Sleep 513/15

Question 1

1. Reasons for morning tiredness

Answer 1

-mental health concerns such as anxiety and depression causing sleep-onset problems and/or sleep maintenance problems -stimulant intake during the evening (eg caffeine, nicotine, illicit stimulants) delaying sleep onset -sleep disorder that fragments sleep (eg insomnia, sleep apnoea, periodic limb movements and nightmares) -disorder of excessive daytime sleepiness (eg narcolepsy) sleeping at the wrong time because of a body clock phase shift called delayed sleep phase disorder (DSPD) -physical disorders such as thyroid dysfunction, fibromyalgia or diabetes.

Question 2

1. Sleep disorders and mental health assessment

Answer 2

The suggestion of mental health/mood problems should NOT stop you from seeking further information about a possible sleep disorder. Treating sleep disorders can prevent the later onset of clinical depression and, to a lesser extent, anxiety disorders in young people. If evidence of significant clinical depression or anxiety these should be treated at the same time as a sleep disorder. Mild depression can be a consequence of sleep loss, whereas sleep anxiety is commonly associated with long periods of lying in bed waiting for sleep onset.

Question 3

1. Assessment of sleep disorder

Answer 3

• history and examination for coexisting medical or psychiatric illness - history of contributing factors - psychosocial - physical and environmental stressors - poor sleep practices/hygiene: - sleep pattern and timings - variability of sleep wake times over 7 days - medication use - substance abuse - stimulant use (coffee, coke, energy drinks, alcohol, smoking - bedtime pattern including phone/computer/television use) - possibly interview family members/partner/caregiver - history of snoring - history of frequent jerking movements: periodic limb movement disorder - falling asleep inappropriate circumstances/unusual times: narcolepsy –> refer to sleep clinic for assessment

Question 4

1. Diagnosis of DSPD (Delayed Sleep Phase Disorder)

Answer 4

sleep onset and wake-up times are delayed by 3–6 hours, compared with conventional times- develops through interaction of: - a delay in the intrinsic circadian rhythm (a biological factor commonly associated with puberty)13 - poor sleep habits (eg staying up increasingly late and being exposed to computer screens). The International Classification of Sleep Disorders criteria - There is a significant delay in the phase of the major sleep episode in relation to the desired or required sleep time and waking time, as evidenced by a chronic or recurrent complaint by the patient or a caregiver of inability to fall asleep and difficulty awakening at a desired or required clock time. - The symptoms are present for at least 3 months. - When patients are allowed to choose their own schedule, they show improved sleep quality and duration for age and maintain a delayed phase of the 24-hour sleep/wake pattern. - Sleep log monitoring for at least 7 days (preferably 14 days) demonstrates a delay in the timing of the habitual sleep period. Work/school days and free days must be included in this monitoring. - The sleep disturbance is not better explained by another current sleep disorder, medical or neurological disorder, mental disorder, medication use, or substance use disorder.

Question 5

1. Treatment of DSPD

Answer 5

• sleep log - morning bright light for at least 1-2 hours can effectively gradually change circadian rhythms (alternative bright light box) - compliance to morning wake time - sleep hygiene - computer screen/blue light suppress melatonin which normally regulates sleep onset time; should cease 2 hours before bed - 1-2 hours relaxing activities (to allowed in lounge room) - avoid caffeine - avoid vigorous exercise within a few hours sleep

Question 6

1. DSPD comorbid with depression: antidepressant choice

Answer 6

No reported evidence for one over another in DSPS or insomnia with depression - should follow guidelines for depression

Question 7

2. Snoring vs OSA

Answer 7

• witnessed apnoeas in OSA - gasping or choking - fragmented sleep - daytime sleepiness - morning headaches - decreased memory or concentration - irritability - lowered mood –> Epsworth sleepiness > 9 (/24) 0: never 1:slight 2:mod 3:high 1. sitting and reading 2. Watching TV 3. Sitting in public place 4. Passenger in car 1 hour 5. Lying down to rest in afternoon 6. Sitting and talking to someone 7. Sitting quietly after a lunch (without ETOH) 8. In car stopped in traffic Both snoring and OSA are worsened by - recent weight gain - nasal obstruction (eg seasonal rhinitis) - alcohol intake before bed

