Sleep Medicine (Oxford Case Histories)

334 OXFORD CASE HISTORIES IN SLEEP MEDICINE efficacy later in the night they are not good at maintaining sleep. However, they are less likely to cause sedation the morning after taking a dose. Longer-acting drugs are good at initiating and maintaining sleep, but are more likely to cause sedation the next day. This is particularly relevant if the person has to be alert in the morning, for example if they drive to work. Table 53.1 shows some commonly used hypnotics with their half-lives. Remember that these are the half-lives, not their duration of action. The duration of action will vary from person to person. The benefit of looking at half-lives is that they give you some indication of the relative duration when comparing the different drugs. Comparing the three ‘z’ drugs is a case in point. Zopiclone is the longest acting of the three and is therefore useful for sleep initiation and sleep maintenance insomnia. However, many patients complain of daytime sedation with it. It is therefore no surprise that it has been shown to have an adverse effect on driving performance the morning after taking a dose. Zolpidem has a medium duration of action and so is good for sleep onset and Table 53.1 Commonly used hypnotics and their half-lives. The wide variation in the half-lives of some substances means that it can be difficult to predict how that drug will affect an individual patient, but overall the half-lives give a reasonable idea of the relative duration of action of the various drugs and their propensity to lead to daytime sedation the next day. Clonazepam is included, as it is widely used in sleep medicine for a number of conditions including parasomnias, restless legs and sleep fragmentation. Drug Half-Life (hours) Zopiclone 3.5–6.5 Zolpidem 1.5–2.5 Zaleplon 1 Temazepam 8–20 Clonazepam 30–40 Promethazine 5–14 Melatonin Modified Release 3.5–4

Case 53 335 confers some benefit for sleep maintenance, though not to the same extent as zopiclone. However, the shorter half-life makes it safer for driving the next morning. Zaleplon is rarely used, but its extremely short duration of action makes it ideal for patients who have no difficulty getting to sleep but who wake up in the middle of the night. Zaleplon can be taken in the middle of the night and will re-establish sleep quickly, but will leave the body quickly enough that there will be little or no hangover on waking in the morning. Additional factors to consider when choosing a hypnotic are the other side effects of each drug. For example, benzodiazepines may be more likely to exacerbate obstructive sleep apnoea, while zopiclone causes an unpleasant metallic after-taste in some (though not all) patients. Whether the risks of addiction are greater with some hypnotics than others is controversial. The addictive potential of the benzodiazepines is well established; some research suggests that the ‘z’ drugs may be less addictive, but not everyone is convinced of this. We discussed the options with Mrs P and, given that she drove to work every morning, we were concerned about her using zopiclone. We decided to switch her to zolpidem 10 mg, which we felt would be sufficient to control her symptoms, as her insomnia was primarily sleep initiation insomnia and when she did wake at night it tended to be in the first half of the night. Mrs P found the zolpidem to be largely effective and she felt much more alert during the day. She was also appreciative of the fact that zolpidem does not cause the metallic after-taste. She did find that once or twice a week she would wake up earlier than usual, but was not too bothered by it. When the summer holidays came around Mrs P asked to remain on the hypnotics. She said she felt so well on the medication that she was reluctant to stop it. She was aware of the risk of addiction, but felt that it was a risk worth taking. We agreed to continue prescribing it, with a number of conditions. First, we asked that the GP prescribe the medication so that he could monitor her use on a regular basis. We arranged to see her three monthly to review whether she still needed the medication and whether there were any adverse side effects. We advised her to try to take regular drug holidays in order to

336 OXFORD CASE HISTORIES IN SLEEP MEDICINE reduce the likelihood of developing tolerance to the drug. Finally, we asked her to attend a course of CBT-I. 4. What is the point of doing CBT-I if the person is taking a hypnotic? First, it is important to remember that a hypnotic is not an anaesthetic. It is unlikely to put a patient to sleep if their physiological and psychological state is not conducive to sleep. A hypnotic should be seen as something that helps someone sleep rather than something that makes them sleep. It is not uncommon for patients to initially have a good response to a hypnotic but to then find that it becomes progressively less effective. This may be a sign of tolerance, but is often actually due to poor sleep habits. Patients may become lazy about their sleep-related behaviours, for example being erratic about their sleep schedules, having caffeine in the evening or watching TV in bed. Therefore, their behaviours counteract the effect of the medication. Doing CBT-I helps patients to optimize their sleep-related behaviours so the medication has the best chance of working. Second, most patients prefer to sleep without medication and they are often under pressure from their GPs to discontinue their hypnotics. It is therefore important to provide them with an alternative treatment. Mrs P found the CBT course extremely helpful. She found that when the medication was combined with the CBT she was able to sleep well on only 5 mg of zolpidem on most nights. She had not been successful in stopping the medication, but was happy with her sleep and how she felt during the day. We followed her up three monthly for a year and over that time there was no loss of efficacy or dose escalation. Learning points The polysomnogram is rarely useful in insomnia, unless the history suggests the presence of another sleep disorder. Insomnia can precede and cause depression, and does not necessarily remit when the depression improves.

