英文條目: https://en.wikipedia.org/wiki/Schizophrenia
中文條目: https://zh.wikipedia.org/wiki/%E7%B2%BE%E7%A5%9E%E5%88%86%E8%A3%82%E7%97%87
中文引言: (2016/10/17已由So47009 重寫引言, 和英文已有相當類似度)
思覺失調症（英語：schizophrenia[1]）是精神疾病的一種，特徵為患者出現異常的社會行為和不能辨別真實與幻想[2]，以往在台灣稱為「精神分裂症」，由英文名稱Schizo+phren+ia直譯而來。常見症狀包括妄想、幻覺、思維混亂、幻聽、社會參與、情緒表達的程度降低和缺乏動力等等[2][3]。思覺失調症患者通常伴有其他心理上的健康問題，如焦慮症、重性抑鬱障礙或物質使用障礙[4]。症狀多半是漸進式地出現，且一般始於成年早期，持續一段長時間[3][5]。
思覺失調症的病因包括環境和遺傳因素[6]，可能的環境因素包含成長於城市中、使用大麻、感染某些傳染病、父母生育年齡和在母體內營養攝取不足[6][7]。遺傳因素包括各種常見和罕見的遺傳變異[8]。思覺失調症的診斷基於觀察患者表現出來的行為及其所報告的個人經歷[5]。在診斷時，亦必須把患者所身處的文化納入考慮範圍[5]。2013年為止，此病並無任何客觀的測試予供作診斷[5]。思覺失調症並不等同「多重人格」或「多重人格障礙」——這種混淆的想法常在公眾認知中出現[9]。
治療的核心是開給患者處方抗精神病藥、安排諮詢、工作培訓與社會康復[2][6]。目前尚不清楚典型抗精神病藥與非典型抗精神病藥兩者間哪種的效果會較佳[10]。在其他抗精神病藥物都無法改善病情的情況下，就可能會使用氯氮平。必要時，患者可能會被強制住院治療，如患者可能會對自身或他人構成傷害這一種情況，但現在的住院時間比以往更為短暫，且強制住院治療的總次數亦較為少[11]。
約0.3-0.7％的人在其一生中受思覺失調症所影響[12] 。2013年，全球估計有2360萬例思覺失調症患者[13]。男性比女性更常受到思覺失調症的影響[2]。大約20％的人康復得很好，一些人亦能完全康復[5]。患者常伴有一定的社會問題，例如長期失業、貧窮和無家可歸[5][14]。患有思覺失調症的人的平均預期壽命比平均值少10年至25年[15]。其背後原因是患者的身體健康問題增加和自殺率較高（約5%）[12][16]。2013年，估計有16,000人死於與思覺失調症有關或由其引起的行為[17]。
For other uses, see Schizophrenia (disambiguation).
Schizophrenia is a mental disorder characterized by abnormal social behavior and failure to understand what is real.[2]Common symptoms include false beliefs, unclear or confused thinking, hearing voices, reduced social engagement and emotional expression, and a lack of motivation.[2][3] People with schizophrenia often have additional mental health problems such as anxiety disorders, major depressive illness, or substance use disorder.[4] Symptoms typically come on gradually, begin in young adulthood, and last a long time.[3][5]
思覺失調症（英語：schizophrenia[1]），有別於人格分裂，是一種以[[社會行為異常]]以及[[認知混亂]]為特徵的[[精神疾病]][2]。在台灣以往稱為精神分裂症（由直譯英文名稱Schizo+phren+ia而來）。思覺失調症的常見症狀包括[[妄想]]、[[思維障礙]]、[[幻聽]]、社交功能障礙、抑鬱以及[[缺乏應有的積極性與主動性]][2][3]。患者同時常伴有其他精神健康問題，包括[[焦慮症]]、[[重性抑鬱障礙]]或[[物質使用疾患(SUD)]][4]。思覺失調症的症狀常始於成年初期，並持續很長時間[3][5]。
The causes of schizophrenia include environmental and genetic factors.[6] Possible environmental factors include being raised in a city, cannabis use, certain infections, parental age, and poor nutrition during pregnancy.[6][7] Genetic factors include a variety of common and rare genetic variants.[8] Diagnosis is based on observed behavior and the person’s reported experiences.[5] During diagnosis a person’s culture must also be taken into account.[5] As of 2013 there is no objective test.[5]Schizophrenia does not imply a "split personality" or "multiple personality disorder"—conditions it is often confused with in public perception.[9]
思覺失調症具體病因尚不明確，目前研究顯示許多生理、[[遺傳]]、心理、及[[環境因素]]都可成為罹患思覺失調症的風險因子[中1]，可能的環境因素包括城市中成長、吸食[[大麻]]、一些特定的感染、父母生育年齡、孕期營養不良等[6][7]，遺傳因素包含許多常見以及罕見的基因突變[8]。診斷思覺失調症主要透過觀察患者行為及聽取患者敘述的經歷[5]，同時必須考慮個案的[[文化習慣]][5]以作診斷。截至2013年，思覺失調症尚無客觀測量方法[5]，思覺失調症（精神分裂症）並不等同於“人格分裂”或“[[解離性人格疾患]]”，這種混淆的想法常在公眾認知中出現[9]。
The mainstay of treatment is antipsychotic medication along with counselling, job training, and social rehabilitation.[2][6] It is unclear if typical or atypical antipsychotics are better.[10] In those who do not improve with other antipsychotics, clozapine may be used.[6] In more serious cases—where there is risk to self or others—involuntary hospitalization may be necessary, although hospital stays are now shorter and less frequent than they once were.[11]
最主要的治療方法為抗精神病藥物治療，同时配合諮詢、工作訓練與社交復原[2][6]，現在還不清楚在於典型或非典型抗精神病藥是否較好[10]；無法因用藥而改善的人們可能可使用氯氮平[6]。多數嚴重的病例中，當患者會造成自己或他人的危害，即使現今住院時間與頻率較早期短且少，患者仍需非自願性住院。[11]。
About 0.3–0.7% of people are affected by schizophrenia during their lifetime.[12] In 2013 there was estimated to be 23.6 million cases globally.[13] Males are more often affected than females.[2] About 20% of people do well and a few recover completely.[5]Social problems, such as long-term unemployment, poverty, and homelessness are common.[5][14] The average life expectancy of people with the disorder is ten to twenty-five years less than the average.[15] This is the result of increased physical health problems and a higher suicide rate (about 5%).[12][16] In 2013 an estimated 16,000 people died from behavior related to, or caused by, schizophrenia.[17]
大約0.3-0.7%的人一生會受到思覺失調症的影響[12]，2013年時估計全球大約有2360萬個病例[13]。男性相對比女性，更常受到其影響[2]。大約20%的人們會改善而少數人能恢復正常[5]。常見的社交問題為長期失業，貧困和無家可歸[5][14]。而患者平均壽命會少於人們的平均壽命十到二十五年[15]。這是因為身體健康問題與高自殺率(大約5%)所造成的。在2013時估計，大約有一萬六千民的患者，死於與思覺失調症相關或者直接造成的行為{17}。
See also: Basic symptoms of schizophrenia
