104年繼續教育藥物濫用之治療本質、政策與復健機構設置

104 年台灣成癮科學學會持續教育 (系列二)
主題：探討藥物濫用之治療本質、政策與醫療復健機構設置
日期：104 年 7 月 4 日 (星期六) PM 13:30~18:30
地點：林酒店 7 樓柏林廳地址：台中市西屯區朝富路 99 號
主辦單位：台灣成癮科學學會
Time Topic Speaker Moderator
13:00-13:30 Registration
13:30-13:35 Opening 衛福部陳快樂司長
The nature of treatment in substance 邱南英院長陳展航主任

13:40-14:30
abuse 彰基鹿東分院台中榮總
14:30-14:40 Break
Neurobiology and management of 黃尚堅主任王作仁副院長

14:40-15:30
Opioids 台灣成癮科學學會部立嘉南療養院
Neurobiology and management of 黃介良主任楊延光教授
15:30-16:20 stimulants (Amphetamine, Ketamine,
中國醫藥學院成大醫學院
Cocaine and club Drug)
16:20-16:40 Break
Rehabilitation settings: from inpatient 林滄耀主任諶立中副局長

16:40-17:30
to Community-based Treatment 部立草屯療養院新北市衛生局
How to establish a consistent policy in 洪嘉均秘書長

黃三原理事長
17:30-18:20 drug intervention: from government 黃三原理事長
台灣成癮科學學會
to popular education. 台灣成癮科學學會
18:20-18:40 Discussion all all
＊台灣成癮科學學會 5 學分、台灣精神醫學會繼續教育 5 學分及衛福部藥癮治療相關繼續教育 5

小時
＊上課資料以 Textbook of substance abuse treatment, AJP 2014 年出版為主; 臨床及研究經驗當輔助
教材; 課後考試以書本一般成癮概念及臨床經驗為主 (每位講師出 6-8 題)
1
Nan-Ying Chiu
邱南英院長簡歷
服務單位：(中文) 彰化基督教醫療財團法人鹿東基督教醫院(英文)
Lutung Christian Hospital
簡歷：邱南英醫師畢業於中山醫學大學醫學系，曾服預備軍官役擔任
陸軍野戰步兵師軍醫官兼衛生排排長，退伍後於彰化基督教醫
院內科部、精神科及台灣大學醫學院附設醫院精神醫學部接受
住院醫師訓練，之後任職為財團法人彰化基督教醫院精神科主
治醫師、精神科主任、睡眠醫學中心主任。財團法人彰化基督
教醫院鹿東分院成立後成為該院院長兼財團法人彰化基督教醫
院體系精神科主任，鹿東分院後更名為鹿東基督教醫院，曾任
該院院長。現為鹿東基督教醫院永久主治醫師。擁有中華民國
醫師執照、中華民國精神科專科醫師執照、台灣老年精神醫學
會老年精神專科醫師證照、台灣成癮科學學會次專科證書、台
灣睡眠醫學學會睡眠醫學專科醫師證書、台灣團體心理治療學
會團體心理治療師證書、台灣團體心理治療學會團體心理治療
督導證書。為中華民國教育部部定助理教授，曾經於曉明女中、
田中少年輔育院、中台醫護技術學院、仁德醫護專科學校、新
竹教育大學、長榮大學任教，現為中山醫學大學、彰化師範大
學兼任助理教授，也在中國醫藥大學、亞洲大學教書。為多個
學會、協會的會員，曾擔任彰化縣康復之友協會理事長、真善
美基金會董事，也曾任台灣憂鬱症防治學會理事、台灣向日葵
全人關懷協會、台灣老年精神醫學會、台灣自殺防治學會理事、
台灣成癮科學學會的理事或監事，目前為台灣精神醫學會、台
灣精神分裂症研究學會、台灣醫界菸害防治聯盟、台灣生物精
神醫學暨神經精神藥理學會的理事或監事。是多家大學的學生
實習督導，亦擔任政府機關多個委員會的委員。曾在美國杜克
大學醫學中心精神醫學與行為科學部擔任研究員。曾為數個期
刊審稿，現為台灣精神醫學期刊執行編輯。研究的興趣為情感
疾患、思覺失調症、菸癮、成癮科學、睡眠醫學、精神治療藥
物…等，迄今共參與 86 案研究計劃，至目前期刊論文有 69 篇，
口頭報告與壁報論文共 171 篇，曾著作「香菸知多少」一書，
其他撰寫及翻譯的書籍章節共 46 種。所獲獎項如法務部和衛生
署獎牌、彰化縣醫療奉獻獎。
The Nature of Treatment in
Substance Abuse
Dr. Nan-Ying Chiu

邱南英醫師
Science in the treatment of

substance abuse
• It is an undeniable fact that substance use disorders (SUDs) were
neglected by organized medicine for many years.
• In the 1930s the founders of Alcoholics Anonymous (AA) realized

that alcoholism is a disease and that it would someday be treated
like other medical illnesses.
• Since the 1970s, science began to be applied to the understanding

and treatment of SUDs, remarkable facts have been learned about
what happens to the brain when addicting drugs are consumed.
1
substance abuse
• The attitude of the physicians toward treatment began to change
with the development of the methadone maintenance treatment
(MMT) in the 1960s.
• The poor treatment given to patients suffering from SUDs in the

United states and the world were seen .
• High relapse rate of the SUDs patients after treatment were noted.
Progress in research of treatment

of substance abuse
• There are specific behavioral and pharmacological approaches to
substance abuse treatment that have been found effective in
numerous randomized controlled trials.
• Only about one in 10 individuals with SUDs receives any treatment,

and those who do usually do not get evidence-based treatment
techniques.
2
Most common treatment of SUDs
• The most common form of treatment for SUDs is probably
detoxification, which, in reality, is not treatment at all.
• Simply reducing withdrawal symptoms by giving a short-term

medication may make the patient more comfortable, but there is no
long-term benefit.
• Addiction is a chronic medical disease of the brain. It makes no

sense to treat addicted patients with detoxification and brief therapy
(28-day inpatient rehabilitation) without long-term follow-up therapy
for at least 6-12 months.
Training of treatment providers

of substance abuse
• Most of those specializing in the treatment of addictive disorders
have no training on the biological basis of addiction and no training
in medications for addiction.
• Many addiction counselors actively try to discourage the use of

medications.
• SUDs are among the most common of all disorders requiring

treatment by physicians.
• The training of treatment providers of SUDs is essential.
• The ethical issue of treatment of SUDs should be considered.
3
substance abuse-key points
• Detoxification is pointless unless followed by long-term treatment of
at least 6-12 months.
• U.S. Food and Drug Administration-approved medications to prevent

relapse are available but rarely used.
• The neuroscience of addiction is very advanced compared with that

of other mental illnesses.

substance abuse-key points
• Addiction should be treated as a chronic disease such as diabetes
or hypertension. Medications may need to be continued indefinitely.
• The Affordable Care Act requires that insurers provide treatment

equal to that available for other chronic diseases such as diabetes
or hypertension.
• There is a great lack of physicians and other therapists educated on

the scientific knowledge already available on the nature of addiction.
All medical schools require training in this subject.
4
Assessment of the
substance abuse patient
• A number of factors influence the accurate identification,
assessment, and diagnosis of substance-related disorders .
• The factors include the clinical setting, the style of interviewing, the
attitude of the clinician, and patient characteristics such as the
presence of co-occurring medical and psychiatric disorders and the
stage of use or abuse of the substance.
The goals of assessing

patients with SUDs
• Identify the presence of substance-related disorder, as well as signs
of harmful or hazardous use so that prevention and early
intervention may take place.
• Make an accurate diagnosis and relating this to any other co-

occurring medical or psychiatric disorders.
• Identify barriers to treatment as well as strengths and supports.
• Assess and enhance the patient’s motivation to change.
• Formulate and help to initiate appropriate evidence-based

interventions and treatments.
5
Eliciting the substance
abuse history
• Interviewing style: The clinician’s attitude and style of history taking
can facilitate a thorough and accurate assessment. Asking questions
in an honest, respectful, and matter-of-fact manner is likely to be
most effective. Maintaining a nonjudgmental stance is helpful to
patients.
• Patient characteristics: Age, gender, partner of marital status, legal

and employment status, culture, and ethnicity; level of insight into as
well as personal explanation for the nature of the problem;
psychiatric or medical comorbidity; stage in the course of illness
(e.g., first treatment, recovery, recent relapse); current phase of use
9e.g., intoxicated, withdrawing, interepisode); stage of readiness for
change.
Diagnosing substance-related
disorders
• Substance use disorder
• Substance intoxication
• Substance withdrawal
• Other substance-induced disorders
6
Substance-related and addictive
disorders in DSM-5
DSM-5物質相關及成癮障礙症
• Substance-related disorders
substance use disorder 物質使用障礙症
substance intoxication 物質中毒
substance withdrawal 物質戒斷
other substance-induced disorders
unspecified substance-related disorders
• Non-substance-related disorders
gambling disorder 嗜賭症
DSM-5診斷的重要改變
• 物質相關及成癮障礙症(substance-related and addictive disorders)含
兩大部份，一為非物質相關疾患只有嗜睹症，另一為物質相關障礙症
(substance related disorder)，下面分為：物質使用疾患(substance
use disorder)、物質中毒、物質戒斷、其他物質引發的疾患、非特定
性物質相關疾患。
• 在DSM-5不再使用濫用(abuse)和依賴(dependence)，診斷標準依有
無戒斷為10或11項，在12個月期間內符合2項及以上就是使用疾患，
但依項次的多少區分成輕度、中度、重度，也需作特別註明。
• 相關的物質有酒精、咖啡因、大麻、幻覺劑、吸入劑、類鴉片製劑、
鎮靜劑、安眠劑、抗焦慮劑、菸草和其他。
7
Substance-related disorders in DSM-5
DSM-5物質相關障礙症
• Alcohol-related disorders
• Caffeine-related disorders
• Cannabis-related disorders
• Hallucinogen-related disorders
• Inhalant-related disorders
• Opioid-related disorders
• Sedative-, hypnotic-, or anxiolytic-related disorders
• Stimulant-related disorders
• Tobacco-related disorders
• Other substance-related disorders
DSM-5物質使用障礙症的診斷準則
一種適應不良的物質使用模式，造成功能明顯減損。一年內有以下兩個
或兩個以上的症狀則屬之。
•比預期花更多時間使用或使用更大量。
•努力想減少或控制使用但不成功。
•花費許多時間以取得該物質。
•強烈渴望使用該物質。
•無法實踐責任。
•重複造成人際關係問題。
•放棄或減少社交、嗜好或工作。
•在對身體有害的情境下仍重複使用。
•即使知道使用物質會引發問題仍繼續使用。
•耐受性。
•(戒斷症狀。)
8
Substance-related disorders in DSM-5
DSM-5物質相關障礙症
• Substance use disorders-no abuse , no dependence,
10-11 symptoms 不再使用濫用和依賴
Current severity:目前的嚴重度
mild: presence of 2-3 symptoms
moderate: presence of 4-5 symptoms
severe: presence of 6 or more symptoms
Specify if: 特别註明 In early remission 早期緩解

In sustained remission 維持緩解
on maintenance therapy 維持治療
In a controlled environment 在控制的環境
• Substance-induced disorders
Substance use disorders in DSM-5

DSM-5物質的種類
• Alcohol
• Cannabis
• Phencyclidine
• Other hallucinogens
• Inhalants
• Opioids
• Sedatives, hypnotics, or anxiolytics
• Stimulants
• Tobacco
• Other (unknown)
9
Substance-induced disorders in DSM-5
DSM-5物質引發的障礙症
• Intoxication: with use disorder, without use disorder, with perceptual

disturbances, without perceptual disturbances
• Withdrawal: without perceptual disturbances, with perceptual

disturbances
• Other substance/medication-induced mental disorders
Substance intoxication in DSM-5

DSM-5物質中毒
• Alcohol
• Caffeine
• Cannabis
• Phencyclidine
• Other hallucinogens
• Inhalants
• Opioids
• Stimulants
• Other (or unknown)
10
Substance withdrawal in DSM-5
DSM-5物質戒斷
• Alcohol
• Caffeine
• Cannabis
• Opioids
• Stimulants
• Tobacco
• Other (or unknown)
DSM-5 Alcohol-related disorders

DSM-5酒精相關的障礙症
• Alcohol use disorder

• Alcohol intoxication
• Alcohol withdrawal
• Other alcohol-induced disorders
• Unspecified alcohol-related disorder
11
DSM-5 Caffeine-related disorders
DSM-5咖啡因相關的障礙症
• Caffeine intoxication
• Caffeine withdrawal
• Other caffeine-induced disorders
• Unspecified caffeine-related disorder
DSM-5 Opioid-related disorders

DSM-5類鴉片相關的障礙症
• Opioid use disorder

• Opioid intoxication
• Opioid withdraawal
• Other opioid-induced disorders
• Unspecified opioid-related disorder
12
DSM-5 Tobacco-related disorders
DSM-5菸草相關的障礙症
• Tobacco use disorder

• Tobacco withdrawal
• Other tobacco-induced disorders
• Unspecified tobacco-related disorder
Other substance/medication-induced
mental disorders in DSM-5
DSM-5其他物質/藥物引發的精神疾患
• Psychotic disorders
• Bipolar and related disorders
• Depressive disorders
• Anxiety disorders
• Obsessive-compulsive and related disorders
• Sleep disorders
• Sexual dysfunctions
• Delirium
• Neurocognitive disorders
13
Content of the interview
for substance abuse
• History of the substance-related disorder
• Psychiatric history
• Medical history
• Family history
• Social and developmental history
• Physical examination
• Mental status examination
• Additional information: a patient’s significant others can often offer
important additional information, biological markers can help in
detecting the degree and regularity of the patient’s substance use.
History of the
substance-related disorder
• Age at first substance use
• Frequency of substance use
• Amount of substance taken during an episode of use
• Route of administration for the substance
• Consequences associated with substance us
• Treatment history
• Periods of abstinence
• Relapses
14
Psychiatric history
• There is an increased prevalence of substance-related disorders
among patients diagnosed with other psychiatric disorders.
• Patients diagnosed with SUDs are more likely to have a co-
occurring psychiatric disorder.
• The co-occurring SUDs and psychiatric disorders can each worsen
the prognosis for the other disorder.
• Integrated treatment improves and enhances outcomes for both
disorders.
• It is import to assess SUDs in patients presenting for treatment of
other psychiatric disorders and equally important to assess
psychiatric disorders among patients presenting for treatment of
Suds.
Medical problems
associated with alcohol
• Blackouts
• Hangovers
• Withdrawal tremors
• Withdrawal seizures
• Delirium tremens
• Aspiration pneumonia
• Cerebellar degeneration
• Gastritis
• Gastroesophageal reflux disease
• Hepatitis
• Pancreatitis
• Wernicke-korsakoff syndrome
15
Signs and symptoms of sedative,
hypnotics, or anxiolytics intoxication
• Slurred speech
• Incoordination
• Nystagmus
• Unsteady gait
• Impairment in cognition (e.g., attention, memory)
• Stupor or coma
Signs and symptoms

of opioids withdrawal
• Dysphoric mood
• Nausea or vomiting
• Muscle aches
• Lacrimation or rhinorrhea
• Pupillary dilation, piloerection
• Diarrhea
• Yawning
• Fever
• Insomnia
16
Assessment of the
-key points
• Successful treatment of substance-related disorders depends on a
careful, accurate assessment and diagnosis.
• Accurate assessment is facilitated by interview settings that provide

privacy and patient confidentiality and that permit adequate time to
ask key questions, to follow up on positive patient responses, and to
give feedback to the patient.
• A substance use history should be obtained from all patients

presenting for treatment.
Assessment of the
-key points
• Patient assessment can be influenced by a number of patient
characteristics, including the patient’s age, gender, ethnicity, and
legal, marital, and employment status; degree of insight into the
nature of the problem; medical or psychiatric comorbidity; stage in
the course of illness (e.g., recovery, recent relapse, first treatment);
current phase of use (e.g., intoxication, withdrawal, interepisode);
and stage of readiness for change and motivation.
17
Assessment of the
-key points
• A complete substance use assessment requires eliciting the history
of use for all the major categories of substances, with a focus on
age at first use, frequency and amount of use, consequences of use,
substance abuse treatment history, and complete psychiatric,
medical and social, and developmental histories.
• Collateral informant interviews, standardized questionnaires, and

biological testing may also provide additional helpful information for
some substance abuse patients.
Screening and brief intervention

• Screening and brief intervention (SBI) is now a well-established
clinical practice supported by evidence from controlled clinical trials.
• SBI is simultaneously a preventive intervention aimed at recurring

behavioral risks and an initial step in the management of moderate
to severe substance use disorders.
18
Screening
• Screening does not simply mean testing. Screening is a clinical
activity performed for patients without known symptoms of the target
condition.
• SBI is not appropriate for people seeking help for symptoms of

substance use disorders; such patients should receive assessments
and treatment.
Screening tools
• Many screening tools have been validated for their accuracy.
• The key issues for selecting a tool for practice are brevity, wide
applicability to populations, and validity for detecting the full
spectrum of unhealthy use.
19
Screening tools
• The CAGE questions (Mayfield et al. 1974).” Have you ever felt you
should Cut down on your drinking? Have people Annoyed you by
criticizing your drinking? Have you ever felt bad or Guilty about your
drinking? Have you ever taken a drink first thing in the morning [Eye-
opener] to steady your nerves or get rid of a hangover?”
• The Michigan Alcoholism Screening test (MAST) (Selzer 1971,

1975).
• Single screening questions (SSQs) are brief and have been

validated in primary medical care settings. “How many times in the
past year have you used an illegal drug or used a prescription
medication for non-medical reason?”
Screening tools
• The Drug Abuse screening Test (DAST) (Skinner 1982).
• The Alcohol Use Disorders Identification Test (AUDIT) (babor et al.

