第1章 精神科藥物的致殘、中毒失認的作用 (p. 1)
CHAPTER 1 The Brain-Disabling, Spellbinding Effects of Psychiatric Drugs
現代精神科藥物治療的可信度來自於專業人士和非專業人士經常接受的一些科學證明的假設。 這些基本假設符合神話：支持信仰體系和一系列實踐的虛構。 與這些神話相反，本書確定了基於科學和臨床證據以及常識的精神藥理學原理。
Modern psychiatric drug treatment gains its credibility from a number of assumptions that professionals and laypersons alike too often accept as scientifically proven. These underlying assumptions qualify as myths: fictions that support a belief system and a set of practices. In contrast to these myths, this book identifies principles of psychopharmacology that are based on scientific and clinical evidence as well as on common sense.
Together, these form the brain-disabling principles or the brain-disabling concept of biopsychiatric treatment. While the book in its entirety provides the evidence for these principles, this chapter will summarize them, including the new principle of intoxication anosognosia, or medication spellbinding (Breggin, 2006d, in press).
從本質上講，大腦功能障礙的概念作為一個整體表明，所有的精神病治療——藥物、電擊和腦葉切除術——都是通過破壞大腦和大腦的功能來發揮作用，產生的效果隨後被解釋（或誤解）為改善。 藥物施法是一種大腦致殘效應，使個體無法感知藥物引起的損傷程度； 使個人不將自己的任何變化歸因於藥物不良反應； 經常使個人認為他們比以往任何時候都做得更好，而實際上他們做得更糟； 在極端情況下，驅使他們從事傷害自己和他人的強迫性活動。
In essence, the brain-disabling concept as a whole states that all psychiatric treatments—drugs, electroshock, and lobotomy—work by disrupting the function of the brain and mind, creating effects that are then interpreted (or misinterpreted) as improvements. Medication spellbinding is a brain-disabling effect that renders individuals unable to perceive the degree of their drug-induced impairment; causes individuals not to attribute any change in themselves to an adverse drug effect; often makes individuals believe that they are doing better than ever, when they are doing worse; and in the extreme, drives them into compulsive activities that harm themselves and others.
大腦功能障礙的四項基本原則 (p. 2)
THE BASIC FOUR BRAIN-DISABLING PRINCIPLES
I.All biopsychiatric treatments share a common mode of action: the disruption of normal brain function.
Pharmacologists speak of a drug’s therapeutic index, the dosage ratio between the beneficial effect and the toxic effect. The first brain-disabling principle of psychiatric treatment reveals that the toxic dose is the therapeutic dose—that brain disability causes the seemingly therapeutic effect.
This same principle applies to electroshock and psychosurgery.
大腦致殘原則指出，一旦達到毒性，藥物就會開始產生精神作用； 也就是說，它開始影響大腦和思想。 沒有毒性，該藥物將沒有精神作用。
The brain-disabling principle states that as soon as toxicity is reached, the drug begins to have a psychoactive effect; that is, it begins to affect the brain and mind. Without toxicity, the drug would have no psychoactive effect.
Psychoactive drugs, including psychiatric drugs, vary in their toxicity.
However, all of the major categories of psychiatric drugs—antidepressants, stimulants, tranquilizers (antianxiety drugs), mood stabilizers, and antipsychotics—are neurotoxic. They poison neurons, and sometimes destroy them.
II. All biopsychiatric interventions cause generalized brain dysfunction.
儘管特定治療確實對大腦產生了明顯不同的影響，但它們都具有產生廣泛性功能障礙的能力，並在情感和智力功能的範圍內造成一定程度的損害。 由於大腦高度集成，因此不可能在不損害各種其他功能的情況下禁用受限的心理功能，通常會導致大腦和思維的普遍功能障礙。 例如，即使產生輕微的情緒遲鈍、嗜睡或疲勞，也可能損害認知功能，如注意力、注意力、警覺性、自我關注或自我意識以及社會敏感性。 這些變化可能是微妙的，著迷的人可能無法察覺它們，但這些變化仍然會對人的生活質量產生不利影響。
Although specific treatments do have recognizably different effects on the brain, they share the capacity to produce generalized dysfunction with some degree of impairment across the spectrum of emotional and intellectual function. Because the brain is so highly integrated, it is not possible to disable circumscribed mental functions without impairing a variety of other functions, typically causing generalized dysfunction of the brain and mind. For example, even the production of a slight emotional dullness, lethargy, or fatigue is likely to impair cognitive functions such as attention, concentration, alertness, self-concern or self-awareness, and social sensitivity. These changes can be subtle, and the spellbound individual may fail to perceive them, but the changes nonetheless adversely affect the person’s quality of life.
Shock treatment and psychosurgery always produce obvious generalized dysfunction. Some medications may not obviously produce these effects in their minimal dose range, but they may also lack any substantial so-called therapeutic effect in that range.
三、 生物精神治療通過損害更高的人類功能來發揮治療效果，包括情緒反應能力、社會敏感性、自我意識或自我洞察力、自主性和自我決定。 更劇烈的影響包括冷漠、欣快和躁狂，1 和腦葉切除樣冷漠。
III. Biopsychiatric treatments exert their therapeutic effect by impairing higher human functions, including emotional responsiveness, social sensitivity, self-awareness or self-insight, autonomy, and self-determination. More drastic effects include apathy, euphoria and mania,1 and lobotomy-like indifference.
由於廣泛的腦功能障礙以及對額葉、邊緣系統和其他結構的特定影響，生物精神干預會損害更高的心理、心理和精神功能。 通常，結果是對自己和對他人的冷漠，就像腦葉切除術一樣——我稱之為失活綜合症。 最近的研究證實，SSRI 抗抑鬱藥（如 Prozac、Zoloft 和 Paxil）會產生這些影響； 興奮劑，如利他林、協奏曲和阿得拉爾； 以及較新的抗精神病藥物，例如利培酮和賽普樂2（見第 2、4 和 7 章）。 長期使用任何精神活性藥物或精神藥物，包括苯二氮卓類藥物和情緒穩定劑，都會產生一定程度的失活。
Higher mental, psycho logical, and spiritual functioning are impaired by biopsychiatric interventions as a result of generalized brain dysfunction as well as specific effects on the frontal lobe, limbic system, and other structures. Commonly, the result is a lobotomy-like indifference to self and to others—a syndrome that I have called deactivation. Recent research confirms that these effects occur with the SSRI antidepressants, such as Prozac, Zoloft, and Paxil; the stimulants, such as Ritalin, Concerta, and Adderall; and the newer antipsychotics, such as Risperdal and Zyprexa2 (see chapters 2, 4, and 7). Chronic use of any psychoactive or psychiatric drug, including the benzodiazepines and mood stabilizers, will produce a degree of deactivation.
自發的、自生的、自主的或自願的活動是生物，尤其是人類的生命本質。 它可以看作是人類活動的最高表現。 因為它需要一個功能齊全的大腦，所以在大腦最高中心（包括額葉和邊緣系統，以及更深的網狀激活系統）受到任何損傷後，都會出現自發行為的損害。
Spontaneous, self-generated, autonomous or voluntary activity is the vital essence of living creatures, and especially human beings. It can be viewed as the highest expression of human activity. Because it requires a fully functioning brain, impairment of spontaneous behavior occurs following any injury to the highest centers of the brain, including the frontal lobes and limbic system, as well as the deeper reticular activating system.
由於較高的大腦功能很脆弱並且依賴於整體的身體健康，自發的、自我產生的行為的失活通常是任何身體損傷或疾病的第一個跡象，從頭部受傷和慢性疲勞到流感樣疾病、荷爾蒙失調 和腦瘤。 同樣，失活是任何精神活性藥物（即任何破壞大腦和思維功能的藥物）的最早和最重要的影響之一，包括所有精神藥物。
Because higher brain functions are fragile and dependent on overall physical well-being, a deactivating loss of spontaneous, self-generated behavior is often the first sign of any physical impairment or illness, from head injury and chronic fatigue to fl ulike illnesses, hormonal disorders, and brain tumors. Similarly, deactivation is one of the earliest and most essential effects of any psychoactive drug—that is, any drug that disrupts the function of the brain and mind—including all psychiatric drugs.
多種藥物不良反應可歸入更廣泛的失活概念。 其中一些反應包括藥物引起的主動性降低、冷漠、冷漠、嗜睡、精神運動遲緩和失去興趣。 藥物引起的抑鬱、鎮靜、嗜睡、情緒遲鈍或遲鈍、不適和被動通常反映了一定程度的失活。 在有關精神藥物作用的動物文獻中，失活被描述為整體活動、自發活動、社會互動和探索的減少。
A variety of adverse drug reactions can be subsumed under the broader concept of deactivation. Some of these reactions include drug-induced diminished initiative, indifference, apathy, lethargy, psychomotor retardation, and loss of interest. Drug-induced depression, sedation, drowsiness, emotional dulling or blunting, malaise, and passivity often reflect a degree of deactivation. In the animal literature concerning psychiatric drug effects, deactivation is described as reductions in overall activity, spontaneous activity, social interactions, and exploration.