Individuals with schizophrenia may experience hallucinations (most reported are hearing voices), delusions (often bizarre or persecutoryin nature), and disorganized thinking and speech. The last may range from loss of train of thought, to sentences only loosely connected in meaning, to speech that is not understandable known as word salad. Social withdrawal, sloppiness of dress and hygiene, and loss of motivation and judgment are all common in schizophrenia.[18] Distortions of self-experience such as feeling as if one’s thoughts or feelings are not really one’s own to believing thoughts are being inserted into one’s mind, sometimes termed passivity phenomena, are also common.[19] There is often an observable pattern of emotional difficulty, for example lack of responsiveness.[20] Impairment in social cognition is associated with schizophrenia,[21] as are symptoms of paranoia. Social isolation commonly occurs.[22] Difficulties in workingand long-term memory, attention, executive functioning, and speed of processing also commonly occur.[12] In one uncommon subtype, the person may be largely mute, remain motionless in bizarre postures, or exhibit purposeless agitation, all signs of catatonia.[23] About 30 to 50 percent of people with schizophrenia fail to accept that they have an illness or comply with their recommended treatment.[24]Treatment may have some effect on insight.[25] People with schizophrenia often find facial emotion perception to be difficult.[26]
==临床表现==
主条目：思觉失调症的基本臨床表現（英文：Basic symptoms of schizophrenia ）
思覺失調症患者常會經歷[[幻覺]]（通常為[[幻聽]]）、[[妄想]]（通常古怪或為[[被害妄想]]），以及[[思維障礙]]。患者的思維障礙可輕至思路不清晰不清晰，重至[[言語雜亂無章或一直重覆]]（分裂性言語，英文：[[word salad]]）。思覺失調症患者會出現社會退縮、個人衛生習慣不良、缺乏動力及及判斷力等狀態[18]。[[自我經驗的扭曲]]，例如覺得自己的想法或感受不屬於自己，乃至於思考被插入自己的心智中（一件不相干的事情突然擾亂思緒，無法繼續思考，即[[思考插入]]）以及被動體驗也是思覺失調症患者的常見症狀[19]。患者的情緒障礙常有一定可觀察的模式，例如反應遲鈍[20]。[[社會認知]]障礙的產生也常與思覺失調症有關，即表現為[[偏執症狀]]。[[社交孤立]]常發生於思覺失調症患者[22]。思覺失調症患者的[[短期]]與[[長期記憶]]、[[注意力]]、[[執行功能]]會受到影響，[[思緒]]也會變得緩慢[12]。患有一種較少見的思覺失調症亞型的患者会突然失語，還會以一個奇怪的姿勢靜止不動，或表現出漫無目的的焦慮狀態，而這些也都為[[緊張症]]的症狀[23]。大約有百分之三十到五十的思覺失調症病人不會接受自己的患病事實，或採取不配合治療的態度。治療也或許會改變病患的患病認識[25]。思覺失調症病患也常會難以做出面部表情[26]。
People with schizophrenia may have a high rate of irritable bowel syndrome but they often do not mention it unless specifically asked.[27]
思覺失調症患者會有很高比例的同時患有[[大腸激躁症]]的概率，但病患常常不會主動提起[27]。
Positive and negative
Schizophrenia is often described in terms of positive and negative (or deficit) symptoms.[28] Positive symptoms are those that most individuals do not normally experience, but are present in people with schizophrenia. They can include delusions, disordered thoughts and speech, and tactile, auditory, visual, olfactory and gustatory hallucinations, typically regarded as manifestations of psychosis.[29]Hallucinations are also typically related to the content of the delusional theme.[30] Positive symptoms generally respond well to medication.[30]
===正性與負性===
思覺失調症常被分為正性與負性（或稱缺陷）症狀[28]。「正性症狀」指的是那些大多數個體不會經歷、但是存在於思覺失調症患者身上的不尋常經驗。它們包括了一些通常會被視為精神病的表現，例如妄想、混亂的思考和言語，以及觸覺、聽覺、視覺、嗅覺和味覺的幻覺[29]，
幻覺經常會跟妄想的主題有關[30]。正性症狀以藥物治療的效果通常很好[30]。
Negative symptoms are deficits of normal emotional responses or of other thought processes, and are less responsive to medication.[18]They commonly include flat expressions or little emotion, poverty of speech, inability to experience pleasure, lack of desire to form relationships, and lack of motivation. Negative symptoms appear to contribute more to poor quality of life, functional ability, and the burden on others than do positive symptoms.[31] People with greater negative symptoms often have a history of poor adjustment before the onset of illness, and response to medication is often limited.[18][32]
「負向症狀」是對於一般情緒反應或其他思維過程有缺陷，而且通常對藥物的反應比較小[18]。通常包括了反應平淡、情感微弱、言語貧乏、無法體驗樂趣，還有缺乏動力。與正性症狀相比，負性症狀通常在生活品質、實用能力上更為低落，而且對旁人造成的負擔較大[31]。具有較重度負向症狀的人，通常在發病之前，就有一段不良的調整歷史，而且藥物治療的效果也通常很有限[18][32]。
Cognitive dysfunction
Deficits in cognitive abilities are widely recognized as a core feature of schizophrenia.[33][34][35] The extent of the cognitive deficits an individual experiences is a predictor of how functional an individual will be, the quality of occupational performance, and how successful the individual will be in maintaining treatment.[36] The presence and degree of cognitive dysfunction in individuals with schizophrenia has been reported to be a better indicator of functionality than the presentation of positive or negative symptoms.[33] The deficits impacting the cognitive function are found in a large number of areas: working memory, long-term memory,[37][38] verbal declarative memory,[39] semantic processing,[40]episodic memory,[36] attention, learning (particularly verbal learning).[37]
