AQA心理 精神分裂症 阳性阴性症状 多巴胺
精神分裂症是 AQA 心理学 7182 第三张卷子里的选修题，Section C 占 24 分，整卷两小时、96 分。这一题的知识点分成四块：分类与诊断、生物学解释、心理学解释、治疗。很多学生以为把症状名词背完就够了，其实 16 分题考的是解释之间的取舍，以及每一项证据的方法学问题。下面按考纲顺序，把 14 个容易被忽略的细节讲清楚。
The schizophrenia option sits in Section C of Paper 3, a two-hour paper marked out of 96, and carries 24 of those marks. High-scoring answers compare explanations instead of listing symptoms, while the weakest ones confuse classification with diagnosis. The notes below follow the specification order and flag the methodological problems behind each piece of evidence.
阳性症状与阴性症状的边界
阳性症状是正常功能之外的增加，幻觉与妄想是两项核心。听幻觉最常见，患者听到评论性或命令性声音，妄想的典型形式是被害与夸大，且不因反证而改变。阴性症状是正常功能的减退，言语贫乏指话少且内容空，意志缺乏指长期无法启动目标行为，情感平淡指表情与语调变化减少。很多学生以为幻觉就是看见不存在的东西，其实视幻觉的比例低得多。阴性症状更依赖观察与家属描述，容易被误读成抑郁或懒散。诊断时两类症状要分别记录，因为预后与用药反应都不同。
Positive symptoms add experience that should not be there, and hallucinations with delusions carry most of the diagnostic weight. Auditory voices are far more common than visual ones, while negative symptoms such as speech poverty, avolition and blunted affect are inferred from observation and family report instead of from what the patient says. That asymmetry matters clinically, because negative symptoms predict poorer functional outcome and respond less well to standard dopamine-blocking drugs, so they are easily mistaken for depression or laziness.
DSM-5 与 ICD-11 的时长门槛
DSM-5 在 2013 年把诊断门槛写成两条以上核心症状，其中至少一条来自妄想、幻觉或言语紊乱。这些症状要在一个月内的大部分时间存在，而整个障碍的连续征象要满六个月，前驱期与残留期都算进去。ICD-11 的口径宽松得多，只要求一个月的精神病性症状。两套标准同时存在，直接导致研究之间难以比较，也让同一个病人在不同国家拿到不同结论。考纲后面提到的分类争议，指向的正是标准不统一的问题。答题时把两个时长写清楚，比笼统说诊断标准严格更有分。
DSM-5, published in 2013, asks for two or more core symptoms present for much of one month, with at least one drawn from delusions, hallucinations or disorganised speech. The wider disturbance must then persist for six months, counting prodromal and residual phases, whereas ICD-11 settles for one month of psychotic symptoms. Because the two manuals disagree on duration, cross-national studies compare populations that were never defined the same way.
共病与症状重叠怎么影响诊断
共病指同一病人同时满足另一种障碍的标准，这会削弱诊断的区分效度。Buckley 等人在 2009 年的综述里给出常见组合，抑郁症状约见于一半患者，物质滥用接近一半，创伤后应激与强迫症状也明显高于一般人群。症状重叠是另一个麻烦，双相障碍的躁狂期可以出现妄想，物质所致精神病与孤独症谱系也会有类似表现。临床上先排除药物与躯体疾病，再谈精神分裂症。这类证据在 16 分题里常被用来质疑分类系统的效度。
Comorbidity means one patient meets criteria for a second disorder at the same time, and it weakens the claim that schizophrenia is a distinct category. Buckley and colleagues reviewed the pattern in 2009 and found depressive symptoms in roughly half of patients and substance misuse in nearly as many. Symptom overlap creates a second problem, since mania, substance-induced psychosis and autism can all produce delusions or flattened affect, which is why clinicians rule out drugs and physical illness first.
