Sleep Disturbances in Fibromyalgia Patients Robert Bennett MD, FRCP, MACR

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Transcript of Sleep Disturbances in Fibromyalgia Patients Robert Bennett MD, FRCP, MACR

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Sleep Disturbances in Fibromyalgia Patients Robert Bennett MD, FRCP, MACR Slide 2 Disclosure Research support : Forest, Jazz, Pfizer Advisory Boards: Lilly, Jazz Speaker Bureaus: None Slide 3 3 Key References 1)Rosenthal MS, Physiology and neurochemistry of sleep. Am. J. Pharm. Educ., 62, 204-208, 1998 2)Passarella S et al. Diagnosis and treatment of insomnia. Am J Health-Syst Pharm. 2008; 65:927-34 3)Moldofsky H. Rheumatic manifestations of sleep disorders. Curr Opin Rheumatol 2010;22(1):59-63 Slide 4 1)Historical aspects of sleep in FM 2)Physiology of sleep 3)Insomnia 4)Disturbed sleep in FM patients 5)Evaluation of disturbed sleep in FM 6)Disturbed sleep and pain 7)Management Objectives Slide 5 1)Historical aspects of sleep in FM 2)Physiology of sleep 3)Insomnia 4)Disturbed sleep in FM patients 5)Evaluation of disturbed sleep in FM 6)Disturbed sleep and pain 7)Management Slide 6 THE PRINCIPLES AND PRACTICE OF MEDICINE DESIGNED FOR THE USE OF PRACTITIONERS AND STUDENTS OF MEDICINE BY WILLIAM OSLER, M. D. FELLOW OF THE ROYAL COLLAGE OF PHYSICIANS, LONDON PROFESSOR OF MEDICINE IN THE JOHNS HOPKINS UNIVERSITY AND PHYSICIAN-IN-CHIEF TO THE JOHNS HOPKINS HOSPITAL, BALTIMORE FORMERLY PROFESSOR OF THE INSTITUTES OF MEDICINE MOOILL UNIVERSITY, MONTREAL AND PROFESSOR OF OLINIOAL MEDICINE 1H THE UNIVERSITY CF PENNSYLVANIA PHILADELPHIA NEW YORK D. APPLETON AND COMPANY 1892 William Osler 1849 - 1919 Slide 7 The Principles and Practice of Medicine William Osler MD, 1892 Neurasthenia: a condition of weakness or exhaustion of the nervous system 1. Sleeplessness is a frequent concomitant 2. The majority are moody or depressed 3. They have weariness on the least exertion 4. The aching pain in the back of the neck is the most constant complaint 5. There are spots of local tenderness in the spine Slide 8 Alpha-delta sleep Slide 9 First Scientific Study in FM Delta (1cps) Alpha + delta Auditory stimulation in a healthy control Moldofsky et al. Psychosomatic Med. 37:341-351, 1975 Slide 10 Objectives 1)Historical aspects of sleep in FM 2)Physiology of sleep 3)Insomnia 4)Disturbed sleep in FM patients 5)Evaluation of disturbed sleep in FM 6)Disturbed sleep and pain 7)Management Slide 11 A.REM sleep B.Non-REM sleep Stage 1 - Transition from wake to sleep Stage 2 Largest percentage of sleep Stages 3 and 4 Restorative sleep There are 4 to 5 cycles of REM and non-REM sleep each night Each cycle lasts 1.5 to 2 hours Sleep stages Slide 12 REM Stage 1 Stage 2 Stage 3 Stage 4 Slide 13 Polysomnography Slide 14 Polysomnographic data is reviewed in 30 second "epochs" Sleep latency Sleep efficiency Percent time in REM and non-REM sleep Percent time in each of the 4 sleep stages Electro-oculogram (EOG) EMG chin EMG tibialis anterior Nasal air flow Chest and abdominal movements Oxygen saturation ECG The number of minutes of sleep divided by the number of minutes in bed. Normal is approximately 85 to 90% or higher. Iber, C et al. The AASM Manual for the Scoring of Sleep: American Academy of Sleep Medicine, Westchester, IL 2007 Slide 15 Sleep architecture Decreasing frequency Increasing amplitude Slide 16 Drowsy EEG During the earliest phases of sleep, when people are drowsy the brain produces beta waves (1335 Hz). As the brain begins to relax slower alpha waves (812 Hz) are produced. During this time when you are not quite asleep, people may experience vivid sensations known as hypnagogic hallucinations. Another very common event is myoclonic jerks. Beta waves (12-30 HZ) Eyes open Eyes closed Alpha waves (8 12 HZ) EEG leads Chin EMG EOG Slide 17 Stage 1 sleep Slow rolling eye movements Theta waves (47.5 Hz) with some alpha Chin EMG EOG EEG leads Stage 1 is a transition period between wakefulness and sleep. In Stage 1, the brain produces high amplitude theta waves (47 Hz), which are very slow brain waves. This period of sleep lasts only 5-10 minutes. If you awaken someone during this stage, they might report that they weren't really asleep. Slide 18 Stage 2 sleep Stage 2 lasts for approximately 20 minutes, mainly theta waves (47 Hz). Then the brain begins to produce bursts of rapid, rhythmic brain wave activity known as sleep spindles and K-complexes. Body temperature starts to decrease and heart rate begins to slow. Minimal eye movement Minimal chin EMG Theta waves (47 Hz) Slide 19 Stages 3 and 4 of non-REM sleep Predominant delta waves (0.53.5 Hz) Stages 3 and 4 are often referred to as delta sleep because slow brain waves known as delta waves (0.1 4 Hz) occur during this time. Stages 3/4 are a deep sleep that lasts for approximately 30 minutes. Bed-wetting, night terrors and sleepwalking are most likely to occur at the end of stage 4 sleep. It is followed by REM sleep. Some eye movement Slide 20 REM sleep Starts after loss of chin EMG Rapid eye movements Bursts of alpha activity Rapid eye movement (REM) sleep is characterized by eye movement, increased respiration rate and increased brain activity.. Vivid dreams often occur in this sleep stage. Dreaming occurs is due to increased brain activity, but voluntary muscles become paralyzed. Slide 21 Sleep control mechanisms Encephalitis lethargica Slide 22 1.A somnolent-opthalmoplegic form with profound sleepiness often leading to coma and death, paralysis of cranial nerves and expressionless faces. 