2001).
• The AUDIT-C (Bradley et al. 2007).
• The 4P’s Plus for screening for alcohol and drug use in pregnancy
(Chasnoff et al. 2007).
20
Assessment of
substance use disorder
• Assessment of use
• Assessment of consequences
• Assessment of the patient’s perception and readiness to change
Brief counseling interventions

• Performing a brief intervention: A brief intervention (BI) involves
counseling to help the patient abstain from or reduce substance use,
or reduce the risk of such use.
• BI consists of feedback, advise, and goal setting. The counseling is

done based on the principles of motivational interviewing.
• After giving advise, the clinician should ask what the patient thinks
and assess what the patient’s goals are and what the patient thinks
might work to achieve them. Telling patients to quit and how to do it
is not likely to be effective.
21
Brief counseling interventions
• Reflective listening is a key skills of motivational interviewing that is
helpful in brief behavior change counseling.
• Once a patient decides to make a change or has changed, working

on motivation to change becomes less the focus and the work is to
assist the patient in figuring out what to do and how to do it.
Evidence for efficacy of brief intervention

among patients identified by screening
• The effect of BI is to decrease risky drinking by about 10%-12% at 1
year and by about 3 drinks per weeks. This is a small effect.
• Data of BI at present are insufficient to draw firm conclusions about

impact on outcomes (e.g., reduction in motor vehicle crashes, less
hospital or emergency department utilization, or even lower
mortality).
• Most studies in trauma centers have been negative, finding no

efficacy of BI.
22
-key points
• Brief screening tools are valid for detecting unhealthy substance use.
• Brief intervention based on the principles of motivational

interviewing can have efficacy for decreasing substance use and its
consequences.

-key points
• Brief intervention for people identified by screening has best proven

efficacy for unhealthy alcohol use (excluding moderate to severe
alcohol use disorder) when done multiple times in primary care.
• The efficacy of screening and brief intervention in hospitals, trauma

settings, and emergency departments, as well as for drugs other
than alcohol, is uncertain.
23
Patient placement criteria
• Patient placement criteria are decision rules that guide care
providers and care managers in assigning patients to the optimal
clinical and cost-effective level of use.
• Extensive reviews of the treatment outcome literature find that

treatment for addictive disorders is effective but that no single
treatment model or level of care is appropriate for all individuals
(Berglund et al. 2003; Institute of Medicine 1990; Miller et al. 2002;
NIDA 2009).
• The most widely used and researched patient placement criteria for
addiction treatment are the patient Placement Criteria (PPC) for the
Treatment of Substance-Related Disorders of the American Society
of Addiction medicine (ASAM 1996; Gasfriend and Mee-Lee 2003).
The ASAM Criteria

Contains information to expand application of the criteria to special
populations:
• Older adults
• Parents receiving addiction treatment concurrently with their children
• People in safety-sensitive occupations
• Criminal justice populations
• Tobacco use disorder
• Gambling disorder
24
Level of care of the ASAM criteria
• Level 0.5: early intervention

• Level 1: outpatient services
• Level 2: intensive outpatient/partial hospitalization
• Level 3: residential/inpatient services
• Level 4: medically managed intensive inpatient services
The ASAM criteria

A comprehensive evaluation of a patient’s immediate and longer-term
needs informs the treatment and service plan regarding the variety
and intensity of interventions necessary and the modalities and
strategies needed.
Principle guiding ASAM development and implications:

• Objectivity
• Choice of treatment levels
• Continuum of care
• Length of stay
25
The ASAM criteria
assessment dimensions
• Acute intoxication and/or withdrawal potential
• Biomedical conditions and complications
• Emotional, behavioral, or cognitive conditions and complications
• Readiness to change
• Relapse, continued use, or continued problem potential
• Recovery environment
Matching assessment and

treatment/placement
• Conduct multidimensional assessment
• Does patient have immediate needs with imminent risk in any of the
6 assessment dimensions?
• If imminent risk in intoxication/ withdrawal potential (Dimension1);

biomedical (Dimension 2); emotional, behavioral, cognitive
(Dimension 3):
Placement is in Level 4: medically managed intensive
inpatient
26
treatment/placement
• If imminent risk in relapse, continued use (Dimension 5); recovery
environment (Dimension 6):
Placement is in Level 3: supportive living environment or
residential level
• If no immediate needs, evaluate multidimensional severity and level

of function to determine treatment priorities and “dose” and intensity
of services needed

treatment/placement
• If dose and intensity of services requires less than 9 hours/week:
Placement is in Level 1: outpatient
If dose requires 9-19 hours/week:
Placement is in Level 2.1: intensive out patient services
If dose is 20 hours/week or more:
Placement is in Level 2.5: partial hospital
27
treatment/placement
• Repeat assessment of multidimensional severity and level of
function to determine need for continued stay in current level of care;
or to transfer or discharge to a less or more intensive level of care
depending on client’s progress of deterioration
Revision of the ASAM Criteria

• The most recent edition of ASAM Criteria established in 2013.
• Level 2 : intensive outpatient care
• Level 2.1: evening care or day treatment programs
• Level 2.5: partial hospitalization
• Level 3 : residential inpatient care
• Level 3.1: supervised domiciliary or working halfway house
• Level 3.3: modified, individualized treatment for cognitively impaired
patients
• Level 3.5: therapeutic community or residential treatment center
• Level 3.7: residential rehabilitation with onsite nursing supervision
28
-key points
• Treatment outcome research demonstrates that treatment for
addictive disorders is effective but that no single model or level of
care is appropriate for all individuals.
• The services themselves and where they are delivered should

therefore be individualized to each patient’s assessed needs.

-key points
• The patient placement criteria incorporate multidimensional

assessments of severity of illness and level of function; problem and
priority identification; treatment matching needs to services; and
level-of-care placement within a broad continuum of care.
• Ongoing assessment of progress and treatment response

determines movement to less or more intensive levels of care.
29
-key points
• The most widely used and researched patient placement criteria tool
for addiction treatment is the American Society of Addiction Medicine
(ASAM) criteria, first published in 1991 and revised in 1996, 2001,
and 2013.
• The ASAM criteria include a broad range of levels of care. Although

this broad range of options could provide longer lengths of care and
monitoring using the same or even fewer resources, benefits plans,
public funding, and provider programs are frequently restricted to a
limited continuum of care.
• Almost 2 decades of research o the ASAM criteria support the

predictive validity and cost-effectiveness of the use of these criteria.
Thank You
for
Your Attention
30
Shang-Chien Huang
黃尚堅主任簡歷
學歷：
陽明大學神經科學研究所暨中研院生醫所合辦分子神經醫學組博士候選人(since 2009)
中國醫藥大學醫學系醫學士
經歷：
現任童綜合醫院精神科主治醫師及藥酒癮精神醫學組負責醫師
現任台灣成癮科學學會常務理事(since 2014)
童綜合醫院人體試驗委員會委員(since 2012)
台中市衛生局藥癮戒治督導考核委員(since 2012)
老年精神專科醫師甄審考試口試委員(since 2013)
Reviewer, British Journal of Psychiatry (SCI IF=7.343)
曾任台灣成癮科學學會理事(2011-2014)
獲獎/榮譽：
童綜合醫院臨床技能中心優良教師(2014)
大台中醫師公會醫療貢獻獎(2013)
教育部獎助出席國際會議發表論文(2009 美國精神醫學會年會)
商業週刊百大良醫推薦好醫師(2009)
專業執照/會員：
精神科專科醫師
成癮專科醫師
老年精神專科醫師
中華民國人類遺傳學會會員
執行中研究計畫：(略)
著作：(略)
興趣： 1. Genetics on neuropsychiatric diseases – Huntington’s disease, heroin
dependence, and schizophrenia
2. Functional image – fMRI and DTI
Neurobiology and Management
of Opioids
童綜合醫院心身科主治醫師暨藥酒癮醫學組負責醫師
國立陽明大學神經科學研究所分子神經醫學組博士候選人
台灣成癮科學學會常務理事
黃尚堅醫師
2015.07.04
Opioid Addiction:
It’s a Brain Disease !
1
Vulnerability
Why do some people become
addicted while others do not?
We Know There’s a
Big Genetic Contribution to
Drug Abuse and Addiction…
….Overlapping with Environmental
Influences that Help Make
Addiction a Complex Disease.
2
Circuits Involved In Drug Abuse and Addiction
All of these must be considered

in developing strategies to
effectively treat addiction
PC
VT
NA
3
Natural Rewards Elevate Dopamine Levels
FOOD SEX
200 200
DA Concentration (% Baseline)
NAc shell
150 150
% of Basal DA Output
100 100
Copulation Frequency
15
Empty 10
50
Box Feeding
5
0 0
0 60 120 180 Female Present
Time (min)
Sample 1 2 3 4 5 6 7 8 Mounts
Number Intromissions
Ejaculations
Di Chiara et al., Neuroscience, 1999. Fiorino and Phillips, J. Neuroscience, 1997.
Endogenous Opioid System
Opioid receptor μ, MOPR, OPRM1 gene

-成癮、止痛、嗜睡、欣快感、癢覺、呼吸抑制
Opioid receptor κ, KOPR, OPRK1 gene

-止痛、嗜睡、利尿、呼吸抑制
Opioid receptor δ, DOPR, OPRD1 gene

-止痛、幻覺
4
9
10
5
11
Neurobiology of Tolerance, Dependence, and

Addiction
 Tolerance – The need for increasing amounts

of compound to achieve a specific physiological
or pharmacological effect.
 Dependence – The appearance of specific

physiological signs and symptoms following
abrupt cessation of chronic administration.
 Addiction – “ drug hunger” or “drug craving”

with compulsive drug seeking and drug taking.
6
Animal Behavioral Models: Addiction-Related
Neurobiology
Drug self-administration.
Impulsivity
Neurobiological changes
Endogenous and Exogenous Opioid Role in

Stress Responsivity
 Stress Responsivity and the Addictions – profound

disruption of the stress-responsive HPA axis, CRF,
ACTH
 Genetic and epigenetic effects on MOPR function –

C17T and A118G SNP, methylation in promotor
regions of the gene encoding for MOPR.
7
Opioid Detoxification
15
16
8
17
18
9
Naloxone Pharmacology
 Acts as a competitive antagonist at the mu receptor
 Binds to the mu receptor
 Prevents binding of other opioid agonists to the
receptor
 Reverses overdose
 Precipitates withdrawal when injected in opioid
dependent individuals
 Short half life (t = 45 minutes)
 Rapidly reaches and binds to the mu receptor when
injected1
 Bioavailability less than 10% via sublingual
administration
1. Gilman et al, (1990) Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 8th Ed, New York: Pergamon Press
替代療法的觀念
 Use long acting opioid medication to replace the
“short acting oipoid (heroin) use behavior”
 以長效的鴉片促動劑藥物維持藥癮個案的生理功
能正常，減少個案對自己及對社會的損害
 Harm reduction approach
 以減輕傷害為出發的一種治療方式，提供有效且
足夠劑量的藥物，以取代非法鴉片類藥物的使用
10
台灣海洛因濫用現況
 海洛因屬第一級毒品(成癮性極高、戒除困難)
 每人每日注射2000-2500元
 海洛因注射人數:10-13萬人(40萬人?)
 自民國73年至99年底，國內愛滋帶原累積通報個案數已
超過2萬(20,057)人，其中藥癮者即有6,448人，佔
32.15%
 透過解毒(detoxification)與戒除(abstinence)療法
成功獲得治療的病人，高達70%以上，將於一到兩年內
復犯(relapse)並使用違禁鴉片
資料來源：行政院衛生署
11
What Is HIV / AIDS?
• Acquired immunodeficiency syndrome (AIDS) is caused by the
human immunodeficiency virus (HIV).
• HIV attacks and destroys white blood cells, causing a defect in
the body’s immune system.
• The immune system of an HIV-infected person becomes so
weakened that it cannot protect itself from serious infections.
When this happens, the person clinically has AIDS.
• AIDS may manifest as early as 2 years or as late as 10 years after
infection with HIV.
24
12
Modes of Transmission
• Sexual – predominant mode of transmission
globally
• Risk per episode

– receptive vaginal intercourse: 0.1-0.2%
– insertive vaginal intercourse: 0.1%
– receptive anal intercourse: 0.1-3%
– insertive anal intercourse: 0.06%
– receptive oral intercourse: 0.04%
Natural History of HIV Infection

Without the Use of Antiretroviral Tx
Primary Death
1200 Infection + Acute HIV syndrome 107
Wide dissemination of virus Opportunistic
1100
Seeding of lymphoid organs Diseases
HIV/RNA Copies per ml Plasma
1000 106
900
Clinical latency
CD4 + T Lymphocyte Count (cells/mmm3)
800
Constitutional 105
700
Symptoms
600
500 104
400
300
103
200
100
0 102
0 3 6 9 12 1 2 3 4 5 6 7 8 9 10 11
Weeks Years
Source: Fauci, A., Pantaleo, D., Stanley S., Weismann, D. Annals of Internal Medicine 124: 6754-3, 1996
13
開始治療時機
臨床症狀 CD4細胞值病毒量建議
症狀出現任何數值任何數值治療服藥
沒有症狀 ≦200 任何數值治療服藥
cells/mm3
沒有症狀 200~350 任何數值大部分醫師建議應該開始治
cells/mm3 療，但有人有不同意見
沒有症狀 >350 >100,000 有些醫師建議開始治療，另
cells/mm3 (RT-PCR) 一些醫師認為可以會延後治
療，繼續追蹤。
沒有症狀 >350 <100,000 大部分醫師可能會延後治療，
cells/mm3 (RT-PCR) 繼續觀察。因為3年進展為
AIDS的機會<15%。。
14
美沙冬替代療法~目的
‧減少非法物質使用
‧增進身體健康
‧減少傳染性疾病傳播如HIV及HCV
‧減少非法活動
‧增加工作機會
‧降低社會成本
‧降低死亡率
‧間接目的包括；諮商、就業服務及空針交換方
案
Methadone Maintenance
 Developed in the mid-1960s
 Day1: 20-30mg (not exceed 40mg), then

increase 5-10mg every 2-7 days
 Maintenance dose: 70-120mg/day generally
15
16
Drugs Interactions with Methadone
Potential Inducers of CYP3A4-Mediated Metabolism — may ↓ methadone level
Methadone Buprenorphine
Efavirenz Methadone level decreased by 60%,
(Stocrit®, opiate withdrawal common, increase
↓Cmin by 49% and
EFV) methadone dose often necessary. AUC by 51%
Titrate methadone dose to effect No withdrawl
demonstrated
Nevirapine Methadone level decreased by 46%, Unknown
(Viramune®, opiate withdrawal common, increase
EFV) methadone dose often necessary.
Titrate methadone dose to effect
Available at: http://aidsinfo.nih.gov/guidelines.
Drugs vs Methadone Interactions

Lopinavir / Methadone level decreased by 53%, No clinically

Ritonavir Opiate withdrawal may occur. Monitor significant effect
(Kaletra®, LPV/r) and titrate dose if needed
Ritonavir Methadone level decreased by 37%, No clinically
(RTV) Monitor and titrate dose if needed significant effect
Nelfinavir Methadone level decreased by 40%, No clinically
(NFV) Opiate withdrawal is rarely occurred significant effect
and priori dosage adjustment are not
needed. Monitor and titrate dose if
needed
Available at: http://aidsinfo.nih.gov/guidelines.
17
Drugs vs Methadone Interactions
Indinavir No interaction Unknown

