Sleep Disorders. Hugh Selsick

Transcription

1 Sleep Disorders Hugh Selsick

2 Obstructive Sleep Apnoea What it is: Repeated narrowing or collapse of the upper airway during sleep. Leads to choking, oxygen desaturations and repeated arousals.

3 Physical effects of OSA Excessive daytime sleepiness (Vaughn, 2011). 6X increased risk of accidents (Teran-Santos, 1999). Significant cardiovascular morbidity impaired left ventricular systolic function,, arrhythmias, atrial fibrillation (Somers, 2011), heart failure, stroke (Shahar, 2001). Impaired glucose control (Polotsky, 2011).

4 OSA and Cognition 80% of OSA patients report subjective cognitive impairment (Guilleminault, 1978). Meta-analyses found consistent deficits in motor coordination, vigilance & executive function. The impact on memory was inconsistent but was there more often than not, and there was no impact on intelligence or verbal abilities (Beebe, 2003; Aloia, 2004). Performance, eg on vigilance tasks, may be normal in short tests but deteriorate in longer tests suggesting that fatigueability is an important factor (Weaver, 2001).

5 Mechanisms of Memory Deficit Sleep disruption leads to reduced potential for learning the following day. This may be due to an unprepared brain. Fatigue leads to reduced attention and reduced memory input. Sleep disruption after learning reduces the opportunity for slow cortical oscillations, spindles and REM which consolidate memory. Intermittent hypoxia can lead to structural damage to the brain which leads to functional consequences.

6 Morphological and Functional Changes Reductions in volume of grey and white matter in multiple regions of the brain. Eg. Cerebellum, middle temporal gyrus, left hippocampus, left posterior parietal cortex, frontal lobe, limbic system, pons, (Morrell, 2014; Macey, 2008). Many of these correlate well with functional deficits. Some of these changes may be reversible with CPAP eg grey matter volume in hippocampampus & frontal lobe (Canessa, 2011), but most are probably not.

7 OSA and Depression The majority of studies support the idea that the prevalence of MDD is higher in OSA than the general population (Gall, 1993). For example, in one study 58% of OSA patients met DSM criteria for MDD (Mosko, 1989) Some studies have found a relationship between OSA severity (both objective and subjective) and risk of MDD while others have found increased risk of MDD in OSA regardless of severity (McCall, 2006; Peppard, 2006).

8 Mechanisms Hypoxia may play a role and white matter lesions correlate with low mood (Harris, 2009; Schroder, 2005)). Sleep fragmentation impairs mood (Martin, 2006). Prevalence of depressive symptoms similar to other sleep disorders that cause sleep fragmentation without hypoxia (Aikens, 1999). OSA may lead to lifestyle changes that increase the risk of depression.

9 OSA and Depression Treating OSA may lead to improvements in depressive symptoms and depression predicts a better response to CPAP (Millman, 1989; Wells, 2007). Or it may not there have been numerous negative studies (Harris, 2009). For example studies on patients with severe OSA showed no improvement on CPAP (Borak, 1996; Munoz, 2000) sign of permanent hypoxic damage?

10 Do We Cause It? Many of the medications we prescribe have weight gain as a side effect. Many of the medications we prescribe lead to sedation and muscle relaxation which may exacerbate OSA. But we may reduce the severity of OSA slightly with some serotonergic antidepressants.

11 Investigations Pulse oximetry Respiratory study Polysomnogram

12 Treatments Weight loss. If position dependent OSA position therapy. Mild moderate OSA: mandibular advancement splint. Moderate severe: Continuous Positive Airway Pressure (CPAP).

13 Crazy Legs (not my term) Restless Legs: subjective sense of discomfort in legs (or anywhere else in the body); worse at night; worse at rest; temporarily relieved by movement. Delays sleep onset leading to initial insomnia. The patient is very aware of the discomfort, can easily localise it, but can very rarely describe it. Periodic Limb Movements: unconscious repetitive clusters of leg movements during sleep. Lead to sleep disruption. Sleepy during day. The patient is very rarely aware of these movements. The bed partner may be, but often they are unaware of them too.

14 Aetiology Hypodopaminergic state in brain. Iron deficiency Pregnancy Diabetes Renal Dysfunction Neuropathy Radiculopathy You!

15 Who? Me? Many psychiatric drugs cause RLS and PLMS: RLS: Escitalopram, Fluoxetine, Mianserin, Mirtazapine, Olanzapine, Quetiapine. PLMS: Citalopram, Fluoxetine, Paroxetine, Sertraline, Venlafaxine, Quetiapine (Krystal, 2010). Any drugs with antidopaminergic or antihistaminergic action can cause or exacerbate RLS/PLMS.

