第3章 抗精神病藥引起的痛苦,包括激動、絕望和抑鬱(第 43 頁)
CHAPTER 3 Neuroleptic-Induced Anguish, Including Agitation, Despair, and Depression (p. 43)

並非所有對中樞神經系統的藥物影響都可以歸類為中毒失知(spellbinding)但都會導致殘疾。 結果通常是患者的整體狀況惡化有時結果是極度痛苦致殘的精神反應。 具有諷刺意味的是,精神科藥物並不能治愈或改善中樞神經系統疾病。他們導致他們(they cause them)

Not all drug effects on the central nervous system can be categorized as spellbinding, but all produce disability. Often the result is a worsening of the patient’s overall condition, and sometimes the result is an extremely distressing or disabling psychiatric reaction. Ironically, psychiatric drugs do not cure or ameliorate central nervous system disorders; they cause them.

儘管對神經安定藥引起的失活產生的類似腦葉切開術的冷漠無動於衷,但許多患者對這些藥物的反應會經歷不同程度的身心痛苦和折磨去激活本身通常被體驗為可怕的,一種活死的(a kind of living death)被囚禁在自己的大腦中(an imprisonment within one’s own brain)

Despite the lobotomy-like indifference to suffering produced by neuroleptic-induced deactivation, many patients experience varying degrees of physical and mental pain and torment in response to these drugs. The deactivation itself is often experienced as dreadful, a kind of living death or an imprisonment within one’s own brain.

本章將描述一些最常見的、可逆的、藥物引起的神經系統反應:急性肌張力障礙; 急性靜坐不能; 帕金森病; 還有一個廣泛的、定義不明確的類別,稱為煩躁不安所有這些都傾向於在治療早期開始,但也可以在以後開始。 第 4 章和第 5 章將回顧有時延遲和經常持續的不良反應,包括不可逆形式的靜坐不能肌張力障礙

This chapter will describe some of the most common, reversible, drug-induced neurological reactions: acute dystonia; acute akathisia; parkinsonism; and a broad, ill-defined category called dysphoria. All of them tend to begin early in treatment but can start later on as well. Chapters 4 and 5 will review the sometimes delayed and often persistent adverse reactions, including irreversible forms of akathisia and dystonia.

大多數與精神抑製藥相關的神經系統疾病屬於錐體外系反應或錐體外系症狀,通常稱為 EPS。 大腦的錐體外係是一個廣泛而復雜的網絡,可以調節和調節運動控制。 系統異常會導致各種功能障礙,包括震顫、肌肉僵硬和痙攣,以及各種不自主運動。

Most of the neurological disorders associated with the neuroleptics fall into the category of extrapyramidal reactions or extrapyramidal symptoms, and are often designated EPS. The extrapyramidal system of the brain is an extensive, complex network that moderates and adjusts motor control. Abnormalities in the system cause a variety of dysfunctions, including tremors, muscular rigidity and spasms, and various involuntary movements.

Casey (1993) 報告說,高達 90% 的接受精神抑製藥的患者會出現急性錐體外係綜合症,通常會導致身體和精神障礙。 不幸的是,儘管有不適和痛苦,醫生經常繼續或增加患者的藥物治療,因為他們將藥物毒性反應誤認為是精神疾病。 一名年輕的男性患者在終止神經安定治療後的幾個月內患有肌張力障礙,導致一隻手臂超過了他的肩膀。 在家庭會議上,他的父母堅持認為這種疾病是一種故意和挑釁的行為。 這些急性症狀在藥物終止後可能會持續相當長的時間,即使對於被認為不太頻繁或強烈產生它們的新型精神抑製藥(Kane 等,1994)。 通常,它們會變成永久性的。

Casey (1993) reported that acute extrapyramidal syndromes occur in up to 90% of patients receiving neuroleptics, often causing physical and mental impairment. Unfortunately, physicians too often continue or increase the patient’s medication, despite discomfort and suffering, because they have mistaken the toxic drug reaction for a psychiatric disorder. A young male patient, for several months after termination of neuroleptic treatment, suffered from a dystonia that caused one arm to rise above his shoulders. In family sessions, his parents persisted in viewing the disorder as a willful and defi ant act. These acute symptoms may linger a considerable time after drug termination, even in regard to newer neuroleptics thought to produce them less frequently or intensively (Kane et al., 1994). Often, they become permanent.

一段時間以來,人們已經知道本章和後續章節中描述的神經毒性作用在老年人中變得更加頻繁和致殘(Gomez 等,1990;Simpson,1977;見第 4 章)。

It has been known for some time that the neurotoxic effects described in this and the following chapters become even more frequent and disabling in the elderly (Gomez et al., 1990; Simpson, 1977; see chapter 4).

對治療的抵抗(第 44 頁)


Van Putten (1974) 評估了 85 名患者對各種抗精神病藥的態度。 焦慮反應者被定義為“習慣性地抱怨藥物作用”、感到“痛苦”和“不斷懇求停藥或減少劑量”的人。 驚人的 38% 的患者屬於這種極端的耐藥性類別。 當耐藥性的標準擴大到包括任何不得不“被迫”服藥的人時,46% 的人被發現表現出“抗藥性”。

Van Putten (1974) evaluated the attitudes of 85 patients toward a variety of neuroleptics. Dysphoric responders were defined as individuals who “habitually complained about the drug effect” and who felt “miserable” and “continually pleaded to have the drug stopped or the dosage reduced.” A remarkable 38% of the patients fell into this extreme category of drug resistance. When the criteria for drug resistance were broadened to include anyone who had “to be pressured” into taking medication, 46% were found to display “drug reluctance.”


The study most likely underestimated the actual percentage of drug reluctance among the total population of patients on the ward. Some, and perhaps many, patients disguised their reluctance to avoid angering the staff, while quietly throwing away their pills.