當醫生和/或患者更喜歡腦功能減弱的狀態，其心智能力或情緒表達範圍較窄或較淺時，生物精神治療被認為是有效的。 如果服藥者報告感覺更有效和更強大，這很可能是基於不切實際的評估、判斷力受損或與藥物魔法相關的欣快感。 當使用所謂的維持劑量的患者沒有出現明顯的效果時，要么劑量太低而無法產生臨床效果，要么患者無法感知藥物的影響，這也是藥物令人著迷的特徵。
Biopsychiatric treatments are deemed effective when the physician and/or the patient prefers a state of diminished brain function, with its narrowed or shallower range of mental capacity or emotional expression. If the drugged individual reports feeling more effective and powerful, it is most likely based on an unrealistic appraisal, impaired judgment, or euphoria associated with medication spellbinding. When patients on so-called maintenance doses do not experience noticeable effects, either the dose is too low to have a clinical effect, or the patient is unable to perceive the drug’s impact, again characteristic of medication spellbinding.
IV. Each biopsychiatric treatment produces its essential or primary brain-disabling effect on all people, including normal volunteers and patients with varied psychiatric diagnoses.
儘管藥物支持者深信不疑，但沒有針對特定精神障礙的特定精神藥物治療。 當然，人們對藥物、休克治療、甚至腦葉切除術或意外頭部受傷的反應方式存在一定的生理和心理差異。 然而，作為一般原則，生物精神干預具有非特異性影響，不依賴於人的精神狀態或狀況。 例如，將顯示神經安定藥和鋰對動物和正常志願者的影響與它們對患者的影響大致相同，部分是通過抑制他們的整體情緒反應。
Despite the deeply held convictions of drug proponents, there are no specific psychoactive drug treatments for specific mental disorders. There is, of course, a certain amount of biological and psychological variation in the way people respond to drugs, shock treatment, or even lobotomy or an accidental head injury. However, as a general principle, biopsychiatric interventions have a nonspecific impact that does not depend on the person’s mental state or condition. For example, it will be shown that neuroleptics and lithium affect animals and normal volunteers in much the same way as they affect patients, in part by subduing their overall emotional responsiveness.
確認大腦功能障礙四項基本原理的說明性研究 (p. 4)
ILLUSTRATIVE RESEARCH CONFIRMING THE BASIC FOUR BRAIN-DISABLING PRINCIPLES
前四個原則是大腦功能障礙概念的核心：基本上，所有精神科藥物都會導致大腦功能的普遍損害，從而降低整體心理和情緒功能； 這種致殘效應也發生在正常志願者身上； 並且該效果對任何精神疾病都沒有特異性。
The first four principles are the heart of the brain-disabling concept: basically, that all psychiatric drugs cause a generalized impairment of brain function that reduces overall mental and emotion function; that this disabling effect occurs, as well, in normal volunteers; and that the effect has no specificity for any psychiatric disorder.
有時，研究直接證實了大腦功能障礙的原理，但並不打算這樣做，也沒有承認這一點。 在某些方面，這是最客觀的研究，因為研究人員不知道他們正在測試的原理。 以下三項研究涉及第二代或非典型精神安定藥利培酮（Risperdal），該藥廣泛用於兒童和成人。
On occasion, research studies directly confirm the brain-disabling principle, but without intending to do so and without acknowledging it. In some ways, this is the most objective kind of research in that the researchers are unaware of the principle that they are testing. The following three studies involve the second-generation or atypical neuroleptic risperidone (Risperdal), which is widely prescribed to children and adults.
Peter Liddle 和他的同事 (2000) 使用正電子發射斷層掃描 (PET) 研究了利培酮對腹側紋狀體、丘腦和額葉皮層代謝率的影響。 他們的受試者是八名被診斷為首發精神分裂症的未使用過神經安定劑的患者。
Peter Liddle and his colleagues (2000) used positron emission tomography (PET) to study the effects of risperidone on the rate of metabolism on the ventral striatum, thalamus, and frontal cortex. Their subjects were eight neuroleptic-naïve patients diagnosed with their first episodes of schizophrenia.
首先，Liddle 等人。 (2000) 發現“單劑量的利培酮會降低腹側紋狀體、丘腦和額葉皮層的新陳代謝。” 作者將該區域確定為皮質-紋狀體-丘腦-皮質反饋迴路。 這包括邊緣系統中的大部分情緒調節中心和額葉中的高級心理中心。 多巴胺能神經傳遞在該系統中起重要作用，並被利培酮嚴重阻斷。 顯然，這證實了利培酮，像所有的精神安定藥一樣，會導致化學性腦葉切除術，不可避免地會產生相對程度的冷漠和冷漠。
First and foremost, Liddle et al. (2000) found that “a single dose of risperidone produced decreases in metabolism in ventral striatum, thalamus and frontal cortex.” The authors identified this region as the cortico–striato–thalamo–cortical feedback loop. This encompasses much of the emotion-regulating centers in the limbic system and higher mental centers in the frontal lobes. Dopaminergic neurotransmission plays a significant role in this system and is profoundly blocked by risperidone. Clearly, this confirms that risperidone, like all neuroleptics, causes a chemical lobotomy, with the inevitable production of relative degrees of apathy and indifference.
此外，根據 Liddle 等人的說法。 （2000 年），“利培酮治療六週後，額葉代謝的下降更為廣泛。” 換句話說，利培酮產生了一種漸進的化學腦葉切除術，抑制了額葉功能。
Moreover, according to Liddle et al. (2000), “after six weeks’ treatment with risperidone, the decreases in frontal lobe metabolism were more extensive.” In other words, the risperidone produced a progressive chemical lobotomy with suppression of frontal lobe function.
Liddle 等人為了符合大腦功能障礙的原則。 （2000）能夠將症狀的進行性抑制與利培酮的暴露聯繫起來。 儘管他們測試了各種症狀，但他們只報告了現實扭曲的嚴重程度有所降低。 事實證明，現實扭曲是對患者妄想和幻覺的全球臨床印象。 毫無疑問，化學腦葉切除術（或外科腦葉切除術）可以減少個體的妄想和幻覺表達。 它通過抑制邊緣系統和額葉功能來做到這一點，導致冷漠和冷漠。 患者不再關心表達他們更華麗的症狀，但他們也不再關心任何事情。 這是全局停用。
In keeping with the brain-disabling principle, Liddle et al. (2000) were able to correlate a progressive suppression of symptoms with the exposure to risperidone. Although they tested for a variety of symptoms, they only reported a decreased severity of reality distortion. Reality distortion turns out to be a global clinical impression of the patient’s delusions and hallucinations. There is certainly no question that a chemical lobotomy (or a surgical lobotomy) reduces the individual’s expression of delusions and hallucinations. It does this by suppressing limbic system and frontal lobe function, causing apathy and indifference. The patients no longer care enough to express their more florid symptoms, but they also no longer care about anything. It is a global deactivation.
利德爾等人。 (2000) 試圖將現實扭曲的減少與海馬體可能過度活躍的區域的抑制聯繫起來，但這是想像力的巨大延伸。 事實很簡單：PET 顯示邊緣系統和額葉的新陳代謝和功能受到全面抑制，在 6 週內對額葉的影響越來越大，這與患者不再交流有關他們的症狀。 這是對神經阻滯劑治療大腦功能障礙概念的展示。
Liddle et al. (2000) try to correlate the reduction in reality distortion with suppression of a presumably overactive region of the hippocampus, but this is a huge stretch of the imagination. The facts are simple: The PET shows a global suppression of metabolism, and hence function, in the limbic system and frontal lobes, with increasing impact on the frontal lobes over a 6-week period, correlated with the patients no longer communicating as much about their symptoms. This is a demonstration of the brain-disabling concept of neuroleptic treatment.
Ngan 等人再次使用 PET。 （2002 年）測量了患者在使用抗精神病藥物之前、初始劑量的利培酮之後和治療 6 週之後的腦代謝活動。 他們發現額葉功能下降，並且根據我在本書 1997 年版中的建議，他們將其稱為失活。 他們得出的結論是，這種額葉代謝的減少是藥物的功能，而不是“精神分裂症”，抗精神病藥物的作用機制是“皮質代謝減少”，尤其是在額葉和顳葉區域。這是大腦致殘概念的支柱：精神藥物通過致殘大腦的較高中心而起作用。 作者指出，需要一個健康的對照組來進一步證明該藥物的主要作用與患者的疾病是分開的，並且會發生在任何人群中，無論是正常的還是異常的。
Again using PET, Ngan et al. (2002) measured cerebral metabolic activity in patients before neuroleptic exposure, after an initial dose of risperidone and after 6 weeks of treatment. They found a reduction of frontal lobe function, and, in keeping with my suggestion in the 1997 edition of this book, they called it deactivation. They concluded that this decrease in frontal lobe metabolism is a function of the drug and not “schizophrenia” and that the mechanism of antipsychotic drug action is a “reduction in cortical metabolism,” especially in the frontal and temporal regions. This is a pillar of the brain-disabling concept: that psychiatric drugs work by disabling the higher centers of the brain. The authors pointed out that a healthy control group is needed to further demonstrate that the drug’s primary effect is separate from the patient’s disorder and would occur in any group of individuals, normal or abnormal.
