2010 mindblock & b-to-b

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2010 MindBlock & B-to-B Sleep & Psychiatry Alan B. Douglass MD, FRCPC, Dip. ABSM Director, Sleep Disorders Clinic & Lab Royal Ottawa Hospital

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2010 MindBlock & B-to-B. Sleep & Psychiatry Alan B. Douglass MD, FRCPC, Dip. ABSM Director, Sleep Disorders Clinic & Lab Royal Ottawa Hospital. Goals for today. Avoid duplicating the Neurology sleep lecture ! Show International Classification of Sleep Disorders (ICSD), with examples. - PowerPoint PPT Presentation

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Page 1: 2010 MindBlock & B-to-B

2010 MindBlock & B-to-BSleep & Psychiatry

Alan B. Douglass MD, FRCPC, Dip. ABSM

Director, Sleep Disorders Clinic & Lab

Royal Ottawa Hospital

Page 2: 2010 MindBlock & B-to-B

Goals for today

• Avoid duplicating the Neurology sleep lecture!

• Show International Classification of Sleep Disorders (ICSD), with examples.

• Show examples specific to psychiatry.

• Physiology of orexin / hypocretin, with narcolepsy as illustration.

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ICSD summary

1990, 1997

(WHM p. 202)

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ICSD 1990, -97International Classification of Sleep Disorders

• DYSSOMNIA: “either too awake at night or too sleepy in the day.” Subtypes:

– Intrinsic (physiological or psychological cause): insomnia, narcolepsy, sleep apnea, PLMD.

– Extrinsic (cause is outside the body): altitude, allergy, alcohol, noise, sleep deprivation.

– Circadian Rhythm Disturbance: jet travel, shift work, delayed sleep phase.

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ICSD, cont’d• PARASOMNIA: a “grab bag” of undesirable

physiology associated with sleep:

– Arousal Disorders: sleepwalking, sleep terrors (“night terrors”), confusional arousals

– Sleep-Wake Transition Disorders: somniloquy, hypnic jerks, rhythmic movement disorder (pediatrics)

– REM Parasomnias: RBD, nightmares, sleep paralysis

– Other: bruxism, enuresis, SIDS

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ICSD, cont’d• MEDICAL-PSYCHIATRIC disorders: a

sleep abnormality is a major symptom of the disorder, but not the primary problem:

– Depression (short RL, high RD, insomnia)– Schizophrenia (long initial insomnia)– Alcoholism (REMS and SWS suppression)– Dementias (“sundowning”, RBD)– Infection (sleeping sickness, encephalitis)

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“Bad Dreams”• PTSD: Traumatic experience that is re-experienced

in the dream. Any sleep stage. Very terrifying, worse

than nightmares. Daytime symptoms also. • Anxiety Dreams: REM, “bad regular dream”

• Nightmares: REM, intense emotion, awaken with full alertness / terrified / emotional++ / SNS active.

• Night Terrors: NREM early in night, mainly kids. Scream++, inconsolable, thrashing, dazed, SNS+++, no

recall in morning. Benign.

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Sleepwalking vs. RBD• Sleepwalking:

– NREM sleep, first 1/3 of night, children and teens; may persist to adulthood. Not a dream. Confused if awoken. Simple to very complex behaviour. Rarely violent.

• Sleep Talking: – Children; NREM; rarely intelligible; often sleepwalk too.

Can persist to adulthood.

• REM Behaviour Disorder: – Old men; brainstem stroke or degeneration; loss of normal

REM paralysis nuclei; frequently severe injuries; mostly last 1/3 of night.

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NARCOLEPSY• Remarkable discovery in 2000: a deficit of

orexin (hypocretin) in lat. (perifornical) hypothalamus is the cause – equal in importance to discovery of DA deficit in Parkinson’s Disease in 1960s.

• 1980-99: HLA-DQB1*0602 shows 90% specificity for narcolepsy in all racial groups, suggesting auto-immune basis (RR highest in all of medicine!)

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. . . Cont’d

• Understanding the deficit in Narcolepsy exposes a previously unknown control system: how circadian information from the SCN is transduced into alertness & sleepiness at appropriate times of day.

• Narcolepsy is nothing more than the randomization of NREM and REM tendency throughout the 24 hours.

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Worm in lateral

hypothalamus causing

narcolepsy.

