DOCSLIB.ORG

Insomnia in Patients with Addictions: a Safer Way to Break the Cycle

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Insomnia in Patients with Addictions: a Safer Way to Break the Cycle Insomnia in patients with addictions: A safer way to break the cycle Fight relapse by improving sleep with nonaddictive agents and behavior therapy ® Dowden Health Media rom alcohol to opioids, most addictive substances can induce sleep disturbances that persist despite Fabstinence and mayCopyright increase theFor risk forpersonal relapse. use only Nearly all FDA-approved hypnotics are Schedule IV controlled substances that—although safe and effective for most populations—are prone to abuse by patients with substance use disorders. You’re not alone if you hesitate to prescribe hypnot- BISSELL ics to these patients; a study of 311 addiction medicine physicians found that they prescribed sleep-promoting medication to only 30% of their alcohol-dependent pa- tients with insomnia.1 IMAGES/CHRISTOPHER This article presents evidence on how alcohol and GETTY other substances disturb sleep in patients with addic- 2008 © tions. We discuss the usefulness of hypnotics, off-label sedatives, and cognitive-behavioral therapy (CBT). Our Deirdre Conroy, PhD Clinical assistant professor of psychiatry goal is to help you reduce your patients’ risk of relapse by addressing their sleep complaints. J. Todd Arnedt, PhD Clinical assistant professor of psychiatry and neurology Kirk J. Brower, MD Workup: 3 principles Associate professor of psychiatry Insomnia is multifactorial. Don’t assume that sub- stance abuse is the only cause of prominent insomnia University of Michigan Ann Arbor complaints. Insomnia in patients with substance use dis- orders may be a manifestation of protracted withdrawal or a primary sleep disorder. Evaluate your patient’s: • other illnesses (psychiatric, medical, and other sleep disorders) • sleep-impairing medications (such as activating Current Psychiatry antidepressants and theophylline) Vol. 7, No. 5 97 continued For mass reproduction, content licensing and permissions contact Dowden Health Media. 097_CPSY0508 097 4/16/08 9:50:41 AM Table 1 Sleep disruptions caused by substances of abuse Substance Effect on sleep Nicotine Diffi culty falling asleep, sleep fragmentation, less restful sleep compared with nonsmokers, increased risk for OSA and SDBa-e Marijuana Short-term diffi culty falling asleep and decreased slow-wave sleep percentage Insomnia during withdrawalf-j and addictions Cocaine Prolonged sleep latency, decreased sleep effi ciency, and decreased REM sleep with intranasal self-administration; hypersomnia during withdrawalk-m Other stimulants Sleep complaints similar to those reported with cocaine use disordersn (amphetamine, methamphetamine, methylphenidate) Opioids Decreased slow-wave sleep, increased stage-2 sleep, but minimal impact on o-t Clinical Point sleep continuity; dreams and nightmares; central sleep apnea OSA: obstructive sleep apnea; SDB: sleep-disordered breathing; REM: rapid eye movement Insomnia is a clinical Source: For reference citations, see this article at CurrentPsychiatry.com diagnosis that does not require • inadequate sleep hygiene Sleep logs are useful. Ask patients to keep overnight sleep • dysfunctional beliefs about sleep. a sleep log for 2 weeks during early recov- laboratory studies Nevertheless, assume that substances ery, after acute withdrawal subsides. These are part of the problem, even if not nec- diaries help assess sleep patterns over time, essarily the only cause of insomnia. Sub- document improvement with abstinence, stance-induced sleep problems usually and engage the patient in treatment. The improve with abstinence but may persist National Sleep Foundation can provide ex- because of enduring effects of chronic drug amples (see Related Resources, page 109). exposure on the brain’s sleep centers. Insomnia is a clinical diagnosis that does Alcohol and sleep disturbances not require an overnight sleep laboratory Insomnia is extremely common in active study (polysomnography [PSG]). Diagnose drinkers and in those who are in treatment insomnia when a patient meets DSM-IV- after having stopped drinking. Across 7 TR criteria (has diffi culty falling asleep or studies of 1,577 alcohol-dependent patients staying asleep or feels that sleep is not re- undergoing treatment, more than one-half freshing for at least 1 month; and the sleep reported insomnia symptoms (mean 58%, problem impairs daytime functioning and/ range 36% to 91%),2,3 substantially higher or causes clinically signifi cant distress). In than the rate in the general population addition, consider: (33%). Nicotine, marijuana, cocaine and • PSG if you suspect other sleep disor- other stimulants, and opioids also can dis- ders, particularly obstructive sleep apnea rupt sleep (Table 1). (OSA) and periodic limb movement disor- der (PLMD) Which came first? Sleep problems may • an overnight sleep study for treat- be a pathway by which problematic sub- ment-resistant insomnia, when you have stance use develops. In 1 study, sleep adequately treated other causes. problems reported by mothers