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1 Sleep Disorders Medicine In Psychiatry Alan B. Douglass MD, FRCPC, Dip. ABPN, Dip. Amer. Board of Sleep Medicine Asst. Professor, Dept of Psychiatry,

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Presentation on theme: "1 Sleep Disorders Medicine In Psychiatry Alan B. Douglass MD, FRCPC, Dip. ABPN, Dip. Amer. Board of Sleep Medicine Asst. Professor, Dept of Psychiatry,"— Presentation transcript:

1 1 Sleep Disorders Medicine In Psychiatry Alan B. Douglass MD, FRCPC, Dip. ABPN, Dip. Amer. Board of Sleep Medicine Asst. Professor, Dept of Psychiatry, University of Ottawa Medical Director, Sleep Disorders Service, Royal Ottawa Hospital

2 2 Introduction Financial Disclosure: Nothing to declare Today we will cover: Basic sleep physiology Narcolepsy – a disorder of the REM control system Periodic Limb Movement Disorder Obstructive Sleep Apnea Insomnia – diagnosis & treatment


4 Great clinical textbook: (Mayo Clinic, 2004)

5 Sleep waveform schematic

6 Sleep Stage % by Age

7 Stg%

8 EEG TypeHz.Sleep Stg. Delta SWS Theta3 - 7REM Alpha8 - 12Wake Beta Wake Spindle Stg Gamma REM, wake EEG Frequencies

9 The “10 – 20” system of EEG electrode placement (C3 / C4 in yellow – where sleep is scored). 10 – 20 electrodes 10-20

10 Wake => Sleep Transition R & K 1968 Wake => Sleep Transition

11 R & K 1968 Stage 2 Sleep

12 Stage 4 Sleep

13 Onset of REM R & K 1968 REM sleep onset

14 Sleep Histogram RL

15 24-hr Sleepiness Profile

16 Multiple Sleep Latency Test (MSLT)

17 MSLT Sleep Restriction

18 Narcolepsy: MSLT, SOREMs

19 mid- saggital section. Netter / CIBA Whole Brain

20 Neurotransmitters in Sleep REM: only time of day when monoamines not firing !

21 REM Control Nuclei “Biological Clock” REM induces muscle paralysis OREXIN

22 SCN clock DA (+) Histamine (+) NA (+) 5HT (+) Orexin / Hypocretin Monoamines controlled by Orexin ~

23 23 REM Control REM Trigger: nucleus reticularis pontis oralis

24 Orexin-Hypocretin projections

25 25 Narcolepsy -- Cataplexy

26 Narcolepsy: night sleep

27 Narcolepsy “Tetrad” (4 symptoms) True sleep attacks Falls asleep without warning, unusual situations Cataplexy Flaccid muscle paralysis; eyes and diaphragm OK; pt. remains awake but paralyzed. Hypnagogic / Hypnopompic hallucinations “Multimodal” – visual, tactile, auditory, smell. Often highly emotional, sexual, frightening Sleep Paralysis Awakes unable to move anything but eyes. Can’t breathe voluntarily or talk. HH often occur here too.

28 Narcolepsy: age of onset Silber 2004, p.97.

29 Narcolepsy Biology HUMANDOG Orexin / Hypo- cretin cells Destroyed by immune system Normal Orexin receptors NormalGenetic abnormality, inactive REM intrusion: (SP, Cataplexy) ++

30 Narcolepsy Treatments: SLEEPINESS: Stimulants (noradrenalin receptor agonists): amphetamine, methylphenidate, modafinil. CATPLEXY: Antidepressants that increase serotonin and or noradrenaline and block ACh, i.e. clomipramine, venlafaxine.

31 31 Narcolepsy versus Schizophrenia Narcolepsy Actually Daytime REM sleep intrusion Apparent “Schizophrenic” Hallucinations 90% aassociation of narcolepsy with an HLA antigen DNA fragment (DQB1*0602) allows “inverse” screening of schizophrenics for narcolepsy Narcolepsy is detectable in sleep lab (MSLT) but pt. must be medication-free for at least 3 weeks.

32 Worm in lateral hypothalamus causing narcolepsy. (neurocysticercosis) J. Clin. Sleep Med. 1(1) 2005, p. 41.

33 33 Obstructive Sleep Apnea


35 Normal

36 Sleep Apnea

37 37 OSA Clinical Symptoms

38 38 Clinical Applicability – Apnea Sleep apnea and depression share clinical features; apnea can produce secondary depression. Serious sleep apnea can cause sufficient impairment to suggest dementia; severe snoring in a “demented” patient could be a treatable illness. Apnea or PLMD can cause sleep deprivation which can cause relapse of mania or depression.