在典型的精神病院裡假裝服藥有多容易? 考慮一下 Rosenhan (1973) 的研究,在該研究中,正常人通過偽裝症狀自己進入了不同的精神病院。 “總而言之,這些假病人服用了近 2,100 顆藥丸,包括依拉維、司特拉津、康帕津和梭嗪,僅舉幾例。 . . . 只吞了兩個。 其餘的要么裝在口袋裡,要么放在馬桶裡。” 這確實是一個了不起的數字:1000 劑中只有不到 1 劑被服用,而醫院工作人員都沒有意識到這一點。 Rosenhan 的研究還披露,普通患者通常會以同樣的方式處理他們的藥物。 羅森漢認為,工作人員未能發現正在發生的事情反映了他們傾向於忽視患者所做的一切,除非它造成了明顯的麻煩。

How easy is it to feign taking medication in a typical psychiatric hospital? Consider the Rosenhan (1973) study, in which normal individuals had themselves admitted to various mental hospitals by faking symptoms. “All told, the pseudopatients were administered nearly 2,100 pills, including Elavil, Stelazine, Compazine, and Thorazine, to name but a few. . . . Only two were swallowed. The rest were either pocketed or deposited in the toilet.” This is a remarkable figure indeed: Less than 1 out of 1,000 doses were taken, and none of the hospital staff were aware of it. The Rosenhan study also disclosed that regular patients were routinely disposing of their medications in the same manner. Rosenhan believed that the failure of the staff to detect what was happening reflected their tendency to ignore everything done by the patients, unless it caused obvious trouble.

急性肌張力障礙反應(第 45 頁)


關於與急性肌張力障礙相關的痛苦的文章很少,這是一種藥物引起的神經系統疾病,會導致疼痛的肌肉痙攣,最常見但不僅限於頸部(斜頸),有時整個背部彎曲成僵硬的弧度。 角弓反張)。 同樣,人們對眼科危機的痛苦也沒有給予足夠的關注,在這種情況下,眼睛會在眼窩處翻捲並鎖定在原位

Very little has been written about the suffering associated with acute dystonia, a drug-induced neurological disorder that causes painful muscle spasms, most commonly, but not exclusively, in the neck (torticollis), and sometimes bending the entire back in a rigid arc (opisthotonus). Similarly, insufficient attention has been paid to the anguish of undergoing an oculogyric crisis, in which the eyes roll up in their sockets and become locked in place.

痙攣會影響任何隨意肌,包括與說話、吞嚥和呼吸以及步態有關的肌肉。 Simpson (1977) 觀察到,“咬肌可能會緊緊收縮,以至於無法張開嘴巴,在極少數情況下,這會導致牙齒、舌頭甚至下頜骨的損傷。 確實存在這種反應可能致命的可能性,特別是如果它們發生在進食期間。”

The spasms can affect any voluntary muscles, including those involved with speech, swallowing, and breathing, as well as gait. Simpson (1977) observed, “The masseter muscles may be tightly contracted so that the mouth cannot be opened and, on rare occasions, this can lead to damage to the teeth, tongue, or even the mandible. The possibility that such reactions can be fatal does exist, particularly if they occur during eating.”

經歷過這些經歷的患者可能會在餘生中以痛苦、恐懼和怨恨來回憶這些經歷。 不用說,如果他們的醫生最初將反應歸咎於患者的精神問題,那麼患者會感到被極大地背叛了通常可以通過適當的醫療干預來中止發作,但如果不治療或發展為不可逆轉的遲發性肌張力障礙,它們可能會無休止地繼續下去(第 4 章)。

Patients who have suffered these experiences may remember them with pain, fear, and resentment for the rest of their lives. Needless to say, if their doctors originally blamed the reactions on the patient’s psychiatric problems, the patient can feel enormously betrayed. Often the attacks can be aborted with proper medical intervention, but they can go on endlessly if untreated or if they develop into an irreversible tardive dystonia (chapter 4).

Silver等人。 (1994) 強調了這些疾病的破壞性影響:

Silver et al. (1994) underscored the devastating impact of these disorders:

該綜合徵最常見的特徵包括無法控制的面部和頸部收緊,以及患者頭部和/或背部的痙攣和扭曲(即角弓反張)。 如果涉及眼外肌,可能會發生眼科危機,其中眼睛被抬高並“鎖定”在該位置。 喉部受累 [痙攣] 可能導致呼吸和換氣困難。 這些反應對於以前沒有這些問題的經驗或不知道這種副作用的患者來說通常是可怕的。 當精神病患者出現肌張力障礙反應時,精神科醫生和患者之間建立的脆弱信任可能會受到不可挽回的破壞。 (第 909-910 頁)

The most common feature of this syndrome includes uncontrollable tightening of the face and neck, and spasm and distortions of the patient’s head and/or back (i.e., opisthotonos). If the extraocular muscles are involved, an oculogyric crisis may occur, wherein the eyes are elevated and “locked” in this position. Laryngeal involvement [spasm] may lead to respiratory and ventilatory difficulties. These reactions are often terrifying to the patient who has no prior experience with these problems or knowledge of this side effect. When a patient with psychosis experiences a dystonic reaction, the fragile trust developed between psychiatrist and patient may be irrevocably damaged. (pp. 909–910)

很多時候,這些反應被錯誤地診斷為精神疾病。 Simpson (1977) 觀察到,“急性肌張力障礙反應是突然發作的,包括奇怪的肌肉痙攣,這些痙攣被誤診為手足抽搐或歇斯底里(特別是因為情緒反應會導致它們的沉澱,而且患者偶爾會被勸說)。 ” 實際上,我從未見過心理反應導致“沉澱”或肌張力障礙反應的開始。 但心理壓力通常會導致或惡化先前存在的藥物引起的肌張力障礙。 壓力會使幾乎所有神經系統疾病惡化。
Too often, these reactions are mistakenly diagnosed as mental illness. Simpson (1977) observed, “Acute dystonic reactions are of sudden onset and consist of bizarre muscular spasms that have been misdiagnosed as tetany or hysteria (particularly because emotional reactions can contribute to their precipitation and because patients can occasionally be talked out of them).” Actually, I have never seen a psychological reaction contribute to the “precipitation” or start of a dystonic reaction; but psychological stress commonly brings out or worsens a preexisting, medication-induced dystonia. Stress will worsen almost any neurological disorder.

與精神病學否認藥物不良反應一致,精神科醫生經常無法診斷肌張力障礙。 在對 1,114 名肌張力障礙患者的調查中,在 279 名看過精神科醫生的患者中,只有 1% 的人得到了正確診斷(“Survey Shows”,1992 年)。 神經科醫生的表現要好得多,他們正確診斷了 44% 的患者。

Consistent with psychiatric denial of adverse drug effects, psychiatrists often fail to diagnose dystonia. In a survey of 1,114 dystonia patients, only 1% of the 279 who saw a psychiatrist were correctly diagnosed (“Survey Shows,” 1992). Neurologists did considerably better, correctly diagnosing 44% of the patients who came to them.