in boys A primary sleep disorder—such as OSA, ages 3 to 5 predicted onset of alcohol and restless legs syndrome (RLS), or PLMD— drug use by ages 12 to 14.4 This relation- typically requires referral to a sleep spe- ship was not mediated by attention prob- cialist. For more information about sleep lems, anxiety/depression, or aggression. disorders—including OSA or RLS—see Re- Thus, insomnia may increase the risk for Current Psychiatry 98 May 2008 lated Resources, page 109. early substance use. 098_CPSY0508 098 4/16/08 9:50:50 AM In an epidemiologic study of >10,000 Box 1 adults, the incidence of new alcohol use Stimulus control: 7 steps disorders after 1 year in those without psy- chiatric disorders at baseline was twice as to a better night’s sleep high in persons with persistent insomnia 5 as in those without insomnia. Step 1. Get into bed to go to sleep only Patients with sleep disturbances may use when you are sleepy alcohol to self-medicate,6 and tolerance to alcohol’s sedating effects develops quickly. As patients consume larger quantities with Step 2. Avoid using the bed for activities other than sleep; for example, do not greater frequency to produce sleep, the risk read, watch TV, eat, or worry in bed. for dependence may increase. Sexual activity is the only exception; on these occasions, follow the next steps Comorbid sleep disorders. Alcohol- when you intend to go to sleep dependent patients with diffi culty fall- ing asleep may have abnormal circadian Step 3. If you are unable to fall asleep rhythms, as suggested by delayed onset of Clinical Point within 15 to 20 minutes, get out of bed 7 nocturnal melatonin secretion. They also and go into another room. Remember, Treating insomnia may have low homeostatic sleep drive, an- the goal is to associate your bed with without treating other factor required to promote sleep.8 falling asleep quickly. Return to bed Habitual alcohol consumption before intending to go to sleep only when you addiction may are very sleepy bedtime (1 to 3 standard drinks) is associ- improve sleep ated with mild sleep-disordered breathing but worsen addiction (SDB) in men but not in women.9 SDB also Step 4. While out of bed during the may be more prevalent in alcohol-depen- night, engage in activities that are quiet dent men age >60.10 but of interest to you. Do not exercise, eat, smoke, or take warm showers or Consuming >2 drinks/day has been as- baths. Do not lie down or fall asleep sociated with restless legs and increased when not in bed periodic limb movements during sleep. Twice as many women reporting high alcohol use were diagnosed with PLMD, Step 5. If you return to bed and still compared with women reporting normal cannot fall asleep within 15 to 20 alcohol consumption.10-11 Recovering alco- minutes, repeat Step 3. Do this as often as necessary throughout the night hol-dependent patients have signifi cantly more periodic limb movements associated with arousals (PLMA) from sleep than Step 6. Set your alarm and get up controls. Moreover, PLMA can predict at the same time every morning, 80% of abstainers and 44% of relapsers af- regardless of how much sleep you got ter 6 months of abstinence.12 during the night. This will help your body acquire a sleep-wake rhythm Multifaceted treatment Step 7. Do not nap during the day A thorough history is essential to evaluate sleep and guide treatment decisions. Refer Source. Adapted from Bootzin R, Nicassio P. Behavioral patients to an accredited sleep disorders treatments for insomnia. In: Hersen M, Eissler R, Miller P, eds. Progress in behavior modifi cation, vol. 6. New York, NY: center if their history shows: Academic Press; 1978:30 • loud snoring • cessation of breathing can be effective for short-term insomnia. • frequent kicking during sleep Keep in mind, however, that treating in- • excessive daytime sleepiness. somnia without addiction treatment may improve sleep but worsen addiction. Tai- Short-term insomnia. Judicious use of lor medications’ pharmacokinetic charac- Current Psychiatry medications with appropriate follow-up teristics to patients’ sleep complaints. For Vol. 7, No. 5 99 099_CPSY0508 099 4/17/08 11:52:09 AM Box 2 Cognitive-behavioral therapy for insomnia (CBT-I): 4 components Stimulus control (SC). Patients with that may help or hinder sleep. Patients chronic insomnia may watch television, with addiction may benefi t from learning talk on the telephone, or worry about not how drug use and withdrawal affects sleeping while lying in bed. The goal of SC sleep or how substance use for sleep Insomnia is to alter this association by reestablishing may exacerbate sleep problems. Other and addictions the bed and bedroom with the pleasant SH recommendations include avoiding experience of falling asleep and staying caffeine, nicotine, and exercise in close asleep.13 Instructions for SC (Box 1, page proximity to bedtime. 99) are commonly provided with sleep Cognitive therapy. Goals are to: restriction. • identify and explore dysfunctional Sleep restriction (SR) addresses the beliefs that cause patients anxiety excessive time that patients with insomnia about sleep problems spend in bed not sleeping.