===認知功能障礙===
認知功能的缺陷廣泛被認定是思覺失調症的核心特徵[33][34][35]。一個人的認知功能缺陷程度可以用來預測他在支持性療法的輔助下，其身體功能性狀況、在職業上的表現，以及此人未來的成就[36]。據報告指出，一個患有思覺失調症的人，其認知功能缺陷的存在以及其程度是比正性或負型症狀更好的功能性指標[33]。認知功能障礙的多項層面包括：[[工作記憶]]、[[長期記憶]][37][38]、口頭[[陳述性記憶]][39]、[[語意處理]][40]、[[情節記憶]][36]、[[注意力]]以及[[學習]](尤其是口語學習)[37]。
Deficits in verbal memory are the most pronounced in individuals with schizophrenia, and are not accounted for by deficit in attention. Verbal memory impairment has been linked to a decreased ability in individuals with schizophrenia to semantically encode (process information relating to meaning), which is cited as a cause for another known deficit in long-term memory.[37] When given a list of words, healthy individuals remember positive words more frequently (known as the Pollyanna principle); however, individuals with schizophrenia tend to remember all words equally regardless of their connotations, suggesting that the experience of anhedonia impairs the semantic encoding of the words.[37] These deficits have been found in individuals before the onset of the illness to some extent.[33][35][41] First-degree family members of individuals with schizophrenia and other high-risk individuals also show a degree of deficit in cognitive abilities, and specifically in working memory.[41]
若不將注意力缺陷納入其中的話，語文記憶缺陷是思覺失調症患者最顯著的認知功能障礙。思覺失調症患者的語文記憶障礙常被解釋為文本製碼能力（將文本信息與含意相連結）的下降，這也被視為使患者產生其他長期記憶缺陷的因素之一[37]：當給健康個體一系列詞彙時，他們常會更快更準地記住令他們感到愉悅的詞彙（即[[波麗安娜效應]]）；但思覺失調症患者則不會因詞彙含義是否令他們愉悅而產生不同的記憶效果，這說明思覺失調症患者的失樂症狀影響了其文本製碼能力[37]。在一定程度上，這些缺陷也在個體發病前出現[33][35][41]。直系親屬患有思覺失調症的個體以及其他的高風險個體也會出現一定程度的認知功能缺陷，特別是工作記憶的缺陷[41]。
A review of the literature on cognitive deficits in individuals with schizophrenia shows that the deficits may be present in early adolescence, or as early as childhood.[33] The deficits which an individual with schizophrenia presents tend to remain the same over time in most patients, or follow an identifiable course based upon environmental variables.[33][37]
一篇对探討思覺失調症患者的認知障礙的相關文獻的討論中称，認知障礙可出現於患者的青春期初期，抑或早至患者童年時出現[33]。隨時間發展，大部分思觉失调症患者所表现出的认知障碍比較穩定，或受環境因素影響按照一定的模式變化[33][37]。
Although the evidence that cognitive deficits remain stable over time is reliable and abundant,[36][37] much of the research in this domain focuses on methods to improve attention and working memory.[37][38] Efforts to improve learning ability in individuals with schizophrenia using a high- versus low-reward condition and an instruction-absent or instruction-present condition revealed that increasing reward leads to poorer performance while providing instruction leads to improved performance, highlighting that some treatments may exist to increase cognitive performance.[37] Training individuals with schizophrenia to alter their thinking, attention, and language behaviors by verbalizing tasks, engaging in cognitive rehearsal, giving self-instructions, giving coping statements to the self to handle failure, and providing self-reinforcement for success, significantly improves performance on recall tasks.[37] This type of training, known as self-instructional (SI) training, produced benefits such as lower number of nonsense verbalizations and improved recall while distracted.[37]
儘管有足夠的可靠證據顯示患者的認知障礙程度會在長時間內保持穩定[36][37]，在此領域中大部分的研究都著力於發展提升患者注意力與工作記憶的方法[37][38]。通過對比高獎勵條件與低獎勵條件，以及有指示与无指示的条件对思觉失调症患者提高学习能力效果的區別，研究證實獎勵增加會導致患者較差的改善效果，而提供指示則會造成比較好的改善效果；這啟發了一些可能可行的提高患者認知能力的治療方法[37]。通過以語言方式呈現的任務、認知演練法、自導法、自我使用因應句型以直面失敗，以及在成功時使用自我增強法等方法，訓練思覺失調症患者以矯正他們的思考、注意以及語言行為，可以極大地改善患者執行回憶任務的表現[37]。這種被稱為自我指導(SI)訓練的訓練方法可以減少患者的無意義語言並提高患者在被干擾時的回憶能力[37]。
Onset
See also: Schizophrenia in children
Late adolescence and early adulthood are peak periods for the onset of schizophrenia,[12] critical years in a young adult’s social and vocational development.[42] In 40% of men and 23% of women diagnosed with schizophrenia, the condition manifested itself before the age of 19.[43] To minimize the developmental disruption associated with schizophrenia, much work has recently been done to identify and treat the prodromal (pre-onset) phase of the illness, which has been detected up to 30 months before the onset of symptoms.[42] Those who go on to develop schizophrenia may experience transient or self-limiting psychotic symptoms[44] and the non-specific symptoms of social withdrawal, irritability, dysphoria,[45] and clumsiness[46] during the prodromal phase.