39 39 Restless Legs Syndrome / Periodic Limb Movement Disorder (RLS-PLMD)

40 Periodic Limb Movement Disorder

41 41 RLS – PLMD: neurochemistry Likely due to iron deficiency in basal ganglia (Fe ++ is co-factor for enzymes that synthesize DA). May predict onset of “syn-nuclein- opathies” (REM behaviour disorder, PSP, Parkinson’s, Lewy Body dementia).

42 42 RLS – PLMD: Sx and Tx SYMPTOMS Late evening / night Legs cramp, squirm, move by themselves Multiple awakenings “Charley Horses” Can’t tolerate legs being immobilized Worse in elderly TREATMENT Check Fe, ferritin, B12, folate Dopamine agonists (L-DOPA, ropinirole, pramipexole) Benzodiazepines or opiates now 2 nd line Quinine obsolete

43 43 Polysomnographic Abnormalities In Psychiatric Patients

44 44 Sleep Abnormalities in Psychiatry Benca, 1992 Meta-analysis of sleep in all major psychiatric disorders showed affective disorders had the largest and most consistent differences from controls. Kaneko, 1981 Extremely short nocturnal REM latency is common to both psychiatric disorders and narcolepsy

45 45 Psychiatric Sleep Measurements Sleep Latency (SL) – sleep onset defined as first 3 contiguous 30-sec. pages of Stage 1 sleep REM Latency (RL) – time from sleep onset to first epoch of REM sleep REM Latency Minus Awake (RLMA) – subtract any interposed pages of waking from the RL Eye Movement Density in REM Sleep (REM Density, RD) – the actual number of eye movements divided by minutes spent in REM

46 46 REM Latency (RL & RLMA) RL varies inversely with age & is highly prevalent in affective disorders. RLMA has statistical properties that are superior to RL (smaller variance, more normal distribution). RL is shortened by cholinergic agonists (arecoline, pilocarpine, physostigmine). Prolonged by anticholinergics (benztropine, trihexyphenidyl, diphenhydramine).

47 47 MDD: sleep features Long initial insomnia, early morning wakening Shallow sleep, easily awakened Non-refreshing sleep Short RL & RLMA; normalized by SSRI (antidepressants are REM suppressants because they increase neurotransmission in serotonergic and adrenergic pathways). High REM density (also a good predictor of eventual depression in a never-ill person)

48 48 MDD (cont.) Some powerful sleep mechanism underlies the expression of depression Total sleep deprivation or selective REM deprivation dramatically improves mood of severely depressed patients (benefit is lost after one night’s sleep or even short nap) Amount of Non-REM sleep in nap predicts worsening of mood

49 49 Bipolar Disorder vs. MDD MDD patients typically have reduced total night sleep, but normal day alertness Depressed bipolar patients in often have excess sleep (up to 18 hours/day), crushing fatigue when awake, ravenous appetite, & weight gain: “atypical depression”. “Switch process” in bipolars often occurs during sleep.

50 50 Bipolar Disorder vs. MDD Excessive sleeping Crushing fatigue Extreme appetite “Atypical Depression” Actually Depressed Phase of Bipolar Disorder DDx: Narcolepsy, Idiopathic Hypersomnolence

51 51 Bipolar Disorder with Narcolepsy Apparent Schizophrenic Hallucinations Narcolepsy Bipolar Disorder + Actually Hypnagogic Hallucinations These 2 illnesses when found together give a misdiagnosis: “psychotic bipolar,” “schizo-affective”

52 52 Alcoholism Acute administration of alcohol produces REM suppression, then: Withdrawal after chronic alcohol intoxication Actually REM sleep without physiological paralysis Hallucination – visual, gustatory, tactile dream- like imagery

53 53 Management of Insomnia

54  Stressful personal events – child is sick, financial crisis, fire damages the house, natural disasters.  Impending stressors – exams, marriage, moving away from home, court appearance.  Acute illness: medical, surgical, especially if painful. Causes of acute insomnia

