躁鬱旅程

相關文章：簡介《謹慎用藥‧小心停藥：給精神科醫師、心理工作者、精神疾病患者和家屬的指南》

資訊要公開，才能守護我們的健康。

我2012-2013年重病時的諸多症狀到現在仍有的殘缺，

（2012重病狀況請見2012病中書信系列〈2012病中書信13-1st〉 共13封）

高度吻合文獻所提的精神科藥物鋰鹽導致不可逆轉的神經毒害

－名為SILENT的症候群 

希望不要再有人遭遇像我這樣的不幸。（我將自己的身體狀況附在翻譯內文對照。）

完成這篇翻譯，是眾人群策群力的成果。

感謝長年住國外的Zen和正在趕藥學碩士畢業論文的Sgnidnuorrus協助翻譯 

感謝Jane提醒注意翻譯著作侵權問題並引介有護理背景的接案譯者Abby，

感謝Abby願意無償協助澄清翻譯疑問處。

感謝百忙之中的小穆提供意見和引介朋友Ping，

感謝正在寫社文所博士論文的Ping協助澄清翻譯疑問處。

感謝來自美國的Linda 跟我分享這篇資料並協助聯繫出版社拿到翻譯同意書

感謝所有協助找尋翻譯者的朋友......

資料來源：

《Brain Disabling Treatments in Psychiatry: Drugs, Electroshock, and the Psychopharmaceutical Complex》

使腦失能的精神病學療法：藥物、電擊療法和精神藥物造成的複合物

Chapter 8: Lithium and Other Drugs for Bipolar Disorder 

第八章：躁鬱症用藥的鋰鹽與其他藥物

作者(author)：Peter R. Breggin MD     出版社（publisher)：Springer Publishing Company,LLC. 

Copyright notice:

Brain-Disabling Treatments in Psychiatry,ISBN:978-082612934-5

Editor:Sheri W. Sussman, Author: Peter R. Breggin

Copyright c 2008 by Springer Publishing Company, LLC, New York, New York 10036. All Rights Reserved.

 The original English language work has been published by Springer Publishing Company,LLC.

No part of this chapter may be reproduced, stored in a retrieval system,

or transmitted in  any form or by any means (electronic, mechanical, photocopying, recording, or otherwise)

without prior permissino from the publisher. 

________________________________________

Book Description 有關此書

From the author of Toxic Psychiatry and Talking Back to Prozac:

"Peter Breggin is the conscience of American psychiatry. Once more he updates us on the real evidence with respect to the safety and effectiveness of specific psychiatric medications and ECT. This information is needed by all mental health professionals, as well as patients and families." --Bertram Karon, Ph.D., Professor of Psychology, Michigan State University, Author of The Psychotherapy of Schizophrenia

作者彼得是美國精神病學界的良知。他不只一次以真實的證據讓我們得知關於特定的精神科藥物的安全性和效能。所有與心理健康領域相關的專家和病人與病人家屬們，都需要來讀一讀這些報告。 －密西根州立大學，心理學教授 Bertram Karon

 "Nowhere does false medical thinking do more harm than in the modern psychiatric argument that mental illness is easily diagnosed and then cured by a side-effect free drug. Nowhere is the correct psychiatric thinking more evident than in the books by Peter Breggin." -- William Glasser, MD, psychiatrist, author of Reality Therapy

在現代精神病學的主張認為：精神疾病易於診斷，且能以無副作用的藥物根治。沒有比這錯誤的醫學思維能造成更大的傷害。Peter Breggin書中正確的精神病學思維，是再清楚明瞭不過的了。