對神經麻痺性帕金森症的絕望(第 46 頁)


帕金森病傾向於在生命的中後期自發發展。 它的症狀包括面具狀或僵硬的臉; 休息時四肢震顫; 四肢間歇性僵硬或痙攣,被動移動時手臂出現齒輪式、棘輪式; 蹣跚、彎腰的步態; 和肌肉或運動活動的整體遲緩。 在其最初或更微妙的形式中,該疾病可能表現為運動緩慢或運動遲緩,稱為運動遲緩。 在其極端形式,運動不能,它嚴重損害所有活動。 抑鬱、腦葉切除樣的不感興趣和某種程度的癡呆症經常伴隨著它。

Parkinson’s disease tends to develop spontaneously in the middle and later years of life. Its symptoms include a masklike or rigid face; a tremor of the extremities at rest; intermittent rigidity or spasms of the limbs, and a cog-wheeling, ratcheting of the arms when passively moved; a shuffling, stooped gait; and overall retardation of muscular or motor activities. In its initial or more subtle forms, the disease may be manifested by a slowness of motion, or motor retardation, called bradykinesia. In its extreme form, akinesia, it grossly impairs all activity. Feelings of depression, lobotomy-like disinterest, and some degree of dementia frequently accompany it.

所有阻斷多巴胺的藥物——包括幾乎所有新舊的精神安定藥——通常都會產生可逆的帕金森綜合徵。 它們還可能導致該綜合徵的不同方面,例如運動遲緩。 Van Putten (1974) 描述了以下反應:

All drugs that block dopamine—including nearly all of the older and newer neuroleptics—commonly produce a reversible parkinsonism syndrome. They can also cause separate aspects of the syndrome, such as bradykinesia. Van Putten (1974) described the following reaction:

7 天后,她抱怨無法忍受的“疲勞”。 . . “我放慢了速度。 我說話慢,動作慢(客觀上,這只有在她引起我們注意之後才明顯)。 我覺得自己像個老太太。 我厭倦了在街區走來走去。 我對未來感到沮喪。 我沒有熱情。 我的工作打字速度幾乎沒有(職員打字員)。 . . 我想要找回自己的個性。” (省略原文)

After seven days she complained of unbearable “fatigue” . . . “I have slowed down. I talk slower and move slower (objectively this was apparent only after she called our attention to it). I feel like an old lady. I get tired from walking around the block. I feel discouraged about the future. I have no enthusiasm. I can’t type nearly as fast at my job (clerk typist) . . . I want my own personality back.” (ellipses original)

藥物引起的帕金森症有時會與抑鬱症或精神分裂症等精神障礙相混淆。 戴維斯等人。 (1975) 警告說,精神科醫生應該“意識到那些表現出冷漠、缺乏自發性、相對無法參與社交活動、沒有生命、像殭屍或昏昏欲睡的患者可能會產生輕微的錐體外系副作用。” 作為拉文(Lavin)等人。 (1992) 證實,當臨床醫生錯誤地將這些症狀歸因於患者的精神障礙時,他們要么增加抗精神病藥的劑量,要么在治療方案中添加抗抑鬱藥或興奮劑,從而進一步損害患者的整體狀況。

Drug-induced parkinsonism is sometimes confused with a mental disorder like depression or schizophrenia. Davis et al. (1975) warned that psychiatrists should “be aware that patients who appear apathetic, lacking in spontaneity, relatively unable to participate in social activities, life-less, zombielike, or drowsy may have subtle extrapyramidal side effects.” As Lavin et al. (1992) confirmed, when clinicians mistakenly attribute these symptoms to the patient’s mental disorder, they either increase the dose of neuroleptic or add an antidepressant or stimulant to the regimen, further impairing the patient’s overall condition.

同樣,美國精神病學出版的臨床精神病學教科書(Marangell et al., 2003)指出:

Similarly, The American Psychiatric Publishing Textbook of Clinical Psychiatry (Marangell et al., 2003) pointed out:

運動不能被定義為一種自發性減弱的行為狀態,其特徵是手勢減少、說話不自發、冷漠和難以開始日常活動。 運動障礙可能會在數週的治療後出現,並且通常是帕金森綜合徵的一個因素。 這種藥物誘發的綜合徵可能被誤認為是抑鬱症或精神分裂症的陰性症狀。

Akinesia is defined as a behavioral state of diminished spontaneity characterized by decreased gestures, unspontaneous speech, apathy and difficulty with initiating usual activities. Akinesia may appear after several weeks of therapy and often is an element of the Parkinsonism syndrome. This drug-induced syndrome may be mistaken for depression or for negative symptoms of schizophrenia.

顯然,這些藥物的壓倒一切的效果是對意志和精神的大腦切開術,產生深刻的魔力。 當以前興奮、發聲或無序的患者因運動不能而被制服時,幾乎總是被認為是一種積極的“治療”效果。 不良反應如此引人入勝,以至於許多患者都淪為殭屍般的狀態,沒有抱怨,也沒有意識到他們失去功能和意志的嚴重性。 從字面上看,精神病院裡擠滿了某種程度的這種可悲狀況的病人。

Obviously, the overriding effect of these drugs is a lobotomy-like crushing of will and spirit, resulting in profound spellbinding. When previously excited, vocal, or disorderly patients become subdued by akinesia, it is almost always considered a positive “therapeutic” effect. The adverse effects are so spellbinding that many patients are reduced to a zombielike condition without complaining and without seeming to perceive the severity of their loss of function and will. Mental hospitals are literally filled with patients in one degree or another of this deplorable condition.

通常,帕金森病會在藥物治療期間持續存在,並且在停藥後需要數天、數週甚至數月才能清除。 Klawans(如 Goetz 等人,1980 年引用的)將延遲清除歸因於藥物在患者體內的持久性。 雖然一些藥物可以改善症狀的強度,但效果通常是部分的,潛在的異常神經系統狀況仍然存在,並且經常發生額外的藥物不良反應。

Typically, the parkinsonism remains for the duration of the drug therapy and takes days, weeks, or even months to clear after discontinuation of the drug. Klawans (as cited in Goetz et al., 1980) attributed the delayed clearing to the persistence of the drug in the patient’s body. Although some medications can ameliorate the intensity of the symptoms, the effect is usually partial, the underlying abnormal neurological condition remains, and additional adverse drug effects frequently occur.