Load more

Recommended publications
  • Journal of Pharmacology and Experimental Therapeutics
    Journal of Pharmacology and Experimental Therapeutics Molecular Determinants of Ligand Selectivity for the Human Multidrug And Toxin Extrusion Proteins, MATE1 and MATE-2K Bethzaida Astorga, Sean Ekins, Mark Morales and Stephen H Wright Department of Physiology, University of Arizona, Tucson, AZ 85724, USA (B.A., M.M., and S.H.W.) Collaborations in Chemistry, 5616 Hilltop Needmore Road, Fuquay-Varina NC 27526, USA (S.E.) Supplemental Table 1. Compounds selected by the common features pharmacophore after searching a database of 2690 FDA approved compounds (www.collaborativedrug.com). FitValue Common Name Indication 3.93897 PYRIMETHAMINE Antimalarial 3.3167 naloxone Antidote Naloxone Hydrochloride 3.27622 DEXMEDETOMIDINE Anxiolytic 3.2407 Chlordantoin Antifungal 3.1776 NALORPHINE Antidote Nalorphine Hydrochloride 3.15108 Perfosfamide Antineoplastic 3.11759 Cinchonidine Sulfate Antimalarial Cinchonidine 3.10352 Cinchonine Sulfate Antimalarial Cinchonine 3.07469 METHOHEXITAL Anesthetic 3.06799 PROGUANIL Antimalarial PROGUANIL HYDROCHLORIDE 100MG 3.05018 TOPIRAMATE Anticonvulsant 3.04366 MIDODRINE Antihypotensive Midodrine Hydrochloride 2.98558 Chlorbetamide Antiamebic 2.98463 TRIMETHOPRIM Antibiotic Antibacterial 2.98457 ZILEUTON Antiinflammatory 2.94205 AMINOMETRADINE Diuretic 2.89284 SCOPOLAMINE Antispasmodic ScopolamineHydrobromide 2.88791 ARTICAINE Anesthetic 2.84534 RITODRINE Tocolytic 2.82357 MITOBRONITOL Antineoplastic Mitolactol 2.81033 LORAZEPAM Anxiolytic 2.74943 ETHOHEXADIOL Insecticide 2.64902 METHOXAMINE Antihypotensive Methoxamine
    [Show full text]
  • Management of Status Epilepticus
    Published online: 2019-11-21 THIEME Review Article 267 Management of Status Epilepticus Ritesh Lamsal1 Navindra R. Bista1 1Department of Anaesthesiology, Tribhuvan University Teaching Address for correspondence Ritesh Lamsal, MD, DM, Department Hospital, Institute of Medicine, Tribhuvan University, Nepal of Anaesthesiology, Tribhuvan University Teaching Hospital, Institute of Medicine, Tribhuvan University,Kathmandu, Nepal (e-mail: [email protected]). J Neuroanaesthesiol Crit Care 2019;6:267–274 Abstract Status epilepticus (SE) is a life-threatening neurologic condition that requires imme- diate assessment and intervention. Over the past few decades, the duration of seizure Keywords required to define status epilepticus has shortened, reflecting the need to start thera- ► convulsive status py without the slightest delay. The focus of this review is on the management of con- epilepticus vulsive and nonconvulsive status epilepticus in critically ill patients. Initial treatment ► neurocritical care of both forms of status epilepticus includes immediate assessment and stabilization, ► nonconvulsive status and administration of rapidly acting benzodiazepine therapy followed by nonbenzodi- epilepticus azepine antiepileptic drug. Refractory and super-refractory status epilepticus (RSE and ► refractory status SRSE) pose a lot of therapeutic problems, necessitating the administration of contin- epilepticus uous infusion of high doses of anesthetic agents, and carry a high risk of debilitating ► status epilepticus morbidity as well as mortality. ► super-refractory sta- tus epilepticus Introduction occur after 30 minutes of seizure activity. However, this working definition did not indicate the need to immediately Status epilepticus (SE) is a medical and neurologic emergency commence treatment and that permanent neuronal injury that requires immediate evaluation and treatment. It is associat- could occur by the time a clinical diagnosis of SE was made.
