DOCSLIB.ORG

Topiramate Pharmacotherapy for Alcohol Use Disorder and Other

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Topiramate Pharmacotherapy for Alcohol Use Disorder and Other CE: ; JAM-D-16-00049; Total nos of Pages: 16; JAM-D-16-00049 REVIEW Topiramate Pharmacotherapy for Alcohol Use Disorder and Other Addictions: A Narrative Review Ajay Manhapra, MD, Anirban Chakraborty, MBBS, and Albert J. Arias, MD, MS 08/15/2018 on pR0X8mps8emMFe6SSjULcOvZdU7Lq92sVezWUqbDpikBtBa8dPs+x8jFMo+CspZ5E+TY5YMZQKrQAwY1b8dC/CITypGBtyI/TuXrHp5+MNSsd6YOAns1MMj9Atc5CqXrWirhh/uUTYs= by https://journals.lww.com/journaladdictionmedicine from Downloaded Downloaded from Patra, 2010). SUDs are often chronic diseases with complex https://journals.lww.com/journaladdictionmedicine Topiramate is a non-benzodiazepine anticonvulsant medication with neurobiological underpinnings resulting in varied behavioral multi-faceted pharmacologic action. It has emerged as an efficacious and psychosocial problems posing significant treatment chal- pharmacotherapeutic option for the treatment of addiction, especially lenges to clinicians. Investigations into pharmacological treat- alcohol use disorder (AUD). We present a broad narrative review of ment of SUDs have not yielded a ‘‘magic bullet,’’ but led to the putative mechanism of action and clinical utility of topiramate the development of multiple pharmacotherapeutic agents, with regard to AUD and other substance use disorders. Collective putatively targeting different components of the disease pro- evidence suggests topiramate is an effective treatment option in cess (ie, craving, euphoria from the substance). AUD, with notable efficacy in reducing harmful drinking patterns Non-benzodiazepine anticonvulsant medications with by pR0X8mps8emMFe6SSjULcOvZdU7Lq92sVezWUqbDpikBtBa8dPs+x8jFMo+CspZ5E+TY5YMZQKrQAwY1b8dC/CITypGBtyI/TuXrHp5+MNSsd6YOAns1MMj9Atc5CqXrWirhh/uUTYs= in AUD. Though not currently approved by the United States Food their effects on glutamatergic and GABAergic neurotransmis- and Drug Administration for the indication of AUD, topiramate sion, have broad therapeutic benefits in the treatment of AUD should be considered as a pharmacological treatment option with with regard to both withdrawal and relapse prevention, and high utility among AUD patients. Early pharmacogenetic studies with varying degrees of effectiveness (Hammond et al., 2015; raise the intriguing possibility of identifying patients likely to Pani et al., 2014). Topiramate appears to be an effective respond to topiramate using genetic testing, and initial studies show treatment option in AUD, and is emerging as a possible option that topiramate may also be useful in treating cocaine use disorder, in the management of other SUDs (Johnson and Ait-Daoud, smoking cessation and behavioral addictions. However, further 2010). Here we provide a narrative review of the possible research is needed in all these areas. utilities of topiramate in AUD and other SUDs. Key Words: alcohol dependence, alcohol use disorder, alcoholism, SEARCH METHODOLOGY anticonvulsant, medication treatment, Topiramate We conducted a series of English-language medical (J Addict Med 2018;xx: xxx–xxx) literature searches using the PubMed, Cochrane Library, and PsycINFO databases using the following search terms: lcohol and other substance use disorders (AUD, SUDs) ‘‘topiramate,’’ ‘‘topiramate þ substance abuse/substance use A are highly prevalent in the United States and also disorder/addiction/withdrawal/side-effects/alcohol/alcohol globally, imposing a tremendous burden on society (Meri- use disorder/alcohol dependence/cocaine/nicotine/smoking/ kangas and McClair, 2012; Sacks et al., 2015; United Nations gambling/eating disorder.’’ Studies involving humans only, Office on Drugs and Crime, 2017). AUD is a significant health published up to September 2017 were included in the review. problem in the United States with a 13.9% 12-month and All study designs, namely meta-analysis, randomized control 29.1% lifetime prevalence (Grant et al., 2015). The 12-month trials, open trials, case series and case reports were included prevalence for AUD reported globally is up to 16% (Rehm and for review. We manually searched the reference lists of pertinent original research articles, review articles, and text- books for additional relevant citations. From the VA Hampton Medical Center, Hampton, VA (AM); VAConnecticut Healthcare System, West Haven (AM, AJA); Department of Psychiatry, MECHANISM OF ACTION Yale School of Medicine, New