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Sleep Medicine on the Fly- What Every Physician Should Know \Integration of Psychiatry into Primary Health Care Conference- January 2014 Raed Hawa MD,

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Presentation on theme: "Sleep Medicine on the Fly- What Every Physician Should Know \Integration of Psychiatry into Primary Health Care Conference- January 2014 Raed Hawa MD,"— Presentation transcript:

1 Sleep Medicine on the Fly- What Every Physician Should Know \Integration of Psychiatry into Primary Health Care Conference- January 2014 Raed Hawa MD, FRCP, DABSM, DABPN Deputy Psychiatrist in Chief- UHN Associate Professor Department of Psychiatry, University of Toronto Diplomate American Board of Psychiatry and Neurology Diplomate American Board of Sleep Medicine Specialty Certification in Psychosomatic Medicine Specialty Certification in Sleep Medicine 1

2 Disclosure: Dr. Raed Hawa
Advisory board, speakers’ bureaus, grant, financial or research support No conflict of interest and no financial interest or other affiliation to declare

3 A Road Map? At the end of today's session participants are expected to: 1. improve their knowledge of sleep medicine as it pertains to their practice 2. become aware of the options that are available to treat these sleep disorders 3. appreciate the complexity and co-morbidity between psychiatric disorders and sleep disorders *It is all about how it applies to your practice*

4 Why should physicians be interested in sleep disorders?
Sleep/tiredness/sleepiness complaints Insomnia is often an early presentation of a psychiatric or medical illness Many sleep disorders may mimic psychiatric illnesses ( sleep apnea and depression) Medications affect sleep Our patient population can benefit from basic sleep hygiene practices

5 QUESTION What is Philagrypnia?

6 Clinical Vingette David, a 48 yo married male, a banker, and a father of 2 ages 14 and 16. Long history of recurrent major depressive episodes with multiple trials of SSRIs, SNRIs and Bupropion Currently of Venlafaxine XR 225mg/day Current complaints of increased irritability and missing work that he attributes to poor sleep What might be the causes for David’s insomnia? Primary sleep disorder Residual depression Medication related ? Poor sleep hygiene Alcohol/caffeine intake Something else

7 Tools to help us

8 SLEEP Awake – low voltage – random, fast
Drowsy – 8 to 12 cps – alpha waves N1-Stage 1 – 3 to 7 cps – theta waves N2-Stage 2 – 12 to 14 cps – sleep spindles and K complexes N3 -Delta Sleep – 1 1/4 to 2 cps – delta waves > 75 mV R-REM Sleep – low voltage – random fast with sawtooth waves

9 Normal Sleep Histogram
REM W N1 N2 N3 1 - light sleep, 5-10% of total sleep time, transition between awake and asleep % of total sleep time 3,4 - deep or delta wave sleep, occurs mostly early in the night REM sleep, 20-25% of sleep All 4 stages repeat in ultradian rhythm of about 90 minutes 1 2 3 4 5 6 7 Hours of Recording

10 Is it a primary sleep disorder?
Obstructive sleep apnea (4-8%) Restless leg syndrome (2-15%) Insomnia (10-30%) Parasomnia ( 5-10% ) EDS ( <5% )

11 OSAS Cessation of breathing lasting at least 10 seconds with desaturations and arousals. Some of the signs and symptoms: Snoring, gasping for air, stopping breathing at night, memory complaints, irritability, depression, morning headaches, sexual problems, restless sleep, and sedation or tiredness during the day.

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13 OSAS Why treat? High blood pressure
Heart problems- 8 to 10 times more likely to have heart attacks or strokes More health care money- 2.5 times more likely to visit a doctor More likely to die in their sleep- 2.5 times more likely Poor quality of life and 3 times more likely to be involved in car accidents

14 OSAS Rx Didgeridoo!! Weight loss/ Bariatric Surgery EPAP
Surgery/ Pillar procedure/ Maxillofacial Dental Device CPAP – gold standard

15 If (s)he snores suspect apnea
ALSO CONSIDER STOPBANG & MALLAMPATI

16 STOP BANG questionnaire
S do you Snore T do you feel Tired, fatigued or sleepy O have you been Observed to stop breathing P high blood Pressure B BMI >35 A Age >50 N Neck circumference >40 G Gender: Male Anesthesiology 2008; 108:

17 MALLAMPATI SCORE

18 Does the patient have apnea?
Her BMI is 22. She is on methadone for prior heroin abuse. She denies sleep difficulties but has been complaining of sleepiness. What would be your clinical concern?

