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Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine
Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine Arash Mosarrezaii1, Mohammad Reza Amiri Nikpour1, Ata Jabarzadeh2 1Department of Neurology, Imam Khomeini Hospital, Urmia University of Medical Sciences, Urmia, Iran, 2Medical Student, Urmia University of Medical Sciences, Urmia, Iran Abstract Background: Migraine is a debilitating neurological condition, which can be categorized into episodic and chronic groups based on its clinical pattern. Avoiding the risk factors exacerbating migraine is not enough to reduce the frequency and severity of migraine headaches, and in the case of non-receiving proper drug treatment, episodic migraines have the potential to become chronic, which increases the risk of cardiovascular complications RESEARCH ARTICLE and leaves great impact on the quality of life of patients and increasing the health-care costs. The objective of this research was to compare the effects of venlafaxine (VFL) and nortriptyline and propranolol in preventing migraines. Methods: This research is an interventional study performed on 60 patients with migraine admitted to the neurological clinic. Patients were visited at 3 time intervals. In each stage, the variables of headache frequency, headache severity, nausea, vomiting, and drowsiness were recorded. Data were analyzed using SPSS 23 software. Results: VFL drug with a daily dose of 37.5 mg is not only more tolerable in the long term but also leaves better effect in reducing the frequency and severity of headaches compared to the combination of nortriptyline and propranolol. Conclusion: VFL is an appropriate, effective, and tolerable alternative to migraine treatment. Key words: Migraine, nortriptyline, propranolol, venlafaxine INTRODUCTION Patients with CM are less likely to have full-time job than patients with episodic type, and they are at risk of job igraine is known as a common incapacity, anxiety, chronic pain, and depression 2 times neurological disorder and causes more than patients with episodic migraine. -
Drug Class Review Antianginal Agents
Drug Class Review Antianginal Agents 24:12.08 Nitrates and Nitrites 24:04.92 Cardiac Drugs, Miscellaneous Amyl Nitrite Isosorbide Dinitrate (IsoDitrate ER®, others) Isosorbide Mononitrate (Imdur®) Nitroglycerin (Minitran®, Nitrostat®, others) Ranolazine (Ranexa®) Final Report May 2015 Review prepared by: Melissa Archer, PharmD, Clinical Pharmacist Carin Steinvoort, PharmD, Clinical Pharmacist Gary Oderda, PharmD, MPH, Professor University of Utah College of Pharmacy Copyright © 2015 by University of Utah College of Pharmacy Salt Lake City, Utah. All rights reserved. Table of Contents Executive Summary ......................................................................................................................... 3 Introduction .................................................................................................................................... 4 Table 1. Antianginal Therapies .............................................................................................. 4 Table 2. Summary of Agents .................................................................................................. 5 Disease Overview ........................................................................................................................ 8 Table 3. Summary of Current Clinical Practice Guidelines .................................................... 9 Pharmacology ............................................................................................................................... 10 Table 4. Pharmacokinetic Properties -
Schizophrenia Care Guide