Haven (AM, AC, AJA); VA New England Mental Illness Research and Education Center, West Haven, CT (AM, Topiramate is a fructose-1,6-diphosphate analogue and AJA). was initially developed as an anti-diabetic drug but was later Received for publication March 1, 2016; accepted June 1, 2018. developed as an anti-convulsant due to its similarity with Ajay Manhapra was supported by the VA/OAA Interprofessional Advanced acetazolamide. Topiramate acts as a positive allostatic mod- Fellowship in Addiction Treatment, and Research in Addiction Medicine on ulator at GABAA receptors, which are activated causing 08/15/2018 Scholars (RAMS) Program, R25DA033211 from the National Institute on Drug Abuse. VA New England Mental Illness Research and Education increased chloride ion influx into neurons, thus increasing Center, West Haven, CT supported this review. overall GABA mediated inhibition (White, 2003). These activ- The authors have no financial or other conflicts of interests to report. ities are probably mediated through non-benzodiazepine bind- Send correspondence to Albert J. Arias, MD, MS, 950 Campbell Rd #116A, ing sites on GABAA receptors (White et al., 2000). GABA West Haven, CT 06516. E-mail: [email protected]. levels in the brain are also increased. Topiramate is a non- Copyright ß 2018 American Society of Addiction Medicine ISSN: 1932-0620/16/0000-0001 competitive antagonist of a-amino-3-hydroxy-5-methyl-4-iso- DOI: 10.1097/ADM.0000000000000443 xazolepropionic acid (AMPA)/kainate mediated glutamate J Addict Med Volume 00, Number 00, Month/Month 2018 1 Copyright © 2018 American Society of Addiction Medicine. Unauthorized reproduction of this article is prohibited. CE: ; JAM-D-16-00049; Total nos of Pages: 16; JAM-D-16-00049 Manhapra et al. J Addict Med Volume 00, Number 00, Month/Month 2018 receptors causing blockage of glutamate-mediated neuroexci- side effect. Carbonic anhydrase (CA) activity inhibition has tation, but has no effect on NMDA-sensitive glutamate recep- been implicated in several of these adverse effects. CA tors (Angehagen et al., 2005). In addition, topiramate limits inhibition in the kidneys is the obvious driver of metabolic depolarization and excitability at voltage-activated Naþ chan- acidosis associated with topiramate and Type 3 renal tubular nels, causing inhibition of high and repetitive action potential acidosis which has also been reported in association with CA discharges. Topiramate also inhibits L-type Ca2þ channels inhibition (Garris and Oles, 2005; Sacre´ et al., 2006). CA reducing neurotransmitter release and Ca2þ-dependent second inhibition locally and preferentially at sensory neuronal end- messenger systems (Zhang et al., 2000). Consistent with its ings leading to acidosis and resulting ectopic activation of structural similarity to acetazolamide, it also inhibits Types II sensory neurons has been implicated in parasthesias (unpleas- and IV carbonic anhydrase, leading to inhibition of hydrogen ant tingling in extremities) associated with topiramate (Fujii ion secretion by renal tubules, and increasing secretion of Naþ, et al., 1993; Spitzer et al., 2002; Swietach et al., 2003). Renal þ À K , HCO3 , and water (Dodgson et al., 2000). calculi occur at a 2- to 4-fold higher rate among those on The effects of topiramate on pathways involved in topiramate, and are thought to be due to an increase in urinary addiction have been elucidated to some extent, but hypotheses pH caused by increased excretion of bicarbonates and about how it affects the addicted brain remain largely specu- decreased citrate excretion that promotes precipitation of lative and have not been fully explored in the context of calcium salts (calcium phosphate) (Welch et al., 2006). translational studies (Johnson, 2005; Johnson and Ait-Daoud, Oligohydrosis is a rare but serious risk of topiramate 2010; Johnson, 2008). Topiramate is thought to alter the treatment. Oligohydrosis (insufficient sweating associated reinforcing properties and subjective experience of drugs with heat or exercise) has been attributed to CA inhibition and alcohol, and probably helps to normalize and restore (Cerminara et al., 2006) and inhibition of aquaporin 5 recep- balance in the reward circuits of the brain, thus restoring tors in sweat glands (Ma et al., 2007). Topiramate is preg- proper hedonic function and stress response among chroni- nancy category D, and cleft palate can occur with fetal cally drug or alcohol using persons. Topiramate putatively exposure. Due caution should be exercised