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Paul Reading Consultant Neurologist The James Cook University Hospital

Sl eep Medicine h ypersomnia and insomnia. Neuropsychiatry Course St Anne’s College Oxford , December 9 th 2011. Paul Reading Consultant Neurologist The James Cook University Hospital. Everyone and every animal needs to sleep!.

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Paul Reading Consultant Neurologist The James Cook University Hospital

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  1. Sleep Medicine hypersomnia and insomnia Neuropsychiatry Course St Anne’s College Oxford, December 9th 2011 Paul Reading Consultant Neurologist The James Cook University Hospital

  2. Everyone and every animal needs to sleep! If sleep doesn’t serve some vital function it is the biggest mistake evolution ever made. Alan Rechtschaffen Sleep is of the brain, by the brain and for the brain William Dement The best bridge for repair between despair and hope is a good night’s sleep Joseph E Crossman

  3. I.Defining a normal night’s sleep • II. How much sleep is needed?some effects of sleep deprivation • III. The effects of aging • IV.Abnormal daytime sleepinesscommon causes • V.Insomnia • VI. Conclusions

  4. WAKING REM REM REM REM REM Sleep I II NREM Sleep Stage normal hypnogram of young adult III IV 1 2 3 4 5 6 7 Time (hours through night)

  5. sleep deprivation “Disorders of arousal”e.g. sleep walking; Hypnicjerks WAKE Cataplexy; Sleep paralysis; Hallucinations;e.g. narcolepsy, PD Lucid dreaming REM NREM “overlap” syndromes or “ambiguous sleep” common in narcolepsy and some dementias (esp DLB)cf delirium

  6. II. How much sleep do we get and how much is needed?

  7. Mortality ↑ by 15% if <4.5h or>8.5h

  8. Disturbed sleep predicts “poor outcome” in elderly(Pollaket al 1990) ~2000 elderly New Yorkers interviewed in depth 4 years later : 16% had died, 4% in care; only insomnia (and cognitive impairment) good predictors (in males)

  9. II. How much sleep is needed to feel refreshed on waking? • Probably between 7 and 7.5 hrs for significant majority“long and “short” sleepers actually quite rarenote: Einstein v Thatcher / Napoleon • Quality probably as important as quantityamount of deep SWS (stage 3/4 non-REM) particularly important REM sleep involved more in memory consolidation? • Concept of widespread chronic “sleep debt” populardo we really sleep less than 100 years ago? (~ 6.8h v 8.2h) • Sleep drive is primarily homeostatic (c.f. hunger and thirst)but also circadian influences, nadirs of alertness at 4am & 3pm are afternoon naps normal and / or beneficial?

  10. II. How much sleep is needed? 0 14 0 14 PVT = psychomotor vigilance test 8 hrs/night 6 hrs/night Data suggest increasing signs of sleepiness with regular 6 hours of nocturnal sleep but subjective sleepiness ≠objective sleepiness 4 hrs/night 0 hrs/night Van Dongenet al 2002 Sleep

  11. II. Sleep Deprivation acute consequences • Sleepinesseye-blinks slower • pupillary “instability” • sleep latency (on MSLT) ~3 minif no previous overnight sleep • Slower reaction times longerbrain “ages” by ~10 yrs for every 90 mins of sleep deprivation • vigilance / sustained attention particularly affected • brain has to work “harder” to complete cognitive tasks • lapses and “micro-sleeps” a common practical concern note the eyes can be open

  12. II. Sleep Deprivation neuropsychology • Hypo-frontalityperseveration/reduced flexibility Harrison and Horne 1999 increased risk taking Venkatramanet al 2007 poor moral judgement Killgoreet al 2007 impaired sense of humour Killgoreet al 2006 reduced “emotional intelligence” van der Helm et al 2010 negative mind set van der Helm and Walker 2010increased distractibility Anderson et al 2011

  13. II. Sleep deprivation & emotional processingincreased affective volatility and irritabilityreduced “emotional intelligence” • after 24h SD, “angry” & “happy” emotions less recognised seen particularly in women full recovery of function seen after sleep period

  14. II. The adverse emotional effects of sleep deprivation • Sleep loss in medical residents amplified negative emotional consequences of disruptive daytime experiences while positive benefits of rewarding activities were blunted (Zohar 2005) • In test of emotional memory, f-MR scans show limbic areas overactive to negative stimuli > 1 night SD (Yooet al 2007) • “hyper-limbic state” • due to loss of functional connectivity with PFC? note similarities to depressionover-reactive to negative events

  15. II. Sleep Deprivation chronic consequences • Metabolic increased insulin resistance abnormal response to hunger signals (leptin, ghrelin) • Immunological increased cytokines (CRP)leucocyctosis >45h SD less successful vaccinations? increased cancer? note Danish ruling re shift workers • Neurotoxicity? particularly in the elderly brain

  16. Is chronic sleep deprivation neurotoxic? possible clinical evidence • grey matter changes in brains of severe OSA in middle-age menEunYeonJooet alSleep 2010

  17. The effects of aging sleep quantity 24 Awake 16 REM sleep Hours in day 8 NREM sleep 0 -1 0 1 10 20 100 Conception Birth Death Age (y) Hobson. Sleep and Dreaming. In: Fundamental Neuroscience 1999. Roffwarg et al. Science 1996;152:604.

