2010 mindblock & b-to-b sleep & psychiatry alan b. douglass md, frcpc, dip. absm director,...

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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-BSleep & 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.

• Show examples specific to psychiatry.

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

ICSD summary

1990, 1997

(WHM p. 202)

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.

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

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)

“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.

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.

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!)

. . . 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.

Worm in lateral

hypothalamus causing

narcolepsy.

(neurocysticercosis)

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

SCNclock

DA (+)

Histam. (+)

NA (+)

5HT (+)

Orexin / Hypocretin

Monoamine Monoamine Control by Control by HypocretinHypocretin

+/-

Onset of REM

Onset of REM Sleep

R & K 1968

Narcolepsy: MSLT, SOREMs

REM- on / off neurons

REM Control Nuclei

PGO waves trigger EMs in REM sleep

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.

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.

Sleep fragmen-tation due to PLMD.

(note Stg. 1%)

PLMs(60 sec.

Page)

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).

REM Behaviour Disorder

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.

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

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.

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.

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

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.

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.

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

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.