, Mannheim.
Schweiz Arch Neurol Psychiatr (1985). 1995;146(5):224-9.
In this paper schizophrenia is taken to be a collection of diseases with similar pathological features, including the core Bleulerian symptoms. The aim is to see how far current research can specify the anatomical regions which are functionally defective in schizophrenia and what transmitter systems may be involved. It appears schizophrenic brains show a tendency toward fewer cells in the temporal region, including limbic system as well as the thalamus. Functional deficits are seen in the dorsolateral frontal cortex, as well as thalamus suggesting a cortical-thalamic-striatal pathway. It is clear that Dopamine disregulation in this pathway leads to psychotic symptoms but probably does not account for the ambivalence, affective blunting or asocial behavior. GABA lesions prenatally could lead to glutamate over activity with potential toxic consequences after puberty leading to a plausible hypothesis as to the central neurochemical defect in schizophrenia, this hypothesis is elaborated.
在本文中，精神分裂症被视为一组具有相似病理特征的疾病，包括核心的布鲁勒症状。目的是探究当前研究在多大程度上能够明确精神分裂症中功能存在缺陷的解剖区域以及可能涉及哪些递质系统。精神分裂症患者的大脑似乎在颞叶区域（包括边缘系统以及丘脑）呈现出细胞数量减少的趋势。在背外侧前额叶皮质以及丘脑可见功能缺陷，提示存在皮质 - 丘脑 - 纹状体通路。显然，该通路中多巴胺调节异常会导致精神病性症状，但可能无法解释矛盾情感、情感迟钝或社交行为障碍。产前的γ-氨基丁酸（GABA）损伤可能导致青春期后谷氨酸过度活跃并产生潜在毒性后果，从而为精神分裂症的中枢神经化学缺陷提出了一个合理的假说，本文对这一假说进行了详细阐述。