  18. The effects of aging sleep timing

  19. The effects of aging sleep “quality” • Sleep less consolidatednocturnal sleep generally less “efficient” (90% in young v <85%)~6 minor EEG arousals during sleep are common if >65yr • Progressive “deterioration” in deep slow wave sleepamplitude of delta waves reduced after 25 yrs earliest biomarker of aging?

  20. The effects of aging sleep “quality” • Phase advance in circadian timing with ageabout 30 minutes per decade • Less robust response / recovery to sleep deprivationshift work and jet lag poorly tolerated? • Symptoms of insomnia in ~30%both sleep onset and maintenance • Periodic limb movements (PLM’s) very common (~30%)regular leg slow jerks resembling flexor withdrawal reflex

  21. The effects of aging PLM’s Periodic leg movement K-complex in light,stage 2nREM sleep EEG arousal (alpha rhythm)

  22. The effects of aging examples of PLM’s • strong link with restless legs syndrome • more common if iron deficient • may respond to dopaminergic drugs • clinical relevance frequently debatedsimply a marker of light sleep?does an arousal precede PLM?

  23. IV. Abnormal daytime sleepinessmeasuring subjective sleepiness The Epworth scale - the likelihood of dozing in the following situations: • Sitting and reading • Watching TV • Sitting inactive in a public place (eg theatre or meeting) • Sitting as a passenger in a car for an hour without a break • Lying down to rest in the afternoon when circumstances permit • Sitting and talking to someone • Sitting quietly after lunch without alcohol • Sitting in a car while stopped for a few minutes in traffic Patient rates each item as 0 (would never doze) to 3 (high chance of dozing) ESS total score: 0  24 (<10 normal?)

  24. IV. Abnormal daytime sleepinessmeasuring objective sleepiness • The Multiple Sleep Latency Test (MSLT) • mean sleep latency and type of sleep onset in 4 or 5 naps • - previous night’s sleep should be monitored • - rigorous and strict routine essential for correct interpretation • agood “gold standard”? • prone to false positive (USA?) and false negative (UK?) results • - activity between naps crucial - age effects generally ignored - drug effects may affect results e.g. anti-depressants what is normal range?

  25. Primary Sleep Disorders • with sleep-wake dysregulation(~2% of sleepy population?) • Narcolepsy • Idiopathic hypersomnolence EDS affects 5% of population? • Sleepiness Secondary to a Chronic Disorder • Obstructive Sleep apnoea/hypopnoea syndrome • Restless legs syndrome • Parkinson’s disease • Depression • Myotonic dystrophy • Multiple sclerosis • Circadian Misalignment • Shift work sleep disorder • Delayed and advanced sleep phase syndromes(strong genetic influences) In real life: (voluntary) sleep restriction the environment (e.g. noise) pain other medical conditions

  26. Medical causes • Obstructive sleep apnoea • Asthma • Oesophageal reflux • Prostatism / nocturia • Pain syndromesdiabetic neuropathy, fibromyalgia reduced daytime wakefulness due to “secondary” insomnia • Neurological causes • Restless legs syndrome • Parkinson’s disease • Dementia • Morvan’s syndrome • Fatal familial insomnia • Psychiatric causes • Medication related(stimulating anti-depressants) • Withdrawal-related • Anxiety disorders • Mood disorders “sleep toxins”

  27. Obstructive Sleep Apnoea (syndrome) • Usually easy to pick up from history / phenotype • male, overweight, neck circumference > 17” • don’t overlook retrognathia, large tonsils 4% middle-aged men (2% women) • unrefreshing sleep with severe snoring/pauses • dry mouth in morning, worse after alcohol • confirmed by investigations (oximetry or ambulatory home study) • treatment options: wtlossCPAP MAD’ssurgery