===初始發作===
{{see also|兒童思覺失調症}}
青春期末以及成年初始是思覺失調症初次發病的高峰時段[12]，同時也是青年社會能力與職業能力發展的關鍵階段[42]。被診斷為思覺失調症的患者中，百分之四十的男性與百分之二十三的女性患者在十九歲前即有思覺失調症的症狀發生[43]。為避免思覺失調症帶來對成長的影響，近年來已經在發現並治療思覺失調症的[[前期徵象]]，即最多在思覺失調症症狀初次發作三十個月前發現其前徵的方面做了大量工作[42]。思覺失調症患者在發病前期可能會經歷短暫或有自限性的精神病症狀[44]以及一些非特異性症狀，後者包括社會退縮、易怒、[[煩躁]][46]以及行动笨拙。
Main article: Causes of schizophrenia
A combination of genetic and environmental factors play a role in the development of schizophrenia.[9][12] People with a family history of schizophrenia who have a transient psychosis have a 20–40% chance of being diagnosed one year later.[47]
==病因==
{{main|思覺失調症的病因}}
遺傳性和環境因素共同擔任思覺失調症發展的關鍵[9][12]。一個具有思覺失調症家族史且患有過渡性精神失調疾病的人，有20-40%的機率病發一年後會被診斷出來[47]。
Genetic
Estimates of heritability vary because of the difficulty in separating genetic and environmental influences;[48] averages of 0.80 have been given.[49] The greatest single risk factor for developing schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of monozygotic twins of those with schizophrenia are also affected.[9]If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%.[49]
===遺傳因素===
因[[難以分離]]遺傳與環境因素的影響，各個對思覺失調症可遺傳性的估計差異較大[48]；對其估計的平均值為0.80[49]。最大的单一风险因子为[[直系亲属]]患有思覺失調症（風險為6.5%）；若是[[同卵雙胞胎]]的一方患有思覺失調症，另一方患病風險則達百分之四十以上[9]。若是父母一方患病，其患病風險為約百分之十三；若父母雙方均患病則風險為將近百分之五十[49]。
Many genes are believed to be involved in schizophrenia, each of small effect and unknown transmission and expression.[8][9] Many possible candidates have been proposed, including specific copy number variations, NOTCH4, and histone protein loci.[50] A number of genome-wide associations such as zinc finger protein 804A have also been linked.[51] There appears to be overlap in the genetics of schizophrenia and bipolar disorder.[52] Evidence is emerging that the genetic architecture of schizophrenia involved both common and rare risk variation.[53]
許多[[基因]]被認為與思覺失調症的發病有關，而每個基因的影響都很有限，且其傳導與表現機制均不明[8][9]。現已提出許多可能造成影響的遺傳學改變，包括特定的[[基因複製數變異]]、[[跨膜受體蛋白NOTCH-4]]、以及組織蛋白等[50]。一些[[全基因組關聯分析]]顯示[[鋅指蛋白804A]]等也與思覺失調症有關[51]。思覺失調症與[[雙向情感障礙]]的遺傳學特徵有一定的重疊性[52]。證據顯示導致思覺失調症的遺傳學特徵包括常見以及不常見的基因突變[53]。
Assuming a hereditary basis, one question from evolutionary psychology is why genes that increase the likelihood of psychosis evolved, assuming the condition would have been maladaptive from an evolutionary point of view. One idea is that genes are involved in the evolution of language and human nature, but to date such ideas remain little more than hypothetical in nature.[54][55]
假設思覺失調症存在遺傳基礎，從[[演化心理學]]角度可思考一個問題：為什麼參與「增加」精神病患病可能性的基因型的變化被假定為[[不適應]]演化的狀態？一個解釋為這些基因參與了人類語言與[[人性]]的演化，但至今為止這樣的解釋仍只停留於假說層次[54][55]。
Environment
Environmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors.[12]
Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents.[9] Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis.[56] Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two,[9][12] even after taking into account drug use, ethnic group, and size of social group.[57] Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.[9][58]
It has been hypothesised that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora.[59] A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.[60]
與思覺失調症發展有關的環境因素包括生活環境、使用娛樂性藥物以及孕期壓力因子[12]。
父母養育子女的方式被認為與思覺失調症的發生應該沒有影響，儘管的確場常表現鼓勵態度的父母的子女相對父母挑剔或常批評的更不容易患病[9]。童年創傷、親人離世以及經受霸凌或虐待等因素增加了患有精神病的風險[56]。即使是在已經考慮到[[使用娛樂性藥物]]、[[種族]]差異以及[[社會群體]]規模的問題的影響後，童年或成年生長在城市環境下還是一致被認為可使患病風險增加兩倍[9][12][57]。其他重要環境因素包括[[社會隔離]]或移民而造成的社會困境、種族歧視、家庭功能失常、失業以及住房條件差等[9][58]。
Substance use
About half of those with schizophrenia use drugs or alcohol excessively.[61] Amphetamine, cocaine, and to a lesser extent alcohol, can result in a transient stimulant psychosis oralcohol-related psychosis that presents very similarly to schizophrenia.[9][62] Although it is not generally believed to be a cause of the illness, people with schizophrenia usenicotine at much higher rates than the general population.[63]
Alcohol abuse can occasionally cause the development of a chronic, substance-induced psychotic disorder via a kindling mechanism.[64] Alcohol use is not associated with an earlier onset of psychosis.[65]
Cannabis can be a contributory factor in schizophrenia,[7][66][67] potentially causing the disease in those who are already at risk.[67] The increased risk may require the presence of certain genes within an individual[67] or may be related to preexisting psychopathology.[7] Early exposure is strongly associated with an increased risk.[7] The size of the increased risk is not clear,[68] but appears to be in the range of two to three times greater for psychosis.[66] Higher dosage and greater frequency of use are indicators of increased risk of chronic psychoses.[66]
Other drugs may be used only as coping mechanisms by individuals who have schizophrenia, to deal with depression, anxiety, boredom, and loneliness.[61][69]
Developmental factors
