Sleep Disorders Preeti Devnani
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Sleep Matters the Impact of Sleep on Health and Wellbeing Mental Health Awareness Week 2011
Sleep Matters The impact of sleep on health and wellbeing Mental Health Awareness Week 2011 Address Mental Health Foundation Sea Containers House 20 Upper Ground London SE1 9QB United Kingdom Telephone 020 7803 1100 Email [email protected] Website www.HowDidYouSleep.org £10 IBSN 978-1-906162-65-8 Registered charity number England 801130 Scotland SC039714 © Mental Health Foundation 2011 Contents 04 Executive summary 08 Introduction 12 Part 01 – Sleeping and sleep patterns 28 Part 02 – Poor sleep 48 Part 03 – Sleeping well 62 Conclusion 66 Useful resources 68 References 72 Appendix: Sleep diary 76 Acknowledgements 01 ‘The main facts in human life are five: E. M. Forster Executive We spend approximately a Poor sleep over a sustained period One of the most widely used and – The new Public Health Outcomes third of our lives asleep. Sleep leads to a number of problems which successful therapies is Cognitive Framework should include a specific Summary are immediately recognisable, including Behavioural Therapy (CBT). This is outcome on reducing sleep problems is an essential and involuntary fatigue, sleepiness, poor concentration, useful even for people who have across the whole population. process, without which we lapses in memory, and irritability. had insomnia for a long period of time. Sleep should also be reflected in cannot function effectively. A full course of such a therapy with new national mental health outcome It is as important to our Up to one third of the population may a sleep specialist is potentially costly, indicators, including improving bodies as eating, drinking suffer from insomnia (lack of sleep and is most appropriate for people sleep for people who experience and breathing, and is vital for or poor quality sleep). -
A Case of Recurrent Sleep Paralysis: Beyond Narcolepsy
Open Access Austin Journal of Clinical Neurology A Austin Full Text Article Publishing Group Case Report A Case of Recurrent Sleep Paralysis: Beyond Narcolepsy Vijaya Yelisetty and Kanika Bagai* Abstract Department of Neurology, Vanderbilt University School of Medicine, Tennessee, USA Isolated episodes of sleep paralysis can occur in healthy people at least *Corresponding author: Kanika Bagai, Department of once in their lifetime; however recurrent isolated sleep paralysis (RISP) events Neurology, Vanderbilt Sleep Disorders Center, Vanderbilt are less common and often worrisome. Recurrent episodes of sleep paralysis University School of Medicine, A- 0118 Medical Center are often seen in patients with narcolepsy. Here, we present a unique case of North, Nashville, TN 37232, Tennessee, USA, Tel: 615- a middle-aged woman who presents with symptoms of RISP in her fifth decade 322-0283; Fax: 615-936-0223; Email: kanika.bagai@ that was not associated with narcolepsy. Vanderbilt.Edu Received: June 20, 2014; Accepted: August 20, 2014; Published: August 22, 2014 Introduction Laboratory data including complete blood count, complete metabolic panel, TSH, Vit B12, Vit D levels were within normal limits We describe a case of a 52-year-old woman who presents with as below: initial symptoms of recurrent isolated sleep paralysis. Complete blood count: WBC: 5.7k/ul; Hemoglobin 12.6 gm/dl, Case Presentation hematocrit 37%, platelets count 258k/ul. A 52 year-old woman presented to the sleep clinic with complaints Chemistries: Sodium 141 mmol/l, potassium 4.1 mmol/l, chloride of sleep difficulties and symptoms of “unable to move her body while 107 mmol/l, bicarbonate 25 mmol/l, glucose 213 mg/dl, BUN 19 mg/ in bed”. -
Using Bright Light and Melatonin to Reduce Jet Lag Helen J
Chapter 16 Using Bright Light and Melatonin to Reduce Jet Lag Helen J. Burgess Biological Rhythms Research Laboratory, Rush University Medical Center, Chicago, IL PROTOCOL NAME Using bright light and melatonin to reduce jet lag. GROSS INDICATION This is generally applicable to phase shifting the circadian clock in patients with circadian rhythm sleep disorders or winter depression. SPECIFIC INDICATION Bright light and melatonin can be used to reduce jet lag after crossing at least two time zones east or west. CONTRAINDICATIONS Bright light should probably not be used in: l people with existing eye disease; l people using photosensitizing medications. Bright light can induce: l migraines (in about one-third of migraine sufferers); l mania (rare). Melatonin should probably not be used in: l people who are driving or operating heavy machinery (unless they have previously tested their response to melatonin and are taking ,0.5 mg of melatonin); l pregnant or nursing women (melatonin will transfer to the fetus/infant); l women seeking to become pregnant; Behavioral Treatments for Sleep Disorders. DOI: 10.1016/B978-0-12-381522-4.00016-X © 2011 Elsevier Inc. All rights reserved. 