Van Putten 和 May (1978) 在接受相對中等劑量的抗精神病藥物或抗精神病藥物治療的 47% 的患者中發現運動遲緩(運動緩慢)和運動不能,這是帕金森症的一個方面。 包括相對較輕的病例,Korcyzn 和 Goldberg (1976) 發現 66 名接受各種抗精神病藥的患者中有 61% 患有帕金森症。 Klawans(如 Goetz 等人,1980 年引用的)指出,文獻中的痛苦率在所有接受治療的患者中從 5% 到 60% 不等,並提供了他自己的 10% 到 15% 的數字來表示“明顯的帕金森病特徵”。 Klawans 還指出,一些藥物比其他藥物更容易產生帕金森綜合徵,並且當使用靈敏的檢測方法時,最常用的一種藥物氟哌啶醇 (Haldol) 可能會在超過 90% 的患者中產生帕金森綜合徵。

Van Putten and May (1978) found bradykinesia (slow movements) and akinesia, aspects of parkinsonism, in 47% of their patients treated with relatively moderate doses of neuroleptic or antipsychotic drugs. Including relatively mild cases, Korcyzn and Goldberg (1976) found parkinsonism in 61% of 66 patients receiving a variety of neuroleptics. Klawans (as cited in Goetz et al., 1980) noted that rates of affliction vary in the literature from 5% to 60% of all patients treated and offered his own figure of 10% to 15% for “clear parkinsonian features.” Klawans also noted that some drugs produce parkinsonism more readily than others and that one of the most frequently used, haloperidol (Haldol), may produce parkinsonism in more than 90% of patients when sensitive detection methods are used.

我與神經科醫生交流過,他們發現神經安定藥引起的帕金森症有時確實會成為永久性的。 這與昏睡性腦炎的教訓是一致的,昏睡性腦炎是 20 世紀早期的一種病毒性流行病,患者因受精神抑製藥損傷的同一大腦區域受損而發展為不可逆轉的帕金森症(見第 4 章和第 5 章)。 雖然在使用安定藥的最初幾十年中,有人對永久性藥物誘發的帕金森症表示擔憂(Crane,1977;Hall 等人,1956;Hornykiewicz,1967;Klawans,如 Goetz 等人,1980 年所引用的;Korczyn 等人) ., 1976; Merritt, 1979; Simpson, 1977),近來很少表達。

I have communicated with neurologists who find that neuroleptic-induced parkinsonism does sometimes become permanent. This is consistent with the lessons of lethargic encephalitis, a viral epidemic from the early twentieth century in which patients developed irreversible parkinsonism from damage to the same regions of the brain that are damaged by the neuroleptics (see chapters 4 and 5). While some concern about permanent drug-induced parkinsonism was voiced in the first few decades of neuroleptic use (Crane, 1977; Hall et al., 1956; Hornykiewicz, 1967; Klawans, as cited in Goetz et al., 1980; Korczyn et al., 1976; Merritt, 1979; Simpson, 1977), little has been expressed in recent times.

帕金森氏症作為腦功能障礙治療的一個方面(第 48 頁)

Parkinsonism as an Aspect of Brain-Disabling Therapy (p. 48)

在該行業意識到改善其公眾和專業形象之前,許多精神病學家將帕金森綜合徵與抗精神病藥的治療效果聯繫起來(Davis et al., 1975; Paulson, 1959)。 Cole (1960) 說,在某些情況下,使用藥物誘發的帕金森症來控制患者相當於使用毒性作為治療。 科爾甚至使用藥理學緊身衣來描述藥物作用

Before the profession became so conscious of improving its public and professional image, many psychiatrists connected the parkinsonism syndrome to the therapeutic effect of neuroleptics (described in Davis et al., 1975; Paulson, 1959). Cole (1960) said that in some cases, the use of drug-induced parkinsonism to control the patient was the equivalent of using toxicity as therapy. Cole went so far as to use the phrase pharmacologic straitjacket to describe the drug effect.

靜坐不能的痛苦(第 48 頁)


靜坐不能是一種藥物引起的反應,其特徵是令人不安、緊張或焦慮的強烈感覺,驅使人們移動他或她的身體(Jeste 等人,1986;Weiner 等人,1983)。 患有靜坐不能的人發現很難坐下或保持雙腳靜止。 有些人會原地踏步,瘋狂地踱步,或者尋找讓他們保持移動的活動。 我評估了患有永久性靜坐不能(遲發性靜坐不能;見第 4 章)的患者,他們終其一生都被困在永久的痛苦中。 這種由藥物引起的疾病所產生的神經系統痛苦會變得如此極端,以至於即使是最著迷、相對冷漠的病人也會感到受到折磨。

Akathisia is a drug-induced reaction characterized by compelling feelings of restlessness, tension, or anxiety that drive a person to move his or her body (Jeste et al., 1986; Weiner et al., 1983). People with akathisia find it difficult to sit or to keep their feet still. Some will walk in place, pace frantically, or search out activities that keep them on the move. I have evaluated patients with permanent akathisia (tardive akathisia; see chapter 4) who, for their entire lives, are trapped in perpetual suffering. The neurological distress produced by this drug-induced condition can become so extreme that even the most spellbound, relatively indifferent patient will feel tortured.

患有靜坐不能的患者經常使用電隱喻或描述例如“電流通過我的血管”或“我的頭部受到衝擊”。 常用的詞有折磨人、折磨人、難以形容。 患者經常說他們寧願死也不願患有靜坐不能,這種疾病會導致自殺。 與患有焦慮症的患者不同,這些人似乎在描述身體現象,就好像他們受到了由內而外的折磨。

Patients suffering from akathisia often use electrical metaphors or descriptions such as “electricity going through my veins” or “shocks in my head.” Words like excruciating, torture, and indescribable are commonly used. Patients often say that they would rather die than live with akathisia, and the disorder can cause suicidality. Unlike patients suffering from anxiety, these individuals seem to be describing physical phenomena as if they are being tortured from the inside out.