精神病學家（醫師）William Glasser 《真實療法》的作者

翻譯內容如下：

藥物迷咒與醫療引發的無助與否認

SPELLBINDING AND IATROGENIC
HELPLESSNESS AND DENIAL

先前引用Judd 的研究證實，鋰鹽所引起的失能在患者的朋友眼裡看來明顯，也可透過心理測驗測得，但專家卻全然無視這些失能。由於病人如被下咒般的藥物迷惑（註1），病人們在服用鋰鹽的情況下，難以評估自己的心神狀態。病人服用鋰鹽數日至數週後，鋰鹽的毒性通常緩慢、不知不覺的加深，致使其判斷能力以一種幾乎無法被察覺的漸進方式被損害。事實上，當病人中毒逐漸嚴重時，他們對病情的陳述就不被信賴，即使這些症狀包括很顯著的腸胃不適、顫抖和精神功能失常。醫師藉由病人的鋰鹽血中濃度，而非病人對自身的感受，來監控病人的狀況。

有研究指出，同上述的藥物迷咒效應，自願受試的正常人在服用低劑量的鋰鹽之後，雖然神經反射能力受到損害，卻毫無所悉或並不承認。報告沒有副作用的服用鋰鹽病患，卻經常出現非常明顯的顫抖症狀，持續規律服用鋰鹽的病人無法察覺到自身神經的缺陷，這可清楚地證明長期以鋰鹽治療，實在是一種藥物迷咒。

對中樞神經系統的毒性 TOXICITY TO THE CENTRAL NERVOUS SYSTEM
認知功能損傷 The Production of Congnitive Deficits

現在社會上已普遍地接受鋰鹽能損害智力功能的這個事實。舉例來說，Shaw在1987年發現服用鋰鹽會造成記憶和手部運動速度的損傷。在全書以生物精神醫學觀點所寫成的《躁鬱症》一書中，Frederick Goodwin 和Kay Jmison（註2）（1990）卻下了鋰鹽確實能造成嚴重的認知功能損害的結論。他們摘要了許多從以前到當時為止的研究文獻並宣稱：

既然這藥物的主要作用是透過中樞神經來調解，那麼鋰鹽能導致種種不同類型、不同嚴重程度的認知損害就不令人意外。事實上，記憶問題是接受鋰鹽治療的病人最常表述的副作用之一。雖然病人主訴認知能力的缺陷也可能是情感性疾患所致，但重要的是要切記，鋰鹽導致智能上的損害並不罕見，此亦促使很多病人不願再服藥。此外，創造力也會因為服用鋰鹽而受影響。

Stip於2000年總結出鋰鹽誘發記憶問題的文獻：
一些研究顯示服用鋰鹽的躁鬱症患者有短期記憶、長期記憶和精神性運動速度的損傷。他們的研究針對正常受試者，進行三週的雙盲檢法（註三）試驗來研究鋰鹽的效果。結果發現：服用鋰鹽治療的受試者，和服用安慰劑者對照下，有長期記憶的缺陷而不易回想起單字。

急性器質性腦部症候群 Acute Organic Brain Syndromes

就鋰鹽因號稱比其他藥物不易產生強烈精神性副作用而被大力推廣來說，知道緊接在鋰鹽上市被使用後，規律接受鋰鹽治療期間發生中毒性譫妄（精神錯亂）的案例有多麼多，就更令人咋舌。（Johnson et al.,1968; Mayfield et al.,1966; Prien et al., 1972; Shopsin et al.,1971; Strayhorn et al.,1977）Prien (1972)發現：接受鋰鹽治療之高積極度的病人當中，有將近三分之一承受著劇烈的藥物反應，包括數種中毒導致的方向感喪失、困惑、缺乏思考的連續性和理解力降低等種種混亂。鋰鹽有高度神經毒性。

SILENT：不可逆轉的，鋰鹽所導致的神經毒害
SILENT:Irreversible Lithium-Induced Neurotoxicity

在1987年，Adityanjee對所謂的鋰鹽中毒進行討論，並下了一個仍適用迄今的評論「人們普遍缺乏對於鋰鹽治療所引發的無法逆轉與治療之併發症的警覺心，儘管證據已經非常清楚。」

