Pregabalin Matches Naltrexone in Lowering Alcohol Craving
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Inhalants Booklet6/4/0712:04Ampage1 Inhalants Inhalants Booklet 6/4/07 12:04 AM Page 2
inhalants booklet6/4/0712:04AMPage1 inhalants inhalants booklet 6/4/07 12:04 AM Page 2 inhalants WHAT ARE INHALANTS? Inhalants are a range of products that are sniffed or inhaled to give the user an immediate head rush or ‘high’. These substances are easily absorbed through the lungs and carried to the brain, where they act to slow down the central nervous system. Many familiar household products are inhalants. Some of the most common are: • Glue • Aerosol spray cans • Cleaning fluids • Felt-tipped pens • Correction fluid (liquid paper) • Chrome-based paints • Paint or paint thinner • Petrol • Anaesthetics Many inhalants are classified as volatile solvents. These change rapidly from a liquid or semi-solid state to a gas when exposed to air. They include chemicals that are found in products such as deodorants, air fresheners, lighter fuels and propellant gases used in aerosols such as whipped cream dispensers. Some volatile solvents are inhaled because of the effects produced not only by the product’s main ingredient, but by the propellant gases, as in aerosols, such as hair spray. Other solvents found in aerosol products such as gold and silver spray paint are sniffed not because of the effects from propellant gases but because of the psychoactive effects caused by the specific solvents necessary to suspend these metallic paints in the spray. The sniffing of metallic paints is known as ‘chroming’. inhalants booklet 6/4/07 12:04 AM Page 3 Another category of inhalant is the nitrites. Amyl, butyl and isobutyl nitrite (collectively known as alkyl nitrites) are clear, yellow liquids which are inhaled for their intoxicating effects. -
An Ecological Investigation of the Time Course of Hangover
AN ECOLOGICAL INVESTIGATION OF HANGOVER SEVERITY AND TIME COURSE _______________________________________ A Dissertation presented to the Faculty of the Graduate School at the University of Missouri-Columbia _______________________________________________________ In Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy _____________________________________________________ by ERIN HUNT-CARTER Dr. Thomas Piasecki, Dissertation Supervisor DECEMBER 2010 The undersigned, appointed by the dean of the Graduate School, have examined the dissertation entitled AN ECOLOGICAL INVESTIGATION OF HANGOVER SEVERITY AND TIME COURSE presented by Erin E. Hunt-Carter, a candidate for the degree of doctor of philosophy, and hereby certify that, in their opinion, it is worthy of acceptance. Professor Thomas M. Piasecki Professor Wendy S. Slutske Professor Kenneth J. Sher Professor Dennis K. Miller Professor Daniel C. Vinson Thank you to my wonderful husband, Brent. I would not have completed this without your endless encouragement and kindness. Thank you to my parents, Toni and John Hunt, and my parents-in-law, Sondra and Guy Carter. Their support and many hours of babysitting were invaluable. Thank you to my sister, Meghan Hunt, for being riotously funny and supporting me through this process. Finally, I’d like to thank my children, Ian and Anna Carter, for keeping me grounded and reminding me what is truly important in life. ACKNOWLEDGEMENTS It is a pleasure to thank those who made this dissertation possible. First, I would like to express my gratitude to my doctoral advisor, Dr. Thomas Piasecki. He generously welcomed me into his lab, and enabled me to gain invaluable experience with ecological momentary assessment. I could not have completed this dissertation without his patient advice, extensive knowledge, and encouragement. -
Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels During Exposure, Short-Term, and Long-Term Withdrawal
Neuropsychopharmacology (2008) 33, 599–610 & 2008 Nature Publishing Group All rights reserved 0893-133X/08 $30.00 www.neuropsychopharmacology.org Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal ,1 1 1 1 Yael Abreu-Villac¸a* , Fernanda Nunes , Fabı´ola do E Queiroz-Gomes , Alex C Manha˜es and 1 Cla´udio C Filgueiras 1 ˆ ˆ Laborato´rio de Neurofisiologia, Departamento de Ciencias Fisiolo´gicas, Instituto de Biologia Roberto Alcantara Gomes, Centro Biome´dico, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short- and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. -
Caffeine and Adenosine
Journal of Alzheimer’s Disease 20 (2010) S3–S15 S3 DOI 10.3233/JAD-2010-1379 IOS Press Review Article Caffeine and Adenosine Joaquim A. Ribeiro∗ and Ana M. Sebastiao˜ Institute of Pharmacology and Neurosciences, Faculty of Medicine and Unit of Neurosciences, Institute of Molecular Medicine, University of Lisbon, Lisbon, Portugal Abstract. Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3, and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors. Caffeine, through antagonism of ARs, affects brain functions such as sleep, cognition, learning, and memory, and modifies brain dysfunctions and diseases: Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Epilepsy, Pain/Migraine, Depression, Schizophrenia. In conclusion, targeting approaches that involve ARs will enhance the possibilities to correct brain dysfunctions, via the universally consumed substance that is caffeine. Keywords: Adenosine, Alzheimer’s disease, anxiety, caffeine, cognition, Huntington’s disease, migraine, Parkinson’s disease, schizophrenia, sleep INTRODUCTION were considered out of the scope of the present work. For more detailed analysis of the actions of caffeine in Caffeine causes most of its biological effects via humans, namely cognition, dementia, and Alzheimer’s antagonizing all types of adenosine receptors (ARs). -