    [Show full text]
  • 2015-16 59. On-Line Learning Bipolar Medications
    Pharmacology/Therapeutics II Block II Handouts – 2015‐16 59. On‐Line learning Bipolar Medications ‐ Schilling 60. On‐Line Learning Anti‐Depressants ‐ Schilling 61. On‐Line Learning Sedative Hypnotics ‐ Battaglia 62. On‐Line Learning Treatment of Insomnia ‐ Battaglia 63. On‐Line Learning AntiPsychotics ‐ Schilling 64. On‐Line Only Drugs of Abuse, tolerance & Dependence – Bakowska 65. Active Learning Session: Mood Disorders & Treatment – Schilling 66. Active Learning Session – Anxiety Disorders – Schilling 67. Active Learning Session – Psychotic Illness & Treatment – Schilling 68. Drugs to Treat Rheumatoid Arthritis & Gout ‐ Clipstone Pharmacology & Therapeutics Bipolar Medications February 15, 2016 David Schilling, M.D. Bipolar Disorder Medications Goals & Objectives: Describe the pharmacologic profiles of major drugs/drug classes used in the treatment of bipolar disorder. These drugs include: Lithium, Divalproex (Depakote), Carbamazepine (Tegretol), Lamotrigine (Lamictal) 1. List the major drugs/drug classes used in the treatment of bipolar disorder 2. Describe the mechanism of action of each of the major drugs/drug classes used in the treatment of bipolar disorder 3. Describe the principle pharmacokinetic properties of the major drugs used to treat bipolar disorder. This includes: half-life & time to steady state, trough levels, metabolic auto-induction, P450 system induction, therapeutic index 4. Describe the pharmacodynamics (common adverse effects) of the major drugs used to treat bipolar disorder. 5. Describe the pharmacodynamics (serious adverse effects) of the major drugs used to treat bipolar disorder. This includes: lithium toxicity, agranulocytosis, aplastic anemia, hepatic failure, exfoliative dermatitis, pancreatitis, Steven’s Johnson syndrome 6. Identify the laboratory tests that may be used to monitor for common and serious major adverse effects of the major drugs used to treat bipolar disorder.
    [Show full text]
  • Insomnia Across the Lifespan: Treating This Common Condition
    2/20/2019 Insomnia Across the Lifespan: Treating This Common Condition Wendy L. Wright MS, ANP-BC, FNP-BC, FAANP, FAAN, FNAP Adult / Family Nurse Practitioner Owner – Wright & Associates Family Healthcare @ Amherst and @ Concord, NH Owner – Partners in Healthcare Education © Wright, 2019 1 1 Disclosures • Speaker Bureau: Pfizer, Merck, Sanofi Pasteur • Consultant: Pfizer, Merck, Sanofi Pasteur © Wright, 2019 2 2 Objectives • Upon completion of this session, the participant will be able to: • Discuss the incidence and prevalence of insomnia across the lifespan • Identify the appropriate work-up of the individual with insomnia • Discuss nonpharmacologic and pharmacologic treatment options for the patient with insomnia © Wright, 2019 3 3 Wright, 2019 1 2/20/2019 What Is Insomnia? • Insomnia: • Difficulty initiating or maintaining sleep; sleep that is nonrestorative despite having an adequate opportunity and no abnormal environmental circumstances; and accompanied by daytime somnolence (Sateia, M.J. et. al, 2017) © Wright, 2019 4 4 What Is Insomnia? • DSM-V definition: • Difficulty initiating and / or • Difficulty maintaining and / or • Waking earlier than desired AND • Occurring at least 3 nights per week for at least 3 months AND • Dissatisfaction with sleep http://www.psychiatrictimes.com/special-reports/review-changes-dsm-5-sleep-wake-disorders accessed 08- 08-2018 © Wright, 2019 5 5 DSM-5 Diagnostic Criteria https://practicingclinicians.com/CE-CME/sleep/enhancing-the-management-of-insomnia-in-older-patients/MPCE90716 © Wright, 2019 6
    [Show full text]
  • Drugs Inducing Insomnia As an Adverse Effect