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20 What About This?

21 Restless leg syndrome First described by Willis in 1672
Diagnostic Criteria ( strictly clinical ): Desire to move limbs ( creepy crawly sensation, itchy and aching feeling, crampy and painful ) with Motor restlessness Worse at rest Temporary relief by activity Worse at night International RLS Study Group 2006

22 Periodic limb movements
PLMS: Diagnosis is based on PSG findings. PLMD: PLMS plus sleep dysfunction. 80% of RLS patients have PLMS Asymptomatic PLMS does not require treatment.

23 RLS Rule out: Iron deficiency, Uremia, RA, Peripheral neuropathy, Diabetes, Pregnancy, Spinal cord lesion, Medications. “The Mimics” Akathisia ( drug induced or positional ), peripheral neuropathy, nocturnal leg cramps, sleep starts, anxiety, and psychosis.

24 Pathophysiology RLS SPECT/PET Reduction of caudate and putamen D2 receptor binding Brain Iron Transport CSF ferritin low- abnormal iron transport fMRI Decreased thalamic blood flow during RLS symptoms

25 Treatment RLS Dopamine Agonists Ropinirole-- 0.25 to 3 mg (D2 agonist)
Pramipexole to 1.5 mg (D2 and D3 agonist) Cabergoline-- 1 to 4 mg Pergolide to 0.75 mg Bromocriptine– 5 to 20 mg Ldopa-carbodopa– 25 to 400 mg

26 Treatment RLS Opioids: Benzodiazepines: Other treatments:
Codeine( mg),Oxycodone( mg), Methadone ( mg) Benzodiazepines: Clonazepam (0.5-2 mg), Temazepam (15-30mg) Other treatments: Gabapentin, Carbamazepine, Clonidine, Baclofen, B12, Folate

27 If your patient has RLS/PLMD?
R/O other causes Check ferritin levels If less than 50 – treat with Fe Add vitamin C If no help, try medications

28 B. Wayne Blount, MD, MPH Professor, Emory S.O.M.
insomnia B. Wayne Blount, MD, MPH Professor, Emory S.O.M.

29 Insomnia- Scope of the Problem
Prevalence: 30% of general population have complaints of sleep disruption and 10% have associated functional impairment Almost all major mental illness is associated with “some” sleep complaint Insomnia can be the presenting complaint for anxiety, depression or a sign of abuse potential Many medical problems can have sleep complaints as part of the presentation Bidirectional model between depression and insomnia, between anxiety and insomnia

30 Insomnia- Definitions
Global dissatisfaction with sleep and one of: 1.Difficulty initiating sleep 2. Difficulty maintaining sleep 3. Early morning awakening With distress or impairment 3 nights/week for 3 months 3 months Despite adequate opportunity for sleep Episodic, persistent or recurrent Transient- do not seek medical attention- usually related to stress/minor event/change in environment Short term and chronic- seek medical attention Primary include idiopathic or sleep state misperception or fatal familial insomnia Secondary- related to psych or medical rpoblems/ meds/circadian problems

31 Pathophysiology of Insomnia
Disorder of hyperarousal - hypervigilance during day with difficulty initiating/maintaining sleep during the night Cognitive model Physiologic model Neuroendocrine model Increased autonomic activity in sleep ( HR, MR, BP,Temperature ,NE secretion, HPA activation) Increased beta/gamma and decreased delta EEG activity Increased brain glucose metabolism Sleep Med Rev (1):9-15 Spielman – behavioural model predisposing factors( heightened arousals, family hx, prior hx,) external factors (stress), produce insomnia perpetuated by maladaptive coping strategies Morin- cognitive model ruminative thoughts around bedtime is the central component; cognitive arousal leads to physiological arousal, with time and repetition there is pairing between temporal and environmental cues and sleeplessness. Physiologic model- RAS interacting with hypothalamus ( anterior) and thalamus. Increased body temp near sleep onset Increased HR during sleep, decreased heart period variability during sleep; increased whole body metabolic rate during sleep in INSOMNIACS Elevated beta activity during NREM in insomnia- this is even more substantiated in insomnia plus depression where there is even more beta activity and metabolic activity in the orbitofrontal cortex ( decreased activity in the dorsolateral prefrontal cortex during wake ) Increased cortisol and ACTH before and during the first half of sleep