(IDV)
Saquinavir / Methadone level decreased by 20%, Unknown
Ritonavir Opiate withdrawal is rarely occurred and
(SQV/r) priori dosage adjustment are not needed.
Monitor and titrate dose if needed
Atazanavir No interaction Unknown
(ATV)
Atazanavir / Unknown May result in
Ritonavir symptoms of
(ATV/r) opiate excess
Available at: http://aidsinfo.nih.gov/guidelines. Revision May 2006.
Contraindications of Methadone
• Hypersensitivity to methadone.
• A history of respiratory depression, especially with
cyanosis, excessive bronchial secretions during acute
asthma attack (as with other opioids).
• Acute alcoholism, head injury, raised intracranial pressure.
• Treatment with MAO inhibitors.
• Active ulcerative colitis or Crohn’s disease.
• Severe hepatic impairment.
• Biliary and renal tract spasm.
Precautions : elderly patients; hepatic impairment
18
Death Attributed to Methadone
• 15% of deaths attributed to methadone occurred during the first
time of MMT, corresponding to 51% of all deaths attributed to
methadone in subjects on MMT.
• About 1/6 of all deaths attributed to methadone occurred during
the first few days on MMT.
Pharmacodynamic Drug Interactions

• Almost all methadone-related deaths occur in the
presence of other CNS depressants.
– Opioids are CNS depressants and may increase the risk of
respiratory depression when used with methadone.
– Benzodiazepines do not usually cause respiratory depression
on their own, but may increase the risk of respiratory
depression when methadone is present.
– Alcohol is a CNS depressant capable of causing respiratory
depression and death. The combination of non-fatal doses of
alcohol and methadone may cause fatal toxicity, particularly in
males.
– Tricyclic antidepressants (TCAs) can cause respiratory
depression and pulmonary edema at high doses, and may
interact with methadone to increase the risk of toxicity. (e.g.
amitirptyline, tofranil, etc.)
19
Buprenorphine Treatment:
Training for Multidisciplinary Addiction Professionals
 Discusses legislation that permits office-based

buprenorphine treatment
 Examines the science of addiction
 Explains how buprenorphine works
 Offers an overview of patient selection issues
 Reviews various patient, counseling, and

therapeutic issues
http://www.drugabuse.gov/sites/default/files/files/BupTx_Factsheet.pdf
Scientific research has led to effective

treatments for opiate addiction:
 In the 1960’s, methadone gained recognition as an
effective treatment for heroin addiction. Administered
daily, methadone treatment is currently regulated so that
only specialized clinics can provide it.
 Naltrexone, an opioid receptor blocker, joined the
medications inventory in 1984. It proved to be highly
effective in reversing the effects of opiate overdose, but
poor treatment adherence has hampered its utility to
promote abstinence.
 Buprenorphine, the newest medication in our toolkit, is
a long-acting partial agonist that acts on the same
receptors as heroin and morphine.
 These medications have also helped reduce the spread of
HIV/AIDS—from a peak of more than 25,000 new cases
in 1993 to fewer than 10,000 cases in 2003.
20
Why Is Buprenorphine Treatment a
Good Choice?
 Buprenorphine is just as effective as moderate
(60 mg per day) doses of methadone.
 Buprenorphine is mildly reinforcing, encouraging
good patient compliance.
 Buprenorphine relieving drug cravings without
producing the same intense “high” or dangerous
side effects.
 Compared to placebo plus counseling, the
majority of patients receiving buprenorphine plus
counseling continue with treatment after one
year (75% retention).
Why Is Buprenorphine Treatment a

Good Choice?
 Buprenorphine is a synthetic opioid medication
that does not produce the euphoria and sedation
caused by heroin or other opioids but is able to
reduce or eliminate withdrawal symptoms
associated with opioid dependence and carries a
low risk of overdose..
 Suboxone, which combines buprenorphine with
the drug naloxone, an antagonist (or blocker) at
opioid receptors. Naloxone has no effect when
Suboxone is taken as prescribed, but if an
addicted individual attempts to inject Suboxone,
the naloxone will produce severe withdrawal
symptoms.
http://www.drugabuse.gov
21
Facts from National Survey on Drug Use
and Health in USA
 In 2010, an estimated 12 million people abused
prescription pain relievers in the past year and
more than 600,000 abused heroin.
 About 2 million people aged 12 or older used a
prescription pain reliever non-medically for the
first time in 2010. Initiation rates for prescription
drug abuse were second only to marijuana rates.
 Treatment admissions for primary abuse of
prescription pain relievers surged from 18, 300 in
1998 to 113, 506 in 2008.
 The number of unintentional overdose deaths
from prescription pain relievers has soared in the
U.S., quadrupling since 1999.
Good experiences in USA

 The FDA approved
Subutex® (buprenorphine)
and Suboxone®
(buprenorphine/naloxone)
in October 2002, making
them the first medications
to be eligible for prescribing
under the DATA (Drug
Addiction Treatment Act)
2000.
 To date, nearly 10,000
physicians have taken the
training needed to prescribe
these two medications.
22
Suboxone SL
 成份: buprenorphine and naloxone in a 4:1
ratio
 劑量/劑型:
 8mg/SL:BPN 8mg and NAL 2mg
 2mg/SL:BPN 2mg and NAL 0.5mg
 適應症：鴉片類物質成癮之替代療法
 第三級管制藥品
 2002, FDA approved
丁基原啡因Buprenorphine
 Suboxone 舌下錠(內含buprenorphine
HCl/Naloxone Dihydrate, 2/0.5及8/2 mg sublingual
tablet)
 Suboxone 添加Naloxone 的用意是防止被個案轉
移為注射使用,避免不當的濫用行為, prevent
diversion
 目前台灣已上市 Available in Taiwan
 Suboxone 8mg , 2mg
 Desud plus 8mg
23
丁基原啡因Buprenorphine
 安全性高 safety profile
 不會過量致死
 對於心臟功能影響小
 藥物交互作用少
 成癮性低 low abuse liability
 戒斷症狀輕微 mild withdrawal symptoms
 引發急性戒斷症狀 precipitated withdrawal
 接受度高，導入快速 easy induction
 濫用問題少 fewer abuse problems,三級管制藥品
schedule III
 價格較高 higher medication cost
Can Opioid Dependence Affect Behavior?
24
How Does SUBOXONE Work?
What Determines Opioid Effects
Receptor affinity (親和力)

–How tightly the drug binds to the
receptor
• Dissociation (解離速度)
–How fast the drug leaves the receptor
Intrinsic activity (內生活性)

–How much the drug stimulates the
receptor
25
Agonist or Antagonist?
 Full Agonist
- binds to the receptor
producing an almost linear
increase in physiological
effect
e.g. Heroin, Methadone,
Morphine
 Partial Agonist
- binds to the receptor but has
a ‘ceiling’ effect on receptor
activation
e.g. Buprenorphine
 Antagonist
- binds to the receptor but do
not produce a biological
response and are able to block
agonist effects
e.g. Naloxone;Naltrexone1;
Buprenorphine Pharmacology
 Semi synthetic opioid
Opiate Receptors
 Agonist (partial) for the mu (μ)
3 main types
opioid receptor and antagonist for
the kappa (κ) receptor Mu (μ)
Analgesia
Euphoria
 High affinity for the mu opiate Respiratory depression
Pupillary Constriction
receptor
Kappa (κ)
 Binds more tightly to the receptor than other Analgesia
opiate agonists or antagonists Dysphoria
Diuresis
Delta (δ)
 Slow dissociation rate from the ? Analgesia
receptor ? Dependence
 Long duration of action, low physical
dependence liability, milder withdrawal
 Highly lipophilic1
1. Lintzeris N et al, National Clinical Guidelines & Procedures for the Use of Buprenorphine in the Treatment of Opioid Dependence (2006).
26
Naloxone Pharmacology
 Acts as a competitive antagonist at the mu receptor
 Binds to the mu receptor
 Prevents binding of other opioid agonists to the
receptor
 Reverses overdose
 Precipitates withdrawal when injected in opioid
dependent individuals
 Short half life (t = 45 minutes)
 Rapidly reaches and binds to the mu receptor when
injected1
 Bioavailability less than 10% via sublingual
administration
Rationale for
Naloxone+Buprenorphine
(Suboxone)
Gordon, 2006 PO IV SL
Incorrect Incorrect Correct

Route Oral IV Sublingual
(diversion)
Buprenorphine NO YES YES
Absorbed?
Naloxone Absorbed? NO YES!!! NO !
Outcome 　　
(No Action) (withdrawal)
27
Blockade Effect
 Buprenorphine demonstrates dose related blockade
effect of other opioids, due to high occupancy rate of
receptors1
 A 16mg dose results in 95% of opiate receptors being occupied
 A 24mg dose results in 100% of opiate receptors being occupied2
Subjective effects:
blockade/tolerance
7 7 7 7
6
Buprenorphine 6
Buprenorphine 6
Buprenorphine 6
Buprenorphine
2 mg 4 mg 8 mg 16 mg
5 5 5 5
Rating
4 4 4 4
3 3 3 3
2 2 2 2
1 1 1 1
0 0 0 0
0 6 18 0 6 18 0 6 18 0 6 18
Cumulative hydromorphone dose (mg)
Adapted from Bickel et al., 1988
1. Bickel WK et al, J Pharmacol Exp Ther (1988) 247:47-53

2. Nutt D, personal communication
“Ceiling” Effects
Ceiling effect on respiratory

Subjective effects: “plateau”
depression
17
50
Drug effect
16
Human respiratory rate 40
15
Breaths/Minute
14 30
Score
13
20
12
10
11
10
0
0 1 2 4 8 16 32 P 1 2 4 8 16 32
PL Buprenorphine (mg, sl) Buprenorphine dose
Adapted from Walsh et al., 1994 Adapted from Walsh et al., 1994
28
舒倍生舌下錠(Suboxone)的特性
 阻擋海洛因發揮作用
 使用Suboxone 後再用海洛因，海洛因無法發揮作用
 病患會有清醒的感覺
 成癮性低
舒倍生舌下錠有頂端效應的特性，服用更高的劑量也不會有更高
的效果，也不會產生欣快感，因此成癮性低
 安全性高
舒倍生舌下錠有頂端效應的特性，呼吸次數不會因為劑量增加而
持續下降，因此服用高的劑量32mg/天，也相當安全
Pharmacokinetics
 Metabolism: Cytochrome P-450 3A4
 Elimination: urine: (30%) and feces (69%)
 Pregnancy Category: C
 Onset: 30- 60 minutes
 Peak: 1- 2 hours
 Elimination half life is 37 hrs
 Duration of action is dose related:
Dose Duration of Action
4 – 8mg 4- 12hrs
>8 – 16mg ~ 24hrs
>16 – 32mg 48 – 72hrs
 Steady state equilibrium is achieved after 3 – 7

days
 considerable individual variability
29
Interactions
 Sedatives e.g. Alcohol, Benzodiazepines
- Creates additive effect on opioid activity eg increase
respiratory depression, increases overdose potential
 Opioid agonists e.g.. Heroin, Methadone

- High affinity of Buprenorphine blocks opioids
binding to the receptors, potentially leading to
precipitate withdrawal
 Opioid antagonists e.g. Naltrexone, Naloxone

- A high dose of naloxone is required to reverse the
effects
 Inducers/Inhibitors of cytochrome P450 hepatic

enzymes e.g. HIV & HCV medications
- Limited clinical impact on Buprenorphine dosing1
Side Effects
 Similar to other opioids
 Constipation 便秘
 Disturbed sleep 睡眠紊亂
 Drowsiness 嗜睡
 Sweating 盜汗
 Headaches 頭痛
 Nausea 噁心嘔吐
 Precipitated withdrawal 加速戒斷症狀
 Experience of side effects can be variable

 side effects maybe experienced with one opioid medication
but not another1
30
Precipitated Withdrawal Graph
16
Severity of opiate withdrawal
Severity opiate withdrawal
14 14 Adapted from Lintzeris et al., 2003

12 12
10 10
8 8
6 6
4 4
2 2
0
0
0 2 04 2 6 4 8 6 128 1412 16
14 1618 18
20 2022 2224 24 2626
Time (hours)
Time (hours)
Precipitated withdrawalNot Not
Precipitated withdrawal enough
enough Buprenorphine
BPN: 4 mg
Not nearly enough BPN: 2 mg Enough BPN: 4 + 4 mg
從海洛因轉換到舒倍生舌下錠
導入期
第一天第二天第三天第四天第五天第六天第七天
第一劑 2mg 8mg 8mg 8mg 8mg 8mg 8mg
第二劑 2mg 2mg 8mg
第三劑 4mg 2mg
總劑量 8mg 12 mg 16 mg 8mg 8mg 8mg 8mg
投藥方式：
須置於舌下，直到完全溶解。若所需劑量超過兩錠，可一次
放入所有需服之藥量於舌下，或一次一錠置於舌下。
無論哪種方式，患者必須將之含住、置於舌下，直到藥物完全溶
解，未溶解前儘量不要吞口水；嚼碎或吞下藥物都會使藥物的生
體可用率降低。
31
從美沙冬轉換到舒倍生舌下錠
導入期
第一天第二天第三天第四天第五天第六天第七天
第一劑 2mg 2mg 4mg 8mg 8mg 8mg 8mg
第二劑 2mg 2mg 4mg
第三劑 2mg 4mg 4mg
第四劑 2mg 4mg 4mg
總劑量 8mg 12 mg 16 mg 8mg 8mg 8mg 8mg
1.美沙冬劑量<30~40mg/day
2.距離上次服用美沙冬的時間，至少24小時
3.首次服藥須COWS>8 始得含服
4.分次含服
Induction vs Retention
As presented by R Schottenfeld at Safer Options Conference, Prague, April 2006.
32
Managing Precipitated Withdrawal
 Be prepared: have contingency plan
 Reassure the patient/care: symptoms time

limited
 Symptomatic medication if severe

-Clonidine (eg: 100-300μgm 4hrly prn for <12hrs)
-Anti-emetics, anti-diarrheal agent, NSAIDS
-BZD- use cautiously
 More BPN? Role is unclear
 More Heroin?
symptoms often relieved by heroin use, but more likely to
again experience precipitated withdrawal with subsequent
BPN dose
Teach them how to use it
Buprenorphine
33
Suboxone vs Methadone
藥品名稱舒倍生舌下錠美沙冬海洛因
對工作的影響彈性且方便的服藥需配合醫院給藥成癮後無法工作，
方式，使您能更專時間，造成您工整天在找錢與找
注於工作作上的不便藥
對身體健康及恢復正常作息及體恢復正常作息及生活失序，體力
生活的影響力，您會感到清醒體力越來越差，易染
上肝炎或愛滋病
或細菌感染
方便性及私密不須天天到院服藥，須每日往返醫院，
性且治療具私密性，產生間接的服藥
同時省下長期交通成本。服藥處無
往返時間及費用隱密性
服藥後再使用不會得到欣快感，使用會有過量致
海洛因可能的舒倍生舌下錠能阻死的風險
反應及風險擋海洛因所發揮的
作用
67
Suboxone vs Methadone
藥品名稱舒倍生舌下錠美沙冬海洛因
管制藥品分類三級管制藥品二級管制藥品一級非法藥品
用藥劑量安全性高，可快速使需緩慢增加劑量，預自行決定劑量，

您達到穩定狀態防過量中毒易過量中毒
用藥方式舌下含服口服注射
每天用藥次數可1~2天服用一次，經 1次/天(不得攜出醫 4-5次/天

醫師評估穩定後，可療機構使用)
帶藥回家服用
戒斷症狀於停止服用後3至5天，於停止服用1至2天後較重，停止服用

出現輕微戒斷症狀，出現戒斷症狀 4-8小時後，出
現嚴重戒斷症狀
其他副作用便秘、頭疼便秘、流汗及皮膚癢副作用類似，但
中毒死亡危險高
34
Thank You for Your Attention !
35
黃介良主任簡歷
學歷：
高雄醫學院醫學系醫學士[1984-1991]
現職：
中國醫藥大學附設醫院精神醫學部主治醫師 [2002 年9 月起]
中國醫藥大學附設醫院精神醫學部成癮防治科主任[2006 年 8 月起]
中國醫藥大學專任講師(講字第 090299 號)[2008 年 8 月起]
經歷：
國立成功大學附設醫院住院醫師[1993-1996]
衛生署朴子醫院精神科主治醫師[1996-2002]
台中市毒品危害防制中心諮詢委員 [2009-2014]
台灣成癮科學會秘書長[2010-2014]
學會會員：
台灣精神醫學會[1993-]
成癮科學會[2008-]
台灣睡眠醫學會[2008-]
NEUROBIOLOGY AND MANAGEMENT OF
STIMULANTS (AMPHETAMINE,
COCAINE,KETAMINE
AND CLUB DRUG)
黃介良醫師
NEUROBIOLOGY OF
STIMULANTS
1
ACUTE STIMULANT EFFECT
Cocaine
1.Cocaine binds to presynaptic dopamine reuptake transporter and
inhibits dopamine reuptake
2.Increase extracellular dopamine level
3.Dose dependence
Methamphetamine
1.binds to dopamine reuptake transporter and vesicular monoamine
transporter
2.Increase extracellular dopamine level by inhibiting reuptake and
increase dopamine efflux
3.High correlated with dopamine release
Metabolism of Methamphetamine is slower than cocaine
Medication treating maybe not effective for different stimulant
Route: smoking>oral or snort
REPEATED STIMULANT
 Addiction
 Sensitization
 Dependence
 Neurotoxicity
 Repeated stimulant exposure induced △FosB

and CaMKII(calcium/calmodulin-dependent
protein kinase) in Nacc.(Robison et al 2013)
 Chromatin regulation (Rogge and Wood 2013)
2
ADDICTION
 Neural area involve:

