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Understanding the Pathogenesis of Insomnia Dr. Jason Ellis.

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1 Understanding the Pathogenesis of Insomnia Dr. Jason Ellis

2 Starting at the end…. Cognitive Behaviour Therapy for Insomnia is: Longer lasting than pharmacotherapy More efficacious and is more effective than pharmacotherapy Cheaper (in the long run) compared to pharmacotherapy Just as effective with complex cases as with ‘pure’ cases So what’s the problem….? Cognitive Behaviour Therapy for Insomnia is: Hampered by very few clinicians Prone to high levels of attrition (50%) and non-adherence Time and labour intensive for the client

3 Why is Addressing Acute Insomnia Important? It is the single biggest predictor of chronic insomnia Acute insomnia is a symptom of many other disorders (e.g. MDD) 10M prescriptions annually in the UK for sleep medications (£15m) Persistence of chronic insomnia (mean 2 years) and associated issues Delivery of preventative intervention would most likely be cheaper than CBT-I Intervention would most likely be less burdensome on the patient (attrition and non-adherence)

4 How do we Conceptualize Acute Insomnia? Spielman et al (1987)

5 How do we Conceptualize Acute Insomnia?

6 Significant Life Event Chronic Stressor Accumulation of Daily Hassles Time Stress Response Stress Response Stress Response Insomnia Threshold Insomnia Threshold Insomnia Threshold Acute Insomnia Trigger 1) Any life event or train of life events which results in a significant reduction in QoL from the individuals Ideal 2) Distress at current situation Minimum Frequency 3 or more nights per week Duration3 days -3 months Course 3 - 14 days Subacute 2 - 4 Weeks Transient 1 - 3 Months Subchronic Qualitative Severity mild / moderate / severe as defined by the patient Quantitative Severity (+30 Minutes SOL; +30 Minutes WASO) What is Acute Insomnia? Ellis, Gehrman, Espie, Riemann & Perlis (2012)

7 Prevalence of Acute Sleep Disturbance USA = 9.47% Acute Sleep Disturbance – Age Category 29-45 UK = 7.85% Acute Sleep Disturbance – Mean Age 31.82 (SD 10.82) Ellis, Perlis et al (under review) 66.85% F Mean Age 32.72 (SD 13.81)

8 Prevalence of Acute Insomnia Ellis, Perlis et al (under review)

9 Incidence of Acute Insomnia Ellis, Perlis et al (under review) 412 Normal Sleepers from General Population Met all criteria for Acute Insomnia: 1 month assessment (N = 412) – 3.39% - 2.67% First episode (57% F) 3 month assessment (N = 295) – 7.80% - 4.75% First episode (61% F) 75% remission from First-episode cases by 3 months 50% remission from Recurrent cases by 3 months = 33% transition rate from Acute to Chronic Insomnia

10 Question: Are there any differences between normal sleepers and people with acute insomnia in how they sleep?

11 Sample 54 Participants (36 Females / 18 Males; Mean age 33.6 SD 13.09) Either no-episode (n = 21 NS) or first-episode insomnia (n = 33 AI) Acute Insomnia (DSM-V Insomnia Disorder + 3 days – 3 months) No self-reported chronic illness or psychiatric illness No gender differences between groups (Chi 2.08, df = 2, p =.35) No age differences between groups (t(52) = -.3, p =.77)

12 Screening / Measures 48hour Urinary Melatonin (aMT6s) – circadian abnormalities Actigraphy (14 days) Sleep Diaries (14 days) Polysomnography (2 nights – 1 st Night full screen / adaptation night) Life Events (LES); Stress (PSS); Psychological Adjustment (HADS)

13 Characterising Sleep Continuity in Acute Insomnia No significant differences

14 Characterising Sleep Architecture in Acute Insomnia No significant differences

15 Characterising Sleep Architecture in Acute Insomnia % N2 (t(52) = 2.22, p<.05) % N3 Significant (t(52) = -2.94, p<.005)

16 Architectural Differences Between Sleeper Groups F(2,51) = 4.75, p<.01

17 Architectural Differences Between Sleeper Groups F(2,51) = 5.68, p<.001

18 Is this a ‘level of stress’ response issue?

19 Is this a ‘sleep propensity’ issue?

20

21 Time in Bed

22 What is this pattern also seen in?

23 Psychological Adjustment

24 New Approaches to Address Attrition in CBT-I? Combining CBT-I with a stimulant Combining CBT-I with a hypnotic Decrease Slow Wave Sleep

25 Question: Are there any relevant daytime factors which relate to this poor psychological adjustment in acute insomnia? Sleep Preoccupation A tendency to be overly preoccupied about sleep during the day, with catastrophic interpretations and counterproductive actions across the 24h cycle. Affective = + worry about short and long-term consequences / anxious at night Behavioural = + drink more coffee / go to bed earlier Cognitive = + concentration difficulties / memory deficiencies

26 722 participants completed the Sleep Preoccupation Scale Poor sleeper (“a current sleep disruption which is negatively affecting the quality, quantity, or timing of your sleep and/or having sleep which is unrefreshing, and occurs at least three nights per week”) Average sleeper (“a current sleep pattern which is sometimes disrupted and/or unrefreshing but occurs less than three nights a week”) Good sleeper (“a current sleep pattern which is not disrupted in its quality, quantity, and timing, and is refreshing”) Ellis et al (2007) Are People With Insomnia Preoccupied with their sleep?

27 Levels of Daytime Sleep Preoccupation

28 Aim to examine the relationship between the Sleep Preoccupation Scale (SPS) and sleep parameters over the course of a semi-natural stressor. The sample was four classes of student nurses and midwives from a West London Teaching Hospital. Students filled in the SPS and a sleep diary every day over the course of their two week exam period (one week before, over the two days of exams as well as three days afterward). All scores are averaged across number of nights. Of the initial sample of 103 students, 92 agreed to take part and returned the questionnaires. Mean age 29.4 (SD 8.3) 80 (86.7%) females, 12 (13.3%) males.

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31 Levels of Daytime Sleep Preoccupation

32 Conclusions Acute Insomnia is:Highly prevalent (7.9%) Annual incidence (31.2%) Increased Stage 2 Sleep Decreased SWS Increased Daytime Preoccupation The transition to Chronic Insomnia is:Highly likely (25-50%) and associated with: Increased REM Latency Decreased SWS Increased Anxiety and Depression and which looks very similar to:The onset of an Affective Disorder

33 How early is early prevention? Ellis, Thomson, Gregory & Sterr (2012) * p<.05

34 University of Surrey Professor Annette Sterr University of Glasgow Professor Colin Espie Dr. Maria Gardani Dr. Amy Thomson University of Everywhere Else in the World Dr. Michael Perlis (U Penn) Professor Celyne Bastien (U Laval) Dr. Phil Gehrman (U Penn) Professor Dieter Riemann (U Freiberg) And the people who fund this work University of London Dr. Alice Gregory

35 jason.ellis@northumbria.ac.uk


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