Factors such as hypoxia and infection, or stress and malnutrition in the mother during fetal development, may result in a slight increase in the risk of schizophrenia later in life.[12]People diagnosed with schizophrenia are more likely to have been born in winter or spring (at least in the northern hemisphere), which may be a result of increased rates of viral exposures in utero.[9] The increased risk is about five to eight percent.[70] Other infections during pregnancy or around the time of birth that may increase the risk includeToxoplasma gondi and Chlamydia.[71]
Main article: Mechanisms of schizophrenia
A number of attempts have been made to explain the link between altered brain function and schizophrenia.[12] One of the most common is the dopamine hypothesis, which attributes psychosis to the mind’s faulty interpretation of the misfiring of dopaminergic neurons.[12]
主條目: [[思覺失調症的機制]]
至今有許多研究嘗試解釋思覺失調症與腦功能變化的關聯性[72]，最廣泛的解釋是[[多巴胺假設(dopamine hypothesis) ]]，此假設將精神疾病如思覺失調症歸因於[[產生多巴胺的神經元(dopaminergic neurons) ]]的失調[12]。
Psychological
Many psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases have been identified in those with the diagnosis or those at risk, especially when under stress or in confusing situations.[72] Some cognitive features may reflect global neurocognitive deficits such as memory loss, while others may be related to particular issues and experiences.[73][74]
Despite a demonstrated appearance of blunted affect, recent findings indicate that many individuals diagnosed with schizophrenia are emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder.[75][76] Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomatology.[77][78][79] The use of "safety behaviors" (acts such as gestures or the use of words in specific contexts) to avoid or neutralize imagined threats may actually contribute to the chronicity of delusions.[80]Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of schizophrenia.[81]
Neurological
Schizophrenia is associated with subtle differences in brain structures, found in forty to fifty percent of cases, and in brain chemistry during acute psychotic states.[12] Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to occur most commonly in the frontal lobes, hippocampus and temporal lobes.[82] Reductions in brain volume, smaller than those found in Alzheimer’s disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or exist prior to the onset of the disease.[46] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[83] Because neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.[84] There has been debate on whether treatment with antipsychotics can itself cause reduction of brain volume.[85]
思覺失調症在40-50%病例中，與不顯著的腦部結構差異及急性精神病狀態的腦部化學有關[12]。以[[神經心理學測試]]和[[腦部造影]]技術，如[[功能性磁振造影[[及[[正電子發射計算機斷層掃描]]，分析腦部功能差異的研究發現，最常見的差異見於[[額葉]]、[[海馬體]]和[[顳葉]][82]。 有報告指在額葉皮層和顳葉出現比在[[阿茲海默症]]較少的腦容量減幅。目前尚 未確 定此腦容量改變為漸進性抑或發病前已經存在[46]。這些異常已被聯繫到普遍跟思覺失調症相關的[[神經認知缺損]][83]。基於神經網路的改變，另有提議指思覺失調症應被視為一系列的神經發展失常[84]。此外，使用抗精神病藥物作治療本身會否造成腦容量減少存在爭議[85]。
Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in schizophrenia.[86] The influential dopamine hypothesis of schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication (atypical antipsychotic medication) can be just as effective as older medication (typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.[87]
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia,[88] and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[89] Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in schizophrenia; this has suggested an important mediating (and possibly causal) role of glutamate pathways in the condition.[90] But positive symptoms fail to respond to glutamatergic medication.[91]
Main article: Diagnosis of schizophrenia
Schizophrenia is diagnosed based on criteria in either the American Psychiatric Association’s fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5), or the World Health Organization’s International Statistical Classification of Diseases and Related Health Problems (ICD-10). These criteria use the self-reported experiences of the person and reported abnormalities in behavior, followed by a clinical assessment by a mental health professional. Symptoms associated with schizophrenia occur along a continuum in the population and must reach a certain severity before a diagnosis is made.[9] As of 2013 there is no objective test.[5]
Criteria
In 2013, the American Psychiatric Association released the fifth edition of the DSM (DSM-5). To be diagnosed with schizophrenia, two diagnostic criteria have to be met over much of the time of a period of at least one month, with a significant impact on social or occupational functioning for at least six months. The person had to be suffering from delusions, hallucinations, or disorganized speech. A second symptom could be negative symptoms, or severely disorganized or catatonic behaviour.[92] The definition of schizophrenia remained essentially the same as that specified by the 2000 version of DSM (DSM-IV-TR), but DSM-5 makes a number of changes.