信度证据：同一病人两个诊断
信度指不同评定者对同一病人给出一致结论的程度。Cheniaux 等人在 2009 年让两位精神科医生用 ICD-10 与 DSM-IV 分别评定同一批 100 名病人，结果一位医生诊断出 26 例精神分裂症，另一位只有 13 例。同一份病历、同样的医生训练，结论差了一倍。DSM-5 的现场试验报告该诊断的 kappa 系数约为 0.46，属于中等偏下的水平。常见的错误是把信度与效度混为一谈，信度低说明工具不稳定，效度低说明工具测错了东西。这两个概念在卷面上必须分开写。
Reliability asks whether two assessors reach the same conclusion about the same patient. Cheniaux and colleagues had two psychiatrists rate 100 patients with both ICD-10 and DSM-IV in 2009, and one diagnosed 26 cases of schizophrenia while the other found 13; the field trial of DSM-5 reported a kappa of about 0.46 for the diagnosis. Reliability and validity are separate questions, and answers that merge them usually lose marks.
文化偏差与性别偏差
诊断标准由西方临床样本发展而来，跨文化使用时会出现系统性偏差。Copeland 在 1971 年把同一批 134 名病人的资料交给英美两国的精神科医生评定，美国医生给出精神分裂症诊断的比例是 69%，英国医生只有 2%。听力幻觉在不同文化里的解释也不同，某些社群把它视为宗教体验。性别偏差体现在发病年龄与症状表达上，男性发病更早、阴性症状更多，女性晚发且情感症状更突出。这些差异让流行病学数据难以直接比较。写评价时点出标准的文化负载，比泛泛批评更有说服力。
Diagnostic manuals were built on Western clinical samples, so transporting them across cultures imports a bias. Copeland gave the same 134 patient records to American and British psychiatrists in 1971, and the American group diagnosed schizophrenia in 69 per cent of cases against 2 per cent for the British group. Sex differences add a second layer, since men tend to develop the disorder earlier with more negative symptoms while women show later onset and stronger affective features.
家系与双生子研究给出的风险梯度
遗传解释依赖三类研究，家系、双生子与收养。Gottesman 在 1991 年汇总的家系研究给出这样一条风险梯度，一般人群的终身风险约 1%，父母一方患病约 13%，父母双方都患病约 46%，同卵双生子约 48%。Joseph 在 2004 年把 2001 年以前的双生子研究合并，同卵一致率 40.4%，异卵 7.4%，差距接近五倍。一致率从来没有到过 100%，说明基因不是全部。双生子研究还有一个隐含假设，同卵与异卵共享环境相同，而现实中同卵被对待得更相似。这条方法学批评在 16 分题里几乎是必写的。
Genetic explanations rest on family, twin and adoption designs. Gottesman pooled family data in 1991 and reported a lifetime risk near 1 per cent in the general population, 13 per cent with one affected parent, 46 per cent with two and 48 per cent for monozygotic co-twins; Joseph merged every twin study published before 2001 and found concordance of 40.4 per cent against 7.4 per cent for dizygotic pairs. Concordance never reaches 100 per cent, and the equal-environment assumption is the standard criticism to raise.
多基因而非单基因
精神分裂症不是单基因病，这一点在近十年的全基因组关联研究里已经清楚。Ripke 等人在 2014 年发表的样本覆盖三万多名患者，定位到 108 个与疾病相关的位点，每个位点的效应都很小。候选基因时代寻找的单一罪魁没有兑现，COMT 与 DISC1 的复制结果一直不稳定。多基因风险评分目前能解释的方差有限，还不能用于个体诊断。对考生来说，这条证据的价值在于支持素质-压力模型，而不是证明基因决定论。
Schizophrenia is polygenic rather than Mendelian, and genome-wide association work has settled that point. Ripke and colleagues analysed more than 30,000 cases in 2014 and identified 108 associated loci, each with a very small effect, which is why single candidate genes such as COMT and DISC1 failed to replicate. Polygenic risk scores still explain little variance and cannot be used diagnostically, so the finding supports a predisposition model rather than genetic determinism.