 Reward: NAcc, ventral pallidum
 Motivation: orbitofrontal cortex,
 Memory: amygdala, hippocampus
 Craving: insula
 Withdrawal: extended amygdala
 Impulse control: prefrontal cortex, cingulate gyrus
ADDICTION
 Reduce stimulant-induced dopamine release predicted poor
treatment outcome (Martinez et al 2011)
 Cue-induced dopamine release in dorsal striatum and drug
craving (volkow et al., 2006)
 dorsal striatum(Fuchs et al., 2006)
 Receives projections from substantia nigra
 Is the primary entry into basal ganglia
 Habitual behavior
3
ADDICTION
 Glutamate in limbic system
 Chronic cocaine result increase GluR1 containing AMPA
receptors, increase AMPA signaling, contribute to relapse
(Kalivas and Volkow et al., 2011)
 Group II mGluRs (GluR2/3) act as inhibitory autoreceptors
that regulate the release of glutamate.
 Chronic cocaine downregulated GluR2/3
ADDICTION
 Dopaminergic and glutamatergic medication may potential
pharmacotherapy to stimulant.
 D1 antagonist, D2 antagonist, agonist, and partial agonist
has show no promise effect on cocaine (Haney and spealman
et al., 2008)
 N-acetylcysteine reduce drug-induced (but not cue-induced)
cocaine craving. (Amen et al., 2011)
 mGluR2/3 agonist and mGluR1 antagonist decrease cocaine
seeking and self-administration, mGluR5 antagonist decrease
methamphetamine self-administration in animal studies
4
ADDICTION
 AMPA antagonist (lamotrigine) decrease cocaine use in
bipolar. (Brown et al., 2012)
 AMPA antagonist (Topiramate, enhance GABA) may promise
on treat cocaine and methamphetamine (Elkashef et al.,
2012).
 GABA agonists as gabapentin, baclofen, vigabatrin, and
tiagabine had shown redued cocaine in human. (Haney et al.,
2006, Hart et al., 2004, 2007, Kahn et al., 2009, Winhusen
et al., 2007)
 Both Glutamate and GABA maybe effect.
 GABA agonists selectively facilitate treatment outcome on
methamphetamine
ADDICTION
 Cocaine and methamphetamine inhibit serotonin reuptake.
 Serotonin reuptake inhibitor did not improve treatment outcome of
cocaine. Serotonin reuptake inhibitor worsened methamphetamine.
(Vocci and Ling et al., 2005)
 NMDA antagonist (memantine) enhance the positive subjective
effects of cocaine and methamphetamine (Collins et al., 2007,
Hart et al., 2002 ).
 GABA agonists as gabapentin, baclofen, vigabatrin, and
tiagabine had shown redued cocaine in human. (Haney et al.,
2006, Hart et al., 2004, 2007, Kahn et al., 2009, Winhusen et al.,
2007)
 Both Glutamate and GABA maybe effect.
 GABA agonists selectively facilitate treatment outcome on
methamphetamine.
5
ADDICTION
STIMULANT- AND CUE- INDUCED DRUG SEEKING
 Hippocampus and basolateral amygdala mediate environmental –

related cue. (Yalachkov et al., 2012)
 Orbitofrontal and anterior cingulate cortex involved in value- and
preference-related signaling.
 Glutamate
 Cocaine had minimal effect on NAcc glutamate release in drug-naïve animal.
 On chronic cocaine exposure animals, basal NAcc glutamate levels are
decrease, glutamate release in response to cocaine is enhanced.
 Both cocaine and cocaine-paired cues activate prefrontal glutamatergic
projections to the NAcc.
 Drug seeking can be elicited by directly stimulating glutamatergic pathways to
the NAcc.
 Blocking or “normalizing” glutamatergic input to the NAcc decrease both
cocaine- and cue-induced glutamate release and cocaine seeking. (Kalivas and
Volkow 2011)
ADDICTION
STIMULANT- AND CUE- INDUCED DRUG SEEKING
 Hypocretin
 Hypocretin increases phasic and tonic dopamine signaling in VTA via
hypocretin receptor on dopamine neurons and indirectly via glutamate.
 Hypocretin antagonist attenuated cocaine seeking elicited by drug cues
but did not affect cocaine seeking triggered by small cocaine
doses(Aston-Jones et al., 2010)
 STRESS- INDUCED DRUG SEEKING

 Extrhypothalamic corticotropin-releasing factor (CRF)
Decreasing stress-induced norepinephrine release with α2-
adrenoceptor agonists also decreases drug seeking. (Erb
2010)
6
ADDICTION
COGNITIVE CONTROL, IMPULSIVITY, DECISION MAKING
 Chronic stimulant abuse is associated with difficulties with

decision making and impulsivity
 Increase capacity to delay gratification predicts longer abstinence from
cocaine. (Washio 2011)
 Stimulant-related increase in ventral striatal activity in combination with
disrupted orbitofrontal function may contribute to increased delay
discounting (Setlow et al., 2009)
 IV cocaine improves inhibition of motor responses in regular cocaine
users, by normalizes hypoactivation in dorsolateral and medial
prefrontal cortical regions subserving this function. (Grarvan et al.,
2008)
SENSITIZATION
 Repeated exposure to cocaine, amphetamine, or stressful stimuli can result in sensitization, or a

heightened sensitivity to convulsant, locomotor, and reforcing effects of subsequent stimulant
administration reflects modulation of AMPA and NMDA receptor and increase expression of
GluR1, GluR2, and GluR2/3 in the Nacc, resulting enhanced dopaminergic response to stimulate
(Carlezon and Nestler, 2008)
 Sensitization play a role at the initiation of drug taking.
 Oral amphetamine to drug-naïve resulted in enhanced psychomotor performance and dopamine
release in NAcc in response to subsequent amphetamine persisting for 1 year. (Boileau et al.,
2006)
 Correlation of striatal dopamine with nondependent and cocaine history following intranasal
cocaine. (Cox et al., 2009)
 Sensitization play a role in development of behavior pathology.
 Methamphetamine-related psychosis may last for weeks, cocaine –related psychosis tends to be
briefer.
 Drug-induce psychosis recurs even under small dose of drug.
7
TOLERANCE
 Larger doses are needed to produce an effect that was previously

obtained at a lower dose.
 First dose produce larger CV and subjective effects than
subsequent doses. (Foltin and Fischman 1991)
DEPENDENCE (WITHDRAWAL)
 Pharmacological dependence is defines as the presence of

withdrawal symptoms upon cessation of drug use.
 Stimulants do not produce neuroadaptions in area mediating
somatic and autonomic function.
 Disorder in mood, depression, fatigue, anxiety and irritability.
 Depression, anxiety, glucose metabolism in limbic, cingulate gyrus,
amygdala, insula (London et al., 2004)
 Dynorphin had role in withdrawal-induced mood dysregulation.
Antagonism of K-opioid receptors reduced depression-like behavior in
rats during cocaine withdrawal. (Chartoff et al., 2012)
8
DEPENDENCE (WITHDRAWAL)
HUMAN
 Β1-adrenergic receptor antagonist blocked CRF signaling in the

amygdala. (Rudoy et al., 2009)
 Stimulant withdrawal associated with increase CRF gene expression in
amygadala, which may contribute to the negative affect and decrease
sensitivity to natural reiforcers accompanying withdrawal.
 Serotonin dysregulation and stimulant withdrawal
 Cocaine users had a blunted neuroendocrine response to D-
fenfluramine for at least 2 weeks of abstinence. /no disruption
of D2 agonist bromocriptine.
 D-fenfluramine is a serotonin releaser and reuptake
inhibitor.(Haney et al., 2001)
 Neurochemical basis of chronic cocaine user had commonly
changes mood during stimulant withdrawal.
TOXICITY
 Chronic stimulant and dopaminergic and serotonergic (not

noradrenergic) neurotoxicity
 Cell death after high –dose methamphetamine (Kraster and
Cadet 2009)
 Comparable dose of methamphetamine on nonhuman primates
decrease dopamine transporter and dopamine axonal markers
(Villemagne et al., 1998)
 In rodents, persistent decreases of dopamine neuron integrity
after self-administration of high methamphetamine doses and with
transient decreases in serotonerguc and norepinephrine neuron
marker. (Krasnova and Cadet 2009) .
9
TOXICITY
 methamphetamine
 In detoxified methamphetamine abusers, decrease dopamine D2
receptors and transporters in striatum persisted months decrease
dopamine transporters correlate with slower motor speed and
poorer verbal memory. (Volkow et al., 2001)
 Evidence of dopaminergic terminal markers recover after
prolonged abstinence. (Volkow et al., 2001)
 In autopsied brains, caudate greater depletion than putamen
which is opposite to the Parkinson’s disease. (Moszczynska et al.,
2004)
TOXICITY
 cocaine
 Cocaine does not appear to produce the same dopaminergic
neurotoxicity as methamphetamine.
 In rodent, cocaine and D-amphetamine produced comparable
levels of behavioral activation, weight loss, and lethality. Only
amphetamine resulted in axonal degeneration in neostriatum and
frontal cortex (Ryan et al., 1998)
 Long-term cocaine associated morphological changes . (Ersche et
al., 2011)
10
TOXICITY
 Dopamine oxidation
 Methamphetamine-induced dopamine release may be auto-oxidized to 6-
hydroxydopamine, resulting in neurodegeneration.
 The destruction of serotonin and dopamine neurons is prevented in animal if
brain dopamine levels are deleted prior to methamphetamine administration.
(Kransnova and Cadet., 2009)
 Glutamate
 Increase glutamate efflux in striatum where neurotoxicity occurs, but not in NAcc.
(Abekawa et al., 1994)
 NMDA antagonists prevent domapinergic and serotonergic neurotoxicity.
(Kransnova and Cadet., 2009)
Stimulant
Conclusion ands key points
 Phamacotherapeutic intervention will not cure a chronic relapsing disorder

(stimulant) but may decrease craving, initiate or prolong abstinence, or block
the acute stimulant effects if the drug being abused.
 Cocaine inhibits the reuptake of dopamine and has relatively short-lasting
effect compared with methamphetamine.
 Methamphetamine blocks reuptake also promotes dopamine release, which
renders more neurotoxic than cocaine.
 Addiction lead by repeated stimulant-induced increases in extracellular
dopamine and glutamate.
22
11
Clinical management: cocaine
23
 1.4 million Americans used cocaine within previous month. (Substance Abuse
and Mental Health Services Administration 2012)
 Consequences:
 HIV
 Hepatitis B or C infection
 Detrimental effect on fetus
 Increase crime and violent
 Medical, financial, psychological problems
24
12
pharmacotherapy
 No medication have shown consistent efficacy, no medication have been

approved by U.S FDA.
 Agonist
 Amphetamines: D-amphetamine (Herin et al., 2010), methamphetamine

(Mooney et al., 2009), methylphenidate (Levin et al., 2007; Schubiner et al.,
2002 )
 Bupropion (Poling et al., 2006)
 Mofafinil (Martinez-Raga et al., 2008) (Dackis et al., 2012)
 Disulfram (Sofuoglu and Sewell 2009)
25

pharmacotherapy
 Agonist
 Amphetamines: D-amphetamine (Herin et al., 2010), methamphetamine
(Mooney et al., 2009), methylphenidate (Levin et al., 2007; Schubiner et al.,
2002 )
 Bupropion (Poling et al., 2006)
 Mofafinil (Martinez-Raga et al., 2008) (Dackis et al., 2012)
 Disulfram (Sofuoglu and Sewell 2009)
26
13
pharmacotherapy
 Neuroadaptation
 Lofexidine: α2-adrenergic receptor agonist (Sinha et al., 2007 )
 Carvedilol: adrenergic blocker (Sofuoglu et al., 2000)
 Doxazosin : α1-adrenergic receptor agonist (Shorter et al., 2013)
 N-acetyl-cysteine (NAC): (Baker et al., 2003)
 Vigabatrin: irreversible GABA tramsaminase inhibitor (Brodie et al., 2009; Somoza et al.,
2013)
 Topiramate: GABA enhence (Kampman et al., 2004; Mariani et al., 2012)
27

pharmacotherapy
 Psychiatric comorbidity
 Schizophrenia, mood and anxiety disorder, depression, ADHD, antisocial personality
(Ford et al., 2009 )
 antidepressants: desipramine (McDowell et al., 2005), imipramine (Nunes et al., 1995),
fluoxetine (Schmitz et al., 2001), sertraline (Oliveto et al., 2012)
 CBT (Carroll et al., 1995)
 methylphenidate (Levin et al., 2007; Schubiner et al., 2002 )
28
14
pharmacotherapy
 Cognitive deficits
 modafinil
 Varencline: partial nicotine acetylcholine receptor agonists, nAChR
 Galantamine: cholinesterase inhibitors, α7 and α4β2 nAChR (Sofuoglu et al., 2011)
 Immunotherapies
 Cocaine vaccine (TA-CD): IIa, (Shen and Kosten 2011)
 Gender-specific hormones
 Oral progesterone among women (Evans and Foltine 2006; Sofuoglu et al., 2002)
29

behavioral therapy
 Behavioral therapy
 12-step facilitation (TSF): TSF v.s. disulfram (Carroll et al., 2012)
 CBT: (Knapp et al., 2007); computerized CBT (Carroll et al., 2008)
 contingency management: (Dutra et al., 2008; Stitzer and Petry

2006)
target behavior (e.g., clean urine)
Reinforcement: voucher without delay
 Effect size: 0.62 (Dutra et al., 2008)
30
15
treatment guideline
 Detoxication
 Acute intoxication
 Hypertension, tachycardia, chest pain, seizures
Avoid β-adrenergic antagonists
Persecutory delusion
Delirium:
BZD are the treatment of choice.
Antipsychotics should be use cautiously because they may worsen hyperthermia.
 Acute withdrawal: mild depressive symptoms, increase appetite, increase sleep,
craving, self-limited
 Initial recovery: motivation, new behavior, reward,
 Relapse prevention
31
Cocaine
 Behavioral treatment including cognitive-behavioral therapies and

contingency management are effective.
 No medication received FDA approval.
 Combined pharmacotherapy and behavioral interventions.
32
16
Clinical management:
methamphetamine
33
Clinical management: methamphetamine
 ATS: amphetamine-type stimulants

 Amphetamine
 Dextroamphetamine
 3,4-methylenedioxymethamphetamine (MDMA)
 Cocaine:
 357,000 persons 12 years or older either dependence or abuse ATS.
(SAMHSA 2011)
 502,000 (SAMHSA 2010)
 52.2 million worldwide (United Nations office on drugs and crime 2012)
34
17
 route
 Inject: immediately
 smoke : immediately
 Snort: 3-5 minutes
 Oral: 20 minutes
 MA inhibits dopamine reuptake, increase dopamine release, and interferes

dopamine transport.
 Dopamine oxidation are toxic to nerve terminals. (Hanson et al., 2004; Pierce
and Kumaresan 2006)
35
 Effect and consequence

