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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.

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slide1

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 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.
narcolepsy
NARCOLEPSY
  • 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.
slide12

SCNclock

DA (+)

+/-

Orexin /

Hypocretin

Histam. (+)

5HT (+)

Monoamine Control by Hypocretin

NA (+)

slide13

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.
insomnia
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
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.
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