Case 53 337 The most important consideration when choosing a hypnotic is the duration of action. Long half-life drugs are good for improving sleep initiation and maintenance, but can lead to daytime sedation. Shorter half-life drugs are good for sleep initiation but less so for sleep maintenance. However, they are less likely to cause daytime sedation. Always consider how important it is for the person to be alert in the morning, particularly if they drive. When starting hypnotics it is tempting to presume that the condition is treated and nothing else needs to be done. In fact, starting a hypnotic should prompt one to redouble one’s efforts to institute non-medical interventions such as CBT-I. Further reading Hall-Porter JM, Curry DT, Walsh JK. Pharmacologic Treatment of Primary Insomnia. Sleep Medicine Clinics 2012;5(4):609–25. Wilson SJ et al. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. Journal of Psychopharmacology 2010 Nov;24(11):1577–601.

Case 54 Please see this patient who is addicted to sleeping pills Mr S is an accountant who presented to the clinic with a complaint of ‘hypnotic addiction’. He had both sleep initiation and sleep maintenance insomnia dating back to his university days. Initially his insomnia was intermittent, but with time it became a consistent feature of his sleep, though the severity varied. Over the years he had been given numerous short courses of hypnotics and, while they had worked well, his insomnia returned as soon as he had finished the course. He managed to function well at work despite his fatigue, though his personal life suffered, as he was often too tired to socialize after work and spent much of the weekend lying in bed trying to catch up on lost sleep (with very little success). Seven years ago he moved to the United States and found the stress of living in a foreign country and the different working conditions very difficult. He was therefore no longer able to function on so little sleep and sought medical help. He was prescribed zolpidem 10 mg which he found very effective. He initially only took it on work nights, but as his job became busier and he started having to work weekends, he started taking it nightly. Six months ago he returned to the United Kingdom. He registered with a GP and approached him for repeat prescriptions for the zolpidem. The GP was reluctant to prescribe the zolpidem for nightly use on a long-term basis and asked Mr S to try stopping it. Mr S explained that he had been taking the zolpidem for six years and had been using it nightly for the last four years. On one occasion he had forgotten to pack it when he went away for a holiday and hardly slept at all for two nights before he was able to obtain a prescription from a local doctor. He has

340 OXFORD CASE HISTORIES IN SLEEP MEDICINE tried sleeping the odd night here and there without the medication but has always had an awful night and gone back to taking the medication the following night.

Case 54 341 1 Why did he have such a poor night’s sleep each time he stopped the medication? 2 Was Mr S addicted to hypnotics? 3 What are the warning signs of hypnotic addiction or misuse? 4 How would you treat Mr S? Questions

342 OXFORD CASE HISTORIES IN SLEEP MEDICINE Answers 1. Why did he have such a poor night’s sleep each time he stopped the medication? The most obvious answer is that he still had an underlying insomnia. But it is more complex than that. He was probably also experiencing an element of rebound insomnia. Rebound insomnia is commonly seen when patients first stop or reduce their hypnotic. Their insomnia gets worse than it would have been had they never taken the hypnotic. Usually this rebound insomnia will recover after a few nights and the insomnia will return to its baseline level. However, many patients are unable to tolerate the wait and go back on to the hypnotic before the rebound insomnia has a chance to improve. They therefore compare their sleep on the hypnotic to their sleep during the rebound insomnia, rather than with their baseline insomnia. This reinforces the idea that they cannot sleep without the hypnotic. It is therefore essential that patients are informed about rebound insomnia when they start on hypnotics and are made aware that it is temporary. Mr S did notice that his insomnia became significantly worse each time he reduced the dose of the medication and that it improved to some extent after a few nights. However, his sleep was never as good as it was on the medication and the cumulative fatigue made him increasingly anxious, which further affected his sleep. The GP became extremely concerned that he had become addicted to the medication and referred Mr S to a substance misuse service to be ‘detoxed’. The substance misuse service put Mr S on a gradual reduction programme with weekly counselling. He successfully managed to stop the hypnotic over a period of eight weeks, but his insomnia became unbearable and he returned to the GP to ask for the prescription to be reinstated. He was unable to function at work and his job was at risk. The GP reluctantly agreed to reinstate the medication on a temporary basis and referred Mr S to the sleep service for a specialist opinion.