 Smoke and inject typically produce well-being, confidence, and euphoria.
 Cardiovascular: caridomyopathy, myocarditis, hypertension, arrhythmia, myocardial infarction,
rapid hear beat, inflammation if t he heart lining (westover et al., 2008)
 Pulmonary: pulmonary edema, dyspnea, bronchitis, pulmonary hypertension, hemoptysis, chest
pain, asthma exacerbation, pulmonary granuloma. Tuberculosis is coomon. High concentration of
MA in lung had been found.(Volkow et al., 2010)
 Neurological: strokes seizure, chronic headache, cerebral swelling and hemorrhage, involuntary
movement and tics.
 Hepatic: MA autopsies: liver disease:40%, cirrhosis9% (Karch 2002)
 Obstetric: low birth weight (Smith et al., 2006)
 Other: skin infection, dental problems (Shetty et al., 2010), anorexia, stomach ulcers, colitis,
kidney failure, blood-borne viruses
36
18
 Psychological effect
 Paranoia, psychosis, depression, anxiety, suicidality, hallucinations, aggression,
and violent.
 Substance use disorder (cannabis, BZD) for Ma-induced side effect.
 ADHD
 gambling disorder
 Sleep disorder
 Eating disorder
 Most common and important: depression and anxiety (McKetin et al., 2011)
37
 Clinical management
 Screening:
 Syndrome
 MA intoxication
1. Agitation, harm to self or other
2. 5 mg haloperidal combine 1-2 mg of lorazepam orally or parenterlly over
12 hours period
3. Atypical neuroleptics orally or parenterlly and 1-2 mg of lorazepam orally
over 12 hours period
4. Hydration and hyperthermia
 MA withdrawal
 Fatigue, depressed mood, clouded thinking
38
19
 Clinical management
 acute and persistent MA psychosis
1. Antipsychotics generally fail to ameliorate long-term post-MA psychosis.
(Freudenmann et al., 2006; Grelotti et al., 2010)
2. Auditaory hallucination with visual sensation (flashing lights, peripheral
artifacts), olfactory and tactile (bug crawling on or below the skin)
3. Acuter psychosis the symptoms often persisted. 28% of the patients had
psychosis lasting longer than 6 months. (Ujike and Sato 2004) Low-doe
antipsychotics may use.
39
20
 MA injectors
 More difficult MA-related disorder
 More craving
 Higher dropout rates
 High hepatitis infection (45% v.s. 15%) (Gonzales et al., 2006)
 MSM (men have sex with men)
 MA-using MSM had 3 times HIV prevalence than non-MA-using MSM.
 women
 Women use MA at rates approaching men. (Brecht et al., 2004).
 Weight loss
 Perinatal exposure
 Growth retardation, premature birth, neurological disorders. (Lucas 1997)
41
 Behavior treatment
 cognitive-behavioral therapies and contingency management
(vocci and montoya 2009)
 cognitive-behavioral therapies had fewer stimulant-positive
urine and contingency management had longer in treatment
program (Rawson et al., 2006)
 Biofeedback-guided neurotraining (Newton et al., 2006; Scott
et al., 2005)
 Matrix model (Rawson et al., 2004)
42
21
 Pharmacotherapy
 No medication received FDA approval.
 Positive: bupropion (McCann and Li 2012), naltrexone (Jayaram-lindstrom et
al., 2008), mirtazapine (Colfax et al., 2011), methylphenidate (Tiihonen et
al., 2007), Lobeline: nicotinic receptor antagonist (Eyerman and Yamamoto
et al., 2005), Topiramate (Johnson et al., 2007), Γ-Viny-Γ-aminobutyric acid
(GVG) (Brodie et al., 2005)
 Negative: aripiprazole (Coffin et al., 2013), modafinil (anderson et al.,
2012), citicoline (Brown and Gabrielson 2012)
 Vaccine: σ receptor ligend AZ66
43
Methamphetamine
 BZD for methamphetamine-related intoxication and withdrawal is the current

accepted practice.
 Special attention in methamphetamine-related consequence on
methamphetamine injectors, adolescents, women, and MSM.
 Psychosocial treatment are effective including cognitive-behavioral therapies
(Matrix model) and contingency management , 12-step facilitation.
 No medication received FDA approval.
 Bupropion plus depot naltrexone
44
22
Hallucinogens and
club drugs
45
Hallucinogens and club drugs
46
23
 Club drug
 LSD, ketamine, MDMA, methamphetamine, GHB, flunitrazepam
 Hallucinogens
 2 chemical classes:
1. Tryptamines: LSD, psiocybin, DMT
2. Phenethylamines:
 Agonists at postsynaptic serotonin 2 receptors (primarily 5-HT2A)
47
 Hallucinogens subjective effect

 Orally, snorted, smoked, or injected
 Perception: visual illusions, intensification of colors, visions of geometric
patterns and detailed scenes with eye closed, synesthesia (e.g., listening to
music produces the perception of seeing colors),
 frank visual and auditory hallucination are uncommon
 Perception of time and space also be strongly altered.
 Intense emotion (Griffiths et al., 2006,2008,2011)
 Physiological effects: dizziness, nausea, drowsiness, parethesia, blurred vision,
dilated pupils, increase heart rate and blood pressure
48
24
 Treatment of acute effect of hallucinogens

 Rarely required medical treatment.
 Verbal reassurance, physical contact, calm environment
 Music, deep breathing, meditation, guided imagery
 No approved medications. BZD may use in severe agitation. Antipsychotics
may also be used.
 Hypertensive crisis
 Serotonin syndrome: autonomic activity increased, delirium, nausea, vomiting.
Cyprohetadine (serotonergic antagonist)
49
 Long-term consequences of hallucinogens

 Classical hallucinogens relatively low physiological toxicity and addiction.
 Hallucinogen–induced psychosis (Strassman et al., 1984)
 Hallucinogen persisting perception disorder: flashbacks of hallucinogen
experience, 4% of 15,00 hallucinogen users
50
25
 Salvia Divinorum 墨西哥鼠尾草

 Psychoactive mint plant in Mexico.
 Main ingredient: Salvinorin A
 Selctive κ–opioid agonist with no acitvity at 5HT2A receptors (Roth et al., 2002)
 Subjective effects:
 Smoking (10-15 minutes), chewing
 At high dose: change visual auditory and tactile perception, disruptions in vestibular
and propriceptive processing, memory impairment, lack of awareness, reliving of
childhood memory, interaction with imaginary beings
 Physiological effect: sweating and chills
 Long-term: some report persisted anxiety, large percentage report persisting positive
psychological effects (Baggott et al., 2010)
51
 MDMA (Ecstasy)
 Synthetic drug similar to both amphetamine and mescaline.
 orally (onset:30-60 minutes, last: 4-6 hours)
 Increase positive mood, interpersonal openness, trust, and empathy
 Physiological effect: dilated pupils, increase heart rate and blood pressure
 Acute treatment: interpersonal support for anxiety and panic, BZD for extreme
agitation, hyperthermia, hyponatremia (Halpern et al., 2011)
 Long-term: changes in attention, memory, mood, anxiety, sleep (McCann et al., 2007)
52
26
 Dissociative amesthetics
 PCP, ketamine, DXM.
 Orally, intravenously, intranasally
 PCP produces brief, dissociative psychotic-like reactions.
 Ketamine and DXM: perceptual distortion, changes in sense of time and space, alterations in body
awareness and spiritual experience. (Reissig et al., 2012)
 Acute treatment:
Naloxone for treatment of DXM overdose. (Chyka et al., 2007)
PCP intoxication exibit dangerous, violent and psychotic-like behaviors. (McCardle et al., 1989)
Haloperidal and lorazepam can be used if serious threat. Continuous cardiac monitor will be needed.
 Long-term:
Ketamine produce memory loss, decrease sociability, physical problems (gastric pain ,cyctitis)
(Muetzelfeldt et al., 2008)
Phencyclidine organic mental disorder: memory deficits, confusion, speech difficult (Weaver et al., 2007 )
53
54
27
 Do not often require pharmacological treatment. BZD and antipsychotics can

be use in cases of extreme agitation.
 Hallucinogens are rug of abuse and also are accepted medical or research
use (ketamine, psilocybin, MDMA ).
 Designer hallucinogens may have physiological toxicity and long-erm risks.
55
THANKS FOR YOUR

LISTENING!
28
Reference
TEXTBOOK OF SUBSTANCE ABUSE

TREATMENT
AJP 2014(FIFTH EDITION)
P169-222
29
林滄耀主任簡歷
學位級別
畢業部定教職
（專科.學士.
最高學畢業學校科系
年月碩士.博士）字號
歷
學士後
國立陽明大學 78.6 學士
醫學系
單位名稱職稱教學實務研究年
現職衛生署草屯療養院成癮治療主任 10 年 10 年 10 年
單位名稱職稱教學實務研究年
衛生署草屯療養院住院醫師、總
4年
醫師
衛生署草屯療養院
主治醫師 10 年 10 年 2
經歷
衛生署草屯療養院成人精神科
2年 2年 2
主任
Part V Rehabilitation settings
from inpatient to Community-
based Treatment
衛生福利部草屯療養院
成癮治療科林滄耀
日期：104年7月 4 日 (星期六)
時間：16:40-17:30
地點：台中市西屯區朝富路99號
摘要
一. Inpatient treatment
二. Community-base Treatment
三. Twelve-Steps Programs
四. Alcoholic Anonymous
五. Therapeutic community
1
一.Inpatient treatment
Minnesota Model
Education, group therapy, peer Orientation of
confrontation, system interventions patients to AA
with family member, and or NA to
establish their
Detoxification employers, recounting of one’s continued
drug and alcohol histories in front involvement
of other patients and staff after
members discharge.
 Developed in the 1950s in Minnesota
 Fixed length of staying(4 weeks mostly)
 Most powerful tool : instillation of hope.
 Emphasize the importance of spirituality in the recovery process.
2
Programs of inpatient treatment
 Program Characteristics
 Integration of employment
 Motivational interview
 Social support
 Adequate counseling
 Treatment satisfaction
 Aftercare
 Case management augmentation strategies
 length of stay: controversial ?
Rational for inpatient treatment

• Permit a high level of medical supervision and safety for
patients with medically dangerous condition, e.g., withdrawals
symptoms
Advantage • Interrupt a cycle of substance use: avoid condition cue.
• Helpful for patients who do not respond to lesser measure
• Experience few drug urge(drug free environment)

• May not be full prepared to handle the more frequent urge
they will experience after discharge.
Disadvantage
• Expense: unable to work, care for their family, study, or
conduct their daily activities, and stigma
Inpatient treatment should be used only when less intensive

treatment has failed or is considered too risky.
3
Indication for Hospitalization
1.The danger that the patient might imminently
experience harm to self or to others.
2 .The likelihood that the patient would achieve

treatment success in less restrictive environment.
Controversy : enormous cost

23% of patients received inpatient rehabilitation
treatment in 2011(Still important)
Outcome of inpatient treatment

• 50-60% at 6-12 months after discharge.(Minnesota
Model)
Abstinence • Co-occurring psychiatric disorder : I year follow-up with
rates abstinence rate of 25%.
• Who completed inpatient alcoholism treatment had lower

Mortality mortality rates in the 3 years after discharge
rates
4
Outcome of inpatient treatment
• Order, more education, employed full time, married, who abuse
alcohol rather than other substance, whose family participate in
treatment.
• More social support, confident in their ability to maintain sobriety,
Better greater motivation to change.
• Severe base line anxiety symptoms
• Mild to moderate levels of psychiatric symptoms
Not better • IDU, antisocial personality disorder, cocaine dependence,

tobacco use
• More severe psychiatric problems
Question about Inpatient treatment
 Implications for the future

 The question should not be:” Is inpatient
treatment effective?”
For which patients is inpatient treatment effective,

at what time or times, and for how long?
10
5
二.Community-Based
Treatment
11
(一) Community
Intervention
12
6
TABLE 35-1 Treatment episodes by referral source, 2010
Criminal justice/driving while intoxicated 36.9%
Health care providers 6.4%
Community referral(57%) School(educational) 1.2%
Employer/employee assistance program 0.5%
Other community referral 12.1%
Other referral (43%) individual 33.1%
Substance abuse providers 9.9%
13
Brief Intervention(BI)
for Alcohol Misuse
 Brief Intervention(BI)
 reducing at-risk drinking(not alcohol use
disorder)
 reduced hospitalization rates
 improve academic problems
 reduce emergency department
14
7
TABLE 35-2 Maximum safe drinking limits
Population Single day Per week
Men<65 years 4 standard drinks 14 standard drinks
Women (all ages)

3 standard drinks 7 standard drinks
Men>65Years
15
Brief Intervention for Alcohol Misuse

Table 35-3 Components of brief intervention for alcohol misuse
1.Screening for at-risk drinking(e g., single question or AUDIT)
2.Quantifying drinks per week
3.Assessing for alcohol use disorder
4. Expressing concern
5.Gauging readiness to change
6.Setting goal
7.Agreeing on a plan
8.Providing educational materials
9.Follow-up with continued support
16
8
Workplace intervention
 Substance use:
 costly to employers , employees, society
 increased worker turnover, accidents, absenteeism, lost
productivity, employee conflict, and increased health
care costs.
 64% full time employees had use alcohol and 8% used an
illicit drug in the previous month(NSDUH,2001).
 Intervention
 Web-based education
 Screening
 Brief intervention
 More confidential and private manner
 EAPs(employee assistance programs)
17
Interventions by the Judicial System

 Drug courts
 Beginning in Miami, Florida, in 1989
 Criminal justices system + addiction treatment
Elements:
 collaboration of judges, prosecutors, public
defenders , community treatment programs
 Programs:
 12-18 months
 random but frequent urine screens
 regular appointments
 referral to social service support
 biweekly judicial hearing
18
9
 Drug courts
 2,459 drug courts in the US(2009)
 increased 40% over the prior 5 years
 charges would be dropped with successful
completion of the program
 Other drug courts
 Juvenile drug courts, college campus
treatment courts, veterans’ treatment
courts
19

 Drug courts outcome
 Decrease crime( Huddleston and Marlowe, 2011)
 45% reduction in crime compared with other
judicial interventions, this decrease to last at least
3 years.
 Significant reduction in drug and alcohol use and
improved family relationships as a result of drug
courts.
 Cost-effectiveness : a saving of $2.21-$3.36 to the
criminal justice system for every $1 invest in drug
court programs.
20
10
(二) Non-Hospital-Based
Service
21
Day Hospital and Intensive

Outpatient Programs
 Day hospital and outpatient services
 less severe substance use
 Definition (ASAM,2001):
 intensive outpatient: 9 hours per week
 partial hospital programs:20 hours per
week
22
11
Community Residential Facilities(CRF)
 Also called “Halfway houses”  Homeless
 Receive patients from inpatient  Improves retention