with topiramate exerts it effects on midbrain dopaminergic (DA) pathways use in women of childbearing potential; a reliable form of projecting from ventral tegmental area (VTA) to the nucleus birth control should be used as well. accumbens (NAcc) by enhancing GABAergic neurotransmis- Acute visual disturbance, myopia and acute angle clo- sion and antagonizing glutamatergic neurotransmission, lead- sure glaucoma all occur infrequently among those receiving ing to suppression of dopaminergic surges at the NAcc. These topiramate, mostly at the beginning of the treatment (Shank proposed effects have not yet been thoroughly investigated in and Maryanoff, 2008). Cognitive impairment
Load more

Recommended publications
  • Eslicarbazepine Acetate: a New Improvement on a Classic Drug Family for the Treatment of Partial-Onset Seizures
    Drugs R D DOI 10.1007/s40268-017-0197-5 REVIEW ARTICLE Eslicarbazepine Acetate: A New Improvement on a Classic Drug Family for the Treatment of Partial-Onset Seizures 1 1 1 Graciana L. Galiana • Angela C. Gauthier • Richard H. Mattson Ó The Author(s) 2017. This article is an open access publication Abstract Eslicarbazepine acetate is a new anti-epileptic drug belonging to the dibenzazepine carboxamide family Key Points that is currently approved as adjunctive therapy and monotherapy for partial-onset (focal) seizures. The drug Eslicarbazepine acetate is an effective and safe enhances slow inactivation of voltage-gated sodium chan- treatment option for partial-onset seizures as nels and subsequently reduces the activity of rapidly firing adjunctive therapy and monotherapy. neurons. Eslicarbazepine acetate has few, but some, drug– drug interactions. It is a weak enzyme inducer and it Eslicarbazepine acetate improves upon its inhibits cytochrome P450 2C19, but it affects a smaller predecessors, carbamazepine and oxcarbazepine, by assortment of enzymes than carbamazepine. Clinical being available in a once-daily regimen, interacting studies using eslicarbazepine acetate as adjunctive treat- with a smaller range of drugs, and causing less side ment or monotherapy have demonstrated its efficacy in effects. patients with refractory or newly diagnosed focal seizures. The drug is generally well tolerated, and the most common side effects include dizziness, headache, and diplopia. One of the greatest strengths of eslicarbazepine acetate is its ability to be administered only once per day. Eslicar- 1 Introduction bazepine acetate has many advantages over older anti- epileptic drugs, and it should be strongly considered when Epilepsy is a common neurological disorder affecting over treating patients with partial-onset epilepsy.
    [Show full text]
  • DESCRIPTION CLINICAL PHARMACOLOGY Mechanism Of
    NDA 20-844/ Topamav Sprinkle Capsules Approved Labeling Text Version: 10/26/98 DESCRIPTION Topiramate is a sulfamate-substituted monosaccharide that is intended for use as an antiepileptic drug. TOPAMAX@ (topiramate capsules) Sprinkle Capsules are available as I5 mg, 25 mg and 50mg sprinkle capsules for oral administration as whole capsules or for opening and sprinkling onto soft food. Topiramate is a white crystalline powder with a bitter taste. Topiramate is most soluble in alkaline solutions containing sodium hydroxide or sodium phosphate and hawng a pH of 9 to IO. It is freely soluble in acetone, chloroform, dimethylsulfoxide, and ethanol. The solubility in water is 9.8 mg/mL. Its saturated solution has a pH of 6.3. Topiramate has the molecular formula C,,H,,NO,S and a molecular weight of 339.37. Topiramate is designated chemically as 2,3:4,5-Di-O-isopropylidene-~- D-fructopyranose sulfamate and has the following structural formula: H3C CH3 TOPAMAX” (topiramate capsules) Sprinkle Capsules contain topiramate coated beads in a hard gelatin capsule. The inactive ingredients are: sugar spheres (sucrose and starch), povidone, cellulose acetate, gelatin, silicone dioxide, sodium lauryl sulfate, titanium dioxide, and black pharmaceutical ink. CLINICAL PHARMACOLOGY Mechanism of Action: The precise mechanism by which topiramate exerts its antiseizure effect is unknown; however, electrophysiological and biochemical studies of the effects of topiramate on cultured neurons have revealed three properties that may contribute to topiramate’s antiepileptic efficacy. First, action potentials elicited repetitively by a sustained depolarization of the neurons are blocked by topiramate in a time-dependent manner, suggestive of a state-dependent sodium channel blocking action.