萊恩等人。 (2004) 進行了一項相關研究，該研究可能是為了測試大腦功能障礙原理的特定目的而計劃的。
Lane et al. (2004) conducted a related study that could have been planned for the specific purpose of testing the brain-disabling principle.
使用 PET，他們測量了單次 2 毫克劑量的利培酮和安慰劑產生的區域代謝變化，這是在一項對九名健康受試者進行的隨機雙盲研究中進行的。 他們的研究結果證實，利培酮對正常人的影響與被標記為精神分裂症的人相同，並且它通過降低對整體心理功能至關重要的區域的大腦功能發揮作用。 他們說，結果：與安慰劑相比，利培酮在健康受試者的左側額葉皮層和右側額葉皮層的新陳代謝方面產生了減少。 聯結分析表明，這些變化發生在與精神分裂症產生利培酮的變化基因座相似的位置。
Using PET, they measured changes in regional metabolism produced by a single 2-mg dose of risperidone and by placebo, administered in a randomized, double-blind study of nine healthy subjects. Their results confirm that risperidone has the same effect on normal people as people labeled schizophrenic and that it acts by reducing brain function in areas critical to overall mental functioning. They stated, Results: Compared with placebo, risperidone produced reductions in metabolism in the left lateral frontal cortex and right medial frontal cortex in healthy subjects. Conjunction analysis reveals that these changes occurred at locations similar to the loci of change produced risperidone with schizophrenia.
The researchers then concluded that there is a link between this reduced metabolism (a brain-disabling effect) and the reduction of clinical symptoms in patients diagnosed with schizophrenia:
Because the reduction in metabolism in the medial frontal cortex produced by risperidone is associated with alleviation of positive symptoms in patients with schizophrenia, the observation of a reduction in metabolism at a similar site in healthy subjects supports the hypothesis that the antipsychotic effect of risperidone arises, at least in part, from a physiologic effect that occurs in both patients with schizophrenia and healthy subjects.
The positive symptoms found in patients diagnosed with schizophrenia, such as hallucinations and delusions, can be suppressed by any brain-disabling trauma, from electroshock and lobotomy to neuroleptic drugs.
這與消極症狀（如冷漠）形成對比，這些消極症狀因禁用或抑制大腦功能而惡化。 如果進行了測量，額葉的失活也與所有自發的心理活動和語言表達的減少相關，這是精神抑制治療期間常見的臨床現象。 這種抑製作用通常被確定為精神運動遲緩、帕金森症狀或冷漠樣冷漠綜合徵。
This is in contrast to the negative symptoms, such as apathy, which are worsened by disabling or suppressing brain function. If it had been measured, the deactivation of the frontal lobes would also have correlated with a reduction in all spontaneous mental activity and verbal expressions, which is a commonly observed clinical phenomenon during neuroleptic treatment. This suppressive effect is often identified as psychomotor retardation, parkinsonian symptoms, or an apathylike syndrome of indifference.
Studies such as these three involving risperidone completely confirm the brain-disabling principles of psychiatric treatment. There should no longer be any scientific doubt about the correctness of the brain-disabling concept, although its general acceptance requires letting go of numerous myths surrounding psychiatric treatment.
六項額外的大腦功能障礙原則 (p. 7)
SIX ADDITIONAL BRAIN-DISABLING PRINCIPLES
The last series of brain-disabling principles describe clinical phenomena associated with treatment-induced brain disability.
V. Patients respond to brain-disabling treatments with their own psychological reactions such as apathy, euphoria, compliance, or resentment.
個體對藥物的反應方式存在一些差異。 例如，同一種抗抑鬱藥會使一個人昏昏欲睡，另一個人精力充沛。 利他林可以讓許多孩子安靜下來，但也讓其他孩子感到不安。
There is some variation in the way individuals respond to drugs. For example, the same antidepressant will make one person sleepy and another energized. Ritalin quiets many children but agitates others.
很難將藥物誘發的反應與心理誘發的反應區分開來。 例如，所有抗抑鬱藥都會引起欣快感和躁狂症。(^3) 同時，一些接受這些藥物的人有自己發展這些精神狀態的傾向。 同樣，多種藥物能夠在患者中產生激動和敵意，但人們可以在沒有藥物的情況下產生這些反應。 服用安定藥後出現的順從性和順從性可能是由藥物引起的失活綜合徵引起的，但也可能是由於患者意識到對精神病學權威和控制的進一步抵抗是徒勞的或危險的。
It can be very difficult to separate out drug-induced from psychologically induced responses. For example, all antidepressants can cause euphoria and mania.(^3) At the same time, some of the people who receive these drugs have their own tendency to develop these mental states. Similarly, a variety of drugs are capable of generating agitation and hostility in patients, yet people can develop these responses without medication. The docility and compliance seen following the administration of neuroleptics can be caused by the drug-induced deactivation syndrome but can also result from the patient’s realization that further resistance to psychiatric authority and control is futile or dangerous.
VI. To the extent that a physical disorder of the brain afflicts the individual, currently available biopsychiatric interventions will worsen or add to the disorder.
目前可用的生物精神治療並非針對任何已知的大腦疾病。 最重要的是，它們會破壞正常的大腦功能，而不會糾正任何大腦異常。 因此，如果患者患有已知的大腦身體疾病，生物精神治療只會惡化或加重病情。 一個典型的例子是讓 Haldol 控制情緒不安的阿爾茨海默氏症患者。 在抑制他們的行為的同時，這種藥物會加重他們的癡呆症（第 2-4 章）。
The currently available biopsychiatric treatments are not specific for any known disorder of the brain. One and all, they disrupt normal brain function, without correcting any brain abnormality. Therefore, if a patient is suffering from a known physical disorder of the brain, biopsychiatric treatment can only worsen or add to it. A classic example involves giving Haldol to control emotionally upset Alzheimer’s patients. While subduing their behavior, the drug worsens their dementia (chapters 2–4).
在製藥公司開發和銷售精神藥物後，試圖在糾正假定的生化失衡的基礎上證明其使用是合理的。 例如，據稱百憂解有助於改善血清素能神經傳遞。 甚至電擊和腦葉切除術也是合理的，因為它們可以糾正生化失衡。 這些入侵不可能糾正生化失衡。 各種各樣的大腦致殘藥物被用於治療相同或相似的疾病——從百憂解到 Xanax 再到電擊的所有藥物都用於治療抑鬱症——每種治療最終都會破壞無數的大腦功能。 實際上，目前所有可用的生物精神干預措施都會對大腦造成直接傷害，從而對大腦造成直接傷害，而不會糾正任何已知的故障。
After psychiatric drugs are developed and marketed by drug companies, attempts are made to justify their use on the basis of correcting presumed biochemical imbalances. For example, it is claimed that Prozac helps by improving serotonergic neurotransmission. Even electroshock and lobotomy are justified on the grounds that they correct biochemical imbalances. There is no likelihood that these intrusions correct a biochemical imbalance. A wide variety of brain-disabling agents are used to treat the same or similar disorders—everything from Prozac to Xanax to electroshock is prescribed for depression—and each treatment ends up disrupting innumerable brain functions. In reality, all currently available biopsychiatric interventions cause direct harm to the brain and hence to the mind, without correcting any known malfunction.
製藥行業一直在努力遊說，讓美國國會、衛生專業人士和公眾相信抑鬱和焦慮等情緒問題是生物起源的。 精神疾病的假定生物學基礎然後被用來證明他們的產品，精神藥物的廣泛銷售是合理的。 但是，即使有一天一種或另一種精神疾病被證明具有生物學基礎，這絕不會證明對這些患者使用精神藥物是合理的，從而使他們潛在的腦部疾病與藥物毒性複合。
The pharmaceutical industry has lobbied hard to convince the U.S. Congress, the health professions, and the public that emotional problems such as depression and anxiety are biological in origin. The supposed biological basis of psychiatric disorders is then used to justify the widespread sale of their products, psychiatric drugs. But even if one or another psychiatric disorder someday turns out to have a biological basis, that in no way would justify inflicting psychiatric drugs on these patients, thereby compounding their underlying brain disorder with drug toxicity.
VII. Individual biopsychiatric treatments are not specific for particular mental disorders.
人們常說，精神病學對特定診斷類別的患者有特定的治療方法，例如“精神分裂症”的抗精神病藥； 抑鬱症的抗抑鬱藥; 用於焦慮的苯二氮卓類鎮靜劑； 鋰用於躁狂症； 和興奮劑，如利他林，用於注意力缺陷多動。 在實際實踐中，許多個體患者一次或多次服用上述所有類別的藥物，而且越來越多的是一次全部服用。 多年來，藥物的推薦使用通常會發生變化。 雖然標記為精神分裂症的患者一般傾向於最初使用抗精神病藥進行治療，或者對抑鬱症患者最初使用抗抑鬱藥，但這在一定程度上是該行業的慣例問題。
It is often said that psychiatry has specific treatments for specific diagnostic categories of patients, for example, neuroleptics for “schizophrenia”; antidepressants for depression; benzodiazepine tranquilizers for anxiety; lithium for mania; and stimulants, such as Ritalin, for attention-deficit hyperactivity. In actual practice, many individual patients are given all of the above categories of drugs at one time or another, and, increasingly so, all at once. Often the recommended use of a drug changes over the years. While there is a general tendency for patients labeled schizophrenic to be initially treated with neuroleptics or for depressed patients to be initially prescribed antidepressants, this is, in part, a matter of convention within the profession.