Question 8

2. OSA History

Answer 8

• usual sleep pattern - bedtime - sleep onset latency (time to fall asleep) - nocturnal wakening - wake up time - total sleep time (reduced total sleep time can contribute to daytime sleepiness - direct questioning sleepiness when driving and about MVA/industrial accidents Risk factors - male gender - middle age - obesity - recent weight gain - increased BMI, neck circumference and waist-hip ratio - upper airway obstruction-tonsillar hypertrophy –> recurrent tonsillitis Complications of OSA - HTN - IHD - CCF - CVA Associated conditions - AF - diabetes DDx - suboptimal sleep hygiene - restless legs syndrome - lowered mood and sedative medications ETOH and sedative medications may worsen OSA by reducing upper airway tone and respiratory drive

Question 9

2. OSA and Driving

Answer 9

OSA increases crash risk x7 The following features x15 risk of a motor vehicle accident: - ESS >16 - previous history of falling asleep at the wheel - a motor vehicle accident (MVA) due to falling asleep. If any of these features are present, an urgent sleep physician referral for assessment and sleep study should be organised. Should be advised not to drive whilst sleepy. He should avoid higher-risk situations (night driving, sleep deprivation, alcohol). State laws require individuals to notify their driver licensing authority of any long-term illness that is likely to affect their ability to drive safely, including OSA. If commercial driver, he must notify his licensing authority and refrain from driving whilst sleepy. He could be subject to legal action if involved in accident due to sleepiness. *fitness to drive

Question 10

2. OSA examination

Answer 10

• BMI (weight kg/m2) should be calculated. (10% increase in body weight = x6 risk OSA - BP should be measured, as up to 50% of OSA patients will have hypertension. - Increased neck circumference (>42 cm men, >41 cm women) is also a risk factor for OSA. - Nasal patency, which may contribute to snoring, should be assessed. - The upper airway should be inspected for tonsillar hypertrophy and the Mallampati score calculated - Retrognathia, rarer craniofacial abnormalities (eg maxillary and mandibular hypoplasia) and endocrine disturbances (acromegaly, hypothyroidism) should be excluded. - Cardiovascular examination should be performed, including looking for atrial fibrillation and congestive heart failure.

Question 11

2. OSA Investigation

Answer 11

Sleep study - apnoea hypopnoea index (AHI) The AHI is the sum of apnoeas (cessation of breathing) and hypopnoeas (reduction in breathing) per hour; AHI of 5–15 indicates mild OSA, 16–30 is moderate and >30 is severe OSA

Question 12

2. Severe OSA

Answer 12

Severe OSA results in - daytime sleepiness, - neurocognitive dysfunction and - impaired quality of life. - increased risk of current and future hypertension, - motor vehicle and occupational accidents, - ischaemic heart disease, - congestive heart failure, - cerebrovascular disease, - atrial fibrillation, - diabetes, - anxiety, - depression, - impotence in men - threefold increase in mortality

Question 13

2. OSA management

Answer 13

• referral to sleep physician - Driving advise; restrictions - Educate and reduce consequences of OSA - Aim total sleep > 7 hours - avoid shift work - lifestyle modification - weight loss - alcohol and smoking - diet and exercise - screen and treat HTN - CPAP for moderate- severe OSA - CPAP adherence should be monitored objectively, using data printouts from his machine - long term adherence 50-70% - If unable to tolerate CPAP therapy his driving risk should be re-evaluated and other options for treatment such as a mandibular advancement splint

Question 14

3. Tiredness/Fatigue History; RLS

Answer 14

• difficulties initiating and maintaining sleep (insomnia), - snoring, - witnessed apnoeas, waking gasping or choking, morning headache and daytime tiredness, which are symptoms of obstructive sleep apnoea (OSA) syndrome. - movements in bed - menstrual history ? menorrhagia females - family history of sleep disorders *