    2 Drugs Inducing Insomnia as an Adverse Effect Ntambwe Malangu University of Limpopo, Medunsa Campus, School of Public Health, South Africa 1. Introduction Insomnia is a symptom, not a stand-alone disease. By definition, insomnia is "difficulty initiating or maintaining sleep, or both" or the perception of poor quality sleep (APA, 1994). As an adverse effect of medicines, it has been documented for several drugs. This chapter describes some drugs whose safety profile includes insomnia. In doing so, it discusses the mechanisms through which drug-induced insomnia occurs, the risk factors associated with its occurrence, and ends with some guidance on strategies to prevent and manage drug- induced insomnia. 2. How drugs induce insomnia There are several mechanisms involved in the induction of insomnia by drugs. Some drugs affects sleep negatively when being used, while others affect sleep and lead to insomnia when they are withdrawn. Drugs belonging to the first category include anticonvulsants, some antidepressants, steroids and central nervous stimulant drugs such amphetamine and caffeine. With regard to caffeine, the mechanism by which caffeine is able to promote wakefulness and insomnia has not been fully elucidated (Lieberman, 1992). However, it seems that, at the levels reached during normal consumption, caffeine exerts its action through antagonism of central adenosine receptors; thereby, it reduces physiologic sleepiness and enhances vigilance (Benington et al., 1993; Walsh et al., 1990; Rosenthal et al., 1991; Bonnet and Arand, 1994; Lorist et al., 1994). In contrast to caffeine, methamphetamine and methylphenidate produce wakefulness by increasing dopaminergic and noradrenergic neurotransmission (Gillman and Goodman, 1985). With regard to withdrawal, it may occur in 40% to 100% of patients treated chronically with benzodiazepines, and can persist for days or weeks following discontinuation.
    [Show full text]
  • Vademecum Agrovet Market Animal Health
    Vademecum Agrovet Market Animal Health We are a Peruvian company focused on the development, production and commercialization of veterinary products, driving its technical and creative development to meet the needs of veterinarians and stock farmers with unique products of high quality. www.agrovetmarket.com Mission l Products of Unique Class Provide veterinary, nutritional and farmaceutical products of unique class; developed in a creative and innovative way, under high standards of quality that allow us to reach international markets and consolidate locally through the formal stablishment of strategical alliances. Antibiotics Line of large animals am Line of companion animals ac Line of poultry and swine av www.agrovetmarket.com Antibiotics ® Agrogenta 11 | Vetigen 11 Injectable Solution Broad-spectrum aminoglycoside Composition: Gentamicin (as sulphate) 110 mg, excipients q.s. ad 1 mL. Indications: Treatment and prevention of infections caused by microorganisms sensitive to gentamicin (of the urogenital, respiratory and gastrointestinal systems). Also useful in cases of mastitis, metritis, post-operatory and cutaneous infections, septicemias, among others.. Dosage and Administration: Cattle, horse, sheep, goat, swine, camelid: 1 mL/27.5 kg of b.w.; young animals, dogs and cats: 1 mL/14 kg; poultry: 0.1 mL/1.4 kg; every 24 hours for 3 to 5 consecutive days by subcutaneous or intramuscular route. Intrauterine or intra-mammary route: Cows: 2 mL diluted in 20 mL of physiological saline solution for 3 to 5 days. Mares: 20 mL diluted in 200 - 500 mL of physiological saline solution for 3 to 5 days (only intrauterine route). Commercial Presentation: Bottle x 100 mL and 250 mL.