Chapter 25 Mechanisms of Action of Antiepileptic Drugs
Chapter 25 Mechanisms of action of antiepileptic drugs GRAEME J. SILLS Department of Molecular and Clinical Pharmacology, University of Liverpool _________________________________________________________________________ Introduction The serendipitous discovery of the anticonvulsant properties of phenobarbital in 1912 marked the foundation of the modern pharmacotherapy of epilepsy. The subsequent 70 years saw the introduction of phenytoin, ethosuximide, carbamazepine, sodium valproate and a range of benzodiazepines. Collectively, these compounds have come to be regarded as the ‘established’ antiepileptic drugs (AEDs). A concerted period of development of drugs for epilepsy throughout the 1980s and 1990s has resulted (to date) in 16 new agents being licensed as add-on treatment for difficult-to-control adult and/or paediatric epilepsy, with some becoming available as monotherapy for newly diagnosed patients. Together, these have become known as the ‘modern’ AEDs. Throughout this period of unprecedented drug development, there have also been considerable advances in our understanding of how antiepileptic agents exert their effects at the cellular level. AEDs are neither preventive nor curative and are employed solely as a means of controlling symptoms (i.e. suppression of seizures). Recurrent seizure activity is the manifestation of an intermittent and excessive hyperexcitability of the nervous system and, while the pharmacological minutiae of currently marketed AEDs remain to be completely unravelled, these agents essentially redress the balance between neuronal excitation and inhibition. Three major classes of mechanism are recognised: modulation of voltage-gated ion channels; enhancement of gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission; and attenuation of glutamate-mediated excitatory neurotransmission. The principal pharmacological targets of currently available AEDs are highlighted in Table 1 and discussed further below. -
“GABA” 'Bout? Pregabalin and Gabapentin Abuse
3/19/18 What’s All the “GABA” ‘Bout? Pregabalin and Gabapentin Abuse Courtney Kominek, PharmD, BCPS, CPE Disclosures .Courtney Kominek, PharmD, BCPS, CPE –Axial Healthcare – Consultant .The views and opinions expressed in this presentation are those of the authors and do not necessarily reflect the official policy or position of any agency of the United States government, including the Department of Veterans Affairs. 1 3/19/18 Learning Objectives .Review the proposed mechanisms of action (MOA) for gabapentin and pregabalin. .Explain the proposed rationale as to why gabapentin and pregabalin have become drugs of abuse. .Identify signs and symptoms of withdrawal that an addicted or tolerant patient may experience upon abrupt discontinuation of gabapentin or pregabalin. .Discuss updates on changes in pain management given the increase in gabapentin and pregabalin abuse. Current Situation Opioid overdose public health crisis Rising use of nonopioid medications including gabapentin Opioids and concomitant gabapentin increase risk for overdose Reports of gabapentinoid abuse Changes in PDMP and scheduling at state level http://www.register-herald.com/news/manchin-asks-fda-dea-to-consider-rescheduling-gabapentin/article_442fa04b-7ed9-5bf8-8d19-b5440e9c278b.html 2 3/19/18 Gabapentin and Pregabalin: Pharmacology and Pharmacokinetics Fact or Alternate Fact? .Gabapentin and pregabalin work on GABA. 3 3/19/18 Mechanism of Action Structurally related to GABA and has GABA-mimetic properties Do not • Alter uptake or breakdown • Convert into GABA • Bind to GABAa or GABAB Binds to the α2-δ subunit of the voltage-gated calcium channel Reduces the Ca2+ -dependent release of pro-nociceptive neurotransmitters Decreases release of glutamate, NE, and substance P Dworkin RH et al. -
Inhalant Abuse Pediatric Care