多巴胺假说从原始版到修订版
原始多巴胺假说来自一项临床观察，能阻断多巴胺受体的药物减轻阳性症状，而增加多巴胺活动的药物会诱发类似症状。问题在于它解释不了阴性症状，抗精神病药对情感平淡与意志缺乏几乎没有作用。修订版由 Davis 等人在 1991 年提出，认为前额叶皮层多巴胺活动过低，皮层下通路活动过高。前者对应阴性症状与认知缺陷，后者对应幻觉与妄想。这一版本把两类症状放进同一个机制，答题时值得单独写一段。
The original dopamine hypothesis grew from a clinical observation: drugs that block dopamine receptors relieve positive symptoms, and drugs that increase dopamine activity can provoke them. It struggled with negative symptoms, which respond poorly to antipsychotics, so Davis and colleagues proposed a revised version in 1991 with too little dopamine in the prefrontal cortex and too much in subcortical pathways. That split maps negative and cognitive features onto the cortical side and hallucinations onto the subcortical side.
神经相关物：脑室与前额叶
神经相关物指与症状稳定相关的脑结构或功能差异。Torrey 在 2007 年汇总的影像研究显示，患者的侧脑室平均比对照组大，灰质体积在前额叶与颞叶偏低。前额叶活动减弱与阴性症状、执行功能受损相关，颞叶与扣带回的异常与听幻觉相关。这些发现属于相关，不能直接读成因果，抗精神病药物的长期使用也可能改变脑结构。作答时先写相关方向，再写因果限制，分数更稳。
Neural correlates are structural or functional differences that travel with the disorder. Torrey reviewed imaging studies in 2007 and reported enlarged lateral ventricles plus reduced grey matter in prefrontal and temporal regions, with prefrontal underactivity linked to negative symptoms and temporal abnormality linked to auditory hallucinations. Correlation is not causation here, since long-term antipsychotic use may itself alter brain structure.
家庭功能解释：双重束缚与高情绪表达
心理学解释的第一条线指向家庭。Fromm-Reichmann 在 1948 年提出精神分裂症母亲的概念，描述一种既控制又拒绝的养育方式，这个说法后来因缺乏证据且责怪母亲而受到批评。Bateson 等人在 1956 年提出双重束缚，孩子收到互相矛盾的指令，无论怎么回应都错。较有实证支持的是情绪表达，Brown、Birley 与 Wing 在 1972 年追踪出院患者九个月，高情绪表达家庭的复发率约 58%，低情绪表达家庭约 10%。相关不等于因果，家庭的高批评也可能是症状造成的。阅卷时常见把这条证据写成纯因果链，那是要扣分的。
The first psychological account points at the family. Fromm-Reichmann described the schizophrenogenic mother in 1948 as controlling and rejecting, an idea later criticised for blaming mothers on thin evidence, and Bateson added the double bind in 1956. Expressed emotion has better support: Brown, Birley and Wing followed discharged patients for nine months in 1972 and found relapse near 58 per cent in high-emotion homes against 10 per cent in low-emotion ones, though the direction of cause remains contested.
认知解释：元表征与推理偏差
认知解释把症状看成信息处理的偏差，而不是家庭关系的产物。Frith 在 1979 年提出注意缺陷，患者无法过滤无关刺激，容易被大量信息淹没。他在 1992 年进一步用元表征解释，元表征指对自己与他人心理状态的表征，这一能力受损会让自我产生的想法被误判为外来声音。Bentall 在 1989 年把妄想解释为推理偏差，患者过早下结论、对外部归因有偏好。认知解释的优势是能解释阳性与阴性症状，也能直接推出 CBTp。局限在于多数证据来自已患病者，无法判断偏差是原因还是结果。
Cognitive accounts treat symptoms as biases in information processing rather than products of family relationships. Frith proposed an attention deficit in 1979 and later argued that a failure of metarepresentation makes self-generated thoughts feel externally generated, which is one route to auditory hallucination. Bentall described delusions as a jumping-to-conclusions bias with an externalising attribution style, and the practical strength of these models is that they generate CBTp, although most evidence is collected after onset.