    [Show full text]
  • 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.
    [Show full text]
  • Clinical Review, Adverse Events
    Clinical Review, Adverse Events Drug: Carbamazepine NDA: 16-608, Tegretol 20-712, Carbatrol 21-710, Equetro Adverse Event: Stevens-Johnson Syndrome Reviewer: Ronald Farkas, MD, PhD Medical Reviewer, DNP, ODE I 1. Executive Summary 1.1 Background Carbamazepine (CBZ) is an anticonvulsant with FDA-approved indications in epilepsy, bipolar disorder and neuropathic pain. CBZ is associated with Stevens-Johnson syndrome (SJS) and Toxic Epidermal Necrolysis (TEN), closely related serious cutaneous adverse drug reactions that can be permanently disabling or fatal. Other anticonvulsants, including phenytoin, phenobarbital, and lamotrigine are also associated with SJS/TEN, as are members of a variety of other drug classes, including nonsteriodal anti-inflammatory drugs and sulfa drugs. The incidence of CBZ-associated SJS/TEN has been considered “extremely rare,” as noted in current U.S. drug labeling. However, recent publications and postmarketing data suggest that CBZ- associated SJS/TEN occurs at a much higher rate in some Asian populations, about 2.5 cases per 1,000 new exposures, and that most of this increased risk is in individuals carrying a specific human leukocyte antigen (HLA) allele, HLA-B*1502. This HLA-B allele is present in about 5- to 20% of many, but not all, Asian populations, and is also present in about 2- to 4% of South Asians/Indians. The allele is also present at a lower frequency, < 1%, in several other ethnic groups around the world (although likely due to distant Asian ancestry). About 10% of U.S. Asians carry HLA-B*1502. HLA-B*1502 is generally not present in the U.S.
    [Show full text]
  • Topiramate (Topamax®)
    June 16, 2020; Page 1 of 3 ® Topiramate (Topamax ) Why is this medication prescribed? • To prevent migraine headaches, treat nerve related pain or control certain types of seizures in patients with epilepsy. How should this medication be used? • Topiramate is available as: o a tablet in the following strengths: 25 mg, 100 mg, or 200 mg o a sprinkle capsule in the following strengths: 15 mg or 25 mg • It can be taken with or without food, but should be taken with water to reduce the risk of developing kidney stones. • It can be taken either once daily or twice daily depending on the dose. To minimize the development of side effects, topiramate is usually started at a low dose and increased in weekly intervals. Doses should be taken at the same time each day. • Examples of topiramate dosing schedules: Example A Example B Week 1: take 25 mg at bedtime Week 1: take 25 mg at bedtime Week 2: take 50 mg at bedtime Week 2: take 25 mg twice daily Week 3: take 75 mg at bedtime Week 3: take 25 mg in morning, 50 mg at bedtime Week 4: take 100 mg at bedtime Week 4: take 50 mg twice a day • Topiramate is NOT a "pain killer" to be taken whenever pain becomes severe or for managing minor aches and pains. Topiramate should be taken on a consistent basis, according to your doctor's orders to help you control long-term pain. • Do NOT abruptly stop taking topiramate without talking to your doctor. If for some reason topiramate is no longer needed, your doctor will reduce your dose gradually to minimize the potential for seizures.