16 Diagnosing RLS/PLMS General physicians correctly diagnose RLS in less than 10% of patients (Hening, 2004). It is surprisingly rare for patients to volunteer RLS symptoms. You need to specifically ask about them. A single question has been shown to have 100% sensitivity and 96.8% specificity for RLS in a neurology outpatient population (Ferri, 2007): When you try to relax in the evening or sleep at night, do you ever have unpleasant, restless feelings in your legs that can be relieved by walking or movement? Possible cause of sundowning in patients with dementia/delirium?

17 Investigations RLS is a clinical diagnosis sleep studies are not needed. PLMS diagnosis needs a sleep study. Bloods: Ferritin (should be >50mcg/l), U&E, folate, B12, glucose

18 Treating RLS & PLM s Treat the blood tests. Change their medication if possible. Dopaminergics eg ropinirole, pramipexole, rotigotine low doses, but risk of psychosis & compulsive behaviours. Anticonvulsants pregabalin, gabapentin Clonazepam Opioids

19 Insomnia Difficulty initiating or maintaining sleep, or sleep of poor quality. Which leads to daytime symptoms.

20 Insomnia is a Serious Disease It is a major risk factor for depression (Breslau, 1996; Ford, 1989; Cho, 2008). Residual insomnia is a risk factor for depressive relapse. It has the same impact on quality of life as congestive heart failure or major depression (Katz, 2002).

21 Assessing Insomnia A good history is usually all that is needed; a sleep diary is helpful. Sleep studies are rarely needed. Screen for comorbid anxiety and depression. But remember that insomnia in the presence of depression or anxiety does not mean it is secondary to depression and anxiety. Screen for restless legs as this may present as insomnia.

22 Medication Melatonin is very safe and well tolerated but very mild. Zopiclone is good for sleep onset and maintenance but can cause daytime drowsiness. 40% of patients get a bitter taste. Zolpidem is good for sleep onset, but less effective for sleep maintenance. It causes less daytime drowsiness. Temazepam has a less predictable duration of action and probably higher potential for respiratory depression and addiction. Anti-histamines are good for sleep maintenance but have numerous side effects. Mirtazapine and trazodone good choices, especially in comorbid depression.

23 Cognitive Behaviour Therapy CBT is cheap and effective: Cheap: can be delivered in a group setting to the majority of patients over 5 sessions by a single therapist. Effective: 70-80% of patients benefit from CBT for Insomnia. This includes insomnia comorbid with physical and psychiatric disease, and improvements are seen in both night time and daytime symptoms.

24 The Homeostatic Sleep Drive From the moment we wake up in the morning we start to accumulate sleepiness. We are filling up our sleep tank with sleep fuel. The chemical substrate of this is probably adenosine. When we sleep at night we use up the fuel. When we run out of fuel in the morning we wake up.

25 Start Filling Your Tank at the Same Time Every Day Set an alarm to wake up and, if possible, get up at the same time every day. If you start to fill your tank at the same time every day, it will reach full at the same time every night. You will therefore feel sleepy at the same time every night and your bed time will become more consistent too.

26 Jealously Guard Your Sleep Fuel Every time you nap (intentionally or unintentionally) you use up some of your sleep fuel. Any sleep during the day is stealing some of your sleep from the night. So avoid napping if possible. Caffeine, which is an adenosine antagonist, can be helpful as long as it is taken early in the day.

27 Go to Sleep When Your Tank is Full Set an earliest bed time which is calculated as follows: Earliest bed = Rising time average sleep time. Only go to bed when you have reached that earliest bed time and you are sleepy. In patients where a temporary reduction in sleep time is dangerous this should be done gradually. As sleep improves the earliest bedtime is gradually moved earlier.

28 Harness the Power of Classical Conditioning 1 Allowed in the Bedroom Sleep Sex Getting dressed and undressed (as long as you don t spend more than a few minutes doing this) Note: This list is complete. There are NO other activities that are allowed in the bedroom. Not Allowed in the Bedroom Reading (yes, reading!) Audiobooks/radio/TV/music Computer/iPad Texting/Talking on the phone Meditation/Prayer Relaxing Exercising Ironing Working/Studying Eating/Drinking Conversations Painting/crosswords/knitting etc. Note: This list is incomplete. ANY other activity you can think of goes in this column!

29 Harness the Power of Classical Conditioning 2 If you are not asleep in about 15 minutes get up, get out of bed, get out of the bedroom and do something relaxing and enjoyable. Do not return to bed until you feel sleepy. If you do not fall asleep within 15 minutes repeat the above. Remember the mantra: I am not doing this tonight to sleep better tonight. I may sleep worse tonight. I am doing this tonight to sleep better in a month.

30 Any Questions?