Question 15

3. Tiredness/Fatigue examination; RLS

Answer 15

OSA examination - Epworth Sleepiness Scale (ESS) score - BMI (weight kg/ height m2)3 - neck circumference (>42 cm men and >41 cm women is a risk factor for OSA)7 - nasal patency and the presence of sinus disease - upper airway examination and a Mallampati score calculated8 - cardiovascular examination, including checking blood pressure (BP) - medications that may contribute to OSA. Iron/ferritin studies Neuro exam; peripheral neuropathy

Question 16

3. DDx Tiredness/Fatigue a/w RLS

Answer 16

Restless Leg Syndrome -recently renamed Willis-Ekbom disease (WED) - OSA- sleep study to confirm/rule out - iron deficiency - akathisia: typically occurs throughout the body and lacks the strong circadian pattern of RLS/WED - painful legs and moving toes (PLMT) and leg cramps: PLMT usually lacks the urge to move and is not relieved by movement; leg cramps have an acute onset and there is palpable muscle contraction - psychogenic: uncommon, but may be difficult to distinguish on symptoms reported - growing pains in children and adolescents: these are not usually characterised by the urge to move; those with attention deficit hyperactivity disorder (ADHD) have a higher incidence of RLS/WED – fidgeting and poor attention may be a symptom of both ADHD and RLS/WED in the young - neuropathy: more likely to involve the feet and not alleviated by movement - multiple sclerosis (MS): there is a higher rate of RLS/WED among patients with MS, particularly in primary progressive MS, in older patients with longer duration of MS and more disabling symptoms of MS - Parkinson’s disease: RLS/WED symptoms more common in Parkinson’s disease, but there is no evidence that having RLS/WED symptoms predicts later onset of Parkinson’s disease.

Question 17

3. RLS/WED

Answer 17

first described by Willis in 1685 significantly reduces quality of life and productivity for patients associated with coronary artery disease and increased mortality affects approximately 7% of the population; the mean age of onset is 34 years and for 3% of patients it is a chronic and persistent condition. RLS/WED can be classified as follows: Primary: no identifiable predisposing factor, positive family history Secondary: ferritin <50 ng/ml Pregnancy: prevalence of 11–27% in pregnancy, especially in the third trimester End-stage renal failure: RLS/WED is reduced in about 40% of dialysis patients following renal transplantation21 Drug-induced: tricyclics, selective serotonin reuptake inhibitors (SSRIs), lithium, dopamine agonists (eg metoclopramide and prochlorperazine) and antihistamines.

Question 18

3. RLS/WED Diagnosis

Answer 18

The diagnostic criteria for RLS/WED can be summarised by the acronym URGES: U urge to move limbs – occurs suddenly and is usually accompanied by uncomfortable and unpleasant sensations R rest or inactivity precipitates or worsens symptoms G getting up or moving improves the situation E evening or nighttime appearance or worsening of symptoms S not solely accounted for by another medical or behavioural condition. The sensations commonly affect the legs, from thigh to ankle, and sometimes the arms. Occasionally, only one leg is affected. They may be painful and, in some people, are also present during the day but worsen in the evening or in periods of stillness (eg in a theatre, on a plane flight, or sitting down to read). A family history is noted in at least two-thirds of patients so the presence of RLS/WED in a first-degree relative supports the diagnosis.

Question 19

3. RLS/WED non pharmacological Management

Answer 19

Most cases of RLSS/WED are mild and do not require treatment. Patients with mild, infrequent symptoms may respond to lifestyle changes alone (eg good sleep hygiene practices); however, where this is ineffective medication could be considered. Other non-pharmacological options include: - stretches, compression stockings, exercise - abstinence from alcohol, caffeine, nicotine - engaging in mentally distracting activities - review of medications (SSRI etc*)) - assess for iron deficiency and institute iron therapy for appropriate patients. The iron story in RLS/WED is evolving and brain iron levels can be low, even in those whose ferritin levels are in the normal range. Iron is an important part of dopamine production in brain tissue. Iron supplementation has been shown to improve RLS/WED symptoms even in patients with a ferritin level of 75 ng/ml. It has been suggested that ferritin levels should maintained at a level at which maximal symptomatic benefit is noted, up to 300 ng/ml. It may take 4–6 weeks of iron therapy before improvement is noted. Iron may be given by infusion or orally, depending on the severity of deficiency.