August 2015 CCHCS/DHCS Care Guide: Schizophrenia SUMMARY DECISION SUPPORT PATIENT EDUCATION/SELF MANAGEMENT GOALS ALERTS Minimize frequency and severity of psychotic episodes Suicidal ideation or gestures Encourage medication adherence Abnormal movements Manage medication side effects Delusions Monitor as clinically appropriate Neuroleptic Malignant Syndrome Danger to self or others DIAGNOSTIC CRITERIA/EVALUATION (PER DSM V) 1. Rule out delirium or other medical illnesses mimicking schizophrenia (see page 5), medications or drugs of abuse causing psychosis (see page 6), other mental illness causes of psychosis, e.g., Bipolar Mania or Depression, Major Depression, PTSD, borderline personality disorder (see page 4). Ideas in patients (even odd ideas) that we disagree with can be learned and are therefore not necessarily signs of schizophrenia. Schizophrenia is a world-wide phenomenon that can occur in cultures with widely differing ideas. 2. Diagnosis is made based on the following: (Criteria A and B must be met) A. Two of the following symptoms/signs must be present over much of at least one month (unless treated), with a significant impact on social or occupational functioning, over at least a 6-month period of time: Delusions, Hallucinations, Disorganized Speech, Negative symptoms (social withdrawal, poverty of thought, etc.), severely disorganized or catatonic behavior. B. At least one of the symptoms/signs should be Delusions, Hallucinations, or Disorganized Speech. TREATMENT OPTIONS MEDICATIONS Informed consent for psychotropic -
Selective Labeling of Serotonin Receptors Byd-[3H]Lysergic Acid
Proc. Nati. Acad. Sci. USA Vol. 75, No. 12, pp. 5783-5787, December 1978 Biochemistry Selective labeling of serotonin receptors by d-[3H]lysergic acid diethylamide in calf caudate (ergots/hallucinogens/tryptamines/norepinephrine/dopamine) PATRICIA M. WHITAKER AND PHILIP SEEMAN* Department of Pharmacology, University of Toronto, Toronto, Canada M5S 1A8 Communicated by Philip Siekevltz, August 18,1978 ABSTRACT Since it was known that d-lysergic acid di- The objective in this present study was to improve the se- ethylamide (LSD) affected catecholaminergic as well as sero- lectivity of [3H]LSD for serotonin receptors, concomitantly toninergic neurons, the objective in this study was to enhance using other drugs to block a-adrenergic and dopamine receptors the selectivity of [3HJISD binding to serotonin receptors in vitro by using crude homogenates of calf caudate. In the presence of (cf. refs. 36-38). We then compared the potencies of various a combination of 50 nM each of phentolamine (adde to pre- drugs on this selective [3H]LSD binding and compared these clude the binding of [3HJLSD to a-adrenoceptors), apmo ie, data to those for the high-affinity binding of [3H]serotonin and spiperone (added to preclude the binding of [3H[LSD to (39). dopamine receptors), it was found by Scatchard analysis that the total number of 3H sites went down to 300 fmol/mg, compared to 1100 fmol/mg in the absence of the catechol- METHODS amine-blocking drugs. The IC50 values (concentrations to inhibit Preparation of Membranes. Calf brains were obtained fresh binding by 50%) for various drugs were tested on the binding of [3HLSD in the presence of 50 nM each of apomorphine (A), from the Canada Packers Hunisett plant (Toronto). -
Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss
Supplemental Material can be found at: /content/suppl/2020/12/18/73.1.202.DC1.html 1521-0081/73/1/202–277$35.00 https://doi.org/10.1124/pharmrev.120.000056 PHARMACOLOGICAL REVIEWS Pharmacol Rev 73:202–277, January 2021 Copyright © 2020 by The Author(s) This is an open access article distributed under the CC BY-NC Attribution 4.0 International license. ASSOCIATE EDITOR: MICHAEL NADER Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss Antonio Inserra, Danilo De Gregorio, and Gabriella Gobbi Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, Montreal, Quebec, Canada Abstract ...................................................................................205 Significance Statement. ..................................................................205 I. Introduction . ..............................................................................205 A. Review Outline ........................................................................205 B. Psychiatric Disorders and the Need for Novel Pharmacotherapies .......................206 C. Psychedelic Compounds as Novel Therapeutics in Psychiatry: Overview and Comparison with Current Available Treatments . .....................................206 D. Classical or Serotonergic Psychedelics versus Nonclassical Psychedelics: Definition ......208 Downloaded from E. Dissociative Anesthetics................................................................209 F. Empathogens-Entactogens . ............................................................209 -
