Module I Chemical Use, Misuse, Abuse, Dependence & Recovery
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Brain Networks Underlying Vulnerability and Resilience to Drug Addiction
Brain networks underlying vulnerability and resilience to drug addiction Karen D. Erschea,b,1,2, Chun Menga,b,1,2, Hisham Ziauddeena,c, Jan Stochla,d, Guy B. Williamse, Edward T. Bullmorea,b,c, and Trevor W. Robbinsb,f aDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0SZ, United Kingdom; bBehavioural and Clinical Neuroscience Institute, Department of Psychology, University of Cambridge, Cambridge CB2 3EB, United Kingdom; cCambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge CB21 5EF, United Kingdom; dDepartment of Kinanthropology and Humanities, Charles University, 16252 Prague, Czech Republic; eDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 3EB, United Kingdom; and fDepartment of Psychology, University of Cambridge, Cambridge CB2 3EB, United Kingdom Edited by Joseph E. LeDoux, New York University, New York, NY, and approved May 8, 2020 (received for review February 11, 2020) Regular drug use can lead to addiction, but not everyone who Much of the neuroscientific research on resilience has been ex- takes drugs makes this transition. How exactly drugs of abuse amined in adolescence (10), which is a period of heightened interact with individual vulnerability is not fully understood, nor is vulnerability and neural plasticity (11). While studies of adoles- it clear how individuals defy the risks associated with drugs or cents are important to inform the development and imple- addiction vulnerability. We used resting-state functional MRI mentation of preventative strategies, we also need to understand (fMRI) in 162 participants to characterize risk- and resilience- how resilience operates in vulnerable adults as the compensatory related changes in corticostriatal functional circuits in individuals mechanisms that have been characterized in adolescents do not exposed to stimulant drugs both with and without clinically di- necessarily translate into adulthood. -
Benzodiazepines
Benzodiazepines Using benzodiazepines in Children and Adolescents Overview Benzodiazepines are group of medications used to treat several different conditions. Some examples of these medications include: lorazepam (Ativan®); clonazepam (Rivotril®); alprazolam (Xanax®) and oxazepam (Serax®). Other benzodiazepine medications are available, but are less commonly used in children and adolescents. What are benzodiazepines used for? Benzodiazepines may be used for the following conditions: • anxiety disorders: generalized anxiety disorder; social anxiety disorder; post-traumatic stress disorder (PTSD); panic attacks/disorder; excessive anxiety prior to surgery • sleep disorders: trouble sleeping (insomnia); waking up suddenly with great fear (night terrors); sleepwalking • seizure disorders (epilepsy) • alcohol withdrawal • treatment of periods of extreme slowing or excessive purposeless motor activity (catatonia) Your doctor may be using this medication for another reason. If you are unclear why this medication is being prescribed, please ask your doctor. How do benzodiazepines work? Benzodiazepines works by affecting the activity of the brain chemical (neurotransmitter) called GABA. By enhancing the action of GABA, benzodiazepines have a calming effect on parts of the brain that are too excitable. This in turn helps to manage anxiety, insomnia, and seizure disorders. How well do benzodiazepines work in children and adolescents? When used to treat anxiety disorders, benzodiazepines decrease symptoms such as nervousness, fear, and excessive worrying. Benzodiazepines may also help with the physical symptoms of anxiety, including fast or strong heart beat, trouble breathing, dizziness, shakiness, sweating, and restlessness. Typically, benzodiazepines are prescribed to manage anxiety symptoms that are uncomfortable, frightening or interfere with daily activities for a short period of time before conventional anti-anxiety treatments like cognitive-behavioural therapy or anti-anxiety takes effect. -
The Effect of Opioids on Emotional Reactivity
