30 Years on: How the Neurodevelopmental Hypothesis of Schizophrenia Morphed Into the Developmental Risk Factor Model of Psychosis

被引:234
作者
Murray, Robin M. [1 ,2 ,3 ]
Bhavsar, Vishal [1 ]
Tripoli, Giada [1 ]
Howes, Oliver [1 ,4 ]
机构
[1] Kings Coll London, Inst Psychiat Psychol & Neurosci, Psychosis Studies Dept, London, England
[2] South London & Maudsley NHS Fdn Trust, Natl Inst Hlth Res NIHR Mental Hlth Biomed Res Ct, London, England
[3] Kings Coll London, London, England
[4] Imperial Coll, Ctr Clin Sci, Psychiat Imaging Grp, London, England
关键词
neurodevelopment; sociodevelopment; dopamine; risk factors; STRIATAL DOPAMINE FUNCTION; CEREBRAL VENTRICULAR SIZE; HIGH-POTENCY CANNABIS; OBSTETRIC COMPLICATIONS; ADULT SCHIZOPHRENIA; GENETIC RISK; EXPERIENCES; CHILDHOOD; SYMPTOMS; BIRTH;
D O I
10.1093/schbul/sbx121
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
At its re-birth 30 years ago, the neurodevelopment hypothesis of schizophrenia focussed on aberrant genes and early neural hazards, but then it grew to include ideas concerning aberrant synaptic pruning in adolescence. The hypothesis had its own stormy development and it endured some difficult teenage years when a resurgence of interest in neurodegeneration threatened its survival. In early adult life, it over-reached itself with some reductionists claiming that schizophrenia was simply a neurodevelopmental disease. However, by age 30, the hypothesis has matured sufficiently to incorporated childhood and adult adversity, urban living and migration, as well as heavy cannabis use, as important risk factors. Thus, it morphed into the developmental risk factor model of psychosis and integrated new evidence concerning dysregulated striatal dopamine as the final step on the pathway linking risk factors to psychotic symptoms.
引用
收藏
页码:1190 / 1196
页数:7
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