151 152 PART I | BSM Treatment Protocols for Insomnia l children (unless they suffer from a neurodevelopmental condition associ- ated with extremely poor sleep); l asthmatics and patients with gastrointestinal disease (melatonin may be inflammatory); l patients using other medications (unless supervised by a physician). RATIONALE FOR INTERVENTION Rapid jet travel across multiple time zones produces a temporary misalign- ment between the timing of the central circadian clock and the desired sleep times in the new time zone. -
The Neurobiology of Narcolepsy-Cataplexy
Progress in Neurobiology Vol. 41, pp. 533 to 541, 1993 0301-0082/93/$24.00 Printed in Great Britain. All rights reserved © 1993 Pergamon Press Ltd THE NEUROBIOLOGY OF NARCOLEPSY-CATAPLEXY MICHAEL S. ALDRICH Department of Neurology, Sleep Disorders Center, University of Michigan Medical Center, Ann Arbor, MI, U.S.A. (Received 17 July 1992) CONTENTS 1. Introduction 533 2. Clinical aspects 533 2.1. Sleepiness and sleep attacks 533 2.2. Cataplexy and related symptoms 534 2.3. Clinical variants 534 2.3.1. Narcolepsy without cataplexy 534 2.3.2. Idiopathic hypersomnia 534 2.3.3. Symptomatic narcolepsy 534 2.4. Treatment 534 3. Pathophysiology 535 4. Neurobiological studies 535 4.1. The canine model of narcolepsy 535 4.2. Pharmacology of human cataplexy 537 4.3. Postmortem studies 537 5. Genetic and family studies 537 6. Summary and conclusions 539 References 539 1. INTRODUCTION 2. CLINICAL ASPECTS Narcolepsy is a specific neurological disorder Narcolepsy has a prevalence that varies worldwide characterized by excessive sleepiness that cannot be from as little as 0.0002% in Israel to 0.16% in Japan; fully relieved with any amount of sleep and by in North America and Europe the prevalence is about abnormalities of rapid eye movement (REM) 0.03-0.06% (Dement et al., 1972; Honda, 1979; Lavie sleep. About two-thirds of patients also have brief and Peled, 1987). The onset of narcoleptic symptoms, episodes of muscle weakness usually brought on by usually in the second or third decade of life, may emotion, referred to as cataplexy. The disorder gener- occur over a few days or weeks or it may be so ally begins in adolescence and continues throughout gradual that the loss of full alertness is unrecognized life. -
Slow-Wave Sleep, Diabetes, and the Sympathetic Nervous System
COMMENTARY Slow-wave sleep, diabetes, and the sympathetic nervous system Derk-Jan Dijk* Surrey Sleep Research Centre, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XP, United Kingdom leep oscillates between two dif- of SWS that has accumulated. The latter less provides supportive evidence for the ferent states: non-rapid eye conclusion was derived from SWS depri- notion that SWS is restorative also for movement (NREM) sleep and vation experiments in which stimuli, usu- the body and that negative effects asso- rapid-eye movement (REM) ally acoustic stimuli [although early on ciated with disruption of this state may Ssleep. Slow-wave sleep (SWS) is a sub- in the history of SWS deprivation, mild extend to the body. state of NREM sleep, and its identifica- electric shocks were used (5)], are deliv- Many other physiological variables are tion is based primarily on the presence ered in response to the ongoing EEG. affected by the behavioral-state sleep, of slow waves, i.e., low-frequency, high- The drive to enter SWS is strong and is the NREM–REM cycle, and SWS. amplitude oscillations in the EEG. Upon the transition from wakefulness to Quantification of SWS is accomplished sleep, heart rate slows down. During by visual inspection of EEG records or Short habitual sleep sleep, the balance of sympathetic and computerized methods such as spectral parasympathetic tone oscillates in syn- analysis based on the fast Fourier trans- has been associated chrony with the NREM–REM cycle. form (FFT). Slow-wave activity (SWA; Analysis of autonomic control of the also referred to as delta power) is a with increased risk variability of heart rate demonstrates quantitative measure of the contribution that, within each NREM episode, as of both the amplitude and prevalence of for diabetes. -