Question 20

3. RLS/WED pharmacological Management

Answer 20

Pharmacological options for RLS/WED include dopaminergic therapy- for more severe symptoms - pramipexole (125–750 µg/day; PBS, restricted benefit for Parkinson’s- if used the RLS/WED rating score must be recorded in the patient’s medical record) - ropinirole (up to 4 mg/day; not PBS listed) - rotigotine as a transdermal patch (4 mg/day; not PBS listed) may be more useful for those who have daytime symptoms Side effects of above meds include - augmentation (an exacerbation of symptoms), which occurs in >20% of patients using these agents in the long term - impulse control disorders (eating, shopping, gambling, sexual activity) and - hypersomnolence, often referred to a sudden sleep attacks. Patients should be asked about these issues at every review. Levodopa+benserizide (100+25–200+50 mg orally) or levodopa+carbidopa (100+25–200+50 mg orally), which are listed on the Pharmaceutical Benefits Scheme (PBS) under the general schedule, may be used if intermittent therapy is required for infrequent limb movements at the time of sleep onset. Some studies have shown a prevalence of up to 25% in pregnancy. Initial treatment should be in avoiding triggers (caffeine, smoking, dopamine antagonists such as metoclopramide) and optimising iron levels. There is a scarcity of pregnancy safety information on first-line medications used in the non-pregnant patient, and medication should be reserved for severe cases. Specialist advice is preferable in these cases.

Question 21

4. Insomnia History

Answer 21

Sleep history should be undertaken to assess disturbance, current and previous sleep patterns: Does she have difficulty falling asleep or maintaining sleep during the night? Is her sleep restorative? How do her sleep problems affect her during the daytime? Common daytime symptoms include: - fatigue - decreased energy - neurocognitive impairment (memory, attention, concentration) - irritability - mood disturbance - anxiety. Were there initial triggering factors? Is there a prior history of sleep disturbance? How long does it take to fall asleep after lights out (sleep onset latency)? What is the number and duration of nocturnal awakenings (wakefulness after sleep onset)? What is her waking up time, total sleep time (TST) and time in bed (TIB)? Calculate ‘sleep efficiency’ (%) using TST/TIB. In addition, assess sleep hygiene, including routine before bedtime, daytime napping and caffeine intake When assessing insomnia ask about predisposing, precipitating and perpetuating factors (the 3Ps). Predisposing factors include: - female gender - advancing age - anxious personality traits. Precipitating factors include: - stress - medical illness (eg pain) - life events (eg separation) - environment (eg temperature, light, noise). Perpetuating factors may include: - sedative or alcohol dependence.

Question 22

4. Insomnia Diagnosis

Answer 22

The diagnostic criteria include: - difficulty initiating and/or maintaining sleep (being awake for longer than 30 minutes) - dissatisfaction with sleep quality (non-restorative sleep) or quantity - impairment in daytime functioning (eg work, study, social). The symptoms occur at least three times per week for longer than 3 months. There may be a prior history of insomnia with a pattern of recurrence. Insomnia commonly co-exists with medical or psychiatric disorders but may occur independently. Cognitive and physiological arousal with negative conditioned responses to the bedroom and falling asleep are often present (‘wired and tired’).

Question 23

4. Insomnia Prevalence

Answer 23

An estimated 6–10% of the general population have symptoms consistent with insomnia disorder. In primary care, 10–20% of patients complain of insomnia symptoms. Insomnia is the most common sleep disorder encountered in general practice in Australia. In 2013–2014, sleep disturbance accounted for 1% of the most frequent problems encountered in general practice in Australia, at a rate of 1.5 per 100 patient encounters. Additionally, sleep disturbance was among the top 10 problems most frequently referred to a medical specialist; 10.9% of patients were referred. Insomnia occurs more often in women (gender ratio 1.5:1) but the prevalence is still high in men.