32 Why care about insomnia?
Insomnia prevalence increases with greater medical comorbidity There is increased prevalence of medical disorders in those with insomnia Insomnia with objective short sleep duration is associated with high risk for hypertension Insomnia with objective short sleep duration is associated with high risk for type 2 diabetes Insomnia with objective short sleep duration is associated with neuropsychological deficits Sleep 2009;32: Sleep 2010;33: Sleep 2007;30920:

33 Treatment Options I. Behavioural and Cognitive therapies
II. Prescription medications

34 Behavioural and Cognitive Therapies Standards of Practice
Stimulus control Relaxation therapy Cognitive behavioural therapy CBT-I Sleep restriction Sleep hygiene Sleep 2006;29: Stimulus control: conditioning between sleep environment and sleepiness HOW- go o bed only when feeling sleepy; in no sleep in minutes then leave bed and bedroom; use bed for sleep; no naps and no snoozes. Bed restriction- increase sleep drive HOW? Strict bedtimes and rising time limited to hours of sleep reported in one night; increase time in bed by advancing bedtime by minutes when efficiency is at least 85%; keep wakeup time fixed; if efficiency is still less than 85% after 10 days, delay bedtime by minutes Sleep hygiene- limit caffeine, alcohol, stimulants; no naps, no clock watching and exercise regularly Relaxation- guided imagery and jacobson’s progressive muscle relaxation Cognitive restructuring- overall overestimation/fear/ apprehension

35 Clinical Practice Point
Most behavioural treatments studied are six one-hour sessions by trained therapists There are a few basic principles that can be utilized in your practice Establish a rapport with your patient, listen, instill hope and follow-up Rely on principle of conditioning and good sleep hygiene practices Self monitoring , treatment rationale, and homework

36 Psychological & Behavioural Treatments For Chronic Insomnia
Standard therapies (Level 1 Evidence) Guideline therapies (Level 2 or 3 Evidence) Psychological / behavioural interventions Stimulus control therapy Relaxation training Cognitive behaviour therapy ± relaxation Sleep restriction Multicomponent* Paradoxical intention Biofeedback KEY MESSAGE: Several types of psychological and behavioural interventions have been shown to be effective for chronic insomnia; the recommendations outlined here may be applied to patients with MDD. For chronic insomnia, CBTi (which includes sleep hygiene practices) is a treatment of choice because its benefits are more long-term compared to medications that can help short-term. ADDITIONAL DISCUSSION NOTES: Stimulus control therapy: interventions that train the insomnia patient to reassociate the bed and bedroom with sleep and reestablish a consistent sleep-wake schedule. Relaxation training: methods aimed at reducing somatic tension (e.g., progressive muscle relaxation, autogenic training) or intrusive thoughts at bedtime that interfere with sleep. Sleep restriction: curtailing the amount of time in bed to the actual amount of time spent asleep, thereby creating a mild sleep deprivation, and then lengthening sleep time as sleep efficiency improves. Cognitive behavioral therapy: various combinations of cognitive and behavioural components aimed at changing patients’ beliefs and attitudes about insomnia, as well as therapies such as stimulus control, sleep restriction, or relaxation training. Sleep hygiene education is also often included. Multicomponent therapy (without CBT): combines stimulus control therapy, relaxation training and sleep hygiene education. Paradoxical intention: instructing the patient to remain passively awake and avoid any effort (i.e., intention) to fall asleep. The goal is to eliminate performance anxiety, as it may inhibit sleep onset. Biofeedback: provides visual or auditory feedback to patients to help them control some physiologic parameters (e.g., muscle tension) in order to seek reduction in somatic arousal. There is insufficient evidence to recommend sleep hygiene education as a single therapy for chronic insomnia Morgenthaler et al. Sleep 2006;11: *stimulus control + relaxation + sleep hygiene OR stimulus control + sleep restriction + sleep hygiene.