    [Show full text]
  • Guideline for Preoperative Medication Management
    Guideline: Preoperative Medication Management Guideline for Preoperative Medication Management Purpose of Guideline: To provide guidance to physicians, advanced practice providers (APPs), pharmacists, and nurses regarding medication management in the preoperative setting. Background: Appropriate perioperative medication management is essential to ensure positive surgical outcomes and prevent medication misadventures.1 Results from a prospective analysis of 1,025 patients admitted to a general surgical unit concluded that patients on at least one medication for a chronic disease are 2.7 times more likely to experience surgical complications compared with those not taking any medications. As the aging population requires more medication use and the availability of various nonprescription medications continues to increase, so does the risk of polypharmacy and the need for perioperative medication guidance.2 There are no well-designed trials to support evidence-based recommendations for perioperative medication management; however, general principles and best practice approaches are available. General considerations for perioperative medication management include a thorough medication history, understanding of the medication pharmacokinetics and potential for withdrawal symptoms, understanding the risks associated with the surgical procedure and the risks of medication discontinuation based on the intended indication. Clinical judgement must be exercised, especially if medication pharmacokinetics are not predictable or there are significant risks associated with inappropriate medication withdrawal (eg, tolerance) or continuation (eg, postsurgical infection).2 Clinical Assessment: Prior to instructing the patient on preoperative medication management, completion of a thorough medication history is recommended – including all information on prescription medications, over-the-counter medications, “as needed” medications, vitamins, supplements, and herbal medications. Allergies should also be verified and documented.
    [Show full text]
  • Pharmacology/Therapeutics II Block III Lectures 2013-14
    Pharmacology/Therapeutics II Block III Lectures 2013‐14 66. Hypothalamic/pituitary Hormones ‐ Rana 67. Estrogens and Progesterone I ‐ Rana 68. Estrogens and Progesterone II ‐ Rana 69. Androgens ‐ Rana 70. Thyroid/Anti‐Thyroid Drugs – Patel 71. Calcium Metabolism – Patel 72. Adrenocorticosterioids and Antagonists – Clipstone 73. Diabetes Drugs I – Clipstone 74. Diabetes Drugs II ‐ Clipstone Pharmacology & Therapeutics Neuroendocrine Pharmacology: Hypothalamic and Pituitary Hormones, March 20, 2014 Lecture Ajay Rana, Ph.D. Neuroendocrine Pharmacology: Hypothalamic and Pituitary Hormones Date: Thursday, March 20, 2014-8:30 AM Reading Assignment: Katzung, Chapter 37 Key Concepts and Learning Objectives To review the physiology of neuroendocrine regulation To discuss the use neuroendocrine agents for the treatment of representative neuroendocrine disorders: growth hormone deficiency/excess, infertility, hyperprolactinemia Drugs discussed Growth Hormone Deficiency: . Recombinant hGH . Synthetic GHRH, Recombinant IGF-1 Growth Hormone Excess: . Somatostatin analogue . GH receptor antagonist . Dopamine receptor agonist Infertility and other endocrine related disorders: . Human menopausal and recombinant gonadotropins . GnRH agonists as activators . GnRH agonists as inhibitors . GnRH receptor antagonists Hyperprolactinemia: . Dopamine receptor agonists 1 Pharmacology & Therapeutics Neuroendocrine Pharmacology: Hypothalamic and Pituitary Hormones, March 20, 2014 Lecture Ajay Rana, Ph.D. 1. Overview of Neuroendocrine Systems The neuroendocrine
    [Show full text]
  • APTIOM (Eslicarbazepine Acetate) Is (S)-10-Acetoxy-10,11-Dihydro-5H­ Dibenz[B,F]Azepine-5-Carboxamide
    HIGHLIGHTS OF PRESCRIBING INFORMATION Monitor and discontinue if another cause cannot be established. (5.2, 5.3, These highlights do not include all the information needed to use 5.4) APTIOM safely and effectively. See full prescribing information for • Hyponatremia: Monitor sodium levels in patients at risk or patients APTIOM. experiencing hyponatremia symptoms. (5.5) • Neurological Adverse Reactions: Monitor for dizziness, disturbance in gait APTIOM® (eslicarbazepine acetate) tablets, for oral use and coordination, somnolence, fatigue, cognitive dysfunction, and visual Initial U.S. Approval: 2013 changes. Use caution when driving or operating machinery. (5.6) • Withdrawal of APTIOM: Withdraw APTIOM gradually to minimize the ---------------------------RECENT MAJOR CHANGES-------------------------­ risk of increased seizure frequency and status epilepticus. (2.6, 5.7, 8.1) Indications and Usage (1) 9/2017 • Dosage and Administration (2) 9/2017 Drug Induced Liver Injury: Discontinue APTIOM in patients with jaundice Warnings and Precautions (5) 9/2017 or evidence of significant liver injury. (5.8) • Hematologic Adverse Reactions: Consider discontinuing. (5.10) ----------------------------INDICATIONS AND USAGE--------------------------­ APTIOM is indicated for the treatment of partial-onset seizures in patients 4 ------------------------------ADVERSE REACTIONS------------------------------­ years of age and older. (1) • Most common adverse reactions in adult patients receiving APTIOM (≥4% and ≥2% greater than placebo): dizziness, somnolence, nausea, headache, ----------------------DOSAGE AND ADMINISTRATION----------------------­ diplopia, vomiting, fatigue, vertigo, ataxia, blurred vision, and tremor. (6.1) • Adult Patients: The recommended initial dosage of APTIOM is 400 mg • Adverse reactions in pediatric patients are similar to those seen in adult once daily. For some patients, treatment may be initiated at 800 mg once patients. daily if the need for seizure reduction outweighs an increased risk of adverse reactions.