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European Review for Medical and Pharmacological Sciences 2012; 16: 1611-1636 The patient with chronic ischemic heart disease. Role of ranolazine in the management of stable angina A. DI MONACO, A. SESTITO Department of Cardiology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy Abstract. – Ischemic heart disease (IHD) is a serve is exhausted2. Symptom severity can be major cause of death in Western Countries and modulated by dynamic vasomotion at the site of accounts for very high costs worldwide. In this re- stenoses and/or by coronary microvascular dys- view we discussed the pathogenesis, symptoms, 1,2 diagnosis, prognosis and management of chronic function . IHD. In particular, we discussed about the percu- In microvascular angina transient myocardial taneous coronary interventions and coronary ischemia is caused by coronary microvascular artery bypass grafting, as well as to clinical trials dysfunction in patients with angiographically that evaluated the advantages of one approach normal epicardial coronary arteries, in the ab- versus another. Pharmacological treatment is 3,4 among major objectives of the review and for sence of any other specific cardiac disease . In each class of therapeutic agents an evaluation of vasospastic angina transient myocardial is- well-conducted clinical trials is provided. The chemia is caused by coronary spasm5. most important drug classes in IHD treatment are Furthermore, angina and transient myocardial betablockers, calcium channel blockers, nitrates, ischemia may also occur in patients with non ath- antiplatelet agents, and ACE-inhibitors. In addition to these agents, also new treatment options are erosclerotic obstructive coronary artery disease, evaluated in patients with stable IHD. -
Guideline- Management of Migraine and Cluster Headache
Hull & East Riding Prescribing Committee Guideline- Management of Migraine and Cluster Headache 1. BACKGROUND Headache is a common neurological condition which accounts for 4.4% of primary care consultations and 30% of neurology appointments. Primary headache disorders include migraine, tension-type and cluster headache. Twice as many women as men are affected by headache disorder. This is thought to be due to changes in hormone levels during the menstrual cycle, which can be more pronounced at puberty and menopause. Recommendations within this guideline are based on best evidence and national/international guidelines. They are followed by consultants and specialist nurses working within the neurology department. Some recommendations may be for medicines prescribed outside their product license i.e. off label. It is noted in the guideline when the medicine is off label and relevant guidelines should be followed when prescribing medicines off label. A number of British Association for the Study of Headache (BASH) leaflets have been linked in this guidance; these can be given to patients and cover the off license use of medicines and information about duration of prophylactic treatments. The colours on the drug names in this guidance refer to the classification in the joint formulary i.e. Red – specialist prescriber only Amber – prescribed in accordance with approved shared care framework Blue - Guideline Led prescribed on advice of specialist or in line with national / local guideline Green – other items listed on formulary suitable for initiation and prescribing by any prescriber If printed in black and white please refer to joint formulary for classification of medicines. Migraine Migraine is often underdiagnosed, misdiagnosed and undertreated. -
Migraine Headache Prophylaxis Hien Ha, Pharmd, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas
Migraine Headache Prophylaxis Hien Ha, PharmD, and Annika Gonzalez, MD, Christus Santa Rosa Family Medicine Residency Program, San Antonio, Texas Migraines impose significant health and financial burdens. Approximately 38% of patients with episodic migraines would benefit from preventive therapy, but less than 13% take prophylactic medications. Preventive medication therapy reduces migraine frequency, severity, and headache-related distress. Preventive therapy may also improve quality of life and prevent the progression to chronic migraines. Some indications for preventive therapy include four or more headaches a month, eight or more headache days a month, debilitating headaches, and medication- overuse headaches. Identifying and managing environmental, dietary, and behavioral triggers are useful strategies for preventing migraines. First-line med- ications established as effective based on clinical evidence include divalproex, topiramate, metoprolol, propranolol, and timolol. Medications such as ami- triptyline, venlafaxine, atenolol, and nadolol are probably effective but should be second-line therapy. There is limited evidence for nebivolol, bisoprolol, pindolol, carbamazepine, gabapentin, fluoxetine, nicardipine, verapamil, nimodipine, nifedipine, lisinopril, and candesartan. Acebutolol, oxcarbazepine, lamotrigine, and telmisartan are ineffective. Newer agents target calcitonin gene-related peptide pain transmission in the migraine pain pathway and have recently received approval from the U.S. Food and Drug Administration; how- ever, more studies of long-term effectiveness and adverse effects are needed. The complementary treatments petasites, feverfew, magnesium, and riboflavin are probably effective. Nonpharmacologic therapies such as relaxation training, thermal biofeedback combined with relaxation training, electromyographic feedback, and cognitive behavior therapy also have good evidence to support their use in migraine prevention. (Am Fam Physician. 2019; 99(1):17-24. -
DBL™ Promethazine Hydrochloride Injection BP
DBL™ Promethazine Hydrochloride Injection BP 1. NAME OF THE MEDICINE Promethazine hydrochloride 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each mL of the solution contains 25.0 mg promethazine hydrochloride, 0.10 mg disodium edetate, 1.30 microlitre glacial acetic acid, 27.2 mg sodium acetate and 1.32 mg sodium metabisulfite in water for injections. Excipient(s) with known effect Sodium metabisulfite For the full list of excipients, see section 6.1 List of Excipients. 3. PHARMACEUTICAL FORM Solution for injection. DBL™ Promethazine Hydrochloride Injection BP is a clear, colourless solution of pH 5.0 to 6.0. 4. CLINICAL PARTICULARS 4.1 Therapeutic Indications DBL™ Promethazine Hydrochloride Injection BP is indicated for the following conditions: Treatment of allergic reactions such as: uncomplicated allergic conditions of the immediate type, e.g., pruritus, urticaria and angioedema, when oral therapy is impossible or contraindicated. Treatment and prevention of vomiting including: motion sickness; drug induced nausea; prevention and control of nausea and vomiting associated with certain types of anaesthesia and surgery, such as procedures with a high incidence of post-operative vomiting (e.g., gynaecological surgery, strabismus or middle ear surgery, and electroconvulsive therapy); in patients with a past history of motion sickness or post- operative vomiting; and in patients in whom avoidance of vomiting is crucial (e.g., neurosurgery and eye surgery). Page 1 of 10 Promethazine has sedative effects and it is also used in: pre-operative, post-operative and obstetric (during labour) sedation. 4.2 Dose and Method of Administration Dosage Allergic conditions Adults: 25 mg to 50 mg by deep intramuscular injection or slow intravenous injection; may be repeated within two hours if necessary. -
Effect of Amitriptyline Antidotes on Repetitive Extrasystole Threshold
Effect of amitriptyline antidotes on repetitive extrasystole threshold The effect ofamitriptyline that leads to ventricular tachycardia was evaluated hy the repetitive extrasystole threshold (RET) technique in 18 dogs. The RET was 28.8 ± 7.9 mamp before and 8.2 ± 5.3 mamp after amitriptyline. p < 0.001. Physostigmine. propranolol. sodium bicarbonate, and left stellate ganglionectomy reversed the effect of amitriptyline on RET. We conclude that amitriptyline overdose predisposes to sudden death by lowering the ventricular fibrillation threshold. This cardiotoxic effect is mediated partly through the central nervous system and can be inhibited by increased plasma binding (bicarbonate), cholinergic stimulation (physostigmine), beta adrenergic blockade (propranolol), and sympathetic denervation (left stellate ganglionectomy). Jonathan M. Tobis, M.D., and Wilbert S. Aronow, M.D. Irvine, Calif. Cardiology Section and Medical Service, University of California, Irvine, and Long Beach Veterans Administration Medical Center The mechanism of tricylic antidepressant ac tyline on the repetinve extrasystole threshold tion is not established. The cardiotoxic proper (RET), Matta et al." have shown that the RET ties have been established.?