2010 MindBlock & B-to-B
1 / 33

2010 MindBlock & B-to-B - PowerPoint PPT Presentation

  • Uploaded on

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.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about '2010 MindBlock & B-to-B' - betha

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
2010 mindblock b to b

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
Goals for today

  • Avoidduplicating 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 summary1990, 1997(WHM p. 202)

Icsd 1990 97 international classification of sleep disorders
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
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 d1
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
“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 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.


  • Remarkable discovery in 2000:adeficit 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
. . . 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
Worm in lateral hypothalamus causing narcolepsy.(neurocysticercosis)J. Clin. Sleep Med. 1(1) 2005, p. 41.

2010 mindblock b to b


DA (+)


Orexin /


Histam. (+)

5HT (+)

Monoamine Control by Hypocretin

NA (+)

2010 mindblock b to b

Onset of REM Sleep

Onset of REM

R & K 1968

Periodic limb movement dis
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
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.

Rem behaviour disorder
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).

Rbd treatment
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.


  • 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
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
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
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
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
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.

Driving sleepiness what kills you
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.