當一種藥物似乎對特定疾病更有效時，它通常取決於它是否對中樞神經系統具有抑製或激發作用。例如，如果抑鬱症患者的情緒和身體已經減慢，給他們服用導致精神運動遲緩的精神抑製藥會使他們看起來更糟。這些患者在人工通電後更有可能得到改善。相反，如果被診斷患有精神分裂症的患者變得煩躁且難以控制，那麼給他們服用興奮劑就沒有意義了。當服用能降低或平緩他們整體情緒反應能力的抗精神病藥時，他們更有可能被判斷為有所改善。同樣，如果孩子在課堂上感到無聊和不安，利他林、Adderall 和 Strattera 等興奮劑會抑制自發行為並強制強迫行為，從而產生進步的錯覺（第 10 章）。然而，這些嚴重的行為影響與針對特定疾病的靈丹妙藥相去甚遠。
When a drug seems more effective for a particular disorder, it often depends on whether it has a suppressive or an energizing effect on the central nervous system. For example, if depressed patients are already emotionally and physically slowed down, giving them a neuroleptic that causes psychomotor retardation would tend to make them look worse. These patients are more likely to seem improved when artificially energized. Conversely, if patients diagnosed with schizophrenia become agitated and difficult to control, it would not make sense to give them stimulants. They are more likely to be judged improved when taking a neuroleptic that reduces or flattens their overall emotional responsiveness. Similarly, if a child is bored and restless in the classroom, stimulants such as Ritalin, Adderall, and Strattera will suppress spontaneous behavior and enforce obsessive–compulsive behavior, giving an illusion of improvement (chapter 10). These gross behavioral effects, however, are a far cry from having a magic bullet for a specific disease.
八。 大腦試圖從物理上補償生物精神干預的致殘效應，經常引起額外的不良反應和戒斷問題。 (p. 9)
VIII. The brain attempts to compensate physically for the disabling effects of biopsychiatric interventions, frequently causing additional adverse reactions and withdrawal problems.
大腦不歡迎精神科藥物作為營養物質。 相反，大腦將它們作為有毒物質做出反應，並試圖克服它們的破壞性影響。 例如，當百憂解在突觸間隙中誘導過量的血清素時，大腦會通過減少神經末梢的血清素輸出、減少突觸中可以接收血清素的受體數量以及增加神經末梢的能力來進行補償。 運輸系統從突觸中去除血清素。 類似地，當利培酮、Zyprexa 或 Haldol 等抗精神病藥物降低多巴胺能係統的反應性時，大腦會進行補償，通過增加多巴胺受體的數量和敏感性在同一系統中產生過度活躍。 所有這些代償性反應都會導致大腦功能出現新的異常，有時會導致不可逆的疾病，例如抗精神病藥物引起的遲發性運動障礙（第 4 章）。
The brain does not welcome psychiatric medications as nutrients. Instead, the brain reacts against them as toxic agents and attempts to overcome their disruptive impact. For example, when Prozac induces an excess of serotonin in the synaptic cleft, the brain compensates by reducing the output of serotonin at the nerve endings, by reducing the number of receptors in the synapse that can receive the serotonin, and by increasing the capacity of the transport system to remove serotonin from the synapse. Similarly, when antipsychotic drugs such as Risperdal, Zyprexa, or Haldol reduce reactivity in the dopaminergic system, the brain compensates, producing hyperactivity in the same system by increasing the number and sensitivity of dopamine receptors. All of these compensatory reactions create new abnormalities in brain function, sometimes causing irreversible disorders, such as antipsychotic drug–induced tardive dyskinesia (chapter 4).
要準確確定服用精神科藥物的人的潛在心理狀況，即使不是不可能，也很困難。 有太多複雜的因素，包括藥物的大腦致殘作用、大腦的代償反應，以及患者對服藥的心理反應。 我評估了許多病例，在這些病例中，患者在多種精神科藥物的衝擊下病情惡化，而處方醫生卻沒有將患者的下降歸因於藥物毒性。 相反，醫生通常將患者病情惡化歸因於“精神疾病”，而實際上患者正遭受藥物不良反應。
It is difficult, if not impossible, to determine accurately the underlying psychological condition of a person who is taking psychiatric drugs. There are too many complicating factors, including the drug’s brain-disabling effect, the brain’s compensatory reactions, and the patient’s psychological responses to taking the drug. I have evaluated many cases in which patients have deteriorated under the onslaught of multiple psychiatric drugs without the prescribing physicians attributing the patients’ decline to drug toxicity. Instead, physicians typically attribute their patients’ worsening condition to “mental illness” when in reality the patient is suffering from adverse drug reactions.
由於大腦試圖補償大多數精神活性藥物的影響，因此患者可能難以戒除這些藥物。 在身體上，大腦不能像停藥一樣迅速地從藥物作用中恢復，因此在停藥後，代償機制可能需要數週或數月才能恢復。 有時，如遲發性運動障礙，大腦無法恢復。 在某些情況下，由於藥物引起的大腦變化產生的情緒不穩定和身體症狀，服用了數月或數年的新型抗抑鬱藥（如 Prozac、Paxil、Zoloft 和 Celexa）的患者無法退出這些藥物。
Because the brain attempts to compensate for the effects of most psychoactive drugs, patients can have difficulty withdrawing from them. Physically, the brain cannot recover from the drug effect as quickly as the drug is withdrawn so that the compensatory mechanisms can require weeks or months to recover after the drug has been withdrawn. Sometimes, as in tardive dyskinesia, the brain fails to recover. In some cases, patients who have taken the newer antidepressants such as Prozac, Paxil, Zoloft, and Celexa for months or years cannot withdraw from them owing to the emotional instability and physical symptoms produced by drug-induced changes in the brain.
九。 開出生物精神干預措施的醫生通常對其風險和收益進行不切實際的評估。 （第 11 頁）
IX. Physicians who prescribe biopsychiatric interventions often have an unrealistic appraisal of their risks and benefits. (p. 11)
可以寫一整本書，講述醫生很少意識到與他們開出的精神科藥物相關的風險，以及他們高估了其有效性的程度。 美國食品藥品監督管理局 (FDA)、醫學和精神病學協會、對推廣藥物有既得利益的專家以及製藥行業——精神藥物綜合體(the psychopharmaceutical complex)——共同推動醫生為兒童和成人開具精神藥物。
An entire book could be written about how little physicians appreciate the risks associated with the psychiatric drugs that they prescribe and how much they overestimate their effectiveness. The Food and Drug Administration (FDA), medical and psychiatric associations, experts with a vested interest in promoting drugs, and the pharmaceutical industry—the psychopharmaceutical complex—combine to push doctors to prescribe psychiatric drugs to children and adults.
個別醫生的臨床判斷如何？ 個別醫生無法評估精神科藥物的有效性。 近年來，甚至有人質疑對照臨床試驗的客觀性，將藥物與安慰劑或替代藥物進行比較（見第 6-7 章）。 調查人員經常受到他們有意識或無意識偏見的影響。
What about the clinical judgment of individual physicians? The individual physician is not in a good position to assess the effectiveness of psychiatric drugs. In recent years, doubt has even been thrown on the objectivity of controlled clinical trials, in which drugs are compared to placebo or to alternative medications (see chapters 6–7). Too often, the investigators are influenced by their conscious or unconscious biases.