treatment or detoxification  Reduces readmission
services  Treatment : from counseling to
 They are not yet ready for highly structured programs
independent living  Approaches using TC,
 Limited sober social supports or psychosocial rehabilitation, 12-
limited sober housing resource step programs, and
 They need the supervision and enhancement of supportive
support of a living environment relationship
committed to sobriety
23
Case Management
TABLE 35-6 Case management function and tasks
Patient advocacy
Shepherding patients through bureaucratic red tape
Improving to fill gaps in service
Outreach to engage and retain patients in treatment
Providing basic services such as transportation
Coordinating multiple providers and agencies
Developing an individualized supportive relationship
24
12
三.Twelve-Steps
Programs
25
(一) The 12 Steps
26
13
The 12 Steps
1. We admitted we were powerless over alcohol—that our
lives had become unmanageable.
2. Came to believe that a Power greater than ourselves could
restore us to sanity.
3. Made a decision to turn our will and our lives over to the
care of God as we understood Him.
4. Made a searching and fearless moral inventory of
ourselves.
5. Admitted to God, to ourselves, and to another human
being the exact nature of our wrongs.
6. Were entirely ready to have God remove all these defects
of character.
27
The 12 Steps
7. Humbly asked Him to remove our shortcomings.
8. Made a list of all persons we had harmed, and became willing
to make amends to them all.
9. Made direct amends to such people wherever possible, except
when to do so would injure them or others.
10. Continued to take personal inventory, and when we were
wrong, promptly admitted it.
11. Sought through prayer and meditation to improve our conscious
contact with God as we understood Him, praying only for
knowledge of His will for us and the power to carry that out.
12. Having had a spiritual awakening as the result of these steps,
we tried to carry this message to alcoholics, and to practice
these principles in all our affairs.
28
14
1. 我們承認我們無能為力對付酒精，而我們的生活已變得不可收拾。
2. 相信有一個比我們本身更大的力量，這個力量能恢復我們心智健康和神智清
明。
3. 作出一個決定，把我們的意志和我們的生活，托付給我們所認識的上帝。
4. 作一次徹底和無懼的自我品格檢討。
5. 向上帝、向自己、向他人承認自己過錯的本質。
6. 要完全準備讓上帝除去自己一切人格上之缺點。
7. 謙遜地祈求上帝除去我們的缺點。
8. 列出一份所有我們所傷害過的人的名單，並使自己甘願對這些人作出補償。
9. 盡可能的話，直接補償他們，除非這樣做會傷害他們或其他人。
10. 繼續經常自我檢討，若有錯失，要迅速承認。
11. 透過禱告與默想，增進我們與自己所認識的上帝有自覺性的接觸，只祈求認
識祂對我們的旨意，並祈求有力量去奉行祂的旨意。
12. 實行這些步驟的結果是我們已經擁有一種精神上的覺醒，我們設法把這個音
訊帶給酒徒，並在我們一切日常生活事物中，去實踐這些原則。
29
12 Traditions
1. Our common welfare should come first; personal recovery depends
upon AA unity.
2. For our group purpose there is but one ultimate authority—a loving God
as He may express Himself in our group conscience. Our leaders are
but trusted servants; they do not govern.
3. The only requirement for AA membership is a desire to stop drinking.
4. Each group should be autonomous except in matters affecting other
groups or AA as a whole.
5. Each group has but one primary purpose—to carry its message to the
alcoholic who still suffers.
6. An AA group ought never endorse, finance, or lend the AA name to any
related facility or outside enterprise, lest problems of money, property,
and prestige divert us from our primary purpose.
30
15
12 Traditions
7. Every AA group ought to be fully self-supporting, declining outside
contributions.
8. Alcoholics Anonymous should remain forever non-professional, but
our service centers may employ special workers.
9. AA, as such, ought never be organized; but we may create service
boards or committees directly responsible to those they serve.
10. Alcoholics Anonymous has no opinion on outside issues; hence the
AA name ought never be drawn into public controversy.
11. Our public relations policy is based on attraction rather than
promotion; we need always to maintain personal anonymity at the
level of press, radio, and films.
12. Anonymity is the spiritual foundation of all our traditions, ever
reminding us to place principles before personalities.
31
十二傳統
1. 我們共同的福利應列第一；個人的康復全賴戒酒無名會的團結一致。
2. 為了我們團體的目的，我們只有一個主要的權威：一個有愛心的上蒼，而祂可以在我們的團體
良心中表達祂自己。我們的領袖只是受委託的僕人，而不管治他人。
3. 作為戒酒無名會成員的唯一要求，就是有停止喝酒的願望。
4. 每一個組別是自治的，足以影響到其他組別或整個戒酒無名會事務者為例外。
5. 每一組別只有一個主要目的：把它的訊息傳遞給那些仍在受苦的酒徒。
6. 任何戒酒無名會組別不應認可、資助或允許任何有關組織或外面的企業機構使用戒酒無名會的
名字，以免因為金錢、物業及聲譽上的問題，將我們轉離了基本的目的。
7. 每一個戒酒無名會組別應自給自足，謝絕外界的捐獻。
8. 戒酒無名會應該永遠保持非專業性，但服務中心可以雇用專門的工作人員。
9. 戒酒無名會就其性質而言，不應該建立組織體系，但我們可以創立服務理事會或委員會，直接
向所服務的對象負責。
10. 戒酒無名會對外界事務不作評論；因此不應該把戒酒無名會的名字捲入公開的爭論中。
11. 我們的公共關係政策是建基於吸引外人參加，而非建基於自我宣傳上；我們在報章、電台和影
視界方面，需要常常保持個人的匿名。
12. 匿名是我們所有傳統中的精神基礎，不斷提醒我們把原則置於個人操守之上。
32
16
(二) Psychological and
Mechanisms
of 12-Srep Programs
33
Theoretical Programs
 Mechanism of recovery
 sequential 12-step program
 “spiritual awakening”
 Spiritual awakening
 “educational variety(as opposed to dramatic
sudden or quantum change)”
 gradual change in attitudes, behaviors, and
world view
 leads to “a profound alternation in one’s
reaction to life”
34
17
 12-step groups emphasize service
work
 service work is seen as part of
members’ recovery
 because it helps members become more
responsible for their personal success
as well as that of the fellowship.
35
 Process of 12-steps
 following the realization of personal “powerlessness”
over the substance(step 1) and
 that the solution lies in finding a “higher power”(step 2),
 member s are asked to make a decision(step 3) about
what to next.
 If the decision is made to trust the AA process(i.e., turn
one’s life and will over to the care of God” as each
member understands” God”), members then complete a
self assessment(step 4),
 discuss it with another person(often a sponsor; step
5)..cont. 6,7,8,9,10,11,12
 The entire process is designed to produce a “spiritual
awakening” sufficient to overcome addiction.
36
18
1. 我們承認我們無能為力對付酒精，而我們的生活已變得不可收拾。
2. 相信有一個比我們本身更大的力量，這個力量能恢復我們心智健康和神智
清明。
3. 作出一個決定，把我們的意志和我們的生活，托付給我們所認識的上帝。
4. 作一次徹底和無懼的自我品格檢討。
5. 向上帝、向自己、向他人承認自己過錯的本質。
6. 要完全準備讓上帝除去自己一切人格上之缺點。
7. 謙遜地祈求上帝除去我們的缺點。
8. 列出一份所有我們所傷害過的人的名單，並使自己甘願對這些人作出補償
。
9. 盡可能的話，直接補償他們，除非這樣做會傷害他們或其他人。
10. 繼續經常自我檢討，若有錯失，要迅速承認。
11. 透過禱告與默想，增進我們與自己所認識的上帝有自覺性的接觸，只祈求
認識祂對我們的旨意，並祈求有力量去奉行祂的旨意。
12. 實行這些步驟的結果是我們已經擁有一種精神上的覺醒，我們設法把這個
音訊帶給酒徒，並在我們一切日常生活事物中，去實踐這些原則。
37
Research on Mechanisms
-Common factors
 Cognitive mechanisms.
 Affective mechanisms
 Social network mechanisms
 12-Steps-Specific Mechanisms
 Spiritual mechanisms
 relationship between 12-step MHOs
involvement and reduced substance use:
evidence is not consistently
38
19
(三) Outcomes of 12-Step
Programs: Efficacy and
Effective
39
Effectiveness Studies
 1- and 3-year follow-up : abstinent
 self-selected into AA/ self-selected into
formal treatment= 48% vs. 21% and 50%
vs. 26%
 8-yearfollow-up: 49% vs. 46%
 Compared
 AA only/ formal treatment + AA : both with
a lower likelihood of drinking problems, at
year 16
40
20
Enhancing Outcomes and
Reducing Health Care Cost
 403 adolescents(12-step groups, 7-year

follow-up ) participated intensive
outpatient programs :
 better substance use outcomes
 lower medical cost
41
Efficacy Studies:12-Step Facilitation

TABLE 38-1 Examples of 12-step facilitation strategies for clinicians
preparation 1. Become familiar with 12-step literature to increase knowledge about
the fellowship and 12-step program
2. Attend several different open meeting to gain a firsthand understanding
of the varying social climates and formats of meeting
3.Keep updated lists of local AA,NA, or other 12-step mutual-help
organization meetings, as well as Web site information, to give to patients
intervention 4. Discussed with patients the rationale for meeting attendance(e.g.,
recovery specific support between sessions, relapse risk appraisal,
remotivation, access to a sober support network)
5.Help patients set goals for meeting attendance, including selecting
particular meeting to try based on patient preferences
6. Link patients with current AA/NA members
7. Monitor and discuss patient concerns, barriers, and attitudes about
AA/Nain session, both before and after AA/NA attendance
8. With adolescent or young patients, get parental support for the
patient’s AA/NA attendance
9. Link patients with group that might be a good fit and enhances of early
42 engagement
21
Efficacy Studies:12-Step Facilitation
TABLE 38-2 Ways for clinicians to implement 12-step facilitation
strategies
Method How it might be implemented
Standard-alone Individual therapy devoted entirely to facilitating 12-step

treatment attendance by promoting an abstinence goal, increasing
willingness to use 12-step attendance as a tool to help achieve
abstinence, and monitoring reaction to 12-step attendance.
Integrated with Within existing treatment, such as cognitive-behavior therapy,

other treatment incorporating encouragement to attend 12-step meeting patients
to agree to attend specific meeting, and discussing 12-step
literature, meeting, and sponsorship
Modular add-on Assertive linkage to specific groups, review of 12-step program

and common concern, direct connection to current 12-step
members, and review of patient attendance and experiences
43
四.Alcoholic Anonymous
44
22
Introduction
 1935, an Akron, Ohio, surgeon named Bob
Smith took his last drink, a beer, to steady
his nerves prior to performing surgery.
 Bill, a New York stockbroker who was newly

sober, was about to drink while in Akron.
Met Bill Wilson, in Akron, Ohio 1935 .
45
AA Survey Data
The increasing transparency between AA and medicine is reflected by the fact that
75% of members’ physicians know they are in AA.
46
23
AA Survey Data
47
Referral to AA
 Over 40% were referred by(2011 )
 treatment facilities
 counseling agencies
 health professionals
 29% were self-motivated
 34% were referred through an AA member
 25% by family
 12% by court order
 4% by an employer or fellow employee
 1% by clergy.
48
24
Length of Sobriety
 Length of Sobriety
 27%: less than 1 year
 24%: 1-5 years
 12%: 5-10 years
 36%: more than 10 years
49
AA Program
 The program of AA is considered a fellowship.
 Fellowship:
 a “mutual association of persons on equal and friendly”
 a mutual sharing, as of experience, activity, or interest.
 Primary focus
 “to stay sober and to help other alcoholics to achieve
sobriety”
 Structured
 Meeting
 AA literature
 the 12-steps and 12 traditions
50
25
AA Program
 Sponsorship is another structured feature of AA.
 The process of AA is a powerful but not fully
understood dynamic
 The process includes
 spiritual growth
 pathological narcissism
 empathy
 interpersonal support
 group adhesion
 unique as each individual participant
51
Meeting
 Speaker meeting:
 tells his or her story to the group
 putting emphasis on what happened(e.g., the effect
of alcohol in that person’s life)
 what was done about it(how the person got sober)
 what is the person doing now to stay sober
 Step meeting: the 12-steps is introduced by a
group leader and discussed by the member.
 Discussion meeting : a group discussion focus
on a salient aspect of recovery.
52
26
AA Literature
 Each AA meeting starts with the leader of the meeting
reading the AA preamble:
Alcoholics Anonymous is a fellowship of men and women
who share their experience, strength, and hope with each
other that they may solve their common problem and help
others to recover from alcoholism. There are no dues or fees
for AA membership; we are self-supporting through our own
contributions. AA is not allied with any sect, denomination,
politics, organization, or institution ; dose not wish to engage
in any controversy, neither endorses nor opposes any
causes. Our primary purpose is to stay sober and help
other alcoholics to achieve sobriety.
53
(一)Psychological
Mechanisms in AA
54
27
 That acquiring a mentor or sponsor in AA
as guide to lead on through the 12steps is
predictive of increased abstinence and
reduction in drinking intensity.
 Individual who has acquired and nurtured a

relationship with a sponsor that explains
reductions in substance use.
55
Psychological
process
1 2
Prescribed Desired
3
AA outcome,
behavior abstinence
4
FIGURE 37-1 Four conditions to establish statistical mediation in
identifying processes of psychological change
56
28
(二) Specific Psychological
Mechanism
57
Cognitive-Based
Psychological Processes
 Compared motivational enhancement
therapy (MET), cognitive behavior
therapy(CBT), TS facilitation(TSF)
 TSF clients report significantly higher rate of
abstinence at 12-month follow-up than did CBT
and MET clients
 All the patients: significant and relatively equal
increases in self-efficacy to remain abstinent
and decreases in positive expectancies
surrounding the use of substance.
58
29
Confidence to Remain Abstinent
 Higher rates of AA meeting attendance
 associated with higher levels of motivation to
abstinence.
 predict higher self-efficacy to remain abstinent
 Increased self-efficacy and powerlessness
over alcohol:
 AA members acknowledging a loss of control
after taking the first drink of alcohol but have
some personal control and/or responsibility in
taking the first drink
59
Spirituality
60
30
Clinical Recommendation
 Practitioners should be familiar with
the core AA literature and should
experience firsthand the environment
and fellowship of AA by attending
several meeting.
61
五.Therapeutic
Community
62
31
Introduction
 TC for psychiatric patients : by Maxwell
Jones and others in the UK(Jones 1953)
 TC for the substance use patients:
 Emerged in the 1960 as a self-help alternative to
existing conventional treatment.
 Recovering alcoholic and drug-addicted
individuals were its first participants
/developers.
 The modern antecedents can be traced to AA
and Synanon
63
Introduction
 Traditional community-based TCs are
similar in
 Structure: decreased from 15-24 months to 9-
15 months
 Staffing pattern
 TC-trained clinicians(with and without recovery
experiences)
 other human service professionals
 Perspective
 Approach
 medical, mental health, vocational, educational,
family, counseling, fiscal, administrative, legal service
 Different in size(from30 to several hundreds)
64
32
(一)The TC Perspective
65
Introduction
 The TC perspective consists four
interrelated views:
1. substance use disorder
2. Individual
3. recovery
4. right living
66
33
View of Disorder
 Drug abuse:
 a disorder of the whole person
 affecting some or all area of function
 The TC and
Cognitive perspective consider the problem
behavior problems:

toThinking
be thebeindividual,
unrealistic or disorganized
not the drug, and
 Value may be confused
addiction is a symptom, not the essence
 Nonexistent
of the disorder.

Antisocial
 Deficits in verbal, reading, writing or marketable skills
 moral or spiritual issue
 The TC perspective:
67
View of the Individual

TC experience
• development for the first time of a

Habilitation socially productive, conventional
lifestyle
• referring to return to lifestyle

Rehabilitation previously lived, known, and
perhaps rejected
68
34
View of the Individual
Table 34-1 Typical behavioral, cognitive, and emotional
characteristics of substance abusers in TC
1. Low tolerance for all forms of discomfort and delay of gratification
2. Problems with authority
3. Inability to manage feelings (particularly hostility/anger, guilt, and anxiety)
4. Poor impulse control (particular sexual or aggressive impulses)
5. Poor judgment and reality testing concerning consequences of actions
6. Unrealistic self-appraisal regarding discrepancies between personal
resource and aspiration
7. Prominence of lying, manipulation, and deception as coping behaviors
8. Personal and social irresponsibility (e.g., inconsistency or failures in
meeting obligations)
9. Marked deficits in learning and in marketable and communication skills
69
View of Recovery
Rehabilitation • in both lifestyle and personal identity
• negative patterns of behavior, thinking

Psychological and feeling that predispose the individual
to drug use
• develop the skills, attitudes, and value of

Social a responsible drug free lifestyle
Enduring • conduct, emotion, skill, attitudes, and

change value
70
35
View of Recovery - Motivation
 Motivation
 external pressure
 Internal motivation: remaining in

treatment
71
View of Recovery –
Self-Help and Mutual Self-Help
 Treatment:
 staff and peer
 daily regime of work, group, meetings,
seminars, and recreation.
 self-help
 mutual self-help
72
36
View of Recovery –Social Learning
 A life style change occurs in a social
context.
 Learning:
 social interaction
 program activities
 taking on various social roles
 Keep a positive social network
73
View of Right Living

 Healthy personal and social living value:
 truth and honesty
 a work ethic
 self reliance
 earned rewards
 achievement
 personal accountability
 responsible
 social manners
 community involvement
74
37
(二)The Therapeutic
Community Approach
75
Introduction
 The TC approach : “community as
method”.
 community itself provides a context of
relationships and activities for social
learning.
 teach individuals to use the community to
change themselves.
 obtain therapeutic and educational impact.
76
38
TC Program Model
 The key components of the program
model:
 social organization (structure)
 work
 peer roles
 staff role
 Functions of components
 understanding of the TC perspective
 affiliation and self-change
77
TC Program Model
- Structure/Social Organization
 Organization
 stratified
 few staff
 resident peers at junior, intermediate, and senior levels
 mutual responsibility.
 Residents perform:
 all house services(e.g., cooking, cleaning, kitchen service,
minor repair)
 serve as apprentices
 run all departments
 conduct house meetings
 certain seminars, and
 peer encounter groups
78
39
TC Program Model
- Structure/Social Organization
 Staffs response
 monitor and evaluate patient status
 supervise resident groups
 assign and supervise resident jobs
 oversee house operations
 conduct therapeutic groups
 provide individual counseling
 organize social and recreational projects
 make decision about resident status, discipline,
promotion, discharge, furloughs, treatment
planning
79
TC Program Model
- Work As Education and Therapy
 Hierarchy:
 according to seniority, clinical progress, and
productivity.
 Job promotion
 Is an explicit measure of the resident’s
improvements and growth
 Lateral or downward job movements also
create situations that require demonstration of
maturity in coping with frustration,
disappointment, and delay of gratification.
80
40
TC Program Model
- Peer as Role Model
 Peer role models

 Primary mediators of the recovery process.
 Expected behaviors
 ”Act as if”: should be, rather than has been
 willingness to confront others
81
TC Program Model
- Staff members as Rational Authorities
 TC residents often have previously

had difficulties with authority.
 Staff members perform as role models
and rational authorities.
82
41
Specific Methods/Interventions
-Therapeutic-Educative Activities
 Group therapy and individual
counseling.
 express feeling and to resolved personal
and social issues
 increase communication and interpersonal
skills
 bring about examination and confrontation
of behavior and attitude
 offer instruction in alternative modes of
behavior
83
-Therapeutic-Educative Activities
 Group activities:
 Encounter, probe, marathons, and
tutorials
84
42
-Community Enhancement Activities
 Community Enhancement Activities
 scheduled
 Morning meeting, seminar, house meeting-held
each day
 General meeting-when needed, negative
behavior, attitudes
 nonscheduled
 informal activities
 related to rituals and traditions, celebrations
(birthday, graduation, phase change),
cremonies….
85
-Community and Clinical Management Elements
 Management Elements
 maintain the physical and psychological safety
 ensure that resident life is orderly and
productive
 staff-managed elements
 Privileges
 Disciplinary sanctions
 Surveillance
 urine test
86
43
Program Stage and Phases
 Stage1: Orientation-Induction(1-60 Days)
 Assimilate the individual into the community
 Stage 2: Primary Treatment(2-12 Months)