如果患者沒有瘋狂地四處走動,醫生通常不願意承認這種疾病是靜坐不能。 一份題為“使用抗精神病藥”(1989)的報告總結了幾位專家的臨床觀察並得出結論:

Doctors are frequently reluctant to acknowledge the disorder as akathisia if the patient is not frantically moving about. A report titled “Using Antipsychotics” (1989) summarized the clinical observations of several experts and concluded,

雖然通常認為靜坐不能的特徵是運動不安的明顯跡象,但應該注意的是,行為症狀可能僅限於焦慮、急躁和敵意的表達。 這種表現常常被誤診為精神病症狀的複發。 (第 2 頁)
While it is commonly believed that akathisia is characterized by obvious signs of motor restlessness, it should be noted that behavioral symptoms may be limited to expressions of anxiety, impatience, and hostility. Too often, this manifestation is misdiagnosed as recurrence of psychotic symptomatology. (p. 2)

靜坐不能在沒有外部身體運動的情況下發生,這在臨床和法律上都很重要。 在臨床上,如果接受藥物治療的患者報告了一種與焦慮不同的內心疼痛或激動感,並且如果描述具有通常與靜坐不能相關的奇怪特徵,那麼警覺的醫生應該考慮診斷為靜坐不能。 這可能導致減少或終止藥物和/或藥物處方以改善症狀。

That akathisia can occur in the absence of external bodily movements is clinically and legally important. Clinically, if medicated patients report a sense of inner pain or agitation that feels different to them than anxiety, and if the descriptions have bizarre qualities often associated with akathisia, alert physicians should consider a diagnose of akathisia. This can lead to a reduction or termination of the medication and/or the prescription of drugs to ameliorate the symptoms.

在法律領域,實施暴力的患者可以使用靜坐不能作為開脫罪責或減輕罪責的因素。 在自殺和暴力事件中,如果藥品製造商未能警告其產品會導致靜坐不能,並且靜坐不能與潛在的災難性後果相關聯,則可能會提起產品責任訴訟。 在沒有外部運動的情況下存在靜坐不能是一個關鍵的診斷問題。

In the legal arena, patients who commit violence may be able to use akathisia as an exculpatory or mitigating factor. In cases of suicide and violence, product liability suits may be brought against drug manufacturers who fail to warn that their products cause akathisia and that akathisia is associated with potentially disastrous consequences. The existence of akathisia in the absence of external movements can be a critical diagnostic issue.

美國精神病學協會 (2000) 的精神疾病診斷和統計手冊 (DSM-IV-TR) 以及早期的 1994 版將靜坐不能描述為由抗精神病藥物和 SSRI 抗抑鬱藥引起的運動障礙。 雖然是由前藥專家撰寫的一份文件,但 DSM-IV-TR 引用了非常高的靜坐不能發生率:“據報導,在接受抗精神病藥物治療的個體中,靜坐不能的患病率差異很大 (20%–70%)。” Sachdev 和 Kruk (1994) 評估了 100 名在澳大利亞新南威爾士大學附屬教學醫院的兩個住院精神病科住院的患者。 41% 的患者出現輕度靜坐不能,21% 出現中度至重度靜坐不能。 他們引用的研究表明,Haldol 和 Prolixin 等高效能神經安定藥的發生率高達 90%。

The American Psychiatric Association’s (2000) Diagnostic and Statistical Manual of Mental Disorders (DSM–IV–TR), as well as the earlier 1994 edition, describe akathisia as a movement disorder caused by both the antipsychotic drugs and the SSRI antidepressants. Although a document written by prodrug experts, the DSM–IV–TR cites very high rates for akathisia: “The reported prevalence of akathisia among individuals receiving neuroleptic medication has varied widely (20%–70%).” Sachdev and Kruk (1994) evaluated 100 patients admitted to two inpatient psychiatric units in teaching hospitals affiliated with the University of New South Wales in Australia. Mild akathisia developed in 41% of patients and moderate-to-severe akathisia in 21%. They cited studies indicating rates as high as 90% with high-potency neuroleptics such as Haldol and Prolixin.

儘管對精神抑製藥引起的靜坐不能發生率的估計差異很大,但即使是較低的估計也會給患者帶來天文數字的風險。 精神病學和醫學對精神安定藥引起的以及抗抑鬱藥引起的靜坐不能給患者造成的痛苦關注太少了。

Although estimates vary widely for the rates of neuroleptic-induced akathisia, even the lower estimates pose an astronomical risk to patients. Psychiatry and medicine have paid far too little attention to the suffering inflicted on patients by neuroleptic-induced, and also antidepressant-induced, akathisia.

DSM-IV-TR 觀察到,非典型抗精神病藥物引起靜坐不能的可能性低於新的非典型藥物,但確實會發生。 以我的經驗,當劑量與舊藥相同時,所謂的非典型藥物,如利培酮和 Zyprexa,同樣可能引起靜坐不能。

The DSM–IV–TR observes that atypical antipsychotic drugs are less likely to cause akathisia than the new atypical drugs but that it does occur. In my experience, so-called atypicals like Risperdal and Zyprexa are equally likely to cause akathisia when given in doses equivalent to those used for the older drugs.

一個單獨的病例報告(Byerly 等,1995)表明,利培酮可產生嚴重的靜坐不能,描述為伴有焦慮和激動的行為刺激。 在一項氯氮平研究中,29 名患者中有 2 名出現靜坐不能,一名輕度,另一名中等強度(Chengappa 等,1994)。

A single case report (Byerly et al., 1995) indicated that risperidone can produce severe akathisia, described as behavioral stimulation with anxiety and agitation. In a study of clozapine, 2 of 29 patients developed akathisia, one mild and the other moderate in intensity (Chengappa et al., 1994).

靜坐不能的後果在個人痛苦以及暴力和自殺的可能性方面可能是毀滅性的。 在“相關特徵和障礙”下,DSM-IV-TR 警告說,“靜坐不能導致的主觀痛苦是顯著的。 . . . 靜坐不能與煩躁、易怒、攻擊性或自殺企圖有關。 精神病症狀或行為失控的惡化可能導致抗精神病藥物的增加。” 值得再次強調的是,靜坐不能導致煩躁、易怒、攻擊性或自殺企圖,以及精神病症狀和行為失控——自殺、暴力和精神惡化的處方。 在 1994 年版的 DSM-IV 中也進行了同樣重要的觀察。

The consequences of akathisia can be devastating in terms of individual suffering and the potential for violence and suicide. Under “Associated Features and Disorders,” the DSM–IV–TR warns that “the subjective distress result from akathisia is significant. . . . Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts. Worsening of psychotic symptoms or behavioral dyscontrol may lead to an increase in neuroleptic medication.” It is worth reemphasizing that akathisia can cause dysphoria, irritability, aggression, or suicide attempts as well as psychotic symptoms and behavioral dyscontrol—a prescription for suicide, violence, and mental deterioration. The same important observations were made in the 1994 edition of the DSM–IV.


Akathisia can cause extreme iatrogenic helplessness and denial and, ultimately, a dangerous degree of medication spellbinding.

