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Sleep Disorders Medicine In Psychiatry

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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, University of Ottawa Medical Director, Sleep Disorders Service, Royal Ottawa Hospital

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

3 DSM-IV-TR

4 Great clinical textbook: (Mayo Clinic, 2004)

5 Sleep waveform schematic

6 Sleep Stage % by Age

7 Stg%

8 EEG Frequencies EEG Type Hz. Sleep Stg. Delta 0.5 - 3 SWS Theta 3 - 7
REM Alpha 8 - 12 Wake Beta Spindle Stg Gamma REM, wake

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

10 Wake => Sleep Transition
R & K 1968

11 Stage 2 Sleep R & K 1968

12 Stage 4 Sleep

13 REM sleep onset Onset of REM R & K 1968

14 Sleep Histogram RL

15 24-hr Sleepiness Profile

16 Multiple Sleep Latency Test (MSLT)

17 Sleep Restriction MSLT

18 Narcolepsy: MSLT, SOREMs

19 Whole Brain mid-saggital section Netter / CIBA

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

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

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

23 REM Control REM Trigger: nucleus reticularis pontis oralis

24 Orexin-Hypocretin projections

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 HUMAN DOG Orexin / Hypo-cretin cells
Destroyed by immune system Normal Orexin receptors Genetic 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 Narcolepsy versus Schizophrenia
Apparent “Schizophrenic” Hallucinations Actually Daytime REM sleep intrusion Narcolepsy 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 Obstructive Sleep Apnea

34

35 Normal

36 Sleep Apnea

37 OSA Clinical Symptoms

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

40 Periodic Limb Movement Disorder

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 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 2nd line Quinine obsolete

43 Polysomnographic Abnormalities In Psychiatric Patients

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

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

53 Management of Insomnia

54 Causes of acute insomnia
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. Instructions on applying the footer to all slides at once can be found here:

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

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

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 Questions ?


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