The Effect of Opioids on Emotional Reactivity Steven M. Savvas, BHSc (Hons) Discipline of Pharmacology, School of Medical Sciences, Faculty of Health Sciences University of Adelaide August, 2013 A thesis submitted in fulfilment of the requirements for the degree of Doctor of Philosophy i Steven M. Savvas, PhD Thesis, 2013 TABLE OF CONTENTS Abstract .................................................................................................................................... xi Declaration ............................................................................................................................ xiii Acknowledgements ............................................................................................................... xiv CHAPTER 1 - INTRODUCTION ...................................................................................... 1 1.1 OPIOIDS AND OPIOID MAINTENANCE TREATMENT ...................................... 1 1.1.1 A BRIEF HISTORY OF OPIOIDS .......................................................................... 1 1.1.2 OPIOID RECEPTORS ............................................................................................ 1 1.1.3 ADAPTATION TO OPIOIDS.................................................................................. 3 1.1.3.1 Tolerance ........................................................................................................ 4 1.1.3.2 Withdrawal ...................................................................................................... 4 1.1.3.3 Dependence -
Module II Opioids
Module II Opioids 101 Module II: Opioids 101 Module II is designed to introduce participants to basic facts about opioids, including information on pharmacology, acute and long-term effects, and basic information about treatments for opioid addiction. This module contains background information necessary to understand the role of buprenorphine in the opioid treatment system. If the audience is already highly knowledgeable about opioid treatment, this module should be abbreviated or omitted. Slide 1: Title Slide Slide 1 The next module provides an overview of opioids and opioid treatment, setting the stage to see the role of buprenorphine in the treatment system. Slide 2: Goals for Module II Slide 2 We are now going to turn a little more directly to the issue of opioid addiction. This module reviews the following: Opioid addiction and the brain Descriptions and definitions of opioid agonists, partial agonists and antagonists Receptor pharmacology Opioid treatment options Page 62 Buprenorphine Treatment: A Training for Multidisciplinary Addiction Professionals Slide 3: Opiate/Opioid: What’s the Difference? Slide 3 Throughout this training we are using the term opioid to define the class of drug with which we are dealing. It is important to understand what this term means. Opiate refers only to drugs or medications that are derived directly from the opium poppy. Examples include heroin, morphine, and codeine. Opioid is a broader term referring to opiates and other synthetically-derived drugs or medications that operate on the opioid receptor system and produce effects similar to morphine. Examples include methadone, buprenorphine, meperidine, and fentanyl. Note to the Trainer(s): All opiates are opioids, but not all opioids are opiates. -
Reinforcement-Based Cognitive Biases As Vulnerability Factors
Reinforcement-based cognitive biases as vulnerability factors in alcohol addiction: From humans to animal models Karolina Noworyta1, Agata Cieslik1, and Rafal Rygula1 1Maj Institute of Pharmacology Polish Academy of Sciences March 15, 2021 Abstract Alcohol use disorder (AUD) is one of the most common but still poorly treated psychiatric conditions. Developing new treatments requires a better understanding of the aetiology of symptoms and evaluation of novel therapeutic targets in preclinical studies. Recent developments in our understanding of the reinforcement-based cognitive biases (RBCBs) that contribute to the development of AUD and its treatment offer new opportunities for both clinical and preclinical research. In this review, we first briefly describe psychological and cognitive theories that implicate various aspects of reinforcement sensitivity in the development, maintenance, and recurrence of alcohol addiction. Furthermore, in separate sections, we describe studies investigating RBCBs and their neural, neurochemical, and pharmacological correlates, and we discuss possible interactions between RBCBs and trajectories of AUD. Finally, we describe how recent translational studies using state-of-the-art animal models can facilitate our understanding of the role of reinforcement sensitivity and RBCBs in various aspects of AUD. Introduction Alcohol addiction is one of the biggest problems of modern society through its impact on health, social cohesion, crime, and its comorbidity with other neuropsychiatric disorders. Major advances in genetics and molecular neurobiology have led to the identification of many of the primary targets of alcohol and revealed neuroadaptations that develop with its chronic consumption. However, understanding pre-existing cognitive deficits that serve as substrates compounding the initiation of alcohol use and the development of alcohol use disorder (AUD) remains a major challenge. -