原本大家認為：除了在少數極端的案例外，鋰鹽導致的神經系統毒害是可逆的。然而，到頭來才發現許多病患顯然發展為不可逆的腦功能損害與官能障礙，且常與小腦有關（Grignon et al.,1996）。最近20年來，研究人員已將這些鋰鹽所致不可逆轉的神經系統毒害的症候群定義為「SILENT 」。Adityanjee et al. (2005)審查了1965年到2004年間，停用鋰鹽後，其神經毒性引起的後遺症卻仍持續至少兩個月以上的案例。他們發現九十個SILENT的案例發生了持續性小腦功能失調，這是最常見的副作用。這些慢性長期地殘障的病人可能需要為步態運動失調(gait ataxia)進行復健；為構音困難做說話的訓練；為痴呆和記憶力受損做認知能力的訓練（p.47）。根據作者群的看法，最可能導致這一切的原因在於，鋰鹽在神經系統及小腦引起的多處神經髓鞘脫失。這並不令人意外，鋰鹽的毒性也可以引起慢性的神經心理的變化，包括受損的記憶、注意力、執行控制力和視覺空間感不足（Brumm et al.,1988）。

只要相當低劑量的鋰鹽血清藥劑，就能導致不可逆的神經毒害。Lang and Davis (2002) 描述「一位服用鋰鹽的44歲男性躁鬱症患者，出現兩個月構音困難、步行失調和雙腳無力等症狀，他有顯著的小腦和錐體路徑功能障礙。他的鋰鹽血清濃度是1.5 mmol/L，略為偏高。（註四）他之後僅部分復原，仍伴隨小腦的運動機能失調。作者們提出警告：在規律服藥的療程中，持續的神經毒性會突如其來地發作。

低劑量鋰鹽療法的神經毒性效果
Neurotoxic Effects in Low-Dosage Maintenaance Therapy

Branchey et al.(1976) 發表了長期服用鋰鹽患者（6個月到7年）的追蹤調查。

36個人中，只有10人無神經性症狀，36個人中包括服用低劑量的患者；另外還有4個人有輕度的震顫麻痺（帕金森）症狀。

（而不幸的我並不只罹患『輕度』的震顫麻痺（帕金森）症狀，

  我震顫無法控制動作的程度，

  讓滿頭白髮的台中榮總的神經內科Dr.C說他行醫多年，

  從來沒看過哪個神經可以讓身體動得那麼厲害的。）

使腦失能的精神病學療法：藥物、電擊療法和精神藥物造成的複合物

髓鞘脫失 (Demyelination)

髓鞘是包覆在神經細胞外的絕緣物質，髓鞘脫失是指髓鞘死亡或損傷。當髓素退化，沿著神經傳輸的信號會被削弱或消失，且神經最後會萎縮。因受影響的細胞功能不同，而產生多樣的症狀。它擾亂了腦與身體其他部位的訊號傳輸，顯現的症狀因人而異。典型的症狀包括：