37 FDA Approved Insomnia Treatment
Immediate Release benzodiazepines Dose (mg) T1/2 (hr) Estazolam (ProSom®) 1, Flurazepam (Dalmane®) 15, Quazepam (Doral®) 7.5, Temazepam (Restoril®) Triazolam (Halcion®) .125, Immediate Release Non-benzodiazepines Eszopiclone (Lunesta®) 1,2,3 5-7 Zaleplon (Sonata®) 5,10 1 Zopiclone (Imovane®*) 5, Zolpidem (Ambien®) (Sublinox *) 5, Selective Melatonin Receptor Agonist Ramelteon (Rozerem®) Doxepin----3m and 6 mg(for maintenance insomnia) * Available in Canada and not in USA

38 Benzodiazepine Receptor Agonists
All BDZ receptor agonists are GABA modulators at the GABAA receptor complex GABAA-receptor: pentamer Allows chloride ions to enter Greater polarization and hence inhibitory Non benzodiazepines have a higher degree of alpha1 subtype selectivity

39 Recommendations For the Management of Insomnia: Pharmacotherapies
Line of therapy Class of medication Example medications 1st line Short-intermediate acting benzodiazepines Melatonin receptor agonist Zolpidem, eszopiclone,* zaleplon,* temazepam Ex: agomelatine* 2nd line Alternate short-intermediate acting benzodiazepines Sedating antidepressants Trazodone, amitriptyline, doxepin, mirtazapine Insomnia + comorbid mood disorder Combined benzodiazepine and sedating antidepressants Anticonvulsants Gabapentin, tiagabine* Atypical antipsychotics Quetiapine, olanzapine KEY MESSAGE: This slide outlines recommended pharmacological treatments for insomnia in the general adult population. Specific recommendations are made for patients with comorbid insomnia and mood disorders, with agents that target both disorders figuring prominently. Short-term hypnotic treatment should be supplemented with behavioural and cognitive therapies when possible Adapted from Schutte-Rodin et al. J Clin Sleep Med 2008;4: *not available in Canada.

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45 Insomnia and Depression
Up to 90% of MDE patients complain of insomnia Up to 40% of patients complaining of insomnia could have a mood disorder Subjective complaints of difficulty initiating, maintaining sleep or early awakening Objective findings: decreased REM latency, increased % REM, increased first REM period and decreased SWS

46 Antidepressants and Sleep
SSRI Venlafaxine Duloxetine BUPROPION MIRTAZAPINE TCA

47 SSRIs and Sleep Idiosyncratic effects: can cause insomnia or agitation in any individual patient Up to 60% of patients on SSRIs are also on a hypnotic All SSRIs decrease SE, suppress REM, delay REM onset, and increase S1 sleep There appears to be a trend where: Fluvoxamine and paroxetine are more sedating Fluoxetine is more stimulating Sertraline, citalopram and escitalopram are neutral Clonazepam plus Prozac- WT Smith 2002 Zolpidem with SSRIs in depression Asnis 1999

48 Clinical Practice Point
Trazodone, TCAs and mirtazapine are commonly used to help insomnia complaints in patients who suffer from depression or anxiety disorders SSRI could be used alone or with a BDZ/hypnotic to help insomnia complaints in depression Adjusting dose or timing can be helpful Combining medication with CBT is an option

49 Are Antidepressants To Blame For Sleep Disturbances?
Class Drug Insomnia Sedation Headache Tremor Dry Mouth Sweating Nausea Diarrhea Constipation Fatigue Anxiety SSRI Citalopram Escitalopram Fluoxetine Fluvoxamine Paroxetine Sertraline SNRI Duloxetine Venlafaxine Desvenlafaxine Others Bupropion Mirtazapine >50% Quetiapine XR KEY MESSAGE: Residual symptoms of sleep disturbance can also be side effects of antidepressant treatment. Insomnia has been associated with many SSRIs and SNRIs, whereas sedation has been associated with all classes of antidepressants. Sertraline having been associated with fatigue and excess sleepiness as well. 0-9% 10-29% ≥30% Data from placebo-controlled trials from respective product monographs; not for direct comparison between agents. Adapted from Lam et al. J Affect Disord 2009:17:S26-43 and Seroquel XR Product Monograph (2011).

50 Role for Antipsychotics
A 45 year-old male was referred to see me for a sleep assessment By the time I saw him he was already put on olanzapine 2.5mg po qhs and has been “doing great”. He was not sure why he needed to see me now What are the effects of antipsychotics on sleep parameters? What is the evidence for use of antipsychotics in insomnia and in complicated insomnia?