範普頓等人。 (1974) 發現 35% 的患者在肌肉注射氟奮乃靜後失代償,通常是由於靜坐不能。 在藥物令人著迷的驚人例證中,甚至患者通常也想將問題歸咎於他或她的精神狀況:
Van Putten et al. (1974) found that 35% of their patients decompensated after one injection of intramuscular fluphenazine, usually as a result of akathisia. In a striking illustration of medication spellbinding, often even the patient wanted to blame the problem on his or her mental condition:

藥物引起的退化與最初的精神病非常相似,以至於在研究開始時,治療團隊(包括病房主任)總是用合理的動態術語解釋失代償。 通常,患者本人同意動態表述。 . . . 思維過程再次變得支離破碎,一些人抱怨他們從未經歷過的極度恐怖。 . . . 諸如“這是一種可怕的感覺”、“我無法描述它”或“如果這種感覺持續下去,我寧願死去”這樣的陳述並不罕見。

The drug-induced regressions resemble the original psychoses so precisely, that at the beginning of the study the treatment team (including the ward director) always explained the decompensation in plausible dynamic terms. Often, the patient himself agreed with the dynamic formulation. . . . Thought processes again became fragmented, and several complained of abject terror, the likes of which they had never experienced. . . . Statements such as “It’s a horrible feeling,” “I can’t describe it” or “If this feeling continues, I’d rather be dead” were not unusual.

這些痛苦的反應很快就開始了。 範普頓等人。 (1980) 還描述了對單劑量氯丙嗪和噻吩的頻繁嚴重煩躁反應。

These anguished responses were rapid in onset. Van Putten et al. (1980) also described frequent severe dysphoric reactions to single doses of chlorpromazine and thiothixene.

Van Putten (1975b) 在對病房人口進行仔細檢查時發現,靜坐不能的發生率非常高,為 45%。 他以圖形的方式描述了痛苦,同時表達了對患者痛苦的關注。 他總結說,

Van Putten (1975b) found an extraordinarily high rate of akathisia, 45%, on close examination of a ward population. He described the distress in graphic terms, while demonstrating concern for the patients’ suffering. He concluded,

由於生活中的許多活動都需要坐著,因此持續的靜坐不能是一種嚴重的困難。 更微妙的靜坐不能被醫生識別——但不能被病人識別! 即使是輕微的靜坐不能,也可能會阻止在晚餐時間、看電影、治療或久坐不動的工作。

Since many of life’s activities require sitting, a sustained akathisia is a severe hardship. The subtler akathisias often go unrecognized by the physician—but not by the patient! Even a mild akathisia can preclude sitting through the dinner hour, a movie, a therapy session, or a sedentary job.

靜坐不能真的會讓一個人發瘋。 Barnes (1992) 指出研究表明靜坐不能誘發精神病。 他引用文獻證實它會導致攻擊性和暴力或自殺(另見 Breggin 等人,1994a,討論靜坐不能和自殺)。 Van Putten 和 Marder (1987) 回顧了文獻並得出結論,靜坐不能“在極端情況下會驅使人們自殺或殺人”。 很多時候,醫生很可能將靜坐不能誤認為是患者的精神障礙而增加用藥,造成惡性循環。

Akathisia can literally drive a person crazy. Barnes (1992) pointed to studies indicating that akathisia can induce psychosis. He cited literature confirming that it can cause aggression and violence or suicide (see also Breggin et al., 1994a, for discussion of akathisia and suicide). Van Putten and Marder (1987) reviewed the literature and concluded that akathisia “in the extreme case, can drive people to suicide or to homicide.” Too often, doctors are likely to mistake the akathisia for the patient’s mental disorder and increase the medication, creating a vicious cycle.

Mayerhoff 和 Lieberman (1992) 觀察到,

Mayerhoff and Lieberman (1992) observed,

許多作者引用的精神抑製藥的一個更麻煩的副作用是一種涉及躁動、興奮和攻擊性行為的綜合症,這可能是也可能不是由靜坐不能引起的。 . . . 有一些證據表明,與中等劑量的低效抗精神病藥相比,中等劑量的氟哌啶醇可能更頻繁地發生暴力行為。

One of the more troublesome side effects of the neuroleptics cited by many authors is a syndrome involving restlessness, excitement and aggressive behavior that may or may not be due to akathisia. . . . There is some evidence to suggest that violent behavior may be more frequent on moderately high-dose haloperidol than on moderate doses of low potency neuroleptics.

氟哌啶醇 (Haldol) 是緊急嘗試控制攻擊性和暴力行為中最常用的藥物之一。 再一次,我們面臨著用可能使病情惡化的藥物治療患者的悲慘諷刺。 當術後患者變得神誌不清時,Haldol 還用於控制重症監護病房的行為,使這些易受傷害的個體面臨相當大的額外風險,並經常加劇他們的破壞性行為。

Haloperidol (Haldol) is among the most frequently used drugs in emergency attempts to control aggressive and violent behavior. Once again, we confront the tragic irony of treating patients with drugs that can worsen their condition. Haldol is also used to control behavior in intensive care units when postsurgery patients become delirious, exposing these vulnerable individuals to considerable additional risk and often exacerbating their disruptive behavior.

正如關於肌張力障礙已經指出的那樣,藥物引起的神經系統異常通常受到某種程度的自我控制。 它們有時可以通過鎮靜劑得到部分緩解,並可能因情緒壓力而惡化。 Sachdev 和 Kruk (1994) 發現,當大多數患者被某事分心時,他們的運動會減弱。

As already noted in regard to dystonia, drug-induced neurological abnormalities are often subject to some degree of self-control. They can sometimes be partially relieved by sedatives and may worsen in reaction to emotional stress. Sachdev and Kruk (1994) found that the movements in most patients would lessen when they were distracted by something.

神經病誘發的抑鬱和自殺(第 51 頁)


在精神病藥物:對大腦的危害 (Breggin, 1983b) 中,我回顧和評估了早期的研究,以記錄精神安定藥引起煩躁和精神病反應的頻率,包括精神分裂樣反應和抑鬱症,伴有或不伴有靜坐不能 (例如,DiMascio,1970;Marsden 等人,1977;Rifkin 等人,1975;Singh,1976;Van Putten 等人,1978)。 這些研究通常涉及仍然常用的藥物,包括 Haldol。 據報導,氯氮平會引起中毒性譫妄,尤其是在老年人中(Pitner 等,1995)。

In Psychiatric Drugs: Hazards to the Brain (Breggin, 1983b), I reviewed and evaluated earlier studies at some length to document the frequency with which neuroleptics can cause dysphoric and psychotic responses, including schizophrenic-like reactions and depression, with or without accompanying akathisia (e.g., DiMascio, 1970; Marsden et al., 1977; Rifkin et al., 1975; Singh, 1976; Van Putten et al., 1978). The studies typically involved drugs that are still commonly in use, including Haldol. Clozapine has been reported to cause toxic delirium, especially in the elderly (Pitner et al., 1995).