（括號內綠色字是慢慢的狀況描述）

◎影響單眼的中心視野模糊，眼球運動時可能伴隨著疼痛
 （這症狀我有；眼睛高壓，酸脹不適，持續疲勞狀態）

◎複視－把一個東西看成兩個東西

◎喪失視力/聽力

◎腳部、手部、胸部或臉部的刺痛疼痛感或麻木無感 /神經病變/
 （這症狀我有；全身爬蟲感、酸麻感、疼痛或麻木無感對冷熱感不明顯知覺麻痺，

  詳情可見部落格文章2012年病中書信）

◎手腳無力感（這症狀我有）

◎認知力損害，包括說話能力受損與記憶喪失
 （這症狀我有；現在說來還很難啟齒，我還沒克服心理障礙，等我準備好了，我會寫出來）

◎對熱敏感－當暴露於熱的環境中，如洗熱水澡，會令症狀惡化或再現。

  (這症狀我有，高溫氧氣少的環境，症狀容易再現或惡化）

◎靈巧度的喪失－尤其手部 

 （這症狀我有；我的手腳反應變慢，我學做粘土勞作連五歲的小女孩都笑我怎麼這麼慢）

◎有身體協調運動和平衡方面的困難
 （這症狀我有；我動作不協調 、走路搖搖晃晃是常態）

◎有控制腸運動或排尿作用的困難
  (這症狀我有，偶會在短時間內頻尿（半小時內可以跑廁所三四次）

◎疲倦感 （這症狀我有；疲勞幾乎如影隨形，沒做什麼就累了）

步行失調 (gait ataxia)：

（這症狀我有；曾有行走困難、舉步維艱，到現在只是步行失調，走路走不快，搖搖晃晃，想走快點動作會變很怪異。）

有腦部位損傷導致的步行失調的人最初顯現的症狀是很差的平衡感，那會以無法單腳站立或無法腳跟接著腳尖走直線。當病情繼續發展，走路會以腳開開的和踮步的步伐和搖搖擺擺、左右搖晃傾斜的方式突顯。轉身也有困難而且可能導致跌倒。

構音困難(dysarthria)：

（這症狀我有；我從從小到大的口齒伶俐、聲若洪鐘，變成說話遲緩（好幾秒鐘才吐得出一個字）和說話結巴的大舌頭、有時想說話卻說不出來、說話聲音很小聲、語調平板、沒辦法控制的音調改變（娃娃音），這些都是曾出現過的症狀，還好現在程度已降低和出現的頻率也降低了）

指一種發生在協助說話運作到的肌肉群發生的問題。它使咬字發音變得非常困難。這和任何認知理解語言的能力無關。而是說話功能的任一個次要系統（如換氣、發音、共鳴、韻律和發音的清晰度）受到影響，導致語音溝通方面的可理解度、能聽度（可聽見的程度）、逼真度和效能方面的損害。

有構音困難的人可能會面臨的挑戰如下：

◎節奏 （我曾好幾秒才能吐出一個字，且有時想講的話卻說不出來，大舌頭、說話結巴。）

◎音質

◎音調（曾說話平板無聲調變化）

◎音量（曾非常小聲，現在較少出現了）

◎換氣－控制呼吸的能力）

（我曾一醒來就無法控制呼吸、過度換氣喘個不停，最嚴重時有喘過一整天。

  現在有時還會出現，慶幸嚴重程度已減緩）

◎速度（我曾說話速度很遲緩，最嚴重時吐出一個字要1-3秒）

◎強度（我曾說話虛弱無力）

◎穩定度（我曾說話忽強呼弱）

◎音域（音域變窄，音平淡，如上，曾說話語調平板）

◎音色 （曾有變過娃娃音，我以前很討厭別人那樣說話，覺得很假）

特別觀察到的案例包括：持續帶著氣音的聲音、不規則地發音中斷、音調平淡(平板音)、扭曲母音、急促無斷句，

以及鼻音過多等方面障礙的不定期出現。

以下註解的部份非原文內容，是慢慢下的註解。

（註1）Spellbinding如下咒般迷住病人的藥物咒縛。

（註2）Kay Jmison ：

       凱‧傑米森博士是約翰‧霍普金斯大學醫學院精神病學系教授。

       曾任加州大學洛杉磯分校情感性疾病門診主任，

       並當選該校「科學女傑」，列名於「全美最佳醫師」內；

       她是美國「國家諮詢委員會人類基因研究」的成員，                               

       同時也是「戴納機構躁鬱症基因基礎」的臨床主任。

       世界躁鬱症研究權威－凱‧傑米森博士…

    （以上內容節錄自《躁鬱之心》作者簡介）Kay Jmison是躁鬱症患者。

（註3）雙盲檢法（double-blind）：

       不告知病人及醫師確切的處方而進行藥物的對照試驗，

       並用統計學理論判定藥效之有無的方法。

（註4）Lang EJ & Davis SM (2002). Lithium neurotoxicity:

    the development of irreversible neurological impairment despite standard 

    monitoring of serum lithium levels. 這篇是case report，

    提到一位44歲的躁鬱症患者，他的"Serum lithium was 1.5 mmol/l,

    a moderate elevation above his usual stable levels of 0.4-0.8 mmol/l."