Sleep 101: the Abcs of Getting Your Zzzs
Sleep 101: The ABCs of Getting Your ZZZs Steven D. Brass, MD MPH MBA Director of Neurology Sleep Medicine Clinic UC Davis Health System November 18, 2014 What you will learn: • Why do we sleep? • How much sleep do we need? • What are the effects of sleep deprivation? • What are the different stages of sleep? • What are the types of sleep problems? • What is sleep apnea and how is it treated? • How can we sleep better? Why do we sleep? • Each of us will spend about 1/3 of our lifetime sleeping! • Sleep helps us with: – Memory consolidation – Immune system – Recharge energy for the day – Growth and development How much sleep do we need? Infants : 14-15 hours National Sleep Foundation Secrets of Sleep; National Geographic Magazine . 2010 Adolescents: 8.5-9.25 hours National Sleep Foundation Secrets of Sleep; National Geographic Magazine . 2010 Adult/Elder Sleep: 7-9 hours National Sleep Foundation Secrets of Sleep; National Geographic Magazine . 2010 What are the different stages of sleep? • Non REM Sleep -75% of the night – Stage 1 – Stage 2 – Stage 3 – Stage 4 • REM Sleep -25% of the night – Dreaming Normal Sleep Patterns in Young Adults REM Stage AWAKE NREM REM 1 2 3 4 1 2 3 4 5 6 7 8 Hours of Sleep Adapted from Berger RJ. The sleep and dream cycle. In: Kales A, ed. Sleep Physiology & Pathology: A Symposium. Philadelphia: J.B. Lippincott; 1969. American Academy of Sleep Medicine Sleep Fragmentation Affects Sleep Quality NORMAL SLEEP = Paged ON CALL SLEEP © American Academy of Sleep Medicine, Westchester, IL Why do we dream? • Everyone -
Jet Lag and Shift Work Sleep Disorders: How to Help Reset the Internal Clock
REVIEW CME EDUCATIONAL OBJECTIVE: Readers will suggest strategies to lessen jet lag and shift work disorders CREDIT BHANU P. KOLLA, MBBS R. ROBERT AUGER, MD Mayo Center for Sleep Medicine, Mayo Center for Sleep Medicine, Department of Psychiatry and Psychology, Department of Psychiatry and Psychology, Mayo Clinic College of Medicine, Mayo Clinic College of Medicine, Rochester, MN Rochester, MN Jet lag and shift work sleep disorders: How to help reset the internal clock ■■ABSTRACT or people who must travel long dis- F tances east or west by air or who must work Jet lag sleep disorder and shift work sleep disorder are the night shift, some relief is possible for the the result of dyssynchrony between the internal clock and grogginess and disorientation that often ensue. the external light-dark cycle, brought on by rapid travel The problems arise from the body’s internal across time zones or by working a nonstandard schedule. clock being out of sync with the sun. Part of Symptoms can be minimized by optimizing the sleep the solution involves helping reset the inter- nal clock, or sometimes, preventing it from environment, by strategic avoidance of and exposure to resetting itself. light, and also with drug and behavioral therapies. This review will focus on jet lag sleep disor- der and shift work sleep disorder, with an em- ■■KEY POINTS phasis on the causes, the clinical assessment, and evidence-based treatment options. Symptoms include daytime anergia, alternating com- plaints of insomnia and hypersomnia, emotional dis- ■ WHEN THE INTERNAL CLOCK turbances, and gastrointestinal distress. The severity IS OUT OF SYNC WITH THE SUN depends on the degree and the duration of dyssynchrony, as well as on innate factors such as age and whether the Circadian rhythm sleep disorders are the re- patient is an “early bird” or a “night owl.” sult of dyssynchrony between the body’s inter- nal clock and the external 24-hour light-dark cycle. -
Parasomnias Revisited New Mexico Thoracic Society Sapna Bhatia Md 02/25/17 Objectives