CLINICAL REPORT Guidance for the Clinician in Rendering Inhalant Abuse Pediatric Care Janet F. Williams, MD, Michael Storck, MD, and the Committee on Substance Abuse and Committee on Native American Child Health ABSTRACT Inhalant abuse is the intentional inhalation of a volatile substance for the purpose of achieving an altered mental state. As an important, yet-underrecognized form of substance abuse, inhalant abuse crosses all demographic, ethnic, and socioeco- nomic boundaries, causing significant morbidity and mortality in school-aged and older children. This clinical report reviews key aspects of inhalant abuse, empha- sizes the need for greater awareness, and offers advice regarding the pediatrician’s role in the prevention and management of this substance abuse problem. TYPES OF CHEMICALS AND PRODUCTS ABUSED The term “inhalant” encompasses a wide range of pharmacologically diverse substances that readily vaporize. Most other substances of abuse are classified by grouping together substances that share a specific central nervous system action or perceived psychoactive effect, but inhalant substances that are abused are grouped by having a common route of drug use. Inhalant abuse, sometimes referred to as solvent or volatile substance abuse, can be better understood when the expansive list of inhalants is classified into 3 groups on the basis of what is currently known pharmacologically: group I includes volatile solvents, fuels, and anesthetics; group II includes nitrous oxide; and group III includes volatile alkyl nitrites (Table 1). This classification is also consistent with reported differences in user populations, patterns of abuse, and associated problems seen clinically.1–3 Drugs that do not www.pediatrics.org/cgi/doi/10.1542/ readily vaporize at room temperature, such as cocaine, heroin, nicotine, or alcohol, peds.2007-0470 can also be abused through inhalation, but characteristic pharmacologic properties doi:10.1542/peds.2007-0470 distinguish these substances from inhalants. -
Expectation Hangover “I Wish I’D Had This Step-By-Step Guide on How to Overcome Huge Obstacles When I Shattered Both My Wrist and My Dreams of Playing for the NFL
Praise for Expectation Hangover “I wish I’d had this step-by-step guide on how to overcome huge obstacles when I shattered both my wrist and my dreams of playing for the NFL. Don’t let your Expectation Hangover control your life — apply what is in this book!” — Lewis Howes, former pro athlete turned lifestyle entrepreneur, host of The School of Greatness podcast “Christine Hassler is the kind of true spiritual guide we all need in our corner — soulful, wise, compassionate, and practical. Her proven methods and deep personal understanding are like the best medicine ever for your heart and soul.” — Christine Arylo, self-love catalyst and author of Madly in Love with ME: The Daring Adventure of Becoming Your Own Best Friend “Christine Hassler continues to be an invaluable voice for every generation. Her insights and observations have changed and enlightened the way I look at my life and the way I raise my children.” — Michael DeLuca, film producer and Columbia Pictures president of production “Disappointment can be a big, ugly monster hiding under our beds. This book is the go-to for getting us through Expectation Hangovers with grace and shining light to cast away those ugly creatures of disappointment!” — Kathryn Budig, author of The Women’s Health Big Book of Yoga “Christine Hassler is brilliant and insightful. Finally, here is the solution for dealing with something that plagues so many, myself included. If you’re hoping to thrive in a world that seems to hand out setbacks at every oppor- tunity, this is the book for you. -
Membrane Stabilizer Medications in the Treatment of Chronic Neuropathic Pain: a Comprehensive Review
Current Pain and Headache Reports (2019) 23: 37 https://doi.org/10.1007/s11916-019-0774-0 OTHER PAIN (A KAYE AND N VADIVELU, SECTION EDITORS) Membrane Stabilizer Medications in the Treatment of Chronic Neuropathic Pain: a Comprehensive Review Omar Viswanath1,2,3 & Ivan Urits4 & Mark R. Jones4 & Jacqueline M. Peck5 & Justin Kochanski6 & Morgan Hasegawa6 & Best Anyama7 & Alan D. Kaye7 Published online: 1 May 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Purpose of Review Neuropathic pain is often debilitating, severely limiting the daily lives of patients who are affected. Typically, neuropathic pain is difficult to manage and, as a result, leads to progression into a chronic condition that is, in many instances, refractory to medical management. Recent Findings Gabapentinoids, belonging to the calcium channel blocking class of drugs, have shown good efficacy in the management of chronic pain and are thus commonly utilized as first-line therapy. Various sodium channel blocking drugs, belonging to the categories of anticonvulsants and local anesthetics, have demonstrated varying degrees of efficacy in the in the treatment of neurogenic pain. Summary Though there is limited medical literature as to efficacy of any one drug, individualized multimodal therapy can provide significant analgesia to patients with chronic neuropathic pain. Keywords Neuropathic pain . Chronic pain . Ion Channel blockers . Anticonvulsants . Membrane stabilizers Introduction Neuropathic pain, which is a result of nervous system injury or lives of patients who are affected. Frequently, it is difficult to dysfunction, is often debilitating, severely limiting the daily manage and as a result leads to the progression of a chronic condition that is, in many instances, refractory to medical This article is part of the Topical Collection on Other Pain management. -