如果臨床和科學研究可能因偏見而扭曲，那麼常規臨床實踐更有可能受到處方醫師的希望和期望的影響。在藥物被證明毫無價值或危險到無法接受之前，大量的醫生多年來一直懷著無限的熱情開藥。例如，多年來，安非他明被免費分發給數百萬抑鬱症和體重控制的患者，但沒有考慮到它們缺乏療效、長期危害和成癮潛力（第 11 章）。近年來，苯二氮卓類藥物（如 Valium 和 Xanax）被過度用於治療焦慮症，儘管它們在長期使用時會加重焦慮，導致持續的記憶和精神缺陷，並經常產生濫用和依賴（第 12 章）。抗抑鬱藥繼續免費提供給兒童和青少年，儘管 FDA 本身承認多項研究未能證明它們有用（第 6 章）。事實上，抗抑鬱藥在治療抑鬱症成人方面的有效性也存在疑問（第 6-7 章），雖然它們的副作用可能會危及生命並使戒斷成為不可能，但大多數醫生認為它們非常安全和有效。在更極端的例子中，儘管對患者的精神生活產生了明顯的破壞性影響並且缺乏經證實的療效（第 9 章），但仍繼續使用精神外科手術和電擊術。
If clinical and scientific studies can be distorted by bias, it is even more likely that routine clinical practice will be affected by the hopes and expectations of the prescribing physician. Physicians in great numbers have prescribed drugs with unbounded enthusiasm for years before the agents have proven to be worthless or unacceptably dangerous. Amphetamines, for example, were freely dispensed for many years to millions of patients for both depression and weight control, without regard for their lack of efficacy, long-term hazards, and addictive potential (chapter 11).Although there has been some increased caution in recent years, benzodiazepines such as Valium and Xanax have been overly prescribed for anxiety, despite the fact that they worsen anxiety in long-term use, cause persisting memory and mental deficits, and frequently produce abuse and dependence (chapter 12). Antidepressants continue to be given freely to children and adolescents, even though the FDA itself has admitted that multiple studies have failed to prove them useful (chapter 6). Indeed, the effectiveness of antidepressants in treating depressed adults is also in doubt (chapters 6–7), while their adverse effects can be life threatening and make withdrawal impossible, yet most physicians think of them as very safe and efficacious. In even more extreme examples, both psychosurgery and electroshock continue to be utilized, despite obviously devastating effects on the mental lives of the patients and the absence of proven efficacy (chapter 9).
X. Patients subjected to biopsychiatric interventions often display poor judgment about the positive and negative effects of the treatment on their mental and emotional functioning, often causing intoxication anosognosia (medication spellbinding).(^4)
Generalized brain dysfunction tends to reduce the individual’s ability to perceive the existence or impact of the dysfunction. This incapacity lies at the heart of spellbinding effects of drugs and is one of the main reasons that patients continue to take psychiatric medications when the drugs are doing more harm than good.
Anosognosia 是指腦損傷導致否認功能喪失的能力。 失認症是任何原因導致的中樞神經系統殘疾的標誌（Breggin，2006d；見後續部分）。
Anosognosia refers to the capacity of brain damage to cause denial of lost function. Anosognosia is a hallmark of central nervous system disability from any cause (Breggin, 2006d; see subsequent sections).
人類在生理和心理上都是複雜的，對藥物的反應各不相同。 因此，沒有兩例藥物咒語是相同的，它們的強度差異很大，而且並非所有病例都會顯示出每一個特徵。 儘管如此，令人著迷是一種易於識別的臨床現象，它可能是所有從輕度到重度的藥物中毒病例的特徵，並且可能在某種程度的精神活性劑對大腦和精神產生影響時被發現。
Human beings are physically and psychologically complex, with varying reactions to drugs. As a result, no two cases of medication spellbinding are identical, they vary widely in intensity, and not all cases will display every characteristic. Nonetheless, spellbinding is a readily identifiable clinical phenomenon that probably characterizes all cases of drug intoxication from mild to severe and probably can be found to some degree whenever a psychoactive agent is having an impact on brain and mind.
The following four characteristics of medication spellbinding are taken from this author’s book Medication Madness (Breggin, in press):
First, spellbound individuals fail to perceive the degree of mental or emotional impairment that the drugs are inflicting on them.
Second, spellbound individuals tend to rationalize and justify their drug-induced mental distress, typically blaming negative feelings on themselves or on something else, sometimes leading to violence against themselves or others.
Third, spellbound individuals often feel as if they are doing better than ever when in reality they are doing worse.
Fourth, extreme spellbinding produces medication madness in which the individual feels driven or compelled to behave in out-of-character and potentially disastrous ways—to murder her beloved mother like Emily Ashton or to drive his car into a policeman like Harry Henderson. The spellbound actions are typically carried out without the individual realizing that he or she is drug impaired and without the individual stopping to consider or grasping the disastrous consequences.
為了練習應用施法的四個原則，讀者可以簡單地回憶一下人們在醉酒時的行為方式。 通常，醉酒的人並沒有意識到他們已經變得多麼受損。 當他們情緒低落時，他們會將其歸咎於酒精中毒以外的某人或某事，通常會變得沮喪或好戰； 他們常常認為自己比以往任何時候都好，但實際上他們有精神障礙和行為不端；
To practice applying the four principles of spellbinding, the reader can simply recall how individuals act when intoxicated with alcohol. Typically, people intoxicated with alcohols do not realize how impaired they have become; when they become emotionally distressed, they blame it on someone or something other than alcohol intoxication, often becoming depressed or belligerent; they often think that they feel better than ever when they are in reality mentally impaired and behaving badly; and finally, they can do stupid things and even perpetrate violence that is wholly out of character for them when sober.
許多長期吸食大麻的人認為大麻可以改善他們的整體心理和社會功能，但如果他們戒掉毒品，他們可能會發現他們的記憶力、精神警覺性、情緒敏感性和社交技能在使用大麻時受到了損害。 藥品。 沉醉於安非他明等興奮劑的人可能會覺得自己擁有超人甚至超人的能力，但他們往往受到嚴重損害。 所有精神科藥物也是如此。 通常，在停藥一段時間且大腦有時間恢復之前，患者對精神或情緒障礙的程度幾乎沒有了解。
Many individuals who chronically smoke marijuana believe that it improves their overall psychological and social functioning, but if they withdraw from the drug, it may become apparent to them that their memory, mental alertness, emotional sensitivity, and social skills have been impaired while using the drug. People intoxicated with stimulants, such as amphetamine, may feel they have superior or even superhuman capacities, when they are often seriously impaired. The same is true of all psychiatric drugs. Often the patient will have little appreciation for the degree of mental or emotional impairment until the drug has been stopped for some time and the brain has had time to recover.
在我的臨床實踐和我作為法律案件醫學專家的工作中，我經常發現人們對安全地停用精神科藥物後他們的功能改善了多少感到沮喪。 這些患者中的許多人多年來一直處於一種或多種精神藥物的嚴重中毒狀態而沒有意識到這一點。 他們將自己的病情歸因於自己的情緒反應或環境中的壓力，他們要求醫生提供更多藥物。
In my clinical practice and in my work as a medical expert in legal cases, I often find that people are dismayed at how much better they function when they have been sa fely withdrawn from psychiatric medications. Many of these patients have remained for years in severe states of intoxication from one or more psychiatric drugs without realizing it. Attributing their condition to their own emotional reactions or to stresses in the environment, they have asked their doctors for more medication.
Owing to brain damage–induced spellbinding, even after a devastating series of shock treatments or psychosurgery, patients may fail to understand the iatrogenic source of their mental dysfunction and instead believe that they need repeated interventions.
藥物拼寫的生物學基礎（第 12 頁）
THE BIOLOGICAL BASIS OF MEDICATION SPELLBINDING (p. 12)
某種程度的引人入勝是額葉功能受損的特徵。 Beer等人。 (2006) 指出，眶額損傷“與客觀的不當社會行為有關”。 患者“意識到親密關係的社會規範”，但“他們不知道他們的任務表現違反了這些規範”。 作者稱這是對自我監控和自我洞察力的損害。 Bach 和 David (2006) 指出，自我意識缺陷在創傷性腦損傷患者中非常常見，是行為障礙發展的關鍵：“我們的研究發現，缺乏社會自我意識可以預測獲得性和創傷性大腦的行為障礙損傷獨立於認知和執行功能。”
Some degree of spellbinding is characteristic of any compromise of frontal lobe function. Beer et al. (2006) noted that orbitofrontal damage is “associated with objective inappropriate social behavior.” The patients “were aware of social norms of intimacy” but “they were unaware that their task performances violated these norms.” The authors call this an impairment of self-monitoring and self-insight. Bach and David (2006) pointed out that self-awareness deficits are very common in patients with traumatic brain injury and key to the development of behavior disturbances: “Our research found that lack of social self-awareness predicts behavioural disturbance in acquired and traumatic brain injury independent of cognitive and executive function.”
腦葉切除或電擊患者以及被神經阻滯劑化學腦葉切除的患者的自我意識嚴重受損。 他們經常無法察覺自己的精神功能障礙，並且會忽略自己身體疾病的警告信號。 與引人入勝的情況一致，他們可能會報告說他們做得比現在更好。 一項對非典型抗精神病藥（包括利培酮、奧氮平和喹硫平）的研究發現，這些患者不切實際地認為自己的生活質量有所改善（Voruganti 等人，2000 年）：“然而，這些感知到的益處並未反映在臨床醫生身上 心理社會功能和生活質量的評定（客觀）測量。
Lobotomized or electroshocked patients as well as patients chemically lobotomized by neuroleptics have greatly impaired self-awareness. They often fail to perceive their mental dysfunction and will neglect warning signs of physical illness in themselves. Consistent with spellbinding, they are likely to report that they are doing better than they are. A study of the atypical neuroleptics, including risperidone, olanzapine, and quetiapine, found that these patients unrealistically rated themselves as improved in quality of life (Voruganti et al., 2000): “These perceived benefits, however, were not reflected in the clinician rated (objective) measure of psychosocial functioning and quality of life.”