ED325463.Pdf
DOCUMENT RESUME ED 325 463 SP 032 697 AUTHOR McCorry, Frank T.T.TLE Preventing Substance kbuse: A Comprehensive Program for Catholic Educators. INSTITUTION National Catholic Educational Association, Washington, DC. Dept. of Elementary Schools. REPORT NO ISBN-1-55833-040-2 PUB DATE 90 NOTE 116p. AVAILABLE FROMNational Catholic Educational Association, Suite 100, 1077 30th St., NW, Washington, DC 20007-3852 ($8.70). PUD TYPE Guides - Non-Classroom Use (055) EDRS PRICE MF01/PC05 Plus Postage. DESCRIPTORS Alcohol AbIlse; *Catholic Educators; *Catholic Schools; *Drug Education; Elementary Secondary Education; Intervention; Parent Role; Prevention; Program Development; Referral; *Substance Abuse; *Teacher Role ABSTRACT This book provides information for teachers about drugs are their effects on body and mind, and explains the role of teachTrs in effective drug education, prevention, and ass:stance programs. Suggestions on preventing drug abuse are also directed to the Catholic community and parents, along with a challenge to introduce programs on the local, regional, and national levels. The book is comprised of 10 chapters: (1) "Understanding the Problem"; (2) "Gateway Drugs: The Beginning of the Problem"; (3) "Cocaine, Crack, Designer Drugs";(4) "Prevention and the 'Prevention, Intervention, Education, and Referral' (PIER) Program";(F) "Education--The Foundation of PIER"; (6) "Prevention--Working with Students";(7) "Intervention and Refel-ral--Timely Help";(8) "The Teacher as Healer"; (9) "PIER--How to Implement :t"; and (10) "The Five Knows -
Drugs, Brains, and Behavior: the Science of Addiction
Drugs, Brains, and Behavior: The Science of Addiction A Research Update from the National Institute on Drug Abuse — January 2007 Is drug addiction a disease? Yes. Addiction is a chronic, relapsing disease that affects the brain and causes compulsive drug seeking and use despite harmful consequences. ¾ How is addiction a disease? Addiction is considered a brain disease because drugs change the brain—in structure and in function. It’s true that for most people, the initial decision to take drugs is voluntary. Over time, however, drug abuse can cause changes to the brain that erode a person’s self control and ability to make sound decisions, while sending intense impulses to take drugs. Many people today do not understand why individuals become addicted to drugs, or how drugs change the brain to foster ¾ What is its course? Drug addiction is a compulsive drug abuse. This new NIDA booklet aims to fill that chronic, relapsing disease––like diabetes, knowledge gap by providing scientific information about the asthma, or heart disease––and it can be disease of drug addiction, including the many harmful consequences and basic approaches to prevent and treat the managed successfully. Treatment helps people disease. http://www.drugabuse.gov/scienceofaddiction to counteract addiction’s powerful disruptive effects and regain control of their lives. And just as with other chronic diseases, relapses are not uncommon. But relapse does not signal failure—rather, it indicates that treatment should be reinstated or adjusted to help the addict fully recover. Why do some people become addicted, while others do not? No single factor can predict whether or not a person will become addicted to drugs. -
Prescription Drug Abuse See Page 10
Preventing and recognizing prescription drug abuse See page 10. from the director: The nonmedical use and abuse of prescription drugs is a serious public health problem in this country. Although most people take prescription medications responsibly, an estimated 52 million people (20 percent of those aged 12 and Prescription older) have used prescription drugs for nonmedical reasons at least once in their lifetimes. Young people are strongly represented in this group. In fact, the National Institute on Drug Abuse’s (NIDA) Drug Abuse Monitoring the Future (MTF) survey found that about 1 in 12 high school seniors reported past-year nonmedical use of the prescription pain reliever Vicodin in 2010, and 1 in 20 reported abusing OxyContin—making these medications among the most commonly