Case 54 343 2. Was Mr S addicted to hypnotics? This is an extremely difficult question to answer. Hypnotics do have the potential to become addictive and addiction to hypnotics is well documented in the literature. However, insomnia is often a longterm condition and once it has become chronic tends not to remit on its own. Therefore, when a patient stops the hypnotic it is to be expected that his insomnia will return and they are therefore likely to request further medication from their doctor. It may therefore be that Mr S was simply seeking the appropriate medication to treat his condition. 3. What are the warning signs of hypnotic addiction or misuse? It is important to note that, as explained, continued use because the patient gets insomnia every time they stop is probably not sufficient to qualify them as misusing, or being dependent on, the drug. However, if the patient decides that they do want to stop the medication and are unable to do so, then clearly their relationship with the medication has become problematic. One of the hallmarks of addiction is continued use despite the drug causing more harm than good. Once again, it is important to differentiate between actual harm from the drug, such as severe side effects, and the doctor’s anxiety about prescribing the drug. Tolerance is always a worrying sign. Patients who find they need to escalate their dose in order to get the same effect are at increased risk of becoming dependent on the medication. One should also be on the lookout for patients who use multiple substances to induce or maintain sleep. Patients may combine prescription hypnotics with alcohol, over-the-counter antihistamines, antidepressants or anxiolytics. This is an extremely dangerous situation and significantly raises the risk of a fatal overdose as well as other adverse outcomes such as falls and car accidents. When patients buy hypnotics on the street or over the Internet this should be addressed as a matter of urgency. The quality and safety of these tablets is always a concern and of course there is no medical monitoring or supervision of their use.

344 OXFORD CASE HISTORIES IN SLEEP MEDICINE Furthermore, one should always be on the lookout for patients who use hypnotics for reasons other than sleep, such as anxiety, or who engage in recreational use. 4. How would you treat Mr S? The first issue to address is whether he needs to be treated. Many patients use hypnotics nightly for years without having any difficulties. However, it is always preferable to use non-medical interventions where possible. Some patients are able to stop hypnotics without medical assistance and some may even find that they sleep as well without medication as they did with it. However, patients are more likely to be successful if they engage in a supervised, gradual withdrawal programme. But withdrawing the medication successfully does not mean the insomnia is well controlled. When withdrawing one treatment, even one that is only partially effective, it makes sense that one should replace it with another effective treatment. Mr S was therefore enrolled in a cognitive behaviour therapy for insomnia (CBT-I) programme. This was a six-week group programme where all the patients were long-term hypnotic users looking to reduce their medication. Studies comparing different reduction regimens for hypnotics are unfortunately lacking. It is therefore not possible to give firm recommendations about how fast one should reduce the medication, whether one should do the reduction before, during or after the CBT-I course, or whether it is better to reduce the medication by gradually reducing the dose or the frequency. In practice, we present all the possibilities to the patients and negotiate a programme that they feel will be realistic and will suit them best. What studies do exist generally use a reduction of 25% of the original dose every one to two weeks, and we use this as a starting point. We set targets and encourage the patient to reduce their medication by a certain amount each fortnight. However, these targets are flexible and sometimes patients will progress more quickly while at other times they may remain on a dose for a bit longer. Most patients choose to do the dose reduction during the CBT-I course, as this allows them to get weekly supervision and support.

Case 54 345 Mr S chose to do this and set a target of reducing by 25% every two weeks. We therefore changed his zolpidem from one 10 mg tablet to two 5 mg tablets. He was therefore able to reduce his dose by 25% by taking one and a half tablets, then one tablet and finally half a tablet. He did experience rebound insomnia after the first dose reduction, but as he now knew about rebound insomnia, and knew it was likely to resolve, he was able to persist with the reduction. The rebound insomnia improved after four nights, though his sleep was not quite as good as it had been on the full dose. However, as he started putting the CBT-I techniques into practice his sleep improved, which gave him the confidence to reduce the dose further. By the end of the CBT-I course he had reduced his medication to 2.5 mg and was sleeping well. We explained that at such a low dose it was unlikely to be having a significant physiological effect and that any perceived benefit was likely to be largely down to a placebo effect. We advised that he start reducing the frequency of the medication and that he make a point of not taking it the night before big meetings or busy days to test his ability to sleep under pressure. However, at this point Mr S was feeling so confident that he decided to stop the medication altogether. He reported having two nights of worse sleep, which he attributed to the anxiety of not taking the medication, but then his sleep settled and at three month follow-up he was still sleeping well without any medication. Learning points Long-term hypnotic use and an inability to sleep well without hypnotics do not necessarily indicate addiction to the hypnotics. Insomnia is often a chronic disorder that requires long-term treatment. However, tolerance, dose escalation, mixing medications or hypnotics with alcohol, or using the hypnotic during the day are warning signs of dependence. If patients want to decrease their hypnotic use the best results are probably achieved through a gradual, supervised withdrawal in combination with CBT-I. If one is withdrawing a treatment, even a partially effective one, one should put another treatment in its place.

346 OXFORD CASE HISTORIES IN SLEEP MEDICINE Rebound insomnia is a common consequence of reducing or stopping