    [Show full text]
  • Drugs That Act in the Cns
    DRUGS THAT ACT IN THE CNS Anxiolytic and Hypnotic Drugs Dr Karamallah S. Mahmood PhD Clinical Pharmacology 1 OTHER ANXIOLYTIC AGENTS/ A. Antidepressants Many antidepressants are effective in the treatment of chronic anxiety disorders and should be considered as first-line agents, especially in patients with concerns for addiction or dependence. Selective serotonin reuptake inhibitors (SSRIs) or serotonin/norepinephrine reuptake inhibitors (SNRIs) may be used alone or prescribed in combination with a benzodiazepine. SSRIs and SNRIs have a lower potential for physical dependence than the benzodiazepines and have become first-line treatment for GAD. 2 OTHER ANXIOLYTIC AGENTS/ B. Buspirone Buspirone is useful for the chronic treatment of GAD and has an efficacy comparable to that of the benzodiazepines. It has a slow onset of action and is not effective for short-term or “as-needed” treatment of acute anxiety states. The actions of buspirone appear to be mediated by serotonin (5-HT1A) receptors, although it also displays some affinity for D2 dopamine receptors and 5-HT2A serotonin receptors. Buspirone lacks the anticonvulsant and muscle-relaxant properties of the benzodiazepines. 3 OTHER ANXIOLYTIC AGENTS B. Buspirone The frequency of adverse effects is low, with the most common effects being headaches, dizziness, nervousness, nausea, and light-headedness. Sedation and psychomotor and cognitive dysfunction are minimal, and dependence is unlikely. Buspirone does not potentiate the CNS depression of alcohol. 4 V. BARBITURATES The barbiturates were formerly the mainstay of treatment to sedate patients or to induce and maintain sleep. Today, they have been largely replaced by the benzodiazepines, primarily because barbiturates induce tolerance and physical dependence and are associated with very severe withdrawal symptoms.
    [Show full text]
  • 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
    [Show full text]
  • Sleep Inducing Toothpaste Made with Natural Herbs and a Natural Hormone
    Sleep inducing toothpaste made with natural herbs and a natural hormone Abstract A toothpaste composition for inducing sleep while simultaneously promoting intraoral cleanliness, which includes toothpaste base ingredients and at least one sleep- inducing natural herb or hormone. The sleep-inducing natural herbs and hormone are selected from the group consisting of Chamomile, Lemon Balm, Passion Flower, and Valerian, and the hormone Melatonin. The sleep-inducing natural herbs are in a range of 0.25% to 18% by weight of the composition. Description of the Invention FIELD OF THE INVENTION The following natural herbs and natural hormone in combination with toothpaste is used at night to improve sleep. The expected dose of toothpaste is calculated at 2 grams. The ingredients have been assessed for range of daily dose for best effects, toxicity in normal range, recommended proportion of each, and water solubility of key constituents. BACKGROUND OF THE INVENTION It is an object of the present invention to provide a sleep-inducing toothpaste or mouth spray which includes sleep-inducing natural herbs and a natural hormone. It is a further object of the present invention to provide a sleep-inducing toothpaste which includes toothpaste base ingredients and natural herbs being Chamomile, Lemon Balm, Passion Flower, Valerian and the natural hormone Melatonin. SUMMARY OF THE INVENTION A toothpaste composition is provided for inducing sleep while simultaneously promoting intraoral cleanliness, which includes toothpaste base ingredients and at least one sleep-inducing natural herb or hormone. The sleep-inducing natural herbs and hormone are selected from the group consisting of the natural herbs Chamomile, Lemon Balm, Passion Flower, and Valerian, and the natural hormone Melatonin.
    [Show full text]
  • THE USE of MIRTAZAPINE AS a HYPNOTIC O Uso Da Mirtazapina Como Hipnótico Francisca Magalhães Scoralicka, Einstein Francisco Camargosa, Otávio Toledo Nóbregaa
    ARTIGO ESPECIAL THE USE OF MIRTAZAPINE AS A HYPNOTIC O uso da mirtazapina como hipnótico Francisca Magalhães Scoralicka, Einstein Francisco Camargosa, Otávio Toledo Nóbregaa Prescription of approved hypnotics for insomnia decreased by more than 50%, whereas of antidepressive agents outstripped that of hypnotics. However, there is little data on their efficacy to treat insomnia, and many of these medications may be associated with known side effects. Antidepressants are associated with various effects on sleep patterns, depending on the intrinsic pharmacological properties of the active agent, such as degree of inhibition of serotonin or noradrenaline reuptake, effects on 5-HT1A and 5-HT2 receptors, action(s) at alpha-adrenoceptors, and/or histamine H1 sites. Mirtazapine is a noradrenergic and specific serotonergic antidepressive agent that acts by antagonizing alpha-2 adrenergic receptors and blocking 5-HT2 and 5-HT3 receptors. It has high affinity for histamine H1 receptors, low affinity for dopaminergic receptors, and lacks anticholinergic activity. In spite of these potential beneficial effects of mirtazapine on sleep, no placebo-controlled randomized clinical trials of ABSTRACT mirtazapine in primary insomniacs have been conducted. Mirtazapine was associated with improvements in sleep on normal sleepers and depressed patients. The most common side effects of mirtazapine, i.e. dry mouth, drowsiness, increased appetite and increased body weight, were mostly mild and transient. Considering its use in elderly people, this paper provides a revision about studies regarding mirtazapine for sleep disorders. KEYWORDS: sleep; antidepressive agents; sleep disorders; treatment� A prescrição de hipnóticos aprovados para insônia diminuiu em mais de 50%, enquanto de antidepressivos ultrapassou a dos primeiros.