    moderate elevation是稍微偏高的意思，因為跟這位患者之前的數值相比，

    1.5 mmol/l是稍高的血清濃度。

   原句有"for the patient"，也就是說：對這位病患來說，1.5 mmol/l是稍微偏高的。

翻譯原文如下：

SPELLBINDING AND IATROGENIC HELPLESSNESS AND DENIAL

The previously cited research by Judd demonstrates how professionals utterly fail to see lithium-induced disabilities that are obvious to friends and detectable with psychological testing. Due to medication spellbinding, patients themselves have difficulty evaluating their mental status on lithium. Toxicity often creeps up slowly over many days or weeks so that their judgment is impaired in an almost imperceptibly gradual manner. In fact, patients cannot be relied on to notice when they are becoming severely toxic, even though the symptoms include marked gastrointestinal disturbances, tremor, and disturbed mental functions. Instead of relying on the perceptions of patients, blood levels must be carefully monitored and the patients carefully watched.

In keeping with this medication spellbinding effect, normal volunteers on small doses suffer impairments of their reflexes but do not realize or acknowledge the impairment ( Linnoila et al., 1974 ). Lithium patients who report no side effects often have grossly obvious tremors. The failure of patients on maintenance therapy to notice their own neurologic defects clearly demonstrates that lone-term treatment with lithium is medication spellbinding.

TOXICITY TO THE CENTRAL NERVOUS SYSTEM

The Production of Cognitive Deficits

It is now generally accepted that lithium can impair intellectual function. For example, Shaw et al. ( 1978 ) found impairments of memory and hand motor speed on lithium. In Manic- Depressive Illness, a book written wholly from a biopsychiatric perspective, Frederick Goodwin and Kay Jamison ( 1990 ) nonetheless concluded that lithium does cause serious cognitive impairments. They summarized much of the literature up to that time and decalred,

Since the drug’s primary action is mediated through the central nervous system, it is not surprising that lithium can cause cognitive impairments of varying types and degrees of severity. Indeed, memory problems are among the side effects of lithium treatment that patients report most frequently. Although affective illness itself contributes both to cognitive deficits and complaints about such deficits, it is important to bear in mind that impairment of intellectual functioning caused by lithium is not uncommaon and, in many patients, leads to noncompliance. Creativity can also be affected. ( p.706 )
More recently, Stip et al. (2000) summarized the literature on lithium – induced memory problems: “ Several studies have shown cognitive impairment in short-term memory, long- term memory and psycho-motor speed in bipolar patients taking lithium.” Their study aimed at testing the effect of lithium in normal subjects in a double-blind, 3-week study. They found that lithium-treated volunteers had long-term memory deficits on recalling words compared to the placebo group.

Acute Organic Brain Syndromes

Considering how vigorously lithium is promoted as relatively free of overpowering mental effects, it is surprising how many cases of toxic delirium during routine lithium therapy were reported soon after the drug came into use ( Johnson te al., 1968; Mayfield te al., 1966; Prien et al.,1972; Shopsin et al.,1971; Strayhorn et al.,1977). Prien et al.(1972) found that almost one-third of the patients in their highly active category suffered “severe” reactions, including several with toxic confusion described as “ disorientation, confusion, lack of continuity of thought, and reduced comprehension.” Lithium is highly neurotoxic.

SILENT: Irreversible Lithium-Induced Neurotoxicity

In 1987, Adityanjee discussed so-called lithium poisoning and made an observation that remains true today: ” There is a general lack of awareness about irreversible and untreatable complications of lithium treatment despite evidence to the contrary.”

