DOCSLIB.ORG

Drug Class Review Newer Drugs for Insomnia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Drug Class Review Newer Drugs for Insomnia Drug Class Review Newer Drugs for Insomnia Final Update 2 Report October 2008 The Agency for Healthcare Research and Quality has not yet seen or approved this report. The purpose of Drug Effectiveness Review Project reports is to make available information regarding the comparative clinical effectiveness and harms of different drugs. Reports are not usage guidelines, nor should they be read as an endorsement of or recommendation for any particular drug, use, or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Update 1: July 2006 Original: December 2005 Susan Carson, MPH Marian S. McDonagh, PharmD Sujata Thakurta, MPA:HA Po-Yin Yen, MS Drug Effectiveness Review Project Marian McDonagh, PharmD, Principal Investigator Oregon Evidence-based Practice Center Mark Helfand, MD, MPH, Director Copyright © 2008 by Oregon Health & Science University Portland, Oregon 97239. All rights reserved. Final Report Update 2 Drug Effectiveness Review Project The medical literature relating to the topic is scanned periodically (see http://www.ohsu.edu/xd/research/centers-institutes/evidence-based-policy- center/derp/documents/methods.cfm for scanning process description). Upon review of the last scan, the Drug Effectiveness Review Project governance group elected not to proceed with another full update of this report based on the information contained in the scan. Some portions of the report may not be up to date. Prior versions of this report can be accessed at the DERP website. Insomnia Page 2 of 87 Final Report Update 2 Drug Effectiveness Review Project TABLE OF CONTENTS INTRODUCTION ............................................................................................................. 6 Scope and Key Questions ....................................................................................................................... 6 METHODS ...................................................................................................................... 9 Literature Search ..................................................................................................................................... 9 Study Selection ........................................................................................................................................ 9 Data Abstraction ...................................................................................................................................... 9 Validity Assessment ................................................................................................................................. 9 Data Synthesis ....................................................................................................................................... 10 RESULTS ..................................................................................................................... 11 Overview of included studies ................................................................................................................. 11 Key Question 1. What is the comparative effectiveness of newer drugs in treating adults and children with insomnia? ....................................................................................................................................... 14 Summary of the Evidence................................................................................................................. 14 Detailed Assessment ........................................................................................................................ 15 Key Question 2. What is the comparative tolerability and safety of Newer Drugs for Insomnia when used to treat patients with insomnia? .................................................................................................... 31 Summary of the Evidence................................................................................................................. 31 Detailed Assessment ........................................................................................................................ 32 Key Question 3. Are there subgroups of patients for which one Newer Drug for Insomnia is more effective or associated with fewer adverse events? .............................................................................. 39 Summary of the Evidence................................................................................................................. 39 Detailed Assessment ........................................................................................................................ 40 SUMMARY .................................................................................................................... 44 REFERENCES .............................................................................................................. 47 FIGURES Figure 1. Newer drugs for insomnia: Results of literature search.......................................................... 12 Figure 2. Subjective sleep latency in placebo-controlled trials of newer insomnia drugs ..................... 23 Figure 3. Subjective sleep duration in placebo-controlled trials of newer insomnia drugs .................... 24 Figure 4. Subjective wake time after sleep onset in placebo-controlled trials of newer insomnia drugs ...................................................................................................................................................... 25 Figure 5. Subjective number of awakenings in placebo-controlled trials of newer insomnia drugs ...... 