abused drugs by adolescents. The abuse of certain prescription drugs— opioids, central nervous system (CNS) depressants, and stimulants—can lead to a variety of adverse health effects, including addiction. Among those who reported past-year nonmedical use of a prescription drug, nearly 14 percent met criteria for abuse of or dependence on it. The reasons for the high prevalence of prescription drug abuse vary by age, gender, and other factors, but likely include greater availability. What is The number of prescriptions for some of these medications has increased prescription dramatically since the early 1990s (see figures, page 2). Moreover, a consumer culture amenable to “taking a pill for drug abuse? what ails you” and the perception of 1 prescription drugs as less harmful than rescription drug abuse is the use of a medication without illicit drugs are other likely contributors a prescription, in a way other than as prescribed, or for to the problem. -
Neurotrophic Factor Expression After CNS Viral Injury Produces Enhanced Sensitivity to Psychostimulants: Potential Mechanism for Addiction Vulnerability
The Journal of Neuroscience, 2000, Vol. 20 RC104 1of5 Neurotrophic Factor Expression After CNS Viral Injury Produces Enhanced Sensitivity to Psychostimulants: Potential Mechanism for Addiction Vulnerability Marylou V. Solbrig,1 George F. Koob,2 Loren H. Parsons,2 Tomoko Kadota,3 Nigel Horscroft,1 Thomas Briese,1 and W. Ian Lipkin1 1Departments of Neurology, Microbiology, and Molecular Genetics, University of California-Irvine, Irvine, California 92697- 4292, 2Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, and 3Department of Anatomy, Chiba University School of Medicine, Chiba 260, Japan Hypothesized risk factors for psychostimulant, amphetamine, specific neurotrophin expression pattern triggered by striatal and cocaine abuse include dopamine (DA) receptor polymor- viral injury that increases tyrosine hydroxylase activity, an early phisms, HIV infection, schizophrenia, drug-induced paranoias, step in DA synthesis, to produce a phenotype of enhanced and movement disorders; however, the molecular, cellular, and amphetamine sensitivity. The reactive neurotrophin pattern pro- biochemical mechanisms that predispose to drug sensitivity or vides a molecular framework for understanding how CNS viral drive the development of addiction are incompletely under- injury, as well as other CNS adaptations producing similar stood. Using the Borna disease rat, an animal model of viral- growth factor activation profiles, may influence psychostimu- induced encephalopathy wherein sensitivity to the locomotor lant sensitivity. and stereotypic behavioral effects of D-amphetamine and co- Key words: virus; encephalitis; neurotrophin; Borna disease; caine is enhanced (Solbrig et al., 1994, 1998), we identify a rat; cocaine; amphetamine; dopamine There is increasing experimental evidence to support a role for with BDV are sensitive to the locomotor and stereotypic behav- neuronal growth factors in the CNS response to drug exposure ioral effects of D-amphetamine and cocaine (Solbrig et al., 1994, that outlasts the acute effects of drug. -
A Unified Framework for Addiction: Vulnerabilities in the Decision Process
BEHAVIORAL AND BRAIN SCIENCES (2008) 31, 415–487 Printed in the United States of America doi:10.1017/S0140525X0800472X A unified framework for addiction: Vulnerabilities in the decision process A. David Redish Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455 [email protected] http://umn.edu/~redish/ Steve Jensen Graduate Program in Computer Science, University of Minnesota, Minneapolis, MN 55455 [email protected] Adam Johnson Graduate Program in Neuroscience and Center for Cognitive Sciences, University of Minnesota, Minneapolis, MN 55455 [email protected] Abstract: The understanding of decision-making systems has come together in recent years to form a unified theory of decision-making in the mammalian brain as arising from multiple, interacting systems (a planning system, a habit system, and a situation-recognition system). This unified decision-making system has multiple potential access points through which it can be driven to make maladaptive choices, particularly choices that entail seeking of certain drugs or behaviors. We identify 10 key vulnerabilities in the system: (1) moving away from homeostasis, (2) changing allostatic set points, (3) euphorigenic “reward-like” signals, (4) overvaluation in the planning system, (5) incorrect search of situation-action-outcome relationships, (6) misclassification of situations, (7) overvaluation in the habit system, (8) a mismatch in the balance of the two decision systems, (9) over-fast discounting processes, and (10) changed learning rates. These vulnerabilities provide a taxonomy of potential problems with decision-making systems. Although each vulnerability can drive an agent to return to the addictive choice, each vulnerability also implies a characteristic symptomology. Different drugs, different behaviors, and different individuals are likely to access different vulnerabilities. -