The ICD-10 criteria are typically used in European countries, while the DSM criteria are used in the United States and to varying degrees around the world, and are prevailing in research studies. The ICD-10 criteria put more emphasis on Schneiderian first-rank symptoms. In practice, agreement between the two systems is high.[96] The current proposal for the ICD-11 criteria for schizophrenia recommends adding self-disorder as a symptom.[19]
If signs of disturbance are present for more than a month but less than six months, the diagnosis of schizophreniform disorder is applied. Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, and various conditions may be classed as psychotic disorder not otherwise specified, while schizoaffective disorder is diagnosed if symptoms of mood disorder are substantially present alongside psychotic symptoms. If the psychotic symptoms are the direct physiological result of a general medical condition or a substance, then the diagnosis is one of a psychosis secondary to that condition.[92] Schizophrenia is not diagnosed if symptoms of pervasive developmental disorder are present unless prominent delusions or hallucinations are also present.[92]
Subtypes
With the publication of DSM-5, the APA removed all sub-classifications of schizophrenia.[97] The five sub-classifications included in DSM-IV-TR were:[98][99]
The ICD-10 defines two additional subtypes:[98]
Sluggish schizophrenia is in the Russian version of the ICD-10. "Sluggish schizophrenia" is in the category of "schizotypal" disorder in section F21 of chapter V.[100]
Differential diagnosis
See also: Dual diagnosis and Comparison of bipolar disorder and schizophrenia
Psychotic symptoms may be present in several other mental disorders, including bipolar disorder,[101] borderline personality disorder,[102] drug intoxication and drug-induced psychosis. Delusions ("non-bizarre") are also present in delusional disorder, and social withdrawal in social anxiety disorder, avoidant personality disorder and schizotypal personality disorder. Schizotypal personality disorder has symptoms that are similar but less severe than those of schizophrenia.[5] Schizophrenia occurs along with obsessive-compulsive disorder (OCD) considerably more often than could be explained by chance, although it can be difficult to distinguish obsessions that occur in OCD from the delusions of schizophrenia.[103] A few people withdrawing from benzodiazepines experience a severe withdrawal syndrome which may last a long time. It can resemble schizophrenia and be misdiagnosed as such.[104]
A more general medical and neurological examination may be needed to rule out medical illnesses which may rarely produce psychotic schizophrenia-like symptoms, such asmetabolic disturbance, systemic infection, syphilis, HIV infection, epilepsy, limbic encephalitis, and brain lesions. Stroke, multiple sclerosis, hyperthyroidism, hypothyroidism anddementias such as Alzheimer’s disease, Huntington’s disease, frontotemporal dementia and Lewy Body dementia may also be associated with schizophrenia-like psychotic symptoms.[105] It may be necessary to rule out a delirium, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, and indicates an underlying medical illness. Investigations are not generally repeated for relapse unless there is a specific medical indication or possible adverse effects from antipsychotic medication. In children hallucinations must be separated from typical childhood fantasies.[5]
Prevention of schizophrenia is difficult as there are no reliable markers for the later development of the disorder.[106] There is tentative evidence for the effectiveness of early interventions to prevent schizophrenia.[107] While there is some evidence that early intervention in those with a psychotic episode may improve short-term outcomes, there is little benefit from these measures after five years.[12] Attempting to prevent schizophrenia in the prodrome phase is of uncertain benefit and therefore as of 2009 is not recommended.[108] Cognitive behavioral therapy may reduce the risk of psychosis in those at high risk after a year[109] and is recommended in this group, by the National Institute for Health and Care Excellence (NICE).[110] Another preventative measure is to avoid drugs that have been associated with development of the disorder, includingcannabis, cocaine, and amphetamines.[9]
Main article: Management of schizophrenia
The primary treatment of schizophrenia is antipsychotic medications, often in combination with psychological and social supports.[12] Hospitalization may occur for severe episodes either voluntarily or (if mental health legislation allows it) involuntarily. Long-term hospitalization is uncommon since deinstitutionalization beginning in the 1950s, although it still occurs.[11] Community support services including drop-in centers, visits by members of a community mental health team, supported employment[111] and support groups are common. Some evidence indicates that regular exercise has a positive effect on the physical and mental health of those with schizophrenia.[112]
Medication
Risperidone (trade name Risperdal) is a commonatypical antipsychoticmedication.
The first-line psychiatric treatment for schizophrenia is antipsychotic medication,[113] which can reduce the positive symptoms of psychosis in about 7 to 14 days. Antipsychotics, however, fail to significantly improve the negative symptoms and cognitive dysfunction.[32][114] In those on antipsychotics, continued use decreases the risk of relapse.[115][116] There is little evidence regarding effects from their use beyond two or three years.[116]
The choice of which antipsychotic to use is based on benefits, risks, and costs.[12] It is debatable whether, as a class, typical or atypical antipsychotics are better.[10][117] Amisulpride, olanzapine, risperidone and clozapine may be more effective but are associated with greater side effects.[118] Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages.[119] There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people.[32] Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia),[120] but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.[9][12][121]
Most people on antipsychotics have side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain.[118] Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.[118] It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome or tardive dyskinesia, a rare but serious neurological disorder.[122]
For people who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be used to achieve control.[123] They reduce the risk of relapse to a greater degree than oral medications.[115] When used in combination with psychosocial interventions they may improve long-term adherence to treatment.[123] TheAmerican Psychiatric Association suggests considering stopping antipsychotics in some people if there are no symptoms for more than a year.[116]
Psychosocial
A number of psychosocial interventions may be useful in the treatment of schizophrenia including: family therapy,[124] assertive community treatment, supported employment,cognitive remediation,[125] skills training, token economic interventions, and psychosocial interventions for substance use and weight management.[126] Family therapy or education, which addresses the whole family system of an individual, may reduce relapses and hospitalizations.[124] Evidence for the effectiveness of cognitive-behavioral therapy (CBT) in either reducing symptoms or preventing relapse is minimal.[127][128] Art or drama therapy have not been well-researched.[129][130] Music therapy has been shown to improve mental state and social functioning when paired with regular care.[131]
Main article: Prognosis of schizophrenia
Disability-adjusted life years lost due to schizophrenia per 100,000 inhabitants in 2004.