26 Figure 6. Withdrawals due to adverse events reported in placebo-controlled trials of newer drugs for insomnia ................................................................................................................................................. 34 TABLES Table 1. Newer drugs for insomnia .......................................................................................................... 8 Table 2. Total numbers of head-to-head trials of newer drugs for insomnia ......................................... 13 Table 3. Head-to-head trials of newer insomnia drugs: Study design and patient characteristics ........ 16 Table 4. Head-to-head comparison of eszopiclone compared with zolpidem on polysomnography- measured outcomes .............................................................................................................................. 17 Table 5. Placebo-controlled trials included in meta-analysis of subjective sleep outcomes ................. 20 Table 6. Adjusted indirect meta-analysis: Summary of results .............................................................. 27 Table 7. Subgroup analysis by elderly and non-elderly adult patients .................................................. 28 Table 8. Placebo-controlled trials of zolpidem extended-release .......................................................... 30 Table 9. Adverse events in head-to-head studies of zaleplon compared with zolpidem ....................... 32 Table 10. Adjusted indirect analysis of placebo-controlled trials: Withdrawals due to adverse events. 35 Table 11. Summary of the evidence by key question ............................................................................ 44 Insomnia Page 3 of 87 Final Report Update 2 Drug Effectiveness Review Project APPENDIXES Appendix A. Literature search strategies ............................................................................................... 60 Appendix B. Quality assessment methods for drug class reviews for the Drug Effectiveness Review Project .................................................................................................................................................... 61 Appendix C. Excluded studies ............................................................................................................... 65 Appendix D. Summary of results of trials comparing newer insomnia drugs compared with benzodiazepines .................................................................................................................................... 84 EVIDENCE TABLES Published in a separate document Insomnia Page 4 of 87 Final Report Update 2 Drug Effectiveness Review Project Suggested citation for this report: Carson S, McDonagh M, Thakurta S, Yen P. Drug class review: Insomnia. 2008. http://www.ohsu.edu/drugeffectiveness/reports/final.cfm Funding: The funding source, the Center for Evidence-based Policy, is supported by 17 organizations, including 15 state Medicaid programs. These organizations selected the topic and had input into the Key Questions of this review. The content and conclusions of the review are entirely determined by the Evidence-based Practice Center researchers. The authors of this report have no financial interest in any company that makes or distributes the products reviewed in this report. Insomnia Page 5 of 87 Final Report Update 2 Drug Effectiveness Review Project INTRODUCTION Insomnia is a serious health problem that affects millions of people. Population surveys have estimated the prevalence of insomnia to be about 30% to 50% of the general population. Variation in estimates depends on different methods of surveying and definitions of insomnia.1 About three-fourths of people who have trouble sleeping say that the problem is “occasional,” averaging about 6 nights per month. The other one-fourth have frequent or chronic insomnia, averaging about 16 nights per month.2
Load more

Recommended publications
  • GABA Receptors
    D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43.
    [Show full text]
  • NINDS Custom Collection II
    ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC
    [Show full text]
  • Prefrontal Α7nachr Signaling Differentially Modulates Afferent
    Research Articles: Systems/Circuits Prefrontal α7nAChR signaling differentially modulates afferent drive and trace fear conditioning behavior in adolescent and adult rats https://doi.org/10.1523/JNEUROSCI.1941-20.2020 Cite as: J. Neurosci 2021; 10.1523/JNEUROSCI.1941-20.2020 Received: 27 July 2020 Revised: 29 November 2020 Accepted: 23 December 2020 This Early Release article has been peer-reviewed and accepted, but has not been through the composition and copyediting processes. The final version may differ slightly in style or formatting and will contain links to any extended data. Alerts: Sign up at www.jneurosci.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Copyright © 2021 the authors 1 Prefrontal α7nAChR signaling differentially modulates afferent drive 2 and trace fear conditioning behavior in adolescent and adult rats 3 4 5 6 7 Running title: Prefrontal α7nAChR control of afferent drive 8 9 10 11 Anabel M. M. Miguelez Fernandez, Hanna M. Molla, Daniel R. Thomases, and Kuei Y. Tseng* 12 13 Department of Anatomy and Cell Biology, University of Illinois at Chicago, IL 14 15 16 17 *Corresponding Author: Kuei Y. Tseng, MD, PhD 18 Department of Anatomy and Cell Biology 19 University of Illinois at Chicago – College of Medicine 20 Chicago, IL 60612, USA 21 Email: [email protected] 22 23 24 Number of figures: 8 25 Number of tables: 0 26 Abstract: 250 27 Main text: 4,030 words (Introduction: 451; Methods: 1,205; Results: 979; Discussion: 1,395) 28 29 30 31 32 Acknowledgements 33 Supported by NIH Grants R01-MH086507 and R01-MH105488 to KYT, and UIC College of Medicine 34 funds to KYT.