51 Antipsychotics and Sleep
Typical antipsychotics Clozapine Risperidone Olanzapine Quetiapine Ziprasidone Total Sleep Time + ++ Sleep Efficiency However consider: Weight gain and therefore worsening of apnea Increased leg restlessness Hyperlipidemia Glucose dysregulation QT prolongation

52 Important Quotes- NIH Chronic Insomnia Panel
“all (antipsychotics) agents have significant risks, and thus their use in the treatment of chronic insomnia cannot be recommended” Eszopiclone and zolpidem extended release are not indicated for “short term” use Intermittent vs regular prescription Short term vs long term prescription

53 Clinical Practice Point
Antipsychotics are commonly used in patients who have psychosis and bipolar illness to help with sleep complaints Antipsychotics are sometimes used in patients whose depression is successfully treated but still complain of their sleep Potential effects on weight, lipids and glucose Quetiapine is commonly used for “psychiatric insomnia”

54 Back to David Is David’s insomnia most likely...
A primary sleep disorder? A residual symptom of depression? Medication-induced? Due to poor sleep hygiene? Due to something else? Use this question as an opportunity for participants to share their experience with one another and to ask expert facilitators for guidance as it relates to challenging cases.

55 Back to David David is exhibiting residual symptoms of depression and mild anxiety His insomnia is affecting his work functioning Would you change his treatment plan? If yes, how? Use this case vignette as an opportunity for participants to share their experience with one another and to ask expert facilitators for guidance as it relates to challenging cases. It is important to address any issues pertaining to sleep hygiene, maladaptive behaviours or cognitive distortions (e.g., I am going to die if I do not sleep).

56 Treatment of Insomnia What is the most common prescribed medication for the treatment of insomnia in the United States? in Kuwait?

57 Clinical aspects of Insomnia
Treatment of insomnia is based upon the following principles: A. Insomnia is always a symptom of a larger psychiatric disorder B. Insomnia may lead to hypertension and diabetes C. Reduction of depressive symptoms can improve insomnia D. Sleep studies are always helpful in confirming the diagnosis of insomnia B and C are right answers

58 Depression and sleep Polysomnographic features of depression seen in 50% of patients diagnosed with depression include: Abbreviated REM sleep onset Increased REM amounts Decreased slow wave sleep Increased sleep fragmentation and arousals Sleep studies are indicated in cases of suspected depression E is incorrect

59 Case of Mr. B Mr. B is a healthy 20 yo male whom you have been seeing in therapy for treatment of anxiety. According to his roommate, the patient has been waking up screaming, with severe sweating and difficulty to communicate with during these episodes. The patient had severe nightmares as a child. The events typically occur after missing his normal amount of sleep because of social events or studying for tests. Q: How would you treat these “nightmares”?

60 Events during sleep Nightmares Night terrors Panic attacks (nocturnal)
REM behaviour disorder Sleep walking Nocturnal seizures CONSIDER: prior history, age, dreaming episode, time of occurrence, ability to console, autonomic arousability, and behaviours during episode.

61 Screening for Parasomnias
1. do you or your bed partner believe that you move your arms, legs, or body too much or have unusual behaviour during sleep? 2. do you move while dreaming as though you are attempting to carry out a dream? 3. have you ever hurt yourself or your partner while asleep? 4. do you eat or drink without full awareness during the night? 5. review medication(hypnotic) list/alcohol intake

62 Events during the night
Fuseli’s Fuseli’s nightmare

63 Nightmares vs Night terrors
REM related Last 1/3 of night Scared Little movement Remember dream Consolable Delayed back to sleep Non REM related First half of night Confused Active Amnesia in morning Not consolable Easy back to sleep

64 Nightmares REM related events Last third of the night Vivid dreams
Dreams are remembered Autonomic hyperarousability- mild No confusion or disorientation

65 Nightmares- cont’d Treatment to be directed for culprit- medications, withdrawal, sleep disorder, sleep deprivation No harm results from awakenings- Reassurance Imagery rehearsal treatment Prazosin in cases of PTSD related n/m Tryptophan?