55 ... acute insomnia #2 Note: all of these conditions are likely to be self- limited, resolving in days to a couple of weeks, and could occur to almost anyone. This matches the federal licensing conditions for all marketed hypnotic drugs ( CPS 2009, p. 1132) : “Treatment with {Imovane} should usually not exceed 7 – 10 consecutive days. Use for more than 2 – 3 consecutive weeks requires a complete reassessment of the patient. Prescriptions should be written for short-term use (7 – 10 days) and should not be prescribed in amounts exceeding a 1-month supply. The use of hypnotics should be restricted to insomnia where disturbed sleep results in impaired daytime functioning.“

56 ... acute insomnia #3 These conditions also illustrate that a state of stress / hyper- arousal is intrinsic in acute insomnia. This has been confirmed by measured elevations of the following in such patients: Whole body metabolic rate Heart rate variability Adrenalin & dopamine metabolites Cortisol, ACTH, and CRF Cerebral glucose metabolism (via PET scan). However, some patients have a chronic trait of hyper-arousal that can lull the doctor into prescribing hypnotics for the long term. This may or may not amount to a psychiatric illness.

57 Chronic Insomnia: Studies indicate that 45 – 85% of chronic insomnia (defined as lasting 6 months or more) is due to psychiatric illness, even if the patient will not endorse or admit it. DSM-IV diagnoses these patients “Insomnia related to another mental disorder,” which includes: Anxiety Disorders: Obsessive compulsive disorder Panic disorder & PTSD Generalized anxiety disorder Hypochondriasis Substance Abuse (especially alcohol & cocaine)

58 ... Chronic insomnia #2 Mood Disorders: Bipolar disorder, especially mania or hypomania Major depression Dysthymic disorder Psychoses: Schizophrenia & Schizo-affective disorder Delusional disorder Psychotic affective disorders. Remaining insomnia patients mainly have painful or disruptive chronic medical conditions (i.e., diarrhea) or a diagnosable sleep disorder (i.e., sleep apnea).

59 ... Chronic insomnia #3 Yet there appears to be a type of patient with chronic insomnia in whom no psychiatric or physical diagnosis can be found. These patients often have: Erratic sleep-wake schedules Poor sleep hygiene Unreasonable expectations about their sleep (“I have to get 9 hours of sleep each night or I’ll get sick”). A belief that they are not sleeping when sleep recordings show that they are. Hyper-vigilance regarding bodily functions Increased sensitivity to the consequences of reduced night sleep (I.e., distorted perception of daytime deficits).

60 ... Chronic insomnia #4 In the International Classification of Sleep Disorders (ICSD), these patients have been variously called “psycho-physiological / learned” insomnia, “sleep state misperception”, “idiopathic insomnia” and “inadequate sleep hygiene.” DSM-IV-TR lumps all of these under “Primary Insomnia” & places the threshold for diagnosis at one month of symptoms or more. Certain patterns of insomnia have diagnostic specificity, I.e., early morning awakening in Major Depression, and initial insomnia in anxiety disorders.

61 Assessment of Insomnia The Interview is critical. It must include: Amount of insomnia (at least 31 min. 3x /week). When did it begin (recent life events and stressors). What time do the lights go out; when does alarm ring in AM? Is there napping in the daytime (causes insomnia at night). Is there Shiftwork? How long on one shift before rotation? In what part of night does insomnia occur? Is it associated with physical or environmental causes? Is there alcohol consumption after 19:00h? Is there caffeine consumption after 14:00h? Is there stimulant drug use or abuse? If indicated, do a full psychiatric diagnostic screening. Consider pain and physical illnesses that could cause it.

62 Treatment Plan for Insomnia Is it ACUTE? Y N Does reassurance & support help? Y N end Rx benzos short-term Identify & treat medical, surgical, or environmental causes No better? Go to next page Is the insomnia acute?

63 Ask psychiatric questions: substance abuse, depression, anxiety + Treat psychiatric illness or refer to psychiatrist. - Ask: sleep hygiene, naps, caffeine, shifts Counsel pt. yourself Refer to sleep psychologist, esp. if “primary insomnia” - + Physical sleep disorders? Refer to sleep lab if (+). +

64 When to refer to sleep clinic Symptoms of sleep apnea (obese, snores, HTN, weight gain, awakens choking, morning headache). Symptoms of RLS / PLMD – legs squirm, cramp, tingle after supper and especially at night If nocturnal injuries – could be sleepwalking, REM Behaviour Disorder, or nocturnal epilepsy. Any chronic insomnia that does not have an obvious cause after reasonable investigations are negative.

65 65 Questions ?

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