    [Show full text]
  • CNS Drug Reviews Vol
    CNS Drug Reviews Vol. 10, No. 1, pp. 45–76 © 2004 Neva Press, Branford, Connecticut Clinical Pharmacology, Clinical Efficacy, and Behavioral Toxicity of Alprazolam: A Review of the Literature Joris C. Verster and Edmund R. Volkerts Utrecht Institute for Pharmaceutical Sciences, Department of Psychopharmacology, University of Utrecht, Utrecht, The Netherlands Keywords: Alprazolam — Benzodiazepines — Anxiety — Depression — Panic — Sedation. ABSTRACT Alprazolam is a benzodiazepine derivative that is currently used in the treatment of generalized anxiety, panic attacks with or without agoraphobia, and depression. Alprazo- lam has a fast onset of symptom relief (within the first week); it is unlikely to produce de- pendency or abuse. No tolerance to its therapeutic effect has been reported. At discontinu- ation of alprazolam treatment, withdrawal and rebound symptoms are common. Hence, alprazolam discontinuation must be tapered. An exhaustive review of the literature showed that alprazolam is significantly superior to placebo, and is at least equally effective in the relief of symptoms as tricyclic antide- pressants (TCAs), such as imipramine. However, although alprazolam and imipramine are significantly more effective than placebo in the treatment of panic attacks, Selective Sero- tonin Reuptake Inhibitors (SSRIs) appear to be superior to either of the two drugs. Therefore, alprazolam is recommended as a second line treatment option, when SSRIs are not effective or well tolerated. In addition to its therapeutic effects, alprazolam produces adverse effects, such as drowsiness and sedation. Since alprazolam is widely used, many clinical studies investi- gated its cognitive and psychomotor effects. It is evident from these studies that alprazo- lam may impair performance in a variety of skills in healthy volunteers as well as in pa- tients.
    [Show full text]
  • In the Treatment of Generalised Anxiety Disorder Does Pharmacology
    Characteristics Table for The Clinical Question: In the treatment of generalised anxiety disorder does 6/18/2010 12:21:10 pharmacology improve outcome? Comparisons Included in this Clinical Question Anticonvulsants versus Placebo Anticonvulsants vs Venlafaxine (SNRI) Antihistamine vs Placebo Benzodiazepines versus vs Placebo Anticonvulsants FELTNER2003 DARCIS1995 KASPER2009 KASPER2009 LADER1998 FELTNER2003 MONTGOMERY2006 MONTGOMERY2006 LLORCA2002 PANDE2003 MONTGOMERY2008 PFIZER2005 PANDE2003 RICKELS2005 PFIZER2005 POHL2005 RICKELS2005 Benzodiazepines versus Azapirones Benzodiazepines versus Placebo Buspirone vs Placebo Duloxetine (SNRI) vs. placebo BOURIN1992 ANDREATINI2002 DAVIDSON1999 HARTFORD2007 ANSSEAU2001 LADER1998 KOPONEN2007 CUTLER1993A MAJERCSIK2003 NICOLINI2009 FELTNER2003 POLLACK1997 RYNN2008 FRESQUET2000 SRAMEK1996 HACKETT2003 LYDIARD1997 MCLEOD1992 MOLLER2001 PANDE2003 PFIZER2008 RICKELS2000B RICKELS2005 Duloxetine (SNRI) vs. Venlafaxine Quetiapine versus Placebo SSRI vs Venlafaxine SSRIs versus Placebo (SNRI) ASTRAZENECA2007A BOSE2008 ALLGULANDER2004 HARTFORD2007 ASTRAZENECA2007B ASTRAZENECA2007A NICOLINI2009 ASTRAZENECA2007C ASTRAZENECA2007B ASTRAZENECA2008 BALDWIN2006 BOSE2008 BRAWMAN-MINTZER2006 DAVIDSON2004 GOODMAN2005 GSK2002 GSK2005 HEWETT2001 LENZE2005 LENZE2009 PFIZER2008 POLLACK2001 RICKELS2003 SSRIs versus SSRIs TCA vs Placebo Venlafaxine (SNRI) versus Azapirones Venlafaxine (SNRI) versus placebo BALDWIN2006 MCLEOD1992 DAVIDSON1999 ALLGULANDER2001 BALL2005 BOSE2008 BIELSKI2005 DAVIDSON1999 GELENBERG2000 HACKETT2003
    [Show full text]
  • Hypnotic Drug Risks of Mortality, Infection, Depression, and Cancer: but Lack of Benefit [Version 3; Peer Review: 2 Approved]