药物治疗：典型与非典型
典型抗精神病药以氯丙嗪为代表，1950 年代进入临床，机制是阻断 D2 受体，对阳性症状有效。副作用包括锥体外系反应、迟发性运动障碍与泌乳素升高，患者常因此不愿坚持服药。非典型药物以氯氮平为代表，同时作用于 5-HT2A 受体，对阴性症状与难治性病例效果更好，代价是粒细胞缺乏，需要定期验血。Leucht 等人在 2012 年合并随机对照试验，维持用药一年的复发率约 27%，安慰剂组约 64%。常见的错误是只写药物有效，不写依从性问题，而依从性恰恰是复发的最大变量。
Typical antipsychotics such as chlorpromazine entered practice in the 1950s and work by blocking D2 receptors, which controls positive symptoms at the cost of extrapyramidal effects and tardive dyskinesia. Atypicals such as clozapine add 5-HT2A blockade and help negative symptoms and treatment-resistant cases, but carry a risk of agranulocytosis that requires blood monitoring. Leucht and colleagues pooled trials in 2012 and put one-year relapse near 27 per cent on maintenance treatment against 64 per cent on placebo, which is why adherence matters more than drug choice.
心理治疗：CBTp、家庭治疗与代币制
CBTp 针对妄想与幻觉的内容做工作，帮助患者检验证据、降低信念的确定性，NICE 官网的指南建议至少 16 次个别会谈。家庭治疗把家属纳入，NICE 给出的做法是持续三个月到一年、至少 10 次会谈，重点是沟通与问题解决。Pharoah 等人在 2010 年的 Cochrane 综述合并五十多项随机对照试验，家庭干预降低了复发。代币制来自 Ayllon 与 Azrin 在 1968 年的病房研究，用即时奖励强化自理与社会行为，对阴性症状与住院适应有帮助。艺术治疗在 NICE 官网的指南里是考虑选项，主要针对阴性症状。心理治疗的共同限制是依赖患者主动参与，急性期很难开展。
CBTp works on the content of delusions and hallucinations, testing evidence and reducing conviction, and NICE advises at least 16 individual sessions. Family intervention involves relatives for between three months and a year with at least 10 planned meetings, and the Cochrane review by Pharoah and colleagues in 2010 pooled more than fifty trials showing lower relapse. Token economies, derived from the ward study by Ayllon and Azrin in 1968, reward self-care immediately, while arts therapies are a considered option aimed mainly at negative symptoms.
素质-压力模型把两边接起来
素质-压力模型认为个体先有易感性，再由环境压力触发。Meehl 在 1962 年提出原始版本，把易感性设想为一种神经系统缺陷。Tienari 等人在 2000 年报告的芬兰收养研究提供了支持，亲生母亲患病的高风险被收养者，在功能不良的收养家庭里出现障碍的比例明显更高，在健康家庭里则接近对照组。这说明基因决定的是阈值，不是结局。AQA 的 16 分题常要求用这个模型整合生物与心理证据，答题时要把两边的证据各写一条，再写交互作用。很多学生以为写一句相互作用就够了，实际上要落到具体变量上。
The diathesis-stress model treats inherited vulnerability as a threshold that environment pushes people across. Meehl framed the original version in 1962 around a neural defect, and Tienari's Finnish adoption study, reported in 2000, supported it: high-risk adoptees raised in dysfunctional families developed the disorder far more often than those raised in healthy homes, where rates approached the control group. Answers that only state that biology and environment interact gain little, because AQA rewards naming both variables and the mechanism between them.
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