- II, 14 The most was a good marker of the ventricular fibrillation common serious clinical arrhythmia is ventricu threshold in 91% of the animals they studied. A lar tachycardia." Several antidotes have been single repetitive extrasystole occurred when reported as successful in reversing the central 66% of the fibrillation current was delivered, nervous system and cardiac manifestations oftri and repeated extrasystoles were induced at 82% cyclic antidepressant overdose, i.e., physo of the fibrillation current. stigmine, propranolol, and sodium bicarbon We then explored the effect of several poten ate,3-5, 10. -
(12) United States Patent (10) Patent No.: US 8,080,578 B2 Liggett Et Al
USO08080578B2 (12) United States Patent (10) Patent No.: US 8,080,578 B2 Liggett et al. (45) Date of Patent: *Dec. 20, 2011 (54) METHODS FOR TREATMENT WITH 5,998.458. A 12/1999 Bristow ........................ 514,392 BUCNDOLOL BASED ON GENETIC 6,004,744. A 12/1999 Goelet et al. ...... 435/5 6,013,431 A 1/2000 Söderlund et al. 435/5 TARGETING 6,156,503 A 12/2000 Drazen et al. ..... ... 435/6 6,221,851 B1 4/2001 Feldman ... 51446 (75) Inventors: Stephen B. Liggett, Clarksville, MD 6,316,188 B1 1 1/2001 Yan et al. .......................... 435/6 6,365,618 B1 4/2002 Swartz ... 514,411 (US); Michael Bristow, Englewood, CO 6,498,009 B1 12/2002 Liggett ............................. 435/6 (US) 6,566,101 B1 5/2003 Shuber et al. 435,912 6,586,183 B2 7/2003 Drysdale et al. .................. 435/6 (73) Assignee: The Regents of the University of 6,784, 177 B2 8/2004 Cohn et al. 514,248 Colorado, a body corporate, Denver, 6,797.472 B1 9/2004 Liggett ......... ... 435/6 6,821,724 B1 1 1/2004 Mittman et al. ... 435/6 CO (US) 6,861.217 B1 3/2005 Liggett ......... ... 435/6 7,041,810 B2 5/2006 Small et al. ... ... 435/6 (*) Notice: Subject to any disclaimer, the term of this 7, 195,873 B2 3/2007 Fligheddu et al. ... 435/6 patent is extended or adjusted under 35 7,211,386 B2 5/2007 Small et al. ....... ... 435/6 7,229,756 B1 6/2007 Small et al. -
Calcium Channel Blockers in Cardiovascular Pharmacotherapy
Cardiovascular Pharmacology Core Review Journal of Cardiovascular Pharmacology and Therapeutics 2014, Vol. 19(6) 501-515 Calcium Channel Blockers in ª The Author(s) 2014 Reprints and permission: Cardiovascular Pharmacotherapy sagepub.com/journalsPermissions.nav DOI: 10.1177/1074248414530508 cpt.sagepub.com Theophile Godfraind1 Abstract This paper summarizes the pharmacological properties of calcium channel blockers (CCBs), their established therapeutic uses for cardiovascular disorders and the current improvement of their clinical effects through drug combinations. Their identification resulted from study of small molecules including coronary dilators, which were named calcium antagonists. Further experiments showed that they reduced contraction of arteries by inhibiting calcium entry and by interacting with binding sites identified on voltage-dependent calcium channels. This led to the denomination calcium channel blockers. In short-term studies, by decreasing total peripheral resistance, CCBs lower arterial pressure. By unloading the heart and increasing coronary blood flow, CCBs improve myocardial oxygenation. In long-term treatment, the decrease in blood pressure is more pronounced in hypertensive than in normotensive patients. A controversy on the safety of CCBs ended after a large antihypertensive trial (ALLHAT) sponsored by the National Heart, Lung, and Blood Institute. There are two main types of CCBs: dihydopyridine and non-dihydropyridine; the first type is vascular selective. Dihydropyrines are indicated for hypertension, chronic, stable and vasospastic angina. Non-dihydropyridines have the same indications plus antiarrythmic effects in atrial fibrillation or flutter and paroxysmal supraventricular tachycardia. In addition, CCBs reduced newly formed coronary lesions in atherosclerosis. In order to reach recommended blood pressure goals, there is a recent therapeutic move by combination of CCBs with other antihypertensive agents particularly with inhibitors acting at the level of the renin-angiotensin system.