    F1000Research 2018, 5:918 Last updated: 03 AUG 2021 REVIEW Hypnotic drug risks of mortality, infection, depression, and cancer: but lack of benefit [version 3; peer review: 2 approved] Daniel F. Kripke University of California, San Diego, La Jolla, CA, 92037-2226, USA v3 First published: 19 May 2016, 5:918 Open Peer Review https://doi.org/10.12688/f1000research.8729.1 Second version: 17 Mar 2017, 5:918 https://doi.org/10.12688/f1000research.8729.2 Reviewer Status Latest published: 12 Nov 2018, 5:918 https://doi.org/10.12688/f1000research.8729.3 Invited Reviewers 1 2 Abstract This is a review of hypnotic drug risks and benefits. Almost every version 3 month, new information appears about the risks of hypnotics (update) report report (sleeping pills). The most important risks of hypnotics include excess 12 Nov 2018 mortality (especially overdose deaths, quiet deaths at night, and suicides), infections, cancer, depression, automobile crashes, falls, version 2 other accidents, and hypnotic-withdrawal insomnia. Short-term use of (update) report one-two prescriptions is associated with even greater risk per dose 17 Mar 2017 than long-term use. Hypnotics have usually been prescribed without approved indication, most often with specific contraindications, but version 1 even when indicated, there is little or no benefit. The recommended 19 May 2016 report report doses objectively increase sleep little if at all, daytime performance is often made worse (not better) and the lack of general health benefits is commonly misrepresented in advertising. Treatments such as the 1. Jerome M. Siegel, University of cognitive behavioral treatment of insomnia and bright light treatment California, Los Angeles, Los Angeles, USA of circadian rhythm disorders offer safer and more effective alternative approaches to insomnia.
    [Show full text]
  • Population-Based Drug-Induced Agranulocytosis
    ORIGINAL INVESTIGATION Population-Based Drug-Induced Agranulocytosis Luisa Ibáñez, MD; Xavier Vidal, MD; Elena Ballarín, RN; Joan-Ramon Laporte, MD Background: Since the publication of a major interna- late (OR, 77.84 [95% CI, 4.50-1346.20]), antithyroid tional case-control study on the risk of agranulocytosis drugs (OR, 52.75 [95% CI, 5.82-478.03]), dipyrone (met- associated with the use of medicines in the 1980s, many amizole sodium and metamizole magnesium) (OR, 25.76 new drugs have been introduced in therapeutics. [95% CI, 8.39-179.12]), and spironolactone (OR, 19.97 [95% CI, 2.27-175.89]). Other drugs associated with a Methods: Seventeen units of hematology contribute to significant risk were pyrithyldione, cinepazide, aprin- the case-control surveillance of agranulocytosis and aplas- dine hydrochloride, carbamazepine, sulfonamides, phe- tic anemia in Barcelona, Spain. After a follow-up of 78.73 nytoin and phenytoin sodium, ␤-lactam antibiotics, eryth- million person-years, 177 community cases of agranu- romycin stearate and erythromycin ethylsuccinate, and locytosis were compared with 586 sex-, age, and hospital- diclofenac sodium. Individual attributable incidences for matched control subjects with regard to previous use of all these drugs, which collectively accounted for 68.6% medicines. of cases, were less than 1:1 million per year. Results: The annual incidence of community-acquired Conclusions: Agranulocytosis is rare but serious. A few agranulocytosis was 3.46:1 million, and it increased with drugs account for two thirds of the cases. Our results also age. The fatality rate was 7.0%, and the mortality rate was provide reassurance regarding the risk associated with a 0.24:1 million.