(neurocysticercosis)

J. Clin. Sleep Med. 1(1) 2005, p. 41.

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SCNclock

DA (+)

Histam. (+)

NA (+)

5HT (+)

Orexin / Hypocretin

Monoamine Monoamine Control by Control by HypocretinHypocretin

+/-

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Onset of REM

Onset of REM Sleep

R & K 1968

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Narcolepsy: MSLT, SOREMs

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REM- on / off neurons

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REM Control Nuclei

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PGO waves trigger EMs in REM sleep

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Periodic Limb Movement Dis.

• Due to low brain iron stores, esp. in basal ganglia. Low ferritin, B12, folate -- these are needed to make dopamine.

• Electrodes on anterior tibialis musc. (shins)• RLS = leg cramps / movements in evening,

before bed. PLMD = same, but in sleep. • Day symptoms similar to UARS – result of

sleep fragmentation, loss of stages 3 & 4.

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PLMD, cont’d

• Worsened by: caffeine, red wine, spices, SSRI antidepressants

• Helped by: exercise, warm baths, opiates, stretching, massage, some sleeping pills

• Medical Treatment: dopamine agonists (ropinirole, pramipexole), or dopamine “feedstock” L-DOPA.

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Sleep fragmen-tation due to PLMD.

(note Stg. 1%)

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PLMs(60 sec.

Page)

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REM Behaviour Disorder

• Older men, esp. those with Parkinson’s, or Lewy Body dementia

• Brainstem damage: n. magnocellularis, n. paramedianus (REM paralytic pathways)

• Severe brain injuries• Usually no daytime psychopathology• This is how the general public conceives of

“sleepwalking” (incorrect: it’s in NREM).

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REM Behaviour Disorder

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RBD, Treatment

• Antidepressants are almost all REM suppressants, but they worsen RBD (not known why).

• Clonazepam (anti-epileptic BZD) is the treatment of choice.

• RBD can be seen in alcohol withdrawal and various drug abuse withdrawal.

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INSOMNIA

• Lifetime prevalence 30 – 35% (“serious” in 15%) Much worse in elderly. Sex ratio: F > M.

• Short-term insomnia: days to a few weeks• Persistent insomnia: months to years. Types:

– 1.) Medical

– 2.) “Psychological” (co-morbid Psychiatric diagnosis)

– 3.) Persistent psycho-physiological +/or substances

– 4.) Primary

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Persistent Insomnia Types

• Due to medical problems (i.e.:pain, PLMD)• 50%+ is due to active psychiatric illness:

(depression, bipolar, schizophrenia). 1/5 depressed patients have hypersomnia (“atypical depression”, associated with bipolar spectrum illness); 4/5 have insomnia. Short RL (<65 min, normal=90), low SWS, high REM density.

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Persistent Insomnia, cont’d

• Psychophysiological (“learned” or “behavioral”) insomnia: patients have chronic muscle tension, use bedroom for all their activities, “can’t turn my mind off,” variable bedtime, start projects in late evening, “neurotic.” May later develop into a recognizable psychiatric illness. Tx: CBT, sleep logs, correct erroneous ideas about sleep need, progressive relaxation, sleep restriction therapy, circadian rhythm hygiene (sleep study is rarely necessary). Use of hypnotics to be short-term only.

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Insomnia, cont’d

• Substance Abuse insomnia: alcohol, sedatives, tranquilizers, MJ, cocaine, etc. Treatment is directed to withdrawal and abstinence. Substances destroy nearly all normal sleep architecture while being abused.

• Primary Insomnia: – Idiopathic, often from childhood– Sleep state misperception

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Insomnia Treatment

• Short-Term Insomnia: forms a huge fraction of general practice (exam stress, marital breakup, illness in family, financial). Rx: BZDs, zopiclone, zaleplon for 1-4 weeks. Talk about the stressor!! Do not Rx too long.

• Persistent Insomnias: Keep up your search for dx of depression, bipolar, anxiety. Rx: sedating antidepressants or mood stabilizers long-term.

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Sleepiness & Driving• Circadian risk:

– shift workers, “on-call” workers (i.e., doctors), start / stop of daylight savings time ( + 7% change in accident rate), long holiday drives.

• Alcohol Analogy: – 17 h without sleep is same as blood alcohol 0.05%

(50 mg. alcohol / 100 ml of blood).

• Duration: – decreased performance persists for a day or two

after sleep recovery.

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Sleep Deprivation & Car Accidents (Silber 2004, p. 66)

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Driving /Sleepiness: What Kills You

• Cumulative sleep loss over a week• Speeding• Micro-sleeps (@ 30 m /sec. highway speed)• Decreased peripheral attention• Reduced reaction time• “Automatic driving”• Arousing activities only mask sleepiness;

any alcohol makes it much worse.