 2-4 months
 5-8 months
 9-12 months: role model
87

 Stage 3: Reentry(13-24 Months)
 Initiate patients return to living in the macro
community.
 2 phases of this stage.
 Early reentry phase(13-18 Months):live in the
facility, is to prepare for separation from
community.
 Later
reentry phase(18-24 months):successful
separation from the community.
88
44
 Graduation:
 the end of active program involvement
 completion, or graduation, is not an end but
a beginning
 Aftercare
 social service
 intensive day treatment
 step-down outpatient ambulatory treatment
 linkages with outside agencies.
89
Patients Admitted to TCs

-Conduct and Referral
 Approximately 25-35% of adult
 a legal status
 being paroled
 probated
 otherwise court ordered to treatment.
 A majority of adolescents admission

to TC are legal referral.
90
45
Patients Admitted to TCs
-Meeting Criteria for Residential Treatment
 Exclusion from the TC

 burden to the staff
 pose threat to security and health of the
community.
 history of arson, suicide attempt,
serious psychiatric disorder.
91
Research: Effectiveness
 Outcomes variables: drug use, criminality,
and employment.
 Relationship between retention in treatment
and positive post-treatment outcomes in
TCs.
 complete treatment
 the longer the better
 Cost-benefit outcome
 reduced criminal activity and gains in
employment
92
46
Evolution of the TC:
Modifications and Applications
 The modalities include short-

term(<90 days), medium-term(6-12
months), and long-term(1-2 years).
93
Evolution of the TC:

The TC Human Service
 Staffs
 Mental health
 Medical
 Educational
 Family
 Social workers
 Case manager
94
47
95
96
48
97
98
49
Prof. San-Yuan Huang
Prof. San-Yuan Huang graduated in medicine at the National Defense Medical Center,
Taipei, Taiwan, ROC. He completed his psychiatry residency at Tri-Service General
Hospital, Taipei, Taiwan. After psychiatry resident training, Dr. Huang received his Ph.D.
degree also from the National Defense Medical Center. His academic research focuses on
gene-gene, and gene-behavior-environment interaction in substance use disorders such as
alcohol dependence, depressive alcoholism and other illegal drug abuse. After Ph.D.
degree, he main academic interests/ research are in gene, brain image with SPECT and
PET, psycho-immunology in addiction and mental related disorder.
Currently Dr. Huang is the president of Taiwanese society of addiction science (TSAS).
He is also a professor in Psychiatry at National Defense Medical Center, and the Director
of the Department of Psychiatry at the Tri-Service General Hospital. He is active in
addiction services, particularly in the rehabilitation of addictive patients and promotion of
mental health in the addiction.
Prof. Huang has published more than one hundred and ten original paper, and he serves
on various journal/ and grant review committees including NSC/ MOD, NHRI and
NRPB….. research study sections.
黃三原近一年代表著作(2015-6-30 更新)

SCI (Original article, First or corespondance, SCI only)
1. Yen CH, Yeh YW, Liang CS, Ho PS, …..Lu RB, *Huang SY (correspondence) Reduced
dopamine transporter availability and neurocognitive deficits in male patients with alcohol
dependence. PLoS One. PLoS One. 2015 Jun 29;10(6):e0131017
2. Yeh YW, Ho PS, Chen CY,…..Lu RB, *Huang SY (correspondence) Suicidal ideation
modulates the reduction in serotonin transporter availability in male military conscripts
with major depression: a 4‐[18F]‐ADAM PET study. World J Biol Psychiatry. 2015 Jun
12:1‐11. (2013 Impact factor: 4.225; 26/134 on psychiatry)
3. Yeh YW, Kuo SC, Chen CY,…..Lu RB, *Huang SY (correspondence) Harm avoidance
involved in mediating the association between nerve growth factor (NGF) gene
polymorphisms and antidepressant efficacy in patients with major depressive disorder J
Affect Disord. J Affect Disord. 2015 May 15;183:187‐194
4. Chang HA, Chang CC, Kuo TB, *Huang SY (correspondence) Distinguishing bipolar II
depression from unipolar major depressive disorder: Differences in heart rate variability.
World J Biol Psychiatry. 2015 Mar 24:1‐10. (2013 Impact factor: 4.225; 26/134 on
psychiatry)
5. Tzeng NS, Lu RB, Yeh HW, Yeh YW, Huang CC, Yen CH, Kuo SC, Chen CY,, , Chang HA, Ho
PS, Cheng S, Shih MC, *Huang SY (correspondence) The dopamine transporter gene may
not contribute to susceptibility and the specific personality traits of amphetamine
dependence. Drug and Alcohol Dependence 2015 Apr 1;149:100‐7. (2013 Impact factor:
3.23; 4/18 on substance abuse)
6. Yeh YW, Ho PS, Kuo SC,….., *Huang SY (correspondence) Disproportional reduction of
serotonin transporter may predict the response and adherence to antidepressants in
patients with major depressive disorder: a positron emission tomography study with 4‐
[18F]‐ADAM. Int J Neuropsychopharmacol. 2015 Jan 18 (7) 1‐12 (2014‐12 accepted)
(2013 Impact factor: 5.264; 18/134 on Psychiatry)
7. Huang CC, Lu RB, Yen CH, ……. Shih MC, *Huang SY (correspondence) Dopamine
transporter gene may be associated with bipolar disorder and its personality traits. Eur
Arch Psychiatry Clin Neurosci. 2015 Jun;265(4):281-90 (2013 Impact factor: 3.355; 39/134 on
Psychiatry)
8. Yeh YW, Chen CJ, Jang FL, Kuo SC, Chen CY, Liang CS, Ho PS, Yen CH, Shyu JF, Wan FJ, Lu
RB, *Huang SY (correspondence) SLC6A2 variants may predict remission from major
depression after venlafaxine treatment in Han Chinese population. J Psychiatr Res. 2015
Feb;61:33‐9. (2013 Impact factor: 4.092; 27/134 on Psychiatry)
9. Liang CS, Ho PS, Yen CH, Yeh YW, Kuo SC, Hung CC, Chen CY, Shih MC, Ma KH Lu RB,
*Huang SY (correspondence) Reduced striatal dopamine transporter density associated
with working memory deficits in opioid‐dependent male subjects: a SPECT study, Addict
Biol (2014‐11 PDF Proof) (2013 Impact factor: 5.929; 1/18 on substance abuse)
10. Yeh YW, Ho PS, Chen CY, Kuo SC, Liang CS, Ma KH, Shiue CY, Huang WS, Cheng CY, Wang
TY, Lu RB, *Huang SY (correspondence) Incongruent reduction of serotonin transporter
associated with suicide attempts in patients with major depressive disorder: a positron
emission tomography study with 4‐[18F]‐ADAM. Int J Neuropsychopharmacol. 2014 Oct
31;18(3)1‐9. (2012 Impact factor: 5.641; 13/135 on Psychiatry)
11. Chang CC, Chang HA, Chen TY, Fang WH, *Huang SY (correspondence) Sex‐Specific
Association Between Nerve Growth Factor Polymorphism and Cardiac Vagal Modulation.
Psychosomatic Medicine, 2014 Oct;76(8):638‐43. (2013 Impact factor: 4.085; 28/134 on
Psychiatry; 11 of 126 in Psychology )
12. Chang CC, Chang HA, Chen TY, Fang WH, *Huang SY (correspondence) Brain‐derived
neurotrophic factor (BDNF) Val66Met polymorphism affects sympathetic tone in a
gender‐specific way. Psychoneuroendocrinology 2014 Sep;47:17‐25. (2013 Impact
factor: 5.591; 13/134 on Psychiatry)
13. Chang HA, Chang CC, Tzeng NS, Kuo TB, Lu RB, *Huang SY (correspondence)
Heart rate variability in unmedicated patients with bipolar disorder in the manic phase.
Psychiatry Clin Neurosci. 2014 Sep;68(9):674‐82.
14. Kuo SC, Yeh YW, Chen CY, Huang CC, Chang HA, Yen CH, Ho PS, Liang CS, Chou HW, Lu
RB, *Huang SY (correspondence). DRD3 variation associates with early‐onset heroin
dependence, but not specific personality traits. Prog Neuropsychopharmacol Biol
Psychiatry. 2014 Jun 3;51:1‐8. (2013 Impact factor: 4.025; 33/194 on clinical neurology;
29/135 on Psychiatry)
How to establish a consistent policy in drug
intervention: from government to popular education.
San-Yuan Huang MD. PhD

Department of Psychiatry
National Defense Medical Center
Tri-Service General Hospital Taipei, Taiwan
大綱
1. 世界各國藥物濫用防制政策？各國治理系絡與毒品控制環境，來討探是否會
因各國國家毒品政策的不同而有不同的面貌。
2. 我國毒品防制政策之背後政策哲學基礎為何？
3. 各地方毒品防制中心防制與執行之重點與困境為何？
4. 現行戒癮治療之法律依據。
1
一、美國毒品防制政策之執行經驗
• 1988年美國成立白宮毒品政策管制辦公室美國緝毒局（DEA
）為該國最主要之毒品問題主管機關.
• 美國反毒政策約可分為三類：
（1）禁止：努力查緝走私，但仍受挫於直線上升的走私數量
（2）執行：美國大約有四成的被捕者都與毒品有關
（3）教育：難以評估其實際效果
二、荷蘭毒品防制政策之執行經驗
• 荷蘭之毒品政策由該國衛生部負責協調。
• 從1970年代開始，荷蘭對毒品政策即採實用的減害取向（
Harm Reduction），導致毒品防治系統優先著重健康照護與
預防，同時，並強力掃蕩組織犯罪，將毒品使用的風險與危
害縮減到最小。
• 毒品政策之主要目的在於預防或限制使用毒品所生之風險
與危害。
2
三、澳洲毒品防制政策之執行經驗
• 毒品法規緊隨國際毒品條約(1925年日內瓦鴉片－與毒品公約之規定)
• 1970年代與1980年代早期，澳洲的毒品政策反映了美國對毒品嚴打的
態度，提高刑度，僅需不高的證據證明力即可定罪，並制訂財產沒收
的法律。
• 1985重要的轉變，其著重於公眾健康及減害，強調毒品問題應被視為
健康議題，
• 1993年持續強調減害計畫（Harm Reduction）的重要性
• 1999年: 非法藥物的使用從刑事司法體系轉向教育與治療，但不適用
於毒品交易的犯行。
四、英國毒品防制政策之執行經驗
• 內政部中設有毒品政策理事會: 負責研擬、指揮、執行毒
品政策，以及研究發展與統計
• 內政部毒品行動組（Drug Action Teams, DATs）是執行
國家毒品策略的地方層級組織，由當地政府（教育、社會服務、住
宅）、健康、觀護、監獄及志工等跨部門合作。毒品行動組（DAT）須對英國
的內政大臣負責.
• 我國縣市政府毒品危害防制中心之構想與設置是我國地方
政府層級組織，亦源自於英國毒品行動組之設置與執行。
3
七、中國毒品防制政策之執行經驗
• 由公安部、衛生部和海關總署等25個部門組成的國家禁毒
委員會，統一領導全國的禁毒工作，負責禁毒國際合作，
辦事機構設在公安部。
• l998年，國務院批准公安部成立禁毒局，該局同時又作為
國家禁毒委員會的辦事機構。
聯合國毒品防制政策之執行經驗
• 1997年11月，聯合國成立了聯合國毒品控制和犯罪預防辦公室
(United Nations Office for Drug Control and Crime
Prevention, UNODC)，是全球在打擊非法毒品和國際犯罪方面的
領導者。辦公室設在維也納。
• 主要任務是預防恐怖主義、在全球進行反洗錢、反腐敗、反有組
織犯罪和反販賣人口等活動，
• 聯合國國際麻醉品管制署和聯合國國際犯罪預防中心，均由毒品
控制和犯罪預防辦公室執行主任領導。
4
• 荷蘭將毒品區分為硬性毒品與軟性毒品,並採取不同的政
策與管制措施，是對軟性毒品的「容忍」。而非對軟性毒品
的「除罪化」。
• 美國對於毒品採取零容忍之態度
• Alex Wodak（2006）分析全球毒品政策的趨勢一逐漸轉向災
害減量
當查緝及治療仍無法解決毒品問題?
• Harm reduction 之毒品策略以成為尋求解決毒品問題之
新思維，以減少成癮行為使用者與其所處社會所帶來的有
害後果。
• 在政策上，當吸毒問題在斷絕供應與減少需求兩大策略下
仍無法有效解決，必須以務實態度面對吸毒問題對社會、
衛生、經濟、社會福利等各方面所產生的各項問題，因此
減少損害也自然成為因應毒品問題的一種思維方式。
5
全球治理毒品問題之政策因應措施
• 整體而言，在減少毒品供應與減少毒品需求之態度是一致的
，
• 差別在於對毒品問題之刑事政策與公共衛生安全之考量，
• 如中國大陸、泰國、馬來西亞對於毒品犯（製造、運輸、販賣
者）採取嚴刑峻罰手段，荷蘭、澳洲對施用大麻，所採取之
容忍態度
• Alex Wodak（2006）分析全球毒品政策的趨勢---逐漸轉向
減害取向(Harm reduction)
國際間所採行之減害計畫
• 主要包括：
• 1、針頭交換計畫；
• 2、海洛因處方計畫；
• 3、替代性治療；
• 4、安全注射室。
6
2. 我國毒品防制政策之背後政策哲學基礎
為何？
各國經驗對我國毒品防制政策之影響：
1. 組織設計之參考世界各國多數皆採行組織設計之任務型編組
方式。
2. 執行機關之層級多數國家在中央與地方皆設有專責的反毒機
關或單位
3. 減害觀點之成效建立衛生單位與藥癮者接觸的平臺，給他們歸復社會的機會，可
以使他們無須過著每天找藥，甚至因而犯罪的生活，讓毒品對國民及社會的傷害降到最低。
4. 政策重點之強調從過去支持的嚴打政策轉變成現今較多數國
家認為較有成效的減害取向。
7
我國毒品防制政策
• 我國以往反毒工作:著重供給面之毒品查緝，而對於需求
面之拒毒及戒毒工作，所投入之資源相對較低
• 95 年「行政院毒品防制會報」:由過去「斷絕供給，降低
需求」，調整為「首重降低需求，平衡抑制供需」，加強
反毒之預防工作，並建立「防毒」、「拒毒」、「戒毒」
及「緝毒」之四大工作區塊
我國反毒策略及組織架構
2008行政院研究發展考核委員會 - 毒品防制政策整體規劃報告
8
毒品防治體系之分工
首重降低需求平衡抑制供需
拒毒預防組毒品戒治組防毒監控組緝毒合作組國際參與組
減少初次施減少再次施管控先驅化查緝境內外結合國際及兩

用毒品者用毒品者學物質毒品供給岸共同反毒
教育部負責衛福部負責法務部負責
3.各地方毒品防制中心防制與執行之重點
與困境為何？
9
毒品危害防制中心設置要點
• 法規位階：行政規則-屬行政程序法第159條第2項第1款規
定之行政規則
• 第2-1條
• 直轄市、縣（市）政府為執行毒品防制工作，應由專責
組織辦理毒品防制工作：；必要時，得由各中央目的事
業主管機關視實際情形酌予補助。
• 目前困境: 人力不足; 戒成專線知名度低
毒品危害防制中心之組織架構
10
地方毒品危害防制中心的困境
• 任務編組的人員配置到反毒業務的金額補助有限，人力不
足
• 工作同仁常面臨吸毒犯強烈的心理依賴與病識感不足的困
境，
• 前者所導致的高再犯率使得民間資源普遍投入的意願不高
。
• 後者則為吸毒者配合意願不高讓政府的輔導措施面臨難以
推動的困境。
102 監察院報告
11
4. 現行戒癮治療之法律依據
管制藥品與毒品關係
管制藥品毒品
適用法律管制藥品管理條例毒品危害防制條例
一、成癮性麻醉藥品。麻醉藥品與其製品及影響精神物質與其製品。
二、影響精神藥品。醫藥及科學上需用之麻醉藥品與其製品及影
定義三、其他認為有加強管理必要之藥品。響精神物質與其製品之管理，另以法律定之。
前項管制藥品限供醫藥及科學上之需用。
分級原則依其習慣性、依賴性、濫用性及社會危害性依其成癮性、濫用性及對社會危害性分為四

