The schizophrenia prodrome revisited: A neurodevelopmental perspective

The schizophrenia prodrome revisited: A neurodevelopmental perspective
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DOI:
10.1093/oxfordjournals.schbul.a007036
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发表时间:
2003-01-01
影响因子:
6.6
通讯作者:
Nakayama, E
Nakayama, E
中科院分区:
医学1区
文献类型:
--
作者:
Cornblatt, BA;Lencz, T;Nakayama, E

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尽管人们普遍接受了这一观点。精神分裂症的神经发育模型,其在疾病前驱期相关研究中的应用有限。对疾病的持久生物脆弱性这一概念几乎没有得到承认,这可能是对早期干预的反应。相反,大多数先兆研究的重点是新出现的阳性症状。识别和预防(RAP)计划遵循同样关注反映核心的非特定症状的战略。精神分裂症和那些与精神病有直接关系的人。数据来自62名青少年(平均年龄=16.4岁),在RAP计划的最初3年试点阶段(1998-2001年)。受试者被分为三个临床高危组,其特征是(1)阴性和非特异性症状(如社交孤立、学业失败),最早的前驱阶段;(2)出现中等强度的减弱的阳性症状;(3)严重减弱(但亚精神病)阳性症状,被认为是最接近精神病的。从神经发育文献中选择了四个危险因素来反映脆弱的核心:认知缺陷、情感障碍、社会孤立和学校失败。在三个风险组中,所有四个领域都同样受损,支持存在潜在的脆弱性核心,而不考虑新出现的阳性症状的严重程度。还进行了一项观察性试点研究,以确定通常用于治疗新出现的阳性症状的药物。抗抑郁药和抗精神病药物一样频繁地用于治疗出现中度缓解阳性症状的青少年。不考虑药物类型,中度症状的青少年在大约一年的随访期内表现得相当好。相比之下,出现更严重(但非精神病)缓解症状的青少年接受抗精神病药物治疗,通常与其他药物联合使用。然而,更有症状的青少年的结果是更谨慎的,近一半(即47%)的小组转变为精神分裂症谱系精神障碍。不坚持服药似乎是这一群体的一个主要危险因素。我们的结论是,精神分裂症的神经发育模型得到了我们的数据的支持,一系列新的治疗策略可能通过直接影响精神分裂症的脆弱核心来起到神经保护作用。
Despite the widespread acceptance of the. neurodevelopmental model of schizophrenia, its application to research concerned with the prodromal phase of illness is limited. Little recognition has been given to the concept of an enduring biological vulnerability to illness that may be responsive to early intervention. Rather, the focus of most prodromal studies is on emerging positive symptoms. The Recognition and Prevention (RAP) program follows the strategy of being equally concerned with the nonspecific symptoms reflecting the core of. schizophrenia and those directly related to psychosis. Data were collected from 62 adolescents (mean age = 16.4 years) during the initial 3-year pilot phase of the RAP program (1998-2001). Subjects were divided into three clinical high-risk groups, characterized by (1) negative and nonspecific symptoms (e.g., social isolation, school failures), the earliest prodrome stage; (2) emerging attenuated positive symptoms of moderate intensity; and (3) severe attenuated (but subpsychotic) positive symptoms, considered most proximal to psychosis. Four risk factors, derived from the neurodevelopmental literature, were selected to reflect the vulnerability core: cognitive deficits, affective disturbances, social isolation, and school failure. All four domains were equally impaired across the three risk groups, supporting the presence of the underlying vulnerability core regardless of the magnitude of emerging positive symptoms. An observational pilot study was also conducted to identify the medications typically used to treat emerging positive symptoms. Antidepressants were used as frequently as antipsychotics to treat adolescents presenting with moderate attenuated positive symptoms. Regardless of type of medication, moderately symptomatic youngsters did quite well over the approximately 1-year followup period. By contrast, adolescents presenting with more severe (but nonpsychotic) attenuated symptoms were treated with antipsychotics, often in combination with other agents. Outcome for the more symptomatic youngsters was, however, more guarded, with nearly half (i.e., 47 %) of the group converting to a schizophrenia spectrum psychotic disorder. Nonadherence to medication appeared to be a major risk factor in this group. We conclude that a neurodevelopmental model of schizophrenia is supported by our data and that a range of novel treatment strategies may be neuroprotective by directly affecting the disorder's vulnerability core.