Individual Differences in Nucleus Accumbens Dopamine Receptors Predict Development of Addiction-Like Behavior: a Computational Approach
LETTER Communicated by A. David Redish Individual Differences in Nucleus Accumbens Dopamine Receptors Predict Development of Addiction-Like Behavior: A Computational Approach Payam Piray [email protected] Control and Intelligent Processing Center of Excellence, School of Electrical and Computer Engineering, University of Tehran, Tehran, Iran Mohammad Mahdi Keramati keramati [email protected] School of Management and Economics, Sharif University of Technology, Tehran, Iran Amir Dezfouli [email protected] Caro Lucas [email protected] Control and Intelligent Processing Center of Excellence, School of Electrical and Computer Engineering, University of Tehran, Tehran, Iran Azarakhsh Mokri [email protected] Department of Psychiatry, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran, and Department of Clinical Sciences, Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran Clinical and experimental observations show individual differences in the development of addiction. Increasing evidence supports the hy- pothesis that dopamine receptor availability in the nucleus accumbens (NAc) predisposes drug reinforcement. Here, modeling striatal-midbrain dopaminergic circuit, we propose a reinforcement learning model for ad- diction based on the actor-critic model of striatum. Modeling dopamine receptors in the NAc as modulators of learning rate for appetitive—but not aversive—stimuli in the critic—but not the actor—we define vulner- ability to addiction as a relatively lower learning rate for the appetitive stimuli, compared to aversive stimuli, in the critic. We hypothesize that an imbalance in this learning parameter used by appetitive and aversive learning systems can result in addiction. We elucidate that the interaction Mohammad Mahdi Keramati and Amir Dezfouli contributed equally to this work. -
Similitude and Rebound Effect of Drugs
son, that its exact opposite, when, as has been observed, there is actually such a thing, is produced in the secondary action Similitude and Rebound by our vital force”. Effect of Drugs (Organon of Medicine, paragraph 65) Based on this postulate or “natural law”, homeopathy makes use of the secondary Scientific Evidence and action of the organism as a therapeutic reaction, and prescribes to ill individuals Therapeutic Application medicines that cause symptoms similar to the disorders they themselves cause (prin- ciple of therapeutic similitude), thus stimu- Marcus Zulian Teixeira, Brazil lating the organism to react against its own disease. In Ancient Greece, Hippocrates classically moted alterations in the different systems taught that there were two approaches to of the human body, and the following sec- Although little was divulged by modern PHILOSOPHY AND DISCUSSION the treatment of disease, namely the princi- ondary action of the organism (vital reaction pharmacology, since it opposes convention- ple of contraries and the principle of simi- or conservation force). The latter acts by al treatment, this same secondary action or lars. Treatment according to the principle neutralising the primary disorders caused homeostatic reaction of the organism has of contraries employs drugs that act con- by drugs, in an attempt to maintain the bal- been observed with the use of several types trary to or by palliating (“anti-”)thesymp- ance of the internal milieu or homeostasis: of modern palliative (antipathic or enantio- toms of the disease (e.g., anti-inflammato- pathic) drugs as a rebound effect or para- ries, antacids, antidepressants, etc.). This is “[…] Excessive vivacity follows the use of doxical reaction of the organism.Wehave the main approach to treatment applied by strong coffee (primary action), but slug- been systematically studying for the last fif- conventional medicine, also known as “al- gishness and drowsiness remain for a long teen years the rebound effect of modern lopathy”.