PARASOMNIAS REVISITED NEW MEXICO THORACIC SOCIETY SAPNA BHATIA MD 02/25/17 OBJECTIVES • Appreciate the clinical semiology to help differentiate between REM and NREM parasomnias • Appreciate the ICSD III Classification Scheme for the major parasomnias • Understand management modalities including behavioral and pharmacological for NREM and REM parasomnias • Understand the difference between parasomnias and seizures WHAT ARE PARASOMNIAS? Undesirable motor, or verbal phenomena that arise from sleep or sleep-wake transition PARASOMNIAS: OVERLAPPING STATES REM PARASOMNIAS WAKE NREM PARASOMNIAS REM NREM PARASOMNIAS: DIFFERENTIAL DIAGNOSIS RBD Confusional Arousals Recurrent Isolated Sleep Paralysis Sleepwalking Nightmare Disorder Sleep Terrors WAKE Sleep Related Eating Disorder REM NREM PYSCHOGENIC SEIZURES SPELLS NFLE Dissociative Disorder ICSD II ICSD III REM Parasomnias • RBD • RBD • Recurrent Isolated Sleep • Recurrent Isolated Sleep Paralysis ICSD II VS ICSDParalysis III CLASSIFICATION• Nightmare Disorder • Nightmare Disorder Disorders of arousal • Confusional Arousals • Confusional Arousals (NREM sleep) • Sleepwalking • Sleep Walking • Sleep Terrors • Sleep Terrors • SRED Other Parasomnias • SRED • Sleep Related Dissociative • Sleep Related Dissociative Disorders Disorders • Sleep Enuresis • Sleep Enuresis • Catathrenia SDB • Catathrenia • Exploding Head Syndrome • Exploding Head syndrome • Sleep Related Hallucinations • Sleep Related Hallucinations • Parasomnia, Unspecified • Parasomnia, Unspecified • Parasomnia due to Drug or • Parasomnia -
Narcolepsy and Other Disorders of Excessive Sleepiness
REVIEW ARTICLE 183 Narcolepsy and other Disorders of Excessive Sleepiness S. Chokroverty NJ Neuroscience Institute at JFK; Seton Hall University, Edison, NJ, USA ○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○○ Indian J Sleep Med 2006; 1.4, 183-188 he French physician Gelineau used the term Genetic Factors of Narcolepsy narcolepsy in 1880 to describe irresistible sleep attacks and “astasia” which has all the features Approximately 1-2% of the first-degree relatives of T narcoleptic patients compared with 0.02-0.18% in the of what was later to be named cataplexy. Reports of a large series of patients in the last century brought the general population manifest the illness, indicating a 10- entity of narcolepsy/cataplexy to the attention of the 40 times higher prevalence than existing in the general medical profession. Sleep attacks, cataplexy, sleep population. Most cases of human narcolepsy are paralysis and hypnagogic hallucinations were all grouped sporadic, but some are dominant. Twin studies of under the term narcoleptic tetrad by Yoss and Daily in narcolepsy document lack of a strong genetic influence. 1957. In 1960 Vogel discovered sleep onset rapid eye The majority of monozygotic twins were discordant for movements (SOREMs). Honda et al. discovered the narcolepsy; only 25-31% have concordance, suggesting presence of HLA-antigens in 100% of Japanese an influence of environmental factors in the etiology of narcoleptics in 1983. Finally, the discovery of narcolepsy. Narcolepsy is thought to be recessive in hypocretin or Orexin systems, reports of canine and Doberman Pinschers and Labrador Retrievers but mouse models of narcolepsy and hypocretin-1 deficiency multifactorial in poodles. Histocompatibility leucocyte in the cerebrospinal fluid of human narcolepsy/cataplexy antigens (HLA) are closely associated with narcolepsy in patients (Mignot et al.; Nishino et al.) brought narcolepsy 95-100% of cases in white and Japanese patients. -
Sleep Disturbances in Patients with Persistent Delusions: Prevalence, Clinical Associations, and Therapeutic Strategies
Review Sleep Disturbances in Patients with Persistent Delusions: Prevalence, Clinical Associations, and Therapeutic Strategies Alexandre González-Rodríguez 1 , Javier Labad 2 and Mary V. Seeman 3,* 1 Department of Mental Health, Parc Tauli University Hospital, Autonomous University of Barcelona (UAB), I3PT, Sabadell, 08280 Barcelona, Spain; [email protected] 2 Department of Psychiatry, Hospital of Mataró, Consorci Sanitari del Maresme, Institut d’Investigació i Innovació Parc Tauli (I3PT), CIBERSAM, Mataró, 08304 Barcelona, Spain; [email protected] 3 Department of Psychiatry, University of Toronto, #605 260 Heath St. West, Toronto, ON M5T 1R8, Canada * Correspondence: [email protected] Received: 1 September 2020; Accepted: 12 October 2020; Published: 16 October 2020 Abstract: Sleep disturbances accompany almost all mental illnesses, either because sound sleep and mental well-being share similar requisites, or because mental problems lead to sleep problems, or vice versa. The aim of this narrative review was to examine sleep in patients with delusions, particularly in those diagnosed with delusional disorder. We did this in sequence, first for psychiatric illness in general, then for psychotic illnesses where delusions are prevalent symptoms, and then for delusional disorder. The review also looked at the effect on sleep parameters of individual symptoms commonly seen in delusional disorder (paranoia, cognitive distortions, suicidal thoughts) and searched the evidence base for indications of antipsychotic drug effects on sleep. It subsequently evaluated the influence of sleep therapies on psychotic symptoms, particularly delusions. The review’s findings are clinically important. Delusional symptoms and sleep quality influence one another reciprocally. Effective treatment of sleep problems is of potential benefit to patients with persistent delusions, but may be difficult to implement in the absence of an established therapeutic relationship and an appropriate pharmacologic regimen. -