    [Show full text]
  • Lunesta: Uses, Dosage, Side Effects ­ Drugs.Com
    4/5/2017 Lunesta: Uses, Dosage, Side Effects ­ Drugs.com Lunesta ﴿Generic Name: eszopiclone ﴾e ZOP i klone Brand Names: Lunesta What is Lunesta? Lunesta ﴾eszopiclone﴿ is a sedative, also called a hypnotic. It affects chemicals in your brain that may be unbalanced in people .﴿with sleep problems ﴾insomnia Lunesta is used to treat insomnia. This medicine causes relaxation to help you fall asleep and stay asleep. Lunesta may also be used for purposes not listed in this medication guide. Important information Lunesta may cause a severe allergic reaction. Stop taking this medicine and get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Lunesta will make you fall asleep. Never take this medication during your normal waking hours, unless you have at least 8 hours to dedicate to sleeping. Some people using this medicine have engaged in activity such as driving, eating, or making phone calls and later having no memory of the activity. If this happens to you, stop taking Lunesta and talk with your doctor about another treatment for your sleep disorder. Lunesta can cause sie effects that may impair your thinking or reactions. You may still feel sleepy the morning after taking the medication. Until you know how this medication will affect you during waking hours, be careful if you drive, operate machinery, pilot an airplane, or do anything that requires you to be awake and alert. Do not drink alcohol while you are taking this medication. It can increase some of the side effects, including drowsiness.
    [Show full text]
  • Repeated Lysergic Acid Diethylamide in an Animal Model of Depression
    JOP0010.1177/0269881114531666Journal of PsychopharmacologyBuchborn et al. 531666research-article2014 Original Paper Repeated lysergic acid diethylamide in an animal model of depression: Normalisation of learning behaviour and Journal of Psychopharmacology 2014, Vol. 28(6) 545 –552 hippocampal serotonin 5-HT signalling © The Author(s) 2014 2 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0269881114531666 jop.sagepub.com Tobias Buchborn, Helmut Schröder, Volker Höllt and Gisela Grecksch Abstract A re-balance of postsynaptic serotonin (5-HT) receptor signalling, with an increase in 5-HT1A and a decrease in 5-HT2A signalling, is a final common pathway multiple antidepressants share. Given that the 5-HT1A/2A agonist lysergic acid diethylamide (LSD), when repeatedly applied, selectively downregulates 5-HT2A, but not 5-HT1A receptors, one might expect LSD to similarly re-balance the postsynaptic 5-HT signalling. Challenging this idea, we use an animal model of depression specifically responding to repeated antidepressant treatment (olfactory bulbectomy), and test the antidepressant-like properties of repeated LSD treatment (0.13 mg/kg/d, 11 d). In line with former findings, we observe that bulbectomised rats show marked deficits in active avoidance learning. These deficits, similarly as we earlier noted with imipramine, are largely reversed by repeated LSD administration. Additionally, bulbectomised rats exhibit distinct anomalies of monoamine receptor signalling in hippocampus and/or frontal cortex; 35 from these, only the hippocampal decrease in 5-HT2 related [ S]-GTP-gamma-S binding is normalised by LSD. Importantly, the sham-operated rats do not profit from LSD, and exhibit reduced hippocampal 5-HT2 signalling. As behavioural deficits after bulbectomy respond to agents classified as antidepressants only, we conclude that the effect of LSD in this model can be considered antidepressant-like, and discuss it in terms of a re-balance of hippocampal 5-HT2/5-HT1A signalling.
    [Show full text]