  28. IV. Daytime sleepinessnormal versus abnormal • Important diagnostic questions : • are you getting at least 6 hrs sleep per night? • are you refreshed in morning if you get 8 hrs sleep? • is there a history of severe snoring/other disturbances? • have you fallen asleep in unusual situations? • do you experience “sleep attacks”? • do you have dreams or unusual experiences in naps? • are your naps fairly short and refreshing? • were you sleepy at school, did you under-achieve? • always ask about possible cataplexy and its triggersdiagnostic for narcolepsy but symptoms can be subtle

  29. 24-hour hypnograms in control anduntreated narcoleptic patients REM Sleep MT W REM Control Sleep stage 1 2 3/4 18.00 20.00 22.00 24.00 02.00 04.00 06.00 08.00 10.00 12.00 14.00 16.00 Time of day REM Sleep MT W REM Untreated narcoleptic 1 Sleep stage 2 3/4 18.00 20.00 22.00 24.00 02.00 04.00 06.00 08.00 10.00 12.00 14.00 16.00 Time of day Adapted from Rogers et al. Sleep. 1994;17:590.

  30. 24-hour hypnograms in control anduntreated narcoleptic patients REM Sleep MT W REM Control Sleep stage 1 2 3/4 18.00 20.00 22.00 24.00 02.00 04.00 06.00 08.00 10.00 12.00 14.00 16.00 Time of day REM Sleep MT W REM Untreated narcoleptic 1 Sleep stage 2 3/4 18.00 20.00 22.00 24.00 02.00 04.00 06.00 08.00 10.00 12.00 14.00 16.00 Time of day Adapted from Rogers et al. Sleep. 1994;17:590.

  31. Idiopathic hypersomnolence • A diagnosis of exclusion • less frequent than narcolepsy (x 3 - 10 times rarer?) • affects same age group as narcolepsy • 57% have (secondary?) psychiatric disorderBassettiet al1997 • In classical IH: • nocturnal sleep is long and unrefreshing but otherwise normal • daytime naps often last over one hour, also unrestorative • “sleep drunkenness” and automatic behaviours common • IH without long sleep time: • formal criteria for narcolepsy not formally met … • … although controversial whether this is atypical narcolepsy

  32. An illustrative case a sleepy caterer… • 20 year-old female caterer with life-long (?) EDS • occasional nightmares as young child otherwise normal • Frequent unusual naps • parked in car; having hair cut • No nocturnal sleep problems • wakes up “grumpy” even > 9 hours nocturnal sleep

  33. Overnight PSG MSLT next morning Mean sleep latency: only 2 minutes; entered stage III in 3 of 4 naps Diagnosis : idiopathic hypersomnolence; responding well to Modafinil

  34. Circadian “dysrhythmias” chronobiology } • jet lag • shift work environmental • “constitutional” clock problemsdelayed / advanced / non-24hr sleep phase syndromes (note schizophrenia...)

  35. The suprachiasmatic nucleus (SCN) the “master clock” Photosensitive retinal ganglion cells containing melanopsin project to SCN

  36. V. Insomnia • Definitions of chronic “primary insomnia” (ICSD-2) : • persistent difficulty with sleep (> 1 month)can be either initiating or maintaining sleep,despite adequate opportunity and desire to do so • consequent sleep-related symptoms produce distress, impaired social and/or occupational functioning • strong correlation with increasing age • female bias • “paradoxical” insomnia may mimic true insomnia

  37. V. “Primary” Insomnia psycho-physiological (Spielman) • Predisposing factorspersonal ‘risk’ factorsconstitutional, innate, anxiety trait • Precipitating factors‘trigger’ eventspregnancy, illness, trauma • Perpetuating factorsmaladaptive learningacquisition of sleep-disruptive habitse.g. languishing in bed

  38. Habits and InsomniaNLSAA: people with insomnia (n = 221) v good sleepers (n = 802) Morgan et al (1988) Age Ageing; 17: 1-7

  39. Psychiatric morbidity survey UK(2007) prevalence of insomnia (n ~7000)

  40. Psychiatric morbidity survey severity of insomnia

  41. Psychiatric morbidity survey reported causes of insomnia noisenocturia medicationchild care

  42. V. Theories of insomnia “Cognitive arousal” interferes with automatic sleepracing mind, ruminations, can’t “switch off” • selective attention to sleep onset • compensatory intention to fall asleep • counterproductive ‘sleep effort’ • how do good sleepers fall asleep? – by not trying(Colin Espie)

  43. VI. Conclusions • Sleep is not simply an absence of wakefulness • Most need at least 7 hrs of good quality sleep • An impaired sleep-wake cycle can :affect brain, mind and bodyincrease rate ofneuro-degeneration? • Defining “abnormal” often a “grey area”: before labelling a pattern of sleep as diseased,consider: age, genes, lifestyle and medication

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