Van Putten 和 May (1978) 發現 47% 的患者出現運動不能,其中大多數人變得抑鬱。 確認大腦功能障礙的原則,當這些患者變得抑鬱時,他們的精神分裂症被評為改善,可能是因為他們變得相對不活躍、遲鈍、孤僻,甚至沉默。

Van Putten and May (1978) found that 47% of their patients developed akinesia and that most of these became depressed. Confirming the brain-disabling principle, as these patients became depressed, they were rated as improved in their schizophrenia, probably because they became relatively inactive, retarded, withdrawn, and even mute.

抑鬱症是對抗精神病藥治療的一種特別嚴重的反應(Aubree 等人,1980;Quitkin 等人,1975;Van Putten 等人,1978)。 Simonson (1964) 描述了他的母親在服用一小劑康普津治療噁心後變得絕望和絕望。 Ayd (1975) 披露:“現在普遍認為,在使用任何長效肌注神經安定劑治療期間,可能會發生輕度至重度抑鬱症,可能導致自殺,就像在使用任何口服神經安定劑治療期間可能發生一樣。”

Depression is an especially serious reaction to neuroleptic treatment (Aubree et al., 1980; Quitkin et al., 1975; Van Putten et al., 1978). Simonson (1964) described how his mother became despairing and hopeless after one small dose of Compazine for nausea. Ayd (1975) disclosed, “There is now general agreement that mild to severe depressions that may lead to suicide may happen during treatment with any depot [long-acting intramuscular] neuroleptic, just as they may occur during treatment with any oral neuroleptic.”

Small 和 Kellams (1974) 注意到患者因使用長效可注射形式的 Prolixin 治療而有自殺傾向的報導。 其他人已經證實,自殺可能是由安定藥引起的抑鬱症引起的(Alarcon 等人,1969 年;Hogan 等人,1983 年)。

Small and Kellams (1974) noted reports of patients becoming suicidal as a result of treatment with the long-acting injectable form of Prolixin. Others have confirmed that suicide can result from neuroleptic-induced depression (Alarcon et al., 1969; Hogan et al., 1983).

Mayerhoff 和 Lieberman (1992) 認為精神安定藥引起的抑鬱症是一個問題,他們指出,據報導,精神安定藥引起的所謂的運動障礙性抑鬱症的發病率高達 50%,平均為 25%。 頻率可能隨著長效肌內神經阻滯劑的增加而增加。

Neuroleptic-induced depression was recognized as a problem by Mayerhoff and Lieberman (1992), who pointed out that reported incidence rates of neuroleptic-induced so-called akinetic depression reach as high as 50%, with an average of 25%. Frequency probably increases with the long-acting intramuscular neuroleptics.

Emerich 和 Sanberg (1991) 在《生物精神病學》上寫了一篇社論,研究了對精神安定藥的煩躁反應。 他們描述了一系列痛苦的反應,包括煩躁、焦慮、激動和恐慌。 兩名志願者正常經歷了嚴重的焦慮以及意志力的喪失。 他們描述了一項研究,其中相對較小劑量的 Haldol(每天 2.5 毫克)會產生“情緒波動、哭泣、悲傷、抑鬱和沮喪”以及“缺乏動力”。 進一步降低劑量減少了反應。 他們總結道:“激動、焦慮發作、驚恐發作、逃避工作、學校恐懼症、分離焦慮和妄想都是抗精神病藥物治療後報告的副作用。”

Emerich and Sanberg (1991) wrote an editorial in Biological Psychiatry that examined dysphoric reactions to neuroleptics. They described an array of anguished reactions, including dysphoria, anxiety, agitation, and panic. Two volunteer normal  experienced severe anxiety as well as loss of willpower. They described a study in which relatively small doses of Haldol, 2.5 mg/day, produced “mood swings, crying, sadness, depression and despondence” as well as “lack of motivation.” Further lowering of the dose reduced the reactions. They summarized, “Agitation, anxiety attacks, panic attacks, work avoidance, school phobia, separation anxiety and delusions are all antipsychotic side effects that have been reported following neuroleptic treatment.”

與非典型抗精神病藥物相關的風險(第 52 頁)


正如前面第 2 章所述,NIMH CATIE 研究總結道,“錐體外系副作用、運動障礙或靜坐不能的發生率之間沒有統計學上的顯著差異”(Nasrallah,2007,第 9 頁)。 同樣,值得重複的是 Lieberman 等人。 (2005a) 指出,“在我們的研究中,接受第一代和第二代藥物治療的患者出現錐體外系症狀的比例沒有顯著差異。”

As previously noted in chapter 2, the NIMH CATIE study summed up, “There were no statistically significant differences between the rates of extrapyramidal side effects, movement disorders, or akathisia” (Nasrallah, 2007, p. 9). Similarly, it is worth repeating that Lieberman et al. (2005a) stated, “The proportion of patients with extrapyramidal symptoms did not differ significantly among those who received fi rst-generation and second-generation drugs in our study.”

儘管迄今為止關於它的報導相對較少,但較新的精神安定藥也會導致運動不能、抑鬱、精神病和自殺。 據報導,阿立哌唑 (Abilify) 會導致或加重精神病(Grover 等人,2006;Raja,2007)。 我見過幾起奧氮平(Zyprexa)引起殭屍樣行為和嚴重抑鬱的案例。 正如第 2 章所記載的,所有較新的精神安定藥,包括利培酮、Geodon 和 Seroquel,都抑制多巴胺能功能(多巴胺 D2),這是這些臨床狀態最可能的神經化學原因(Wu 等人,2007 年)。

Although relatively little has thus far been written about it, the newer neuroleptics can also cause akinesia, depression, psychosis, and suicidality. Aripiprazole (Abilify) has already been reported to cause or worsen psychosis (Grover et al., 2006; Raja, 2007). I have seen several cases in which olanzapine (Zyprexa) has caused zombielike behavior and profound depression. As chapter 2 also documented, all of the newer neuroleptics, including Risperdal, Geodon, and Seroquel, suppress dopaminergic function (dopamine D2 ), the most probable neurochemical cause of these clinical states (Wu et al., 2007).