2.A hyperkinetic form with restlessness, twitching of muscles, anxiety and severe insomnia. 3.An akinetic form with muscle weakness, rigidity, and severe insomnia (postencephalitic parkinsonism). An epidemic that spread throughout the world from 1977 to 1928. Sleep control mechanisms Encephalitis lethargica Postulated cause is a mutation of the H1N1 influenza virus ? N-methyl-D-aspartate (NMDA) receptor antibody mediated Slide 23 Sleep control mechanisms Constantin von Economo 1876 - 1931 Von Economo, reported that encephalitis lethargica was due to injury to the posterior hypothalamus and rostral midbrain. He recognized that one group of individuals infected during the same epidemic instead had the opposite problem: a prolonged state of insomnia that occurred with lesions of the pre-optic area and basal forebrain. He hypothesized that lesions of the posterior hypothalamus could cause the disease we now call narcolepsy. Based on his observations, von Economo predicted that the region of the hypothalamus near the optic chiasma would contain sleep- promoting neurons, whereas the posterior hypothalamus would contain neurons that promote wakefulness. Slide 24 Sleep control mechanisms Orexin neuronal projectins Orexin neurons originating in the posterior hypothalamus regulate sleep and wakefulness by sending excitatory projections to the entire CNS, with particularly dense projections to monoaminergic and cholinergic nuclei in the brain stem. Slide 25 Sleep Awake Sleep control mechanisms VLPO = ventrolateral pre-optic nucleus (GABA & galanin) ORX = orexin nucleus (orexins) LC = locus ceruleus (nor-adrenaline) Raphe = raphe magnus (serotonin) TMN = tubermammilary nucleus (histamine) Slide 26 Objectives 1)Historical aspects of sleep in FM 2)Physiology of sleep 3)Insomnia 4)Disturbed sleep in FM patients 5)Evaluation of disturbed sleep in FM 6)Disturbed sleep and pain 7)Management Slide 27 DSM-IV criteria for primary insomnia: 1) A complaint of difficulty falling asleep, staying asleep or non-restorative sleep 2) Duration of 1 month 3) Causes clinically significant distress or impairment 4) Does not occur exclusively during the course of a mental disorder 5) Is not due to another medical or sleep disorder or effects of medications/substance abuse Insomnia definition Slide 28 Riemann et al. Pharmacopsychiatry. 2011 Jan;44(1):1-14. Insomnia - consequences 1) Fatigue / malaise 2) Impaired attention, concentration, memory 3)Vocational dysfunction 4)Daytime sleepiness 5) Motivation / energy / initiative reduction 6) Proneness for errors / accidents at work or while driving 7) Tension headache 8) Obesity / diabetes 9) Hypertension 10) Depression / anxiety 11) Coronary heart disease 12) Increased mortality Sleep loss may transiently improve depression Slide 29 Hyperarousal Sleep disturbance Neurobiological alterations Dysfunctional behavior Stressors Long-term consequences Insomnia mechanisms Slide 30 Am J Psychiatry 2004; 161:21262129 Insomnia mechanisms Slide 31 (A)Patients with insomnia: brain areas where metabolism was not decreased in waking and sleep states (B)Healthy subjects: brain areas where metabolism, while awake, was higher than in patients with insomnia Insomnia mechanisms Interacting neural networks are involved in the neurobiology of insomnia: 1. General arousal system (ascending reticular formation and hypothalamus), 2. Emotion-regulating system (hippocampus, amygdala, and anterior cingulate cortex), 3. Cognitive system (prefrontal cortex) Slide 32 Objectives 1)Historical aspects of sleep in FM 2)Physiology of sleep 3)Insomnia 4)Disturbed sleep in FM patients 5)Evaluation of disturbed sleep in FM 6)Disturbed sleep and pain 7)Management Slide 33 Sleep disturbances in FM Insomnia intrusion rhythm cyclic alternating rhythm (CAP) Periodic limb movements (PLM/RLS) Snoring and arousals Apnea and hypopnea Periodic breathing Bruxism Slide 34 First Scientific Study in FM (1975) Delta (1cps) Alpha + delta Moldofsky et al. Psychosomatic Med. 37:341-351, 1975 Auditory stimulation in healthy controls Slide 35 ECG R. leg L. leg Chin EMG EEG leads Normal sleep -EEG sleep Alpha delta sleep Slide 36 Cyclic alternating pattern (CAP) in FM J Rheumatol 2004; 31:11939 Cyclic Alternating Pattern: A New Marker of Sleep Alteration in Patients with Fibromyalgia? Maurizio Rizzi, Piercarlo Sarzi-puttini, Fabiola Atzeni, Franco Capsoni, Arnaldo Andreoli, Marica Pecis, Stefano Colombo, Mario Carrabba, Margherita Sergi Found CAP pattern in 68% FM patients vs 45% controls. Hypothesized that CAP in FM maybe a result of chronic pain reducing sleep efficien