ADULT SCHIZOPHRENIA FOLLOWING PRENATAL EXPOSURE TO AN INFLUENZA EPIDEMIC
ADULT SCHIZOPHRENIA FOLLOWING PRENATAL EXPOSURE TO AN INFLUENZA EPIDEMIC
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DOI：
10.1001/archpsyc.1988.01800260109013
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发表时间：
1988-02-01
影响因子：
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通讯作者：
BONETT, D
中科院分区：
文献类型：
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作者：
MEDNICK, SA;MACHON, RA;BONETT, D
在芬兰出生队列的背景下，我们测试了这样的假设，即在胎儿发育的后三分之二期间病毒感染会增加成人精神分裂症结局的风险。1957年A型流感流行期间，大赫尔辛基地区所有胎儿的精神病院诊断都有记录。那些在胎儿发育的第二个三个月期间接触到病毒流行病的人，被诊断为精神分裂症而被送往精神病院的风险更高。男性和女性都是如此，在几家精神病院中也是如此。第二个三个月的影响体现在精神病院住院的精神分裂症患者比例上升，以及赫尔辛基市每1000名活产儿中精神分裂症的比例更高。这项研究有几个局限性：(1)我们没有直接证据表明受试者确实受到了病毒感染。(2)精神病学资料仅适用于26岁56天以下的受试者。(3)调查结果是基于医院的诊断。(4)在接触疫情时确定怀孕阶段是以出生日期为依据的。病毒感染可能发生在官方的流行窗口之外；婴儿可能早产或早产。然而，这些错误的来源不应该用来加强调查结果。观察到的病毒效应被解释为许多潜在的妊娠干扰之一。我们认为，在确定精神分裂症的风险方面，与胎儿神经发育过程中的干扰类型相比，这种干扰的类型更为关键。
In the context of a Finnish birth cohort, we tested the hypothesis that viral infection during the latter two thirds of fetal development would increase the risk of adult schizophrenic outcome. Psychiatric hospital diagnoses were recorded for all individuals in greater Helsinki who were fetuses during the 1957 type A2 influenza epidemic. Those exposed to the viral epidemic during their second trimester of fetal development were at elevated risk of being admitted to a psychiatric hospital with a diagnosis of schizophrenia. This was true for both males and females and independently in several psychiatric hospitals. The second-trimester effect was seen in the elevated proportion of schizophrenics among those admitted to a psychiatric hospital and also in higher rates of schizophrenia per 1000 live births in the city of Helsinki. The study has several limitations: (1) We have no direct evidence that the subjects actually suffered a viral infection. (2) The psychiatric data were obtained only for subjects up to the age of 26 years, 56 days. (3) The findings are based on hospital diagnoses. (4) The determination of stage of gestation at time of exposure to the epidemic is based on date of birth. The viral infection might have occurred outside the official epidemic window; the infant may have had a preterm or postterm delivery. These sources of error, however, should not serve to enhance the findings. The observed viral effect is interpreted as being one of many potential perturbations of gestation. We suggest that it is less the type than the timing of the disturbance during fetal neural development that is critical in determining risk for schizophrenia.