額葉的這些嚴重破壞，包括安定藥毒性，通常會制服個體，使他們變得溫順，從而防止在沒有自我監控和自我洞察力的情況下可能發生的危險解除抑制。 然而，許多精神活性藥物，包括抗抑鬱藥、苯二氮卓類鎮靜劑和興奮劑，可以顯著抑制和/或激發個體以強迫性破壞性方式行事，有時會導致犯罪行為、自殺和暴力（Breggin, 2006d, in press）。 當神經安定藥引起靜坐不能時，它們也可以驅使個體走向失控的行為。
These gross disruptions of the frontal lobes, including neuroleptic toxicity, usually subdue individuals, making them docile, thereby preventing dangerous disinhibition that might otherwise occur in the absence of self-monitoring and self-insight. However, many psychoactive drugs, including antidepressants, benzodiazepine tranquilizers, and stimulants, can markedly disinhibit and/or energize and drive the individual to act in a compulsively destructive manner, sometimes leading to criminal behavior, suicide, and violence (Breggin, 2006d, in press). When neuroleptics cause akathisia, they can also drive individuals toward out-of-control behaviors.
The biological bases for the individual’s failure to perceive adverse drug effects on his or her mental life include the following interrelated phenomena:
• 藥物引起的混亂。 幾乎所有的生物精神干預有時都會引起混亂，損害患者對藥物引起的精神功能障礙的認識。
• Drug-induced confusion. Almost all biopsychiatric interventions can at times induce confusion, impairing the patient’s awareness of the drug-induced mental dysfunction.
• 藥物引起的短期記憶喪失。 精神活性藥物經常會損害回憶並擾亂過去記憶的順序，使個人更難識別藥物如何影響他們。
• Drug-induced short-term memory loss. Psychoactive drugs frequently impair recall and also disrupt the order of past memories, making it more difficult for individuals to recognize how a drug has been affecting them.
• 藥物引起的精神障礙，尤其是不同程度的冷漠和躁狂。 所有的精神科藥物都可以產生冷漠或欣快感，許多——例如，新的抗抑鬱藥、興奮劑和苯二氮卓類藥物——可以同時產生這兩種藥物。 冷漠和冷漠使人們對藥物引起的損傷不太了解和擔心。 如果這個人遭受了很大的痛苦，那麼冷漠可能會受到歡迎。 欣快感和躁狂症超越了任何損害感，反而使個人感覺比以往任何時候都更好、更強壯、更有能力。
• Drug-induced mental disturbances, especially various degrees of apathy and mania. All psychiatric drugs can produce either indifference or euphoria, and many—for example, the newer anti-depressants, the stimulants and the benzodiazepine Xanax—can produce both. Apathy and indifference make people less aware of and less concerned about drug-induced impairments. If the person is suffering a great deal, the apathy may be welcomed. Euphoria and mania override any sense of impairment, instead making the individual feel better, stronger, and more able than ever.
• 藥物引起的虛構。 虛構是具有明顯記憶障礙的廣泛性腦功能障礙的症狀。 患者使用合理化和各種掩護故事來向自己和他人隱藏精神功能障礙的程度。 虛構在精神病學和神經病學中得到了很好的理解，但在治療引起的影響方面通常被忽略。 許多患者虛構藥物治療的良好效果，儘管他們顯然受到了損害。
• Drug-induced confabulation. Confabulation is a symptom of generalized brain dysfunction with marked memory impairment. The patient uses rationalizations and various cover stories to hide the extent of mental dysfunction from himself and others. Confabulation is well understood in psychiatry and neurology but is generally ignored in regard to treatment-induced effects. Many patients confabulate good results from drug therapy, although they are obviously impaired by it.
對藥物拼寫的心理影響（第 14 頁）
PSYCHOLOGICAL INFLUENCES ON MEDICATION SPELLBINDING (p. 14)
Psychological influences also play a role in the patient’s tendency to misperceive or misjudge the effects of drugs, but they are not central to the concept of medication spellbinding, which is biologically based. Psychological influences include the following:
• 心理否認。 被情緒痛苦所克服的個體可能會否認他們心理功能障礙的程度。 他們不想承認自己有嚴重的精神障礙。 如果他們希望在使用藥物後感覺更好，或者如果藥物最初引起欣快或情緒麻醉，他們的否認可能會進一步加強。
•Psychological denial. Individuals overcome by emotional suffering are likely to deny the degree of their psychological dysfunction. They do not want to admit to being severely mentally impaired. If they are hoping to feel better with the use of a drug, or if the drug initially caused euphoria or emotional anesthesia, their denial can be further reinforced.
•Placebo effect. Patients have faith that biopsychiatric interventions will be helpful, rather than harmful, encouraging them to disregard drug-induced dysfunction or to mistakenly attribute it to their emotional problems.
•遵守。 在很大程度上，患者會告訴醫生醫生想聽什麼。 如果精神科醫生明確希望聽到藥物是有用的，而不是有害的，許多患者會通過提供虛假信息或隱瞞相互矛盾的證據來遵守。
•Compliance. To an extraordinary extent, patients will tell doctors what the doctors want to hear. If a psychiatrist clearly wants to hear that a drug is helpful, and not harmful, many patients will comply by giving false information or by withholding contradictory evidence.
• 心理引起的混亂。 情緒低落的人很容易失去對病情惡化原因的判斷。 他們很容易將負面藥物作用誤認為是情緒問題的惡化，例如苯二氮卓類鎮靜劑（如 Xanax 或 Ativan）或精神抑製藥（如 Risperdal 或 Abilify）引起的反彈焦慮。 通常，他們責怪自己而不是藥物。 當醫生誇大藥物的益處並且沒有告知患者其潛在的副作用時，這種混淆就會被助長。
•Psychologically induced confusion. Emotionally upset individuals can easily lose their judgment concerning the cause of their worsening conditions. They can easily mistake a negative drug effect, such as rebound anxiety from a benzodiazepine tranquilizer like Xanax or Ativan or depression from a neuroleptic like Risperdal or Abilify, for a worsening of their emotional problems. Typically, they blame themselves rather than the medication. This confusion is abetted when the physician exaggerates the drug’s benefits and fails to inform the patient of its potential adverse effects.
權威精神病學中的醫源性無助和否認（第 14 頁）
IATROGENIC HELPLESSNESS AND DENIAL IN AUTHORITARIAN PSYCHIATRY (p. 14)
In the previous edition of Brain-Disabling Treatments in Psychiatry, I introduced the term iatrogenic helplessness and denial in authoritarian psychiatry to designate a guiding principle of biopsychiatric interventions (see also Breggin, 1983a). Although they may not recognize or admit what they are doing, biological psychiatrists use authoritarian techniques, enforced by brain-disabling interventions, to produce increased helplessness and dependency on the part of the patient. In their journals and conferences they frequently speak of obtaining “medication compliance”—getting the patient to take drugs. In an effort to push their patients to take medications, biological psychiatrists convince them that they have biochemical imbalances, and even genetic disorders, that require treatment with drugs. This creates a submissive, dependent relationship with the prescribing physician. Physically, the psychiatrist prescribes multiple drugs or electroshock, causing brain damage and dysfunction that increases the patient’s tendency to be submissive and dependent. Often these doctors encourage their patients to enter mental hospitals, and sometimes they force them into hospitals or into outpatient commitment in which they are required to submit against their will to medication.
This may seem like a harsh indictment, but it is instead a harsh reality. While most psychiatrists may not realize that they are causing dependency and helplessness, millions of patients throughout the nation are misled into believing that they have biological and genetic defects that can be corrected by medication or electroshock, in effect making them feel helpless and dependent on their doctors and on physical treatments. When many of these patients become worse as a result of treatment, they are told that their underlying “mental illness” is surfacing. When multiple drugs lead to escalating adverse emotional effects, more drugs are added to the regimen, and too often the patient is hospitalized. Rarely do these doctors admit that the drugs are the source of the patients’ worsening problems and that a drug-free period of time may lead to recovery. Throughout the process, the patients remain so spellbound that they cannot perceive how badly there are doing or that the drugs are ruining their lives.
醫源性無助和否認的概念包括患者和醫生對治療的破壞性影響的相互否認，以及對患者潛在的心理和情境問題的相互否認。 總體而言，醫源性無助和否認是精神病學能夠利用腦損傷技術（如電擊和心理外科）以及有毒藥物的頻率的原因。 Spellbinding 解釋了藥物的生物學影響如何強化醫源性無助和否認。
The concept of iatrogenic helplessness and denial includes the patient’s and the doctor’s mutual denial of the damaging impact of the treatment as well as their mutual denial of the patient’s underlying psychological and situational problems. Overall, iatrogenic helplessness and denial accounts for the frequency with which psychiatry has been able to utilize brain-damaging technologies, such as electroshock and psychosurgery, as well as toxic medications. Spellbinding explains how the biological impact of the medication reinforces iatrogenic helplessness and denial.