RBD, Sexsomnia, Sleepwalking, and Sleep Paralysis Comorbidities: Relevance to Pulmonary, Dental, and Behavioral Sleep Medicine
87 EDITORIALRBD, sexsomnia, sleepwalking, and sleep paralysis comorbidities: relevance to pulmonary, dental, and behavioral sleep medicine RBD, sexsomnia, sleepwalking, and sleep paralysis comorbidities: relevance to pulmonary, dental, and behavioral sleep medicine Carlos H. Schenck INTRODUCTION This issue of Sleep Science contains three reports1-3 on diverse REM and NREM parasomnias that serve as illuminating entry points to a broad range of comorbidities that are interlinked with the parasomnias, with relevance to multiple sleep medicine subspecialties. Minnesota Regional Sleep Disorders Center, Departments of Psychiatry, Hennepin Besides the fascinating mechanistic questions raised by this interlinking, there are also County Medical Center and University of important clinical management issues that need to be considered. Parasomnias, to a surprising Minnesota Medical School, Minneapolis, extent, are situated at the core of sleep medicine. The International Classification of Sleep USA Disorders, 3rd Edition (ICSD-3)4 recognizes that instinctual behaviors can be pathologically released with the parasomnias, involving locomotion (sleepwalking), aggression (RBD and NREM parasomnias), eating (sleep related eating disorder), and sex (sexsomnia) that carry the potential for adverse physical, psychological, and interpersonal consequences. Central pattern generators (CPGs) in the brainstem, subserving primitive behaviors, are inappropriately activated with the parasomnias. Figure 1 provides a useful and scientifically sound framework for understanding parasomnia behavioral release and their triggers, based on the seminal work of Tassinari et al. (2005)5 and Tassinari et al. (2009)6 from Bologna related to CPGs, parasomnias, and nocturnal seizures. In regards to the NREM parasomnias, the factors that predispose, prime and precipitate these parasomnias have been comprehensively reviewed by Pressman (2007)7. -
Original Articles
ORIGINAL ARTICLES Improvement in Cataplexy and Daytime Somnolence in Narcoleptic Patients with Venlafaxine XR Administration Rafael J. Salin-Pascual, M.D., Ph.D. Narcoleptic patients have been treated with stimulants for sleep attacks as well as day- time somnolence, without effects on cataplexy, while this symptoms has been treated with antidepressants, that do not improve daytime somnolence or sleep attacks. Venlafaxine inhibits the reuptake of norepinephrine, serotonin, and to lesser extent dopamine, and also suppressed REM sleep. Because some of the symptoms of nar- colepsy may be related to REM sleep deregulation, venlafaxine was studied in this sleep disorder. Six narcoleptic patients were studied, they were drug-free and all of them had daytime somnolence and cataplexy attacks. They underwent the following sleep proce- dure: one acclimatization night, one baseline night, followed by multiple sleep latency test. After two days of the sleep protocol, patients received 150 mg of venlafaxine XR at 08:00 h. Two venlafaxine sleep nights recordings were performed. Patients were fol- lowed for two months with weekly visits for clinical evaluation. Sleep log and analog- visual scale for alertness and somnolence were performed on each visit. Venlafaxine XR was increase by the end of the first month to 300 mg/day. Sleep recordings showed that during venlafaxine XR two days acute administration the following findings: increase in wake time and sleep stage 1, while REM sleep time was reduced. No changes were observed in the rest of sleep architecture variables. Cataplexy attacks were reduced since the first week of venlafaxine administration. Daytime somnolence was reduced also, but until the 7th week and with 300 mg/day of venlafaxine XR administration.