    [Show full text]
  • Journal of Central Nervous System Disease a Review Of
    Journal of Central Nervous System Disease OPEN ACCESS Full open access to this and thousands of other papers at EXPERT REVIEW http://www.la-press.com. A Review of Eslicarbazepine Acetate for the Adjunctive Treatment of Partial-Onset Epilepsy Rajinder P. Singh and Jorge J. Asconapé Department of Neurology, Stritch School of Medicine, Loyola University Medical Center, Maywood, Illinois 60153, USA. Corresponding author email: [email protected] Abstract: Eslicarbazepine acetate (ESL) is a novel antiepileptic drug indicated for the treatment of partial-onset seizures. Structurally, it belongs to the dibenzazepine family and is closely related to carbamazepine and oxcarbazepine. Its main mechanism of action is by blocking the voltage-gated sodium channel. ESL is a pro-drug that is rapidly metabolized almost exclusively into S-licarbazepine, the biologically active drug. It has a favorable pharmacokinetic and drug-drug interaction profile. However, it may induce the metabolism of oral contraceptives and should be used with caution in females of child-bearing age. In the pre-marketing placebo-controlled clinical trials ESL has proven effective as adjunctive therapy in adult patients with refractory of partial-onset seizures. Best results were observed on a single daily dose between 800 and 1200 mg. In general, ESL was well tolerated, with most common dose-related side effects including dizziness, somnolence, headache, nausea and vomiting. Hyponatremia has been observed (0.6%–1.3%), but the incidence appears to be lower than with the use of oxcarbazepine. There is very limited information on the use of ESL in children or as monotherapy. Keywords: eslicarbazepine, licarbazepine, dibenzazepine, voltage-gated sodium channel, partial-onset seizures, epilepsy Journal of Central Nervous System Disease 2011:3 179–187 doi: 10.4137/JCNSD.S4888 This article is available from http://www.la-press.com.
    [Show full text]
  • Beyond Amitriptyline
    children Review Beyond Amitriptyline: A Pediatric and Adolescent Oriented Narrative Review of the Analgesic Properties of Psychotropic Medications for the Treatment of Complex Pain and Headache Disorders Robert Blake Windsor 1,2,*, Michael Sierra 2,3, Megan Zappitelli 2,3 and Maria McDaniel 1,2 1 Division of Pediatric Pain Medicine, Department of Pediatrics, Prisma Health, Greenville, SC 29607, USA; [email protected] 2 School of Medicine Greenville, University of South Carolina, Greenville, SC 29607, USA; [email protected] (M.S.); [email protected] (M.Z.) 3 Division of Child and Adolescent Psychiatry, Department of Psychiatry, Prisma Health, Greenville, SC 29607, USA * Correspondence: [email protected] Received: 30 October 2020; Accepted: 25 November 2020; Published: 2 December 2020 Abstract: Children and adolescents with recurrent or chronic pain and headache are a complex and heterogenous population. Patients are best served by multi-specialty, multidisciplinary teams to assess and create tailored, individualized pain treatment and rehabilitation plans. Due to the complex nature of pain, generalizing pharmacologic treatment recommendations in children with recurrent or chronic pains is challenging. This is particularly true of complicated patients with co-existing painful and psychiatric conditions. There is an unfortunate dearth of evidence to support many pharmacologic therapies to treat children with chronic pain and headache. This narrative review hopes to supplement the available treatment options for this complex population by reviewing the pediatric and adult literature for analgesic properties of medications that also have psychiatric indication. The medications reviewed belong to medication classes typically described as antidepressants, alpha 2 delta ligands, mood stabilizers, anti-psychotics, anti-sympathetic agents, and stimulants.