藥物治療與醫源性無助和否認之間的關係（第 15 頁）
RELATIONSHIP BETWEEN MEDICATION SPELLBINDING AND IATROGENIC HELPLESSNESS AND DENIAL (p. 15)
藥物魔法的概念擴展或闡述了醫源性無助和否認的概念。 它特別觀察到暴露於精神藥物、電擊或腦葉切除術的患者表現出以下無助和否認跡象：（a）他們感知治療引起的精神功能障礙的能力受損； (b) 無法確定藥物、休克或腦葉切除術正在導致他們惡化，並且傾向於將他們的痛苦歸因於其他原因，例如他們自己的所謂精神疾病或其他人對他們的痛苦影響； (c) 不切實際地認為自己比以往任何時候都做得更好，而實際上他們做得更糟； (d) 在極端情況下，發展成強迫性的、破壞性的、自我外星的行為，有時具有躁狂的性質。
The concept of medication spellbinding expands or elaborates on the concept of iatrogenic helplessness and denial. It specifically observes that patients exposed to psychiatric drugs, electroshock, or lobotomy display the following indications of helplessness and denial: (a) impairment in their ability to perceive their treatment-induced mental dysfunction; (b) inability to identify that the drug, shock, or lobotomy is causing their deterioration and a tendency to attribute their distress to some other source, such as their own so-called mental illness or someone else’s distressing effect on them; (c) an unrealistic belief that they are doing better than ever, when they are doing worse; and (d) in extreme cases, the development of compulsive, destructive, ego-alien actions, sometimes of a manic quality.
大多數尋求精神治療的人已經很容易變得無助和依賴。 在潛在患者遇到精神科醫生之前，他或她通常會感到無助一段時間。 在我的表述中，正如《樂於助人的心》（1997b）中所描述的，無助是所有心理失敗的共同點。 無助是大多數自我挫敗的生活方式的核心。 感到無助的人傾向於放棄用理性、愛和自決來克服他們的情感痛苦、內心衝突和現實生活中的壓力。 相反，他們從外部尋求答案。 在現代，這通常意味著來自所謂的專家。
Most people who seek psychiatric treatment are already vulnerable to becoming helpless and dependent. Before the potential patient encounters a psychiatrist, he or she has usually been feeling helpless for some time. In my formulation, as described in The Heart of Being Helpful (1997b), helplessness is the common denominator of all psychological failure. Helplessness is at the core of most self-defeating approaches to life. People who feel helpless tend to give up using reason, love, and self-determination to overcome their emotional suffering, inner conflicts, and real-life stresses. They instead seek answers from outside themselves. In modern times, this often means from so-called experts.
醫源性無助和否認，以及藥物治療，遠遠超出了相對溫和的建議（如用於醫學和精神病學，例如，幫助克服身體疼痛）。 首先，在醫源性無助和否認中，包括藥物令人著迷，精神科醫生損害了患者的大腦，通過精神和身體功能障礙迫使患者服從建議。 其次，在醫源性無助和否認中，精神科醫生對自己或她自己否認治療的破壞性影響以及患者持續的心理或情境問題。
Iatrogenic helplessness and denial, and medication spellbinding, go far beyond relatively benign suggestion (as used in medicine and psychiatry, e.g., to help overcome physical pain). First, in iatrogenic helplessness and denial, including medication spellbinding, the psychiatrist compromises the brain of the patient, enforcing the patient’s submission to suggestion through mental and physical dysfunction. Second, in iatrogenic helplessness and denial, the psychiatrist denies to himself or herself the damaging effects of the treatment as well as the patient’s continuing psychological or situational problems.
Brain damage and dysfunction from any cause, including accidents and illness, frequently produce helplessness and denial, but only in psychiatry is damage and dysfunction used as treatment to produce these disabling, spellbinding effects.
通過生物精神病學干預常規治療的精神和情緒痛苦沒有已知的遺傳或生物原因（第 16 頁）
MENTAL AND EMOTIONAL SUFFERING ROUTINELY TREATED WITH BIOPSYCHIATRIC INTERVENTIONS HAVE NO KNOWN GENETIC OR BIOLOGICAL CAUSE (^5) (p. 16)
請記住，大腦功能障礙概念的有效性並不取決於精神疾病的起源，而是取決於生物精神治療的已知效果。 即使一種或另一種精神疾病應該證明有生物學基礎，也不能證明使用目前的藥物是合理的，所有這些藥物都會使大腦喪失功能。 儘管大多數尋求精神科治療的人的大腦功能沒有問題，但有些人可能有潛在的身體疾病（不是神話般的生化失衡）。 例如，如果患者患有導致抑鬱情緒的甲狀腺疾病或糖尿病，則應給予患者適當的醫療以糾正潛在的身體疾病，而不是使用抗抑鬱藥物。
Keep in mind that the validity of the brain-disabling concept does not depend on the origin of psychiatric disorders but rather on the known effects of biopsychiatric treatment. Even if one or another psychiatric disorder should turn out to have a biological basis, it would not justify using current medications, all of which disable the brain. Although most people who seek psychiatric care have nothing wrong with their brain function, some may have an underlying physical disorder (not a mythical biochemical imbalance). If, for example, a patient has a thyroid disorder or diabetes that is causing feelings of depression, the patient should be given proper medical treatment to correct the underlying physical disorder and not antidepressant drugs.
所謂的精神分裂症通常被認為是基於生物和遺傳的精神疾病的最佳模型。 對於精神分裂症遺傳學的批評，參見 Breggin (1991b) 和最近的 Joseph (1999, 2004a, 2004b, 2006)。 對於精神分裂症的腦疾病模型（參見，例如，Siebert，1999）和精神疾病的生化理論（Breggin，出版中；Colbert，2001）有許多詳細的批評。
So-called schizophrenia is usually put forward as the best model for a biological and genetically based psychiatric disorder. For critiques of the genetics of schizophrenia, see Breggin (1991b) and, more recently, Joseph (1999, 2004a, 2004b, 2006). There are many detailed criticisms of the brain disease model for schizophrenia (see, e.g., Siebert, 1999) and for biochemical theories of psychiatric disorders (Breggin, in press; Colbert, 2001).
Timothy Crow (2007) 的文章“遺傳聯繫如何以及為什麼沒有解決精神病問題：回顧和假設”證實，即使是遺傳研究人員也承認他們沒有發現精神分裂症的遺傳聯繫。 與此同時，尋找抑鬱症的生物學基礎或生物學標記也繼續擱淺。 “我們對重度抑鬱症的神經生物學了解了什麼？” Maria Oquendo 和 Ramin Parsey (2007) 證明，截至 2007 年 4 月，尚未發現任何遺傳或生物學原因。 與往常一樣，社論談到了必須如何進行搜索。 當然，所有這一切都會讓大多數醫療保健提供者在智力上感到不安，他們被教導相信精神疾病有已知的生物學和遺傳原因。
Timothy Crow’s (2007) article “How and Why Genetic Linkage Has Not Solved the Problem of Psychosis: Review and Hypothesis” confirmed that even the genetic researchers admit they have not found a genetic linkage for schizophrenia. Meanwhile, the search for a biological basis, or a biological marker, for depression also continues to run aground. ”What Have We Learned About the Neurobiology of Major Depression?” by Maria Oquendo and Ramin Parsey (2007) demonstrated that as of April 2007, no genetic or biological causes have as yet been discovered. As always, the editorial talks about how the search must go on. All of this, of course, will feel intellectually jarring to most health care providers, who have been taught to believe that psychiatric disorders have known biological and genetic causes.
儘管進行了 200 多年的深入研究，但沒有任何常見的診斷精神疾病被證明是遺傳或生物學起源的，包括精神分裂症、重度抑鬱症和雙相情感障礙的診斷類別、各種焦慮症和兒童障礙，例如 注意缺陷多動。
Despite more than 200 years of intensive research, no commonly diagnosed psychiatric disorders have been proven to be either genetic or biological in origin, including the diagnostic categories of schizophrenia, major depressive disorder and bipolar disorder, the various anxiety disorders, and childhood disorders such as attention-deficit hyperactivity.
目前，典型的精神病患者的大腦中沒有已知的生化失衡——直到他們被給予精神病藥物。 斷言像百憂解這樣的抗抑鬱藥可以糾正不活躍的 5-羥色胺能神經傳遞（一种血清素生化失衡），或者像利培酮或 Seroquel 這樣的安定藥可以糾正過度活躍的多巴胺能神經傳遞（一種多巴胺不平衡）是推測性的，甚至是幼稚的。 儘管經過數十年的努力，但未能證明精神病患者存在任何大腦異常，這表明這些缺陷並不存在。
At present, there are no known biochemical imbalances in the brain of typical psychiatric patients—until they are given psychiatric drugs. It is speculative and even naïve to assert that antidepressants such as Prozac correct underactive serotonergic neurotransmission (a serotonin biochemical imbalance) or that neuroleptics such as Risperdal or Seroquel correct overactive dopaminergic neurotransmission (a dopamine imbalance). The failure to demonstrate the existence of any brain abnormality in psychiatric patients, despite decades of intensive effort, suggests that these defects do not exist.
It seems theoretically possible that some of the problems treated by psychiatrists and other health practitioners could eventually be proven to have a biological basis. As already mentioned, mental function often improves when certain physical disorders, such as hypothyroidism or Cushing’s syndrome, are adequately treated with appropriate medical interventions.