    [Show full text]
  • Drug Class Review on Newer Sedative Hypnotics
    Drug Class Review on Newer Sedative Hypnotics Final Report December 2005 The Agency for Healthcare Research and Quality has not yet seen or approved this report The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Susan Carson, MPH Po-Yin Yen, MS Marian S. McDonagh, PharmD Oregon Evidence-based Practice Center Oregon Health & Science University Mark Helfand, MD, MPH, Director Copyright © 2005 by Oregon Health & Science University Portland, Oregon 97201. All rights reserved. Final Report Drug Effectiveness Review Project TABLE OF CONTENTS Introduction....................................................................................................................... 4 Scope and Key Questions ............................................................................................. 4 Methods.............................................................................................................................. 6 Literature Search........................................................................................................... 6 Study Selection ............................................................................................................
    [Show full text]
  • Belsomra: a First Look Sleep Medicine’S Newest Addition Has a Novel Mechanism and an Undecided Future
    COVER FOCUS Belsomra: A First Look Sleep medicine’s newest addition has a novel mechanism and an undecided future. BY ZAC HAUGHN, SENIOR ASSOCIATE EDITOR n the early 2000s, investment analysts anticipated a boom THE LITERATURE in the insomnia drug market.1 Indiplon and ramelt- The FDA considered Belsomra effective after it was eon (Rozerem) were on the verge of release, and Serpacor studied in three clinical trials involving more than 500 par- was testing eszopiclone, a nonbenzodiazepine hypnotic ticipants. In the studies, patients taking the drug fell asleep Iagent that a glowing “luna moth” would introduce to the faster and spent less time awake during the remainder of public as Lunesta in one of the most memorable pharma- the night compared to people taking placebo.4 The Agency ceutical ad campaigns in recent history. noted Belsomra was not compared to other drugs approved Despite Lunesta’s success and Rozerem’s approval, the to treat insomnia, so it is unknown if there are differences in anticipated boom was barely audible. Indiplon fizzled out safety or effectiveness between Belsomra and other insom- and the FDA made more sleep medicine headlines for rolling nia medications. back dosing than rolling out approvals. All of which makes The trials included two similarly designed, three-month, their recent approval of suvorexant (Belsomra) more intrigu- randomized, double-blind, placebo-controlled, parallel- ing: the oral drug is a substantially different product. group studies. Researchers examined Belsomra 20 and 40mg New to pharmacy shelves in early 2015, Belsomra is indi- in patients in non-elderly adults (age < 65 years) and 15 and cated for the treatment of insomnia characterized by dif- 30mg in elderly patients (age ≥ 65 years).2 Belsomra was ficulties with sleep onset and/or sleep maintenance in four superior to placebo for sleep latency as assessed both objec- different strengths: 5, 10, 15, and 20 milligrams; it is contra- tively by polysomnography and subjectively by patient-esti- indicated in patients with narcolepsy.
    [Show full text]
  • (Mmnm) and Auditory Evoked Field Component N100m
    Neuropsychopharmacology (2004) 29, 1723–1733 & 2004 Nature Publishing Group All rights reserved 0893-133X/04 $30.00 www.neuropsychopharmacology.org Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m Timm Rosburg*,1,2,3, Varvara Marinou1, Jens Haueisen2, Stefan Smesny1 and Heinrich Sauer1 1 2 Department of Psychiatry, Friedrich-Schiller-University Jena, Jena, Germany; Biomagnetic Center, Department of Neurology, Friedrich-Schiller- University Jena, Jena, Germany; 3Department of Epileptology, University of Bonn, Bonn, Germany The mismatch negativity (MMN) as an auditory evoked potential is thought to reflect an early, preconscious attention process. While this component has gained great importance in studies on clinical populations and in basic research on auditory information processing, the involvement of different neurotransmitters in the generation of this component is less well understood. We investigated the impact of the benzodiazepine lorazepam as a GABA agonist on the neuromagnetic MMN (MMNm) and auditory evoked field component N100m. A group of 12 healthy subjects was studied in single blind trials under the following three conditions: after the intake of 1.25 mg lorazepam, 100 mg caffeine or placebo. Neuromagnetic recordings were obtained before drug intake and three times after it. Controlled visual attention was tested additionally using a version of the Continuous Performance Test (CPT). The neuromagnetic activity was reconstructed by a single moving dipole, and the dipole moment and its latency were compared between conditions and time points of measurement. Lorazepam diminished the signal detection performance in the CPT 25 min after drug intake. The source of the field component N100m was attenuated, most significantly in the recording 105 min after lorazepam intake.