The Role of Alcohol Metabolism in the Pathology of Alcohol Hangover
Journal of Clinical Medicine Review The Role of Alcohol Metabolism in the Pathology of Alcohol Hangover 1, 1,2, 1,3 1 Marlou Mackus y, Aurora JAE van de Loo y , Johan Garssen , Aletta D. Kraneveld , Andrew Scholey 4 and Joris C. Verster 1,2,4,* 1 Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, 3584CG Utrecht, The Netherlands; [email protected] (M.M.); [email protected] (A.J.v.d.L.); [email protected] (J.G.); [email protected] (A.D.K.) 2 Institute for Risk Assessment Sciences (IRAS), Utrecht University, 3584CM Utrecht, The Netherlands 3 Global Centre of Excellence Immunology, Nutricia Danone Research, 3584CT Utrecht, The Netherlands 4 Centre for Human Psychopharmacology, Swinburne University, Melbourne, VIC 3122, Australia; [email protected] * Correspondence: [email protected]; Tel.: +31-30-2536-909 Both authors contributed equally to the manuscript. y Received: 31 August 2020; Accepted: 22 October 2020; Published: 25 October 2020 Abstract: The limited number of available studies that examined the pathology of alcohol hangover focused on biomarkers of alcohol metabolism, oxidative stress and the inflammatory response to alcohol as potentially important determinants of hangover severity. The available literature on alcohol metabolism and oxidative stress is reviewed in this article. The current body of evidence suggests a direct relationship between blood ethanol concentration and hangover severity, whereas this association is not significant for acetaldehyde. The rate of alcohol metabolism seems to be an important determinant of hangover severity. That is, fast elimination of ethanol is associated with experiencing less severe hangovers. -
Pregabalin for the Treatment of Drug and Alcohol Withdrawal Symptoms: a Comprehensive Review
CNS Drugs (2016) 30:1191–1200 DOI 10.1007/s40263-016-0390-z REVIEW ARTICLE Pregabalin for the Treatment of Drug and Alcohol Withdrawal Symptoms: A Comprehensive Review 1 2,3 4 5 Rainer Freynhagen • Miroslav Backonja • Stephan Schug • Gavin Lyndon • 6 6 6 Bruce Parsons • Stephen Watt • Regina Behar Published online: 16 November 2016 Ó The Author(s) 2016. This article is published with open access at Springerlink.com Abstract Treatments for physical dependence and asso- treatment of physical dependence and accompanying ciated withdrawal symptoms following the abrupt discon- withdrawal symptoms associated with opioids, benzodi- tinuation of prescription drugs (such as opioids and azepines, nicotine, cannabinoids, and alcohol, although benzodiazepines), nicotine, alcohol, and cannabinoids are data from randomized controlled studies are sparse. How- available, but there is still a need for new and more ever, the current evidence is promising and provides a effective therapies. This review examines evidence sup- platform for future studies, including appropriate random- porting the potential use of pregabalin, an a2d voltage- ized, placebo- and/or comparator-controlled studies, to gated calcium channel subunit ligand, for the treatment of further explore the efficacy and safety of pregabalin for the physical dependence and associated withdrawal symptoms. treatment of withdrawal symptoms. Given the potential for A literature search of the MEDLINE and Cochrane Library pregabalin misuse or abuse, particularly in individuals with databases up to and including 11 December 2015 was a previous history of substance abuse, clinicians should conducted. The search term used was ‘(dependence OR exercise caution when using pregabalin in this patient withdrawal) AND pregabalin’. -
Alcohol Withdrawal
Alcohol withdrawal TERMINOLOGY CLINICAL CLARIFICATION • Alcohol withdrawal may occur after cessation or reduction of heavy and prolonged alcohol use; manifestations are characterized by autonomic hyperactivity and central nervous system excitation 1, 2 • Severe symptom manifestations (eg, seizures, delirium tremens) may develop in up to 5% of patients 3 CLASSIFICATION • Based on severity ○ Minor alcohol withdrawal syndrome 4, 5 – Manifestations occur early, within the first 48 hours after last drink or decrease in consumption 6 □ Manifestations develop about 6 hours after last drink or decrease in consumption and usually peak about 24 to 36 hours; resolution occurs in 2 to 7 days 7 if withdrawal does not progress to major alcohol withdrawal syndrome 4 – Characterized by mild autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia), mild tremor, anxiety, irritability, sleep disturbances (eg, insomnia, vivid dreams), gastrointestinal symptoms (eg, anorexia, nausea, vomiting), headache, and craving alcohol 4 ○ Major alcohol withdrawal syndrome 5, 4 – Progression and worsening of withdrawal manifestations, usually after about 24 hours from the onset of initial manifestations 4 □ Manifestations often peak around 50 hours before gradual resolution or may continue to progress to severe (complicated) withdrawal, particularly without treatment 4 – Characterized by moderate to severe autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia, fever); marked tremor; pronounced anxiety, insomnia,