Question 24

4. Insomnia comorbidities

Answer 24

Comorbidities (eg pain, fibromyalgia, arthritis, diabetes, COPD, coronary artery disease, depression, anxiety, bipolar disorder) are often present. Insomnia - doubles the risk of depression developing in the future - is associated with impaired quality of life, - work absenteeism and - hypertension The current paradigm is that insomnia co-exists with these disorders rather than being a primary or secondary phenomenon.1

Question 25

4. Insomnia DDx

Answer 25

• ‘Short sleepers’ are those who regularly have less sleep than an average person of their age group, have no problems falling asleep or maintaining sleep and have no functional impairment during the day. This pattern can be considered as a variant of normal sleep duration. - Acute situational insomnia lasts days to weeks and is triggered by a precipitating event (eg recent bereavement) or change in sleep schedule (eg overseas trip). - Delayed sleep phase syndrome is a circadian rhythm disorder that is characterised by a late bedtime and getting up time with no daytime dysfunction if the individual is able to sleep in later. A sleep diary can assist with the diagnosis. - Daytime sleepiness and napping are atypical for insomnia and should raise suspicion for other sleep disorders including obstructive sleep apnoea (OSA). - Restless legs syndrome (RLS), now called Willis-Ekbom Disease (WED), is characterised by an unusual feeling in the legs that is relieved by movement during wakefulness and is often associated with periodic limb movements during sleep. - Chronic alcohol dependence, stimulant usage (eg amphetamines) and caffeine can lead to sleep disruption or poor quality sleep. - Comorbid conditions may present with insomnia.

Question 26

4. Insomnia Inx

Answer 26

• Sleep diary for 2 weeks - Insomnia severity index; questionnaire that can screen for insomnia in a community and clinic setting - Sleep studies/polysomnography only if suspect OSA

Question 27

4. Insomnia Management

Answer 27

Non-pharmacological treatments are first-line options for the management of insomnia. - Cognitive behaviour therapy for insomnia (CBTi) is an evidence-based, effective therapy that should be used as a first-line treatment for chronic insomnia. - produces significant improvements in sleep that are sustained at 12 months. - Components include stimulus control, sleep restriction, relaxation techniques, cognitive therapy and sleep hygiene education (Table 1). - A clinical psychologist trained in the management of insomnia provides individual or group therapy over 4–6 sessions (see Resources section). - Online resources are also available as part of a ‘stepped-care’ approach. A Medicare rebate is available under the Chronic Disease Management or Better Access to Mental Health Care schemes. Despite the benefits of CBTi, over 90% of patients seeing a GP with sleeping difficulties are prescribed a benzodiazepine. The Bettering the Evaluation and Care of Health (BEACH) 2013/14 publication reported that two of the top 30 drugs prescribed overall during the study period were benzodiazepines (diazepam accounted for 1.5% of prescriptions and temazepam for 1.2%). Benzodiazepines can improve insomnia in the short term but long-term efficacy is lacking and dependence and tolerance may develop. The benzodiazepine-receptor agonist zolpidem is an alternative option and has longer-term efficacy data and less risk of dependence, but parasomnias are a side effect. Melatonin is approved for use in the short-term treatment of insomnia for those aged over 55 years, but has a modest sedative effect. A trial of sedating antidepressants (eg doxepin, amitriptyline, mirtazapine, agomelatine) may be considered where insomnia and depression co-exist. Valerian is a complementary therapy promoted for improving sleep, but data for its efficacy is limited. Current guidelines recommend short-term use of hypnotics or melatonin for acute or chronic insomnia, where non-pharmacological strategies have been ineffective. A preference for intermittent dosing and overall use for less than 2 weeks is cited. Advice on good sleep practices and counselled about the risks of using alcohol as a sedative, including detrimental effects on slow wave (deep) sleep. Regular follow-up, particularly monitoring for relapse of her insomnia, which commonly occurs in the setting of new environmental stressors.