66 Night terrors Occur out of SWS ( N3 )* First half of the night
Positive hx of sleep walking Behaviour is stereotypical Extreme autonomic discharge Difficult to console Potential self harm/ harm to others * in children out of N1/N2 High amplitude and Hypersynchroonous bursts of slow waves preceed the abnormal behaviours In children can occur out of stage 1 and 2 Tachycardia, tachypnea, prespiratoin, screaming with confusion, glassy eyes, pick at blankets, get up and walk around. Family history of sleepwalking- Incidence of somnambulism and related parasomnias increases aqs follows: 22% when remote relative has it 44% when one parent has it and 60% when both parents affected

67 Night terrors- cont’d May be triggered by: febrile illness, alcohol, sleep deprivation, stress. Medications can induce such events- hypnotics/neuroleptics/stimulants/anti-histamines and antiarrhythmic meds R/O brain insult, brain glioma, epilepsy, cardiac insufficiency.

68 Night terrors- cont’d Treatment of NREM Parasomnia
Education and reassurance Safety precautions- if sleep walking BDZ/ TCA Relaxation Hypnosis

69 Unusual dreams A 66 yo male who you see for depression presented to your office with bruises to his hands and feet after falling off the bed few days earlier. He recalls having a dream where he had to defend himself from a snake. On further inquiry he indicated that his wife has been scared to sleep with him in the same bed due to his excessive movements at night. His sleep record epoch shows the following: 2/3 of males above 50 with RBD will develop Parkinsonian type disorder within a mean interval of 13 years.

70 Unusual dreams

71 Unusual dreams A 66 yo male who you see for depression presented to your office with bruises to his hands and feet after falling off the bed few days earlier. He recalls having a dream where he had to defend himself from a snake. On further inquiry he indicated that his wife has been scared to sleep with him in the same bed due to his excessive movements at night.This man likely: Has loss of muscle atonia during his REM sleep Has REM sleep behaviour disorder (RBD) Would benefit from an SSRI Will develop neuropathy with Guillain Barre-like illness Will benefit from Clonazepam 2/3 of males above 50 with RBD will develop Parkinsonian type disorder within a mean interval of 13 years.

72 ONE LAST, VERY EFFECTIVE TREATMENT OPTION
For apnea, RLS, Insomnia, parasomnias with com0rbid depression and anxiety is:

73 ONE LAST, VERY EFFECTIVE TREATMENT OPTION
For apnea, RLS, Insomnia, parasomnias and com0rbid depression with anxiety is: Review this lecture

74 EXTRAs If we have time we can cover: Excessive Daytime Sleepiness

75 Excessive Daytime Sleepiness

76 Sleepy!

77 Sleepy! The "switch" for sleep is considered to be the ventrolateral preoptic nucleus (VLPO) of the anterior hypothalamus. VLPO uses GABA and galanin to initiate sleep by inhibiting the arousal regions of the brain. VLPO inhibits the wake-promoting regions of the brain including the tuberomammillary nucleus, lateral hypothalamus, locus coeruleus, dorsal raphe, laterodorsal tegmental nucleus, and pedunculopontine tegmental nucleus. Hypocretin (orexin) neurons in the lateral hypothalamus help to stabilize this switch

78 EDS A 45 yo female has been referred to a sleep clinic for assessment of day time sleepiness and fatigue. How do you differentiate between EDS and fatigue? Is there a role for a sleep study? MSLT? MWT? What are the causes for EDS?

79 The Epworth Sleepiness Scale

80 FSS

81 From: Multiple Sleep Latency Test and Maintenance of Wakefulness Test
Date of download: 2/16/2013 Copyright © American College of Chest Physicians. All rights reserved. From: Multiple Sleep Latency Test and Maintenance of Wakefulness Test CHEST. 2008;134(4): doi: /chest Figure Legend: MSLT protocol. Adapted from Littner et al.1

82 Excessive Daytime Sleepiness

83 Final question Of the following which is the most specific finding in a patient who is known to have narcolepsy? MSLT with average sleep onset of 6 minutes Improvement of EDS when drinking coffee Sleep paralysis Hypnagogic Hallucinations Cataplexy

84 Bibliography An update on the dopaminergic treatment of restless legs syndrome and periodic limb movement disorder. Sleep 2004:27(3): Brower KJ. Alcohol’s effects on sleep in alcoholics. Alcohol Research and Health ;25(2): Kushida CA,Littner MR,Hirshkowitz M etal. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep related breathing disorders. Sleep 2006:29(3): Morgenthaler T,Kapen S,Lee-Chiong T etal. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep 2006;29(8): Morin CM,Bootzin RR,Buysse DJ etal. Psychological and behavioural treatment of insomnia. Update of the recent evidence. Sleep 2006;29(11): Neubauer DN. The evolution and development of insomnia pharmacotherapies. JCSM ;3(5): S11-S15 Peterson MJ and Benca RM. Sleep in mood disorders. Psychiatr Clin N 2006;29: Roth T. Insomnia: Definition, prevalence, etiology, and consequences. JCSM 2007;3(5): S7- S10 Schenck C, Mahowald M. Parasomnias. Post Med 2000;107(3): Silber MH. Chronic insomnia. NEJM. 2005;353:803-10