新舊抗精神病藥物在阻斷多巴胺引起不良神經系統影響方面的任何差異充其量只是程度問題。例如,Seeman (2002) 認為,“較新的非典型抗精神病藥。 . .與較老的精神安定藥相比,它們與多巴胺的結合更鬆散。根據這一理論,它們在較短的時間內佔據其封鎖位置,從而產生較少的不利影響,例如 EPS Weiden (2007b) 指出,“理論上”有可能用較新的非典型患者治療患者,而不會引起盡可能多的 EPS 效應。但他總結說:“然而,在實踐中,即使在非典型或第二代抗精神病藥時代,EPS 仍然是一個重大問題……因為所有氯氮平後 SGA [第二代抗精神病藥] 仍然影響多巴胺 D2 受體,它可能更準確地說,這些藥物比早期的抗精神病藥物具有更低的 EPS 負債(第 13 頁)。然而,這種治療希望假設新藥沒有以較大劑量給藥以達到與舊藥相同的效果,從而產生相同的副作用。 4 章將研究表明精神安定藥引起的精神病可以以遲發性精神病和遲發性癡呆的形式成為永久性的證據,導致症狀惡化需要更大劑量的違規藥物的悲慘情況。

Any difference between the older and the newer antipsychotic drugs in regard to blocking dopamine and causing adverse neurological effects is at best a matter of degree. Seeman (2002), for example, argued that “the newer, atypical antipsychotics . . . all bind more loosely” to dopamine than the older neuroleptics. According to this theory, they occupy their blockading position for a briefer period of time, thereby producing fewer adverse effects, such as EPS. Weiden (2007b) noted that “in theory” it might be possible to treat patients with the newer atypicals without causing as many EPS effects. But he concluded, “In practice, however, EPS remain a significant problem even in the era of atypical or second generation antipsychotics.… Because all of the post-clozapine SGAs [second-generation antipsychotics] still affect the dopamine D2 receptor, it may be more accurate to say these medications have lower EPS liabilities” than the earlier antipsychotics (p. 13). However, this therapeutic hope assumes that the newer drugs are not being given in larger doses to achieve the same effect as the older drugs, thereby producing the same adverse effects. Chapter 4 will examine evidence indicating that neuroleptic-induced psychoses can become permanent in the form of tardive psychosis and tardive dementia, leading to a tragic situation in which worsening symptoms require greater doses of the offending medication.

強制問題(第 53 頁)


本章回顧的研究均未考慮患者是否希望接受治療或是否被脅迫。 沒有人提到這些患者在法律上是自願的還是非自願的,更不用說表面上自願的患者是否像經常發生的那樣在脅迫下接受治療。 在耐藥性和痛苦的藥物不良反應是正在研究的問題的研究中,這種考慮的缺失尤其令人吃驚。 精神科醫生似乎常常認為抵抗完全是精神疾病的問題,因此患者是否討厭被迫住院、服藥甚至電擊都無關緊要。 這些研究也沒有考慮到患者互相警告不要抱怨治療,理由是抱怨會導致藥物劑量增加或其他懲罰性結果。

None of the studies reviewed in this chapter considered whether the patients wanted to be in treatment or whether they were being coerced. None mentioned whether the patients were legally voluntary or involuntary, let alone whether ostensibly voluntary patients were undergoing treatment under duress, as frequently happens. The absence of such considerations is particularly startling in studies in which drug resistance and painful adverse drug reactions are the issues under investigation. Psychiatrists too often seem to believe that resistance is wholly a matter of mental illness so that it does not matter if the patient resents being forcibly subjected to hospitalization, medication, or even electroshock. Nor do these studies take into account the reality that patients warn each other against complaining about treatment on the grounds that complaints lead to increased doses of drugs or other punishing results.

四十多年前發表的我 1964 年的研究“開放醫院中自願患者的強制”仍然是唯一一篇經過同行評審的科學文章,系統地研究了用於控制精神病患者的各種威脅和直接形式的強制,包括藥物、電擊、 和承諾。

Publishing more than four decades ago, my 1964 study “Coercion of Voluntary Patients in an Open Hospital” remains the only peer-reviewed scientific article that systematically investigated the various threats and outright forms of coercion used to control mental patients, including drugs, electroshock, and commitment.

最後,精神安定藥會導致大量的身體和情感痛苦,包括痛苦和精神病。 通常,這些藥物會產生一種死氣沉沉和抑鬱的感覺,並且會導致自殺。 痛苦通常與錐體外系反應有關,例如帕金森症、肌張力障礙和靜坐不能。 在大多數情況下,結果是醫源性無助和否認的深刻狀態。 患者在沒有意識到發生了什麼的情況下情緒崩潰。 很多時候,患者變得神魂顛倒,無法識別自己的損傷程度,無法將精神崩潰歸因於藥物,有時認為自己做得更好,但實際上情況更糟,有時,尤其是在靜坐不能的情況下 ,進行強迫性自殺或暴力行為。

In conclusion, the neuroleptics cause an enormous amount of physical and emotional suffering, including anguish and psychosis. Frequently, the drugs produce a feeling of deadness and depression, and they can cause suicide. Often the suffering is associated with extrapyramidal reactions such as parkinsonism, dystonia, and akathisia. The result in most cases is a profound state of iatrogenic helplessness and denial. The patient is emotionally devastated without realizing what has happened. Many times, the patients become spellbound, failing to recognize their degree of impairment, failing to attribute their mental collapse to the drug, sometimes believing that they are doing better when they are in fact worse, and, on occasion, especially when driven by akathisia, committing compulsive suicide or violence.

不幸的是,這些疼痛和精神障礙的神經系統反應,包括肌張力障礙和靜坐不能,也可能是由新型抗抑鬱藥如 Paxil、Prozac、Zoloft 和 Celexa 引起的。 這些令人痛苦的藥物不良反應有時會導致或導致暴力和自殺行為(第 6 章和第 7 章)。

Unfortunately, some of these painful and mentally disabling neurological reactions, including dystonia and akathisia, can also be caused by the newer antidepressants such as Paxil, Prozac, Zoloft, and Celexa. These distressing adverse drug reactions sometimes contribute to or cause violent and suicidal behavior (chapters 6 and 7).

By bangqu