    [Show full text]
  • Drug and Medication Classification Schedule
    KENTUCKY HORSE RACING COMMISSION UNIFORM DRUG, MEDICATION, AND SUBSTANCE CLASSIFICATION SCHEDULE KHRC 8-020-1 (11/2018) Class A drugs, medications, and substances are those (1) that have the highest potential to influence performance in the equine athlete, regardless of their approval by the United States Food and Drug Administration, or (2) that lack approval by the United States Food and Drug Administration but have pharmacologic effects similar to certain Class B drugs, medications, or substances that are approved by the United States Food and Drug Administration. Acecarbromal Bolasterone Cimaterol Divalproex Fluanisone Acetophenazine Boldione Citalopram Dixyrazine Fludiazepam Adinazolam Brimondine Cllibucaine Donepezil Flunitrazepam Alcuronium Bromazepam Clobazam Dopamine Fluopromazine Alfentanil Bromfenac Clocapramine Doxacurium Fluoresone Almotriptan Bromisovalum Clomethiazole Doxapram Fluoxetine Alphaprodine Bromocriptine Clomipramine Doxazosin Flupenthixol Alpidem Bromperidol Clonazepam Doxefazepam Flupirtine Alprazolam Brotizolam Clorazepate Doxepin Flurazepam Alprenolol Bufexamac Clormecaine Droperidol Fluspirilene Althesin Bupivacaine Clostebol Duloxetine Flutoprazepam Aminorex Buprenorphine Clothiapine Eletriptan Fluvoxamine Amisulpride Buspirone Clotiazepam Enalapril Formebolone Amitriptyline Bupropion Cloxazolam Enciprazine Fosinopril Amobarbital Butabartital Clozapine Endorphins Furzabol Amoxapine Butacaine Cobratoxin Enkephalins Galantamine Amperozide Butalbital Cocaine Ephedrine Gallamine Amphetamine Butanilicaine Codeine
    [Show full text]
  • Foods, Drugs, Oils, and Compounds Chapter 198 1
    Foods, Drugs, Oils, and Compounds Chapter 198 1 FOODS, DRUGS, OILS, AND COMPOUNDS CHAPTER 198 SENATE BILL NO. 2218 (Senators J. Lee, Kilzer, Robinson) (Representatives Glassheim, N. Johnson, R. Kelsch) AN ACT to create and enact a new section to chapter 19-02.1 and section 19-03.1-22.4 of the North Dakota Century Code, relating to requirements for prescribing and dispensing controlled substances and certain other specified drugs and requirements for dispensing controlled substances by means of the internet; to amend and reenact subsection 2 of section 19-02.1-15 and section 19-03.1-23 of the North Dakota Century Code, relating to the exclusion from the exemption for dispensing certain drugs and penalties for unlawful distribution or dispensing of controlled substances and counterfeit controlled substances by means of the internet; and to provide a penalty. BE IT ENACTED BY THE LEGISLATIVE ASSEMBLY OF NORTH DAKOTA: SECTION 1. A new section to chapter 19-02.1 of the North Dakota Century Code is created and enacted as follows: Requirements for dispensing controlled substances and specified drugs - Penalty. 1. As used in this section: a. "Controlled substance" has the meaning set forth in section 19-03.1-01. b. "In-person medical evaluation" means a medical evaluation that is conducted with the patient in the physical presence of the practitioner, without regard to whether portions of the evaluation are conducted by other practitioners, and must include one of the following actions: (1) The prescribing practitioner examines the patient at
    [Show full text]