Originally, it was thought that, except in extreme cases, lithium-induced neurotoxicity was reversible. However, it eventually became apparent that many patients develop irreversible brain damage and dysfunction, often involving the cerebellum (Grignon et al., 1996). In the last two decades, researchers have defined a syndrome of irreversible lithium-effectuated neurotoxicity (SILENT). Adityanjee et al.(2005) reviewed the literature from 1965 to 2004 for cases of lithium neurotoxicity with persistence of sequelae for at least 2 months after cessation of treatment. They found 90 cases of SILENT, with persistent cerebellar dysfunction as the most commonly reported persistent aftereffect. These chronically disabled patients may need “ physical rehabilitation for gait ataxia, speech training for dysarthria, and cognitive training for dementia and memory impairments” (p.47) The most cause, according to the authors, is “demyelination caused by lithium in multiple sites in the nervous system, including the cerebellum.” Not surprisingly, lithium toxicity can also cause chronic neuropsychological changes, including impaired memory, attention, executive control functions, and visuospatial deficits ( Brumm et al.,1998).

Irreversible neurotoxicity can occur at relatively low serum doses. Lang and Davis (2002) described “ the case of a 44 year old man who presented with a two-month history of dysarthria, ataxia and leg weakness whilst on maintenance lithium for bipolar disorder.” He had significant cerebellar and pyramidal dysfunction. His serum lithium was 1.5 mmol/L, a moderate elevation for this patient. His recovery was only partial, leaving him mainly with cerebellar ataxia. The authors warned about the insidious onset of persistent neurotoxicity during routine treatment.

Neurotoxic Effects in Low-Dosage Maintenance Therapy

Branchey et al,( 1976) published a follow-up of patients on long-term lithium maintenance (6 months to 7 years). Only 10 of 36 were “ free of neurologic symptoms,” even with the low maintenance doses employed. Four of 36 patients had parkinsonian symptoms at a “ low level of severity.”

The production of the myelin sheath is called myelination

Demyelination
Demyelination is the loss of the myelin sheath insulating the nerves. When myelin degrades, conduction of signals along the nerve can be impaired or lost and the nerve eventually withers. This results in diverse symptoms determined by the functions of the affected neurons. It disrupts signals between the brain and other parts of the body; symptoms differ from patient to patient

Typical symptoms include:

• blurriness in the central visual field that affects only one eye, may be accompanied by pain upon eye movement
• double vision
• loss of vision/hearing
• odd sensation in legs, arms, chest, or face, such as tingling or numbness (neuropathy) 

• weakness of arms or legs

• cognitive disruption, including speech impairment and memory loss
• heat sensitivity (symptoms worsen or reappear upon exposure to heat, such as a hot shower)
• loss of dexterity

• difficulty coordinating movement or balance disorder

• difficulty controlling bowel movements or urination

• fatigue

gait ataxia: 
People with cerebellar ataxia may initially present with poor balance, which could be demonstrated as an inability to stand on one leg or perform tandem gait. As the condition progresses, walking is characterized by a widened base and high stepping, as well as staggering and lurching from side to side.[1]Turning is also problematic and could result in falls.

dysarthria: 

a condition in which problems occur with the muscles that help one talk; this makes it very difficult to pronounce words. It is unrelated to any problem with understanding cognitive language.[3] Any of the speech subsystems (respiration, phonation, resonance, prosody, and articulation) can be affected, leading to impairments in intelligibility, audibility, naturalness, and efficiency of vocal communication.

Individuals with dysarthria may experience challenges in the following:

• Timing
• Vocal quality
• Pitch
• Volume
• Breath control
• Speed
• Strength
• Steadiness
• Range
• Tone

Examples of specific observations include a continuous breathy voice, irregular breakdown of articulation, monopitch, distorted vowels, word flow without pauses, and hypernasality.