Schizophrenia has great human and economic costs.[12] It results in a decreased life expectancy by 10–25 years.[15] This is primarily because of its association with obesity, poor diet, sedentary lifestyles, and smoking, with an increased rate of suicideplaying a lesser role.[12][15][132] Antipsychotic medications may also increase the risk.[15] These differences in life expectancy increased between the 1970s and 1990s.[133]
Schizophrenia is a major cause of disability, with active psychosis ranked as the third-most-disabling condition afterquadriplegia and dementia and ahead of paraplegia and blindness.[134] Approximately three-fourths of people with schizophrenia have ongoing disability with relapses[32] and 16.7 million people globally are deemed to have moderate or severe disability from the condition.[135] Some people do recover completely and others function well in society.[136] Most people with schizophrenia live independently with community support.[12] About 85% are unemployed.[6] In people with a first episode of psychosis a good long-term outcome occurs in 42%, an intermediate outcome in 35% and a poor outcome in 27%.[137] Outcomes for schizophrenia appear better in the developing than the developed world.[138] These conclusions, however, have been questioned.[139][140]
There is a higher than average suicide rate associated with schizophrenia. This has been cited at 10%, but a more recent analysis revises the estimate to 4.9%, most often occurring in the period following onset or first hospital admission.[16][141]Several times more (20 to 40%) attempt suicide at least once.[5][142] There are a variety of risk factors, including male gender, depression, and a high intelligence quotient.[142]
Schizophrenia and smoking have shown a strong association in studies world-wide.[143][144] Use of cigarettes is especially high in individuals diagnosed with schizophrenia, with estimates ranging from 80 to 90% being regular smokers, as compared to 20% of the general population.[144] Those who smoke tend to smoke heavily, and additionally smoke cigarettes with high nicotine content.[145] Some evidence suggests that paranoid schizophrenia may have a better prospect than other types of schizophrenia for independent living and occupational functioning.[146] Among people with schizophrenia use of cannabis is also common.[61]
Main article: Epidemiology of schizophrenia
Schizophrenia affects around 0.3–0.7% of people at some point in their life,[12] or 24 million people worldwide as of 2011.[147] It occurs 1.4 times more frequently in males than females and typically appears earlier in men[9]—the peak ages of onset are 25 years for males and 27 years for females.[148] Onset in childhood is much rarer,[149] as is onset in middle or old age.[150]
Despite the prior belief that schizophrenia occurs at similar rates worldwide, its frequency varies across the world,[5][151] within countries,[152] and at the local and neighborhood level.[153] This variation has been estimated to be fivefold.[6] It causes approximately one percent of worldwide disability adjusted life years[9] and resulted in 20,000 deaths in 2010.[154] The rate of schizophrenia varies up to threefold depending on how it is defined.[12]
In 2000, the World Health Organization found the percentage of people affected and the number of new cases that develop each year is roughly similar around the world, with age-standardized prevalence per 100,000 ranging from 343 in Africa to 544 in Japan and Oceania for men, and from 378 in Africa to 527 in Southeastern Europe for women.[155] About 1.1% of adults have schizophrenia in the United States.[156]
Main article: History of schizophrenia
The term "schizophrenia" was coined by Eugen Bleuler.