    [Show full text]
  • Topamax® Tablets and Sprinkle Capsules Topiramate New Zealand Data Sheet
    TOPAMAX® TABLETS AND SPRINKLE CAPSULES TOPIRAMATE NEW ZEALAND DATA SHEET 1. PRODUCT NAME TOPAMAX® 25 mg, 50 mg, 100 mg & 200 mg film-coated tablets TOPAMAX® Sprinkle 15 mg, 25 mg & 50 mg hard capsules 2. QUALITATIVE AND QUANTITATIVE COMPOSITION TABLETS Each tablet contains 25 mg, 50 mg, 100 mg or 200 mg of topiramate. Excipient(s) with known effect: Lactose monohydrate For a full list of excipients, see section 6.1. SPRINKLE CAPSULES Each capsule contains 15 mg, 25 mg or 50 mg of topiramate. Excipients with known effect: Sugar For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM TABLETS 25 mg: Round, white, film-coated tablets, marked “TOP” on one side and “25” on the other. 50 mg: Round, light-yellow, film-coated tablets, marked “TOP” on one side and “50” on the other 100 mg: Round, yellow, film-coated tablets, marked “TOP” on one side and “100” on the other 200 mg: Round, salmon, film-coated tablets, marked “TOP” on one side and “200” on the other. SPRINKLE CAPSULES Hard capsules enclosing small, white to off-white spheres. Each gelatin capsule consists of a clear (natural) capsule cap and a white capsule body. 15 mg: imprinted with “TOP” on cap and “15 mg” on body 25 mg: imprinted with “TOP” on cap and “25 mg” on body 50mg: imprinted with “TOP” on cap and “50mg” on body (not marketed). CCDS201005v23 1 TOPAMAX(201215)ADS 4. CLINICAL PARTICULARS 4.1 THERAPEUTIC INDICATIONS EPILEPSY TOPAMAX is indicated in adults and children, 2 years and over: • as monotherapy in patients with newly diagnosed epilepsy • for conversion to monotherapy in patients with epilepsy • as add-on therapy in partial onset seizures, generalised tonic-clonic seizures or seizures associated with Lennox-Gastaut syndrome.
    [Show full text]
  • Serotonin Syndrome in the Setting of Lamotrigine, Aripiprazole, and Cocaine Use
    Hindawi Publishing Corporation Case Reports in Medicine Volume 2015, Article ID 769531, 3 pages http://dx.doi.org/10.1155/2015/769531 Case Report Serotonin Syndrome in the Setting of Lamotrigine, Aripiprazole, and Cocaine Use Anupam Kotwal1 and Sarah L. Cutrona2 1 Internal Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Room H6-531, Worcester, MA 01655, USA 2Division of General Medicine and Primary Care, Meyers Primary Care Institute, University of Massachusetts Medical School, 365 Plantation Street, Biotech 1, Suite 100, Worcester, MA 01655, USA Correspondence should be addressed to Anupam Kotwal; [email protected] Received 10 June 2015; Accepted 22 July 2015 Academic Editor: Yedidia Bentur Copyright © 2015 A. Kotwal and S. L. Cutrona. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Serotonin syndrome is a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system. It is classically associated with the simultaneous administration of two serotonergic agents, but it can occur after initiation of a single serotonergic drug or increasing the dose of a serotonergic drug in individuals who are particularly sensitive to serotonin. We describe a case of serotonin syndrome that occurred after ingestion of higher than prescribed doses of lamotrigine and aripiprazole, in addition to cocaine abuse. The diagnosis was established basedn o Hunter toxicity criteria and severity was classified as mild. The features of this syndrome resolved shortly after discontinuation of the offending agents. Serotonin syndrome is characterized by mental status changes, autonomic hyperactivity, and neuromuscular abnormalities along a spectrum ranging from mild to severe.
    [Show full text]