85 Fun Websites The sleep IQ test:
Sleep meditation quilt square: A couple of simple things to remember and a cool site. t/Water_files/water14_help_with_sleep/help_with_sleep.html Practice parameters for treating chronic primary insomnia in the elderly. Nat’l. Guideline Clearinghouse;

86 QUESTIONS If you have any questions I could be reached at the following address: Raed Hawa MD FRCPC DABPN DABSM Associate Professor, Department of Psychiatry Deputy Psychiatrist in Chief, University Health Network Deputy Clerkship Director, UME, University of Toronto Director, Undergraduate Psychiatry Program, UME, University of Toronto

87 Extra Slides

88 Agomelatine and Sleep B A SLEEP EFFICIENCY SLEEP LATENCY 29.7 29.9 80 78.9 78.9 30 28.4 78.8 78.3 78.4 26.7 28.1 27.8 79 78.2 78 77.2 25 23.5 77 76 22.5 Sleep Efficiency (%) 75 76.5 76.4 20 75.8 75.7 74 75.1 75.2 19.5 19.6 20.2 74.8 18.8 18.8 18.9 73 15 Agomelatine 72 Agomelatine Sertaline Sertaline 71 70 10 1 2 3 4 5 6 1 2 3 4 5 6 Week Week P value <.0001 .018 .001 <.001 .007 Agomelatine n 117 112 105 99 88 Sertraline n 114 113 101 93 87 79 71 KEY MESSAGE: Although not yet available in Canada (except through a Special Access program), agomelatine has a favourable effect on the relative amplitude of the circadian rest-activity/sleep-wake cycle in depressed patients as early as week 1, reflecting improvement in sleep and daytime functioning. P value <.001 .003 .005 Agomelatine n 117 112 105 99 88 Sertraline n 114 113 101 93 87 79 71 Double-blind, randomized, controlled clinical trial of agomelatine mg/d (n=154) vs. sertraline mg/d (n=159) over 6 weeks. Agomelatine is only available in Canada through a Special Access program. Kasper et al. J Clin Psychiatry 2010:71:

89 Efficacy of Adjunctive Modafinil In Partial Responders To SSRIs With Persistent Fatigue & Sleepiness
Placebo 6 8 10 12 14 16 18 Mean = SEM HAM-D-17 Score * Week 1 2 4 Final Visita Baseline Other significant improvements for adjunctive modafinil vs. placebo: ↑ CGI-I scores ↓ fatigue KEY MESSAGE: This study supports the efficacy and safety of modafinil as augmentation therapy in patients who are partial responders to SSRI therapy. Benefits were noted in terms of both depressive symptomatology, fatigue / sleepiness, and overall clinical condition. Double-blind, randomized, placebo-controlled clinical trial of 60 depressed, insomniac outpatients receiving open-label fluoxetine plus add-on eszopiclone 3 mg or placebo at bedtime for 8 weeks. CGI-I: Clinical Global Impression – Improvement. *P=0.07; † p=0.06; ‡p<0.08. Fava et al. J Clin Psychiatry 2005:66:85-93.

90 Quetiapine XR: Significant Effect On Sleep In Patients With MDD
Pooled analysis of two 8 week†, RCTs of quetiapine XR in patients with MDD (n=968) KEY MESSAGE: In this pooled analysis of two of the registration studies for quetiapine XR, sleep quality was significantly improved by both doses of the active agent compared to placebo. *p<0.001; †6 week randomization phase, 2 week discontinuation phase; results shown are at week 6. PSQI: Pittsburg Sleep Quality Index. Weisler et al. Int Clin Psychopharmacol 2012; 27:

91 ZOPICLONE ZALEPLON ESZOPICLONE TRAZADONE RAMELTEON MODAFANIL SODIUMOXYBURATE TEMAZEPAM ************** ZOLPIDEM AGOMELATIN


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