In the early 20th century, the psychiatrist Kurt Schneider listed the forms of psychotic symptoms that he thought distinguished schizophrenia from other psychotic disorders. These are called first-rank symptoms or Schneider’s first-rank symptoms. They include delusions of being controlled by an external force, the belief that thoughts are being inserted into or withdrawn from one’s conscious mind, the belief that one’s thoughts are being broadcast to other people, and hearing hallucinatory voices that comment on one’s thoughts or actions or that have a conversation with other hallucinated voices.[157] Although they have significantly contributed to the current diagnostic criteria, the specificity of first-rank symptoms has been questioned. A review of the diagnostic studies conducted between 1970 and 2005 found that they allow neither a reconfirmation nor a rejection of Schneider’s claims, and suggested that first-rank symptoms should be de-emphasized in future revisions of diagnostic systems.[158]The absence of first-rank symptoms should raise suspicion of a medical disorder, however.[19]
The history of schizophrenia is complex and does not lend itself easily to a linear narrative.[159] Accounts of a schizophrenia-like syndrome are thought to be rare in historical records before the 19th century, although reports of irrational, unintelligible, or uncontrolled behavior were common. A detailed case report in 1797 concerning James Tilly Matthews, and accounts by Philippe Pinel published in 1809, are often regarded as the earliest cases of the illness in the medical and psychiatric literature.[160] The Latinized term dementia praecox was first used by German alienist Heinrich Schule in 1886 and then in 1891 by Arnold Pick in a case report of a psychotic disorder (hebephrenia). In 1893 Emil Kraepelinborrowed the term from Schule and Pick and in 1899 introduced a broad new distinction in the classification of mental disorders betweendementia praecox and mood disorder (termed manic depression and including both unipolar and bipolar depression).[161] Kraepelin believed thatdementia praecox was probably caused by a long-term, smouldering systemic or "whole body" disease process that affected many organs and peripheral nerves in the body but which affected the brain after puberty in a final decisive cascade.[162] His use of the term "praecox" distinguished it from other forms of dementia such as Alzheimer’s diseasewhich typically occur later in life.[163] It is sometimes argued that the use of the term démence précoce in 1852 by the French physician Bénédict Morel constitutes the medical discovery of schizophrenia. However, this account ignores the fact that there is little to connect Morel’s descriptive use of the term and the independent development of thedementia praecox disease concept at the end of the nineteenth century.[164]
Molecule of chlorpromazine (trade name Thorazine), which revolutionized treatment of schizophrenia in the 1950s
The word schizophrenia—which translates roughly as "splitting of the mind" and comes from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind")[165]—was coined by Eugen Bleuler in 1908 and was intended to describe the separation of function between personality, thinking, memory, and perception. American and British interpretations of Bleuler led to the claim that he described its main symptoms as four A’s: flattened affect, autism, impaired association of ideas, and ambivalence.[166][167] Bleuler realized that the illness was not a dementia, as some of his patients improved rather than deteriorated, and thus proposed the term schizophrenia instead. Treatment was revolutionized in the mid-1950s with the development and introduction of chlorpromazine.[168]
In the early 1970s, the diagnostic criteria for schizophrenia were the subject of a number of controversies which eventually led to theoperational criteria used today. It became clear after the 1971 US–UK Diagnostic Study that schizophrenia was diagnosed to a far greater extent in America than in Europe.[169] This was partly due to looser diagnostic criteria in the US, which used the DSM-II manual, contrasting with Europe and its ICD-9. David Rosenhan’s 1972 study, published in the journal Science under the title "On being sane in insane places", concluded that the diagnosis of schizophrenia in the US was often subjective and unreliable.[170] These were some of the factors leading to the revision not only of the diagnosis of schizophrenia, but the revision of the whole DSM manual, resulting in the publication of the DSM-III in 1980.[171]
The term schizophrenia is commonly misunderstood to mean that affected persons have a "split personality". Although some people diagnosed with schizophrenia may hear voices and may experience the voices as distinct personalities, schizophrenia does not involve a person changing among distinct, multiple personalities; the confusion arises in part due to the literal interpretation of Bleuler’s term "schizophrenia" (Bleuler originally associated schizophrenia with dissociation, and included split personality in his category of schizophrenia).[172][173] Dissociative identity disorder (having a "split personality") was also often misdiagnosed as schizophrenia based on the loose criteria in the DSM-II.[173][174] The first known misuse of the term to mean "split personality" was in an article by the poet T. S. Eliot in 1933.[175] Other scholars have traced earlier roots.[176] Rather, the term means a "splitting of mental functions", reflecting the presentation of the illness.[177]
See also: Social construction of schizophrenia, List of people with schizophrenia, and Religion and schizophrenia
In 2002, the term for schizophrenia in Japan was changed from seishin-bunretsu-byō (精神分裂病?, lit. "mind-split disease") to tōgō-shitchō-shō(統合失調症?, lit. "integration disorder") to reduce stigma.[178] The new name was inspired by the biopsychosocial model; it increased the percentage of people who were informed of the diagnosis from 37 to 70% over three years.[179] A similar change was made in South Korea in 2012.[180] A professor of psychiatry, Jim van Os, has proposed changing the English term to "psychosis spectrum syndrome".[181]
In the United States, the cost of schizophrenia—including direct costs (outpatient, inpatient, drugs, and long-term care) and non-health care costs (law enforcement, reduced workplace productivity, and unemployment)—was estimated to be $62.7 billion in 2002.[182] The book and film A Beautiful Mind chronicles the life of John Forbes Nash, a Nobel Prize–winning mathematician who was diagnosed with schizophrenia.
Violence
Individuals with severe mental illness, including schizophrenia, are at a significantly greater risk of being victims of both violent and non-violent crime.[183] Schizophrenia has been associated with a higher rate of violent acts, although this is primarily due to higher rates of drug use.[184]Rates of homicide linked to psychosis are similar to those linked to substance misuse, and parallel the overall rate in a region.[185] What role schizophrenia has on violence independent of drug misuse is controversial, but certain aspects of individual histories or mental states may be factors.[186]
Media coverage relating to violent acts by individuals with schizophrenia reinforces public perception of an association between schizophrenia and violence.[184] In a large, representative sample from a 1999 study, 12.8% of Americans believed that individuals with schizophrenia were "very likely" to do something violent against others, and 48.1% said that they were "somewhat likely" to. Over 74% said that people with schizophrenia were either "not very able" or "not able at all" to make decisions concerning their treatment, and 70.2% said the same of money-management decisions.[187] The perception of individuals with psychosis as violent has more than doubled in prevalence since the 1950s, according to one meta-analysis.[188]
See also: Animal models of schizophrenia
Research has found a tentative benefit in using minocycline to treat schizophrenia.[189] Nidotherapy or efforts to change the environment of people with schizophrenia to improve their ability to function, is also being studied; however, there is not enough evidence yet to make conclusions about its effectiveness.[190] Negative symptoms have proven a challenge to treat, as they are generally not made better by medication. Various agents have been explored for possible benefits in this area.[191] There have been trials on drugs with anti-inflammatory activity, based on the premise that inflammation might play a role in the pathology of schizophrenia.[192]