然而，絕大多數通常被視為所謂的精神障礙的問題與大腦或身體的疾病並不相像。 例如，它們不會產生短期記憶中的認知缺陷或腦部疾病的抽象推理特徵。 它們不伴有發燒或實驗室疾病跡象。 與許多神經系統疾病不同，它們不是退化的。 相反，神經學和神經心理學測試通常表明即使不是優越的大腦功能也是正常的，並且身體是健康的——直到開始對大腦造成損害的治療。 任何常規治療的精神問題似乎都不太可能是基於大腦功能障礙，而不是大腦正常個體的生活經歷。
However, the vast majority of problems routinely treated as so-called mental disorders do not remotely resemble diseases of the brain or body. For example, they do not produce the cognitive deficits in short-term memory or abstract reasoning characteristic of brain disorders. They are not accompanied by fever or laboratory signs of illness. Unlike many neurological disorders, they are not degenerative. To the contrary, neurological and neuropsychological testing usually indicates normal if not superior brain function, and the body is healthy—until the brain-damaging treatments are begun. There seems little likelihood that any of the routinely treated psychiatric problems are based on brain malfunction, rather than on the life experiences of individuals with normal brains.
聲稱一種非理性或情緒低落的狀態，無論多麼極端，本身就等於大腦功能受損，這是完全錯誤的。 與電視機和計算機的類比可以說明為什麼會這樣。 如果電視節目或互聯網站點具有攻擊性或不合理，並不表示電視機的電子設備或計算機的硬件有任何問題。 將糟糕的編程或有問題的 Internet 站點歸咎於佈線錯誤是沒有意義的。 同樣，一個人可能在心理上非常不安，而大腦的線路沒有任何相應的缺陷。
To claim that an irrational or emotionally distressed state, however extreme, in itself amounts to impaired brain function is simply false. An analogy to television sets and computers may illustrate why this is so. If a TV program or Internet site is offensive or irrational, it does not indicate that anything is wrong with the electronics of the television set or the hardware of the computer. It makes no sense to attribute the bad programming or the offending Internet site to bad wiring. Similarly, a person can be very disturbed psychologically, without any corresponding defect in the wiring of the brain.
然而，這個論點是沒有實際意義的，因為當代的生物精神病學干預措施無法像專家修復損壞的電視機或計算機那樣真實地聲稱可以糾正大腦故障。 相反，我們盲目地對大腦施加有毒物質，這種物質比電視或電腦的硬件更微妙、更容易受到傷害。 我們甚至以使電視機或電腦維修人員或其客戶感到震驚的方式電擊或破壞大腦，他們都會立即意識到這些治療正在毀壞他們的電視機或電腦。
However, the argument is moot since no contemporary biopsychiatric interventions can truthfully claim to correct a brain malfunction the way an expert can fix a broken TV set or computer. Instead, we blindly inflict toxic substances on a brain that is far more subtle and vulnerable to harm than the hardware of a TV or computer. We even shock or mutilate the brain in ways that would appall TV or computer repair persons or their customers, all of whom would instantly recognize that these treatments were ruining their TV sets or computers.
通常認為患有極端情緒障礙的人，例如幻覺和妄想或自殺和殺人衝動，已經足夠異常，需要對其心理過程或行為進行生物學解釋。 然而，人類的情感生活始終包括廣泛的心理和行為活動。 個人保持理性和控制情緒的意願或能力差異很大。 特定的精神狀態或行為特別不合理或具有破壞性，這本身並不表示物理起源。 如果極端需要生物學解釋，那麼將極端道德、理性和愛的行為歸因於遺傳和生物學原因會更有說服力，因為它們在人類生活中尤其罕見。
It is often suggested that persons suffering from extremes of emotional disorder, such as hallucinations and delusions or suicidal and murderous impulses, are sufficiently abnormal to require a biological explanation for their mental processes or behavior. However, the emotional life of human beings has always included a wide spectrum of mental and behavioral activity. Individual willingness or ability to remain rational and to control one’s emotions varies enormously. That a particular mental state or action is especially irrational or destructive does not, per se, indicate a physical origin. If extremes require biological explanation, then it would be more compelling to ascribe extremely ethical, rational, and loving behaviors to genetic and biological causes since they are especially rare in human life.
藥物起作用的事實——即以看似積極的方式影響大腦和思維——並不能證實個體患有潛在的生物疾病。 在有記載的歷史中，人們出於各種精神和心理原因服藥，從追求更高的意識狀態到想讓生活更容易忍受的願望。 人們通常飲用酒精飲料、咖啡和茶、煙草和大麻來改善他們的健康感。 然而，沒有理由相信他們獲得的結果是由於潛在的生化失衡。
The fact that a drug works—that is, influences the brain and mind in a seemingly positive fashion—does not confirm that the individual suffers from an underlying biological disorder. Throughout recorded history, individuals have medicated themselves for a variety of spiritual and psychological reasons, from the quest for a higher state of consciousness to a desire to make life more bearable. Alcoholic beverages, coffee and tea, tobacco, and marijuana are commonly consumed by people to improve their sense of wellness. Yet there is no reason to believe that the results they obtain are due to an underlying biochemical imbalance.
正如我在之前的書籍中所討論的（Breggin, 1991a; Breggin et al. 1994a, 1994b），我認為精神疾病和精神障礙的概念具有誤導性，並且精神科醫生通常治療的問題都不是遺傳或生物學起源的 . 例如，注意力缺陷多動障礙、精神分裂症和重度抑鬱症等術語都是基於其有效性很容易受到質疑的概念。 然而，大腦功能障礙的原則仍然有效，即使正在治療的一些心理現象被證明具有遺傳或生物學基礎。 所有目前可用的生物精神治療——藥物、電擊和心理外科——通過損害或禁用正常的大腦功能，導致醫源性無助和否認，更具體地說，中毒失認症（藥物迷惑），具有它們的主要或“治療”效果。
As I have discussed in earlier books (Breggin, 1991a; Breggin et al. 1994a, 1994b), I believe that the concepts of mental illness and mental disorder are misleading and that none of the problems commonly treated by psychiatrists are genetic or biological in origin. The terms attention-deficit hyperactivity disorder, schizophrenia, and major depressive disorder, for example, are based on concepts whose validity can easily be challenged. However, the brain-disabling principles remain valid, even if some of the mental phenomena that are being treated turn out to have a genetic or biological basis. All of the currently available biopsychiatric treatments—drugs, electroshock, and psychosurgery—have their primary or “therapeutic” effect by impairing or disabling normal brain function, causing iatrogenic helplessness and denial and, more specifically, intoxication anosognosia (medication spellbinding).
1. 精神病學中使用的“欣快”一詞表示一種誇大的、非理性的或不切實際的幸福感。 它可能起源於心理，但通常是由腦損傷或藥物毒性引起的。
1. The term euphoria as used in psychiatry indicates an exaggerated, irrational, or unrealistic sense of well-being. It can be psychological in origin but is commonly caused by brain damage or drug toxicity.
2. 因為大多數外行和許多醫生不知道藥物的通用名稱，所以我會在本書中偶爾使用商品名稱，例如百憂解和利培酮。 但是，附錄提供了按類別列出的精神科藥物清單，包括商品名稱和通用名稱。
2. Because most laypersons and many physicians do not know the generic names for drugs, I will occasionally use trade names, such as Prozac and Risperdal, throughout the book. However, the appendix offers a list of psychiatric drugs by category, including both trade and generic names.
3. 由於對中樞神經系統的抑製作用，接受抗精神病藥治療的患者出現欣快感並不常見（見第 2 章）。 在接受抗抑鬱藥、興奮劑和苯二氮卓類鎮靜劑（尤其是阿普唑侖）治療的患者中更為常見。 藥物引起的躁狂症是藥物引人入勝的極端。
3. Euphoria is unusual in patients treated with the neuroleptics because of the suppressive effects on the central nervous system (see chapter 2). It is more common among patients treated with antidepressants, stimulants, and benzodiazepine tranquilizers, especially alprazolam. Drug-induced mania is an extreme of medication spellbinding.
4.當我在寫一本新書《藥物瘋狂》（Breggin，出版中）的過程中回顧一生的臨床和法律案例時，我想到了藥物魔法的概念，其中描述了我個人評估的大約 70 個案例（ 另見 Breggin, 2006e)。
4. The concept of medication spellbinding occurred to me when I was reviewing a lifetime of clinical and legal cases in the process of writing a new book, Medication Madness (Breggin, in press), which describes approximately 70 cases that I had personally evaluated (see also Breggin, 2006e).
5. 在本書的上一版中，這個副標題是大腦功能障礙的原理之一，但我將其從原理中刪除了，因為即使未來的某些精神疾病被證明具有遺傳或生物學基礎，目前的治療方法 儘管如此，使用仍會保持毒性並導致大腦殘疾。
5. In the previous edition of this book, this subtitle was one of the brain-disabling principles, but I have removed it from the principles because, even if some future psychiatric disorder proves to have a genetic or biological basis, the current treatments in use will nonetheless remain toxic and cause brain disability.