之程度，分四級管理。級。
審議由中央衛生主管機關設置管制藥品審議委員由法務部會同衛生福利部組成審議委員會，
委員會會審議後，報請行政院核定公告之。每三個月定期檢討，報由行政院公告調整、
增減之
罰則行政罰(罰鍰) 刑罰(判刑或罰金)、行政罰(罰鍰)
12
Law and Policy
‧81年肅清煙毒條例 (22條)
‧88年毒品危害防制條例 (Narcotics Hazard Prevention Act
36條毒品之分級及品項, 2015-2 更新公告)
目的:防制毒品危害，維護國民身心健康
‧毒品戒癮治療實施辦法及完成治療認定標準 (15 條)
依毒品危害防制條例第二十四條第三項規定訂定
(2013年6月更新公告)
25
毒品危害防制條例
(Narcotics Hazard Prevention Act)
第1條（立法目的）第14條(持有或轉讓罌粟、古柯、大麻種子罪）第27條（勒戒處所之設立）
第2條（毒品之分級及品項）第15條（公務員加重其刑),第16條（刪除）第28條（戒治處所之設立）
第17條（減輕其刑）
第2條之1（毒品防制專責組織之成立及應辦事項）第29條（觀察、勒戒及強制戒治
第3條（適用範圍）第18條（專供製造或施用毒品之器具罪）執行之規定）
第19條（犯罪所用或因犯罪所得之財物沒收）第30條（觀察、勒戒及強制戒治
第4條（販運製造毒品罪）
第20條（施用毒品者送勒戒處所觀察、勒戒）費用）
第5條（意圖販賣而持有毒品罪）第30條之1（請求返還已繳納之觀察、
第20條之1（重新審理之聲請）
第6條（強迫或欺瞞使人施用毒品罪) 戒或強制戒治費用）
第21條（施用毒品自動請求治療者）第22條第31條（工業原料之種類及申報
第7條（引誘他人施用毒品罪）第23條（強制戒治期滿之裁定）、檢查）
第8條（轉讓毒品罪）第23條之1（拘提逮捕者之裁定觀察、勒戒）第32條（獎懲辦法）
第9條（加重其刑）第23條之2（觀察、勒戒或強制戒治者之裁定第32條之1（偵查計畫書之提出）
第10條（施用毒品罪）處分）第32條之2（偵查計畫書應載事項
第24條（戒癮治療之緩起訴處分） )
第11條（持有毒品罪）
第11條之1（不得擅自持有毒品及器具）第24條之1（觀察、勒戒或強制戒治處分
第33條（特定人員及採驗尿液實施辦法
之執行時效）第34條（施行細則,法務,內政,衛福）
第12條（栽種罌粟、古柯、大麻罪）
第25條（強制採驗尿液）第35條（本條例繫屬施用毒品案件之處理）
第13條（販運罌粟、古柯、大麻種子罪） 26
第26條（行刑權時效）第36條（施行日）
13
毒品戒癮治療實施辦法及完成治療認定標
第1條: 法源(依毒品危害防制條例第二十四條第三項規定) ‧第9條:治療屆滿(連驗尿三次)
第2條: 實施對象(1,2級) ‧第10條:治療停止，應通知該
第3條: 治療之方式 ‧ 管檢察機關
第4條: 機構設置與教育8小時 ‧第11條:
第5條: 設置專責聯繫人員 ‧第12條:撤銷治療之4種情形
第6條: 參加治療被告之同意 ‧第13條:治療期滿送交成果
第7條: 治療之期程(一年) ‧第14條:費用負擔
第8條: 檢驗、檢查 ‧第15條:公佈或修正日期
27
替代治療執行機構之醫療團隊
（一）中央衛生主管機關指定藥癮戒治醫院
1、應有受過藥癮治療相關訓練之團隊，包括精神科專科醫師、
藥師、護理人員、臨床心理師、職能治療人員及社會工作人
員至少各一名。
2、精神科專科醫師應具有管制藥品使用執照。
（二）其他醫院、診所或衛生所：
1、應有醫師、藥師及護理人員，至少各一名。
2、醫師應具有管制藥品使用執照。
3、不能提供臨床心理、職能治療或社會工作等相關服務者，應
與前款中央衛生主管機關指定藥癮戒治醫院建立合作關係。
執行替代治療之各類人員，每年應接受替代治療繼續教育講習至少八小時。
14
臨床問題一:為何施用第一級毒品可緩起訴
但施用二級不可緩起訴?
修正前修正後說明與修正前後差異
（1998年10月30日起） (2013年6月26日起) （本會諮詢主管機關後補充）
第二條第二條說明：
戒癮治療之實施對象，為施用第一戒癮治療之實施對象，為施用第一常見第二級毒品包含安非他命
級毒品海洛因、嗎啡、鴉片及其相級毒品海洛因、嗎啡、鴉片及前開 (Amphetamine)、大麻(Cannabis)、
類製品者。相類製品與第二級毒品者。古柯(Coca)、可待因(Codeine)、罌
被告有下列情事之一時，不適合為被告有下列情事之一時，不適合為粟(Opium poppy)、麥角乙二胺
附命完成戒癮治療之緩起訴處分，附命完成戒癮治療之緩起訴處分。 (LSD)、液態快樂丸(GHB)、搖頭
但無礙其完成戒癮治療之期程者，但無礙其完成戒癮治療之期程者，丸(MDMA)、大麻脂(Cannabis
不在此限：不在此限： resin)、芬那多松(Phenadoxone)等。
一、緩起訴處分前，因故意犯他罪，一、緩起訴處分前，因故意犯他罪，其他品項以法務部公布之〈毒品危
經檢察官提起公訴或判決有罪經檢察官提起公訴或判決有罪確害防制條例〉為準，可上全國法規
確定。定。。資料庫查詢。
二、緩起訴處分前，另案撤銷假釋，二、緩起訴處分前，另案撤銷假釋，
等待入監服刑。等待入監服刑。差異：
三、緩起訴處分前，另案羈押或執三、緩起訴處分前，另案羈押或執明確規定第二級毒品於戒癮治療
行有期徒刑。行有期徒刑。範圍內。
29
臨床問題二:戒癮治療僅可用藥物治療嗎?
戒癮治療之方式如下：
一、藥物治療。
第 3 條二、心理治療。
三、社會復健治療。
前項各款之治療方式應符合醫學實證，具
有相當療效或被普遍採行者。
30
15
臨床問題三:醫療人員每年接受相同的美沙冬藥癮
相關持續教育八小時有意義嗎?
醫療機構置有曾受藥癮治療相關訓練之精神科專科醫師、藥
師、護理人員、臨床心理師、職能治療人員及社會工作人員
各一名以上，且其精神科專科醫師領有管制藥品使用執照者
得向中央衛生主管機關申請認定為戒癮
第 4 條治療機構（以下稱治療機構）。
前項人員每年應接受藥癮治療相關繼續教育八小時。
中央衛生主管機關得依戒癮治療需求，依第一項所定資格指
定治療機構；其於醫療資源不足地區指定之治療機構，得不
受第一項所定條件之限制。
31
臨床問題四:要治療多久才算完成?
第 7 條戒癮治療之期程以連續一年為限。
32
16
臨床問題五:每一樣檢查有規定都要做嗎?
第八條第八條說明：
接受戒癮治療者於治療前接受戒癮治療者於治療前應使戒癮治療更符合個案需
應由治療機構進行下列檢由治療機構評估後，視需要求並避免戒癮治療因個案
驗、檢查：進行下列檢驗、檢查：身體狀況所產生的影響。
一、尿液毒品及其代謝物一、尿液毒品及其代謝物檢本法並未明文規定個案需
檢驗。驗。要或不需要檢查的標準，
二、肝功能檢驗。二、肝功能檢驗。評估與決定權在於戒癮治
三、B型肝炎表面抗原及三、B型肝炎表面抗原及其療機構或提供戒癮治療的
其抗體檢驗。抗體檢驗。醫療院所之醫師。
四、C型肝炎抗體檢驗。四、C型肝炎抗體檢驗。
五、人類免疫缺乏病毒感五、人類免疫缺乏病毒感染差異：
染檢驗。檢驗。加入醫療人員依個案需求
六、梅毒血清檢驗。六、梅毒血清檢驗。進行評估。
七、胸腔X光檢查。七、胸腔X光檢查。
八、心電圖檢查。八、心電圖檢查。 33
臨床問題六:未依指定時間接受藥物治療逾七日
就要退出嗎?
第十二條第十二條說明：
被告於緩起訴期間，有下列情被告於緩起訴期間，有下列情形未接受治療的原因可能是個案
形之一者，視為未完成戒癮治療之一者，視為未完成戒癮治療，得身體其他問題、工作繁忙、委任
得撤銷緩起訴處分。撤銷緩起訴處分：出差或其他不可抗因素，本條文
一、於治療期間，未依指定時一、於治療期間，無故未依指修正允許個案有條件的延期。
間接受藥物治療逾七日。定時間接受藥物治療逾七日。超過七日未接受治療者得檢附
二、於治療期間，無故未依指二、於治療期間，無故未依指定延期相關證明(如看診紀錄、工
定時間接受心理治療或社會時間接受心理治療或社會復健作或會議記錄、出差紀錄)等交
復健治療逾三次。治療逾三次。由戒癮治療機構或看診醫院之醫
三、對治療機構人員有強暴、三、對治療機構人員有強暴、脅師報予檢察官以繼續緩起訴。
脅迫、恐嚇等行為。迫、恐嚇等行為。
四、於緩起訴期間，經檢察機四、於緩起訴期間，經檢察機關差異：
關或司法警察機關採尿送驗，或司法警察機關採尿送驗，呈增加未接受藥物治療的條件為
呈毒品陽性反應。毒品陽性反應。「無故未接受治療」。
34
17
臨床問題七:戒癮治療期為什麼突然被抓?
第十三條第十三條說明：
被告於戒癮治療期被告於戒癮治療期程主要是告知機構個
程屆滿後，依治療屆滿後，依治療機構案的費用可以結算、
機構函送之檢驗結函送之檢驗結果或診紀錄可以結案，以
果或診斷證明，未斷證明，未完成戒癮利後續作業。
完成戒癮治療者，治療者，得撤銷緩起差異：
得撤銷緩起訴處分。訴處分。緩起訴處分之撤銷，
檢察機關於撤銷緩起後會由檢察官通知
訴處分後，應即通知戒癮治療機構。
戒癮治療機構。 35
臨床問題八:戒癮治療費用由誰負擔?
第十四條第十四條說明：
戒癮治療費用，戒癮治療費用除經同時提醒個案有
由接受戒癮治療公私立機構補助減可以尋找的管道。
者自行負擔。免外，由接受戒癮差異：
治療者自行負擔。明確提到公立機
構補助情形(低收
或其他條件)。
36
18
管制藥品管理架構
• 習慣性
• 管制藥品登記證(機構、業 • 依賴性
者) • 濫用性
• 管制藥品使用執照(醫師等 • 社會危害性
專業人員) 分級
• 輸出、輸入、製造同意書
(源頭管理)
管理
• 相關證照：運輸憑照、醫藥
教育研究試驗使用核准函
流向
管理
簿冊登錄申報制度勾稽查核
機構業者衛生機關
新興濫用藥物列管程序管制藥品
法務部毒品審衛生福利部管制藥
毒品
議委員會品審議委員會
• 成癮性科學需用
• 濫用性
無例：Mephedrone
新興濫用藥物
• 對社會危害性
5-MeO-DIPT
醫療用途
2C-B
PMEA
• 習慣性
• 依賴性
有
管制藥品
• 濫用性法務部毒品審
毒品
• 社會危害性議委員會
衛生福利部管制藥例：Zaleplon
品審議委員會 Modafinil
Butorphanol
19
新興濫用物質列為管制藥品之原則
一、無醫療用途：無醫療用途之新興濫用藥物，則依毒品列管級
別，列屬相同級別。
二、有醫療用途：
1.聯合國新列管之麻醉藥品，依前述分級原則，分
屬第二至第三級管制藥品；聯合國新列管之影響
精神藥品，列屬第三至四級。
2.聯合國未列管，但我國有濫用傾向之品項，則參照其他國家(美、
英等)，並依結構或成癮性相近品項之級別列管。
Amphetamine
Methamphetamine is metabolized to amphetamine;
both can be present in urine after
methamphetamine use.
Methamphetamine Levoamphetamine : Dextroamphetamine
Para-
Hydroxylation
Amphetamine Beta-
Hydroxylation
• Methylphenidate :
Ritalin© or Concerta Oxidative
Deamination
• Lisdexamphetamine
Nor-ephedrine
20
各國新興濫用物質列管模式
列管模式說明舉例
單一物質列管模式根據聯合國三大公約精神所制定的法律
(The List Model) a.標準程序：傳統列管方式
b.緊急列管程序：如美國及英國的暫時列管措施
c.快速程序：與緊急列管類似，但此程序屬於永久列管無期限，如日本指定藥
物
類似物質列管模式廣義的化學結構相似性為原則，若某一物
(The Analogue System 質符合(a)實質結構相似性(b)實質化學相
Model) 似性，類似於目前已被列管的非法物質則
此物質即可以此模式列管
通用結構列管模式以物質結構式為原則，列管一連串家族類
(The Generic Legislation 似物質，此模式係一種防範於未來的工具，
Model) 在所有可能被合成的非法藥物尚未合成前
即預先列管的方法
台灣地區濫用藥物尿液檢驗檢體
檢體是誰送的? 身為專家的你送過嗎 ?
21
衛福部每年通報數據如何來?
謝謝大家為台灣成癮防治業務而努力
22

104年繼續教育 藥物濫用之治療本質、政策與復健機構設置

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104 年台灣成癮科學學會 持續教育 (系列二)

Time Topic Speaker Moderator

13:30-13:35 Opening 衛福部 陳快樂司長

The nature of treatment in substance 邱南英院長 陳展航主任

Neurobiology and management of 黃尚堅主任 王作仁 副院長

Rehabilitation settings: from inpatient 林滄耀主任 諶立中副局長

How to establish a consistent policy in 洪嘉均秘書長

18:20-18:40 Discussion all all

＊台灣成癮科學學會 5 學分、台灣精神醫學會繼續教育 5 學分及衛福部藥癮治療相關繼續教育 5

口頭報告與壁報論文共 171 篇，曾著作「香菸知多少」一書，

Dr. Nan-Ying Chiu

Science in the treatment of

• In the 1930s the founders of Alcoholics Anonymous (AA) realized

• Since the 1970s, science began to be applied to the understanding

• The poor treatment given to patients suffering from SUDs in the

Progress in research of treatment

• Only about one in 10 individuals with SUDs receives any treatment,

• Simply reducing withdrawal symptoms by giving a short-term

• Addiction is a chronic medical disease of the brain. It makes no

Training of treatment providers

• Many addiction counselors actively try to discourage the use of

• SUDs are among the most common of all disorders requiring

• The training of treatment providers of SUDs is essential.

• The ethical issue of treatment of SUDs should be considered.

• U.S. Food and Drug Administration-approved medications to prevent

• The neuroscience of addiction is very advanced compared with that

Science in the treatment of

• The Affordable Care Act requires that insurers provide treatment

• There is a great lack of physicians and other therapists educated on

The goals of assessing

• Make an accurate diagnosis and relating this to any other co-

• Identify barriers to treatment as well as strengths and supports.

• Assess and enhance the patient’s motivation to change.

• Formulate and help to initiate appropriate evidence-based

• Patient characteristics: Age, gender, partner of marital status, legal

Specify if: 特别註明 In early remission 早期緩解

Substance use disorders in DSM-5

• Intoxication: with use disorder, without use disorder, with perceptual

• Withdrawal: without perceptual disturbances, with perceptual

• Other substance/medication-induced mental disorders

Substance intoxication in DSM-5

DSM-5 Alcohol-related disorders

• Alcohol use disorder

DSM-5 Opioid-related disorders

• Opioid use disorder

• Tobacco use disorder

Signs and symptoms

• Accurate assessment is facilitated by interview settings that provide

• A substance use history should be obtained from all patients

• Collateral informant interviews, standardized questionnaires, and

Screening and brief intervention

• SBI is simultaneously a preventive intervention aimed at recurring

• SBI is not appropriate for people seeking help for symptoms of

• The Michigan Alcoholism Screening test (MAST) (Selzer 1971,

• Single screening questions (SSQs) are brief and have been

• The Alcohol Use Disorders Identification Test (AUDIT) (babor et al.

• The AUDIT-C (Bradley et al. 2007).

• Assessment of the patient’s perception and readiness to change

104年繼續教育藥物濫用之治療本質、政策與復健機構設置

104年繼續教育藥物濫用之治療本質、政策與復健機構設置

104年繼續教育藥物濫用之治療本質、政策與復健機構設置

104 年台灣成癮科學學會持續教育 (系列二)

13:30-13:35 Opening 衛福部陳快樂司長

The nature of treatment in substance 邱南英院長陳展航主任

Neurobiology and management of 黃尚堅主任王作仁副院長

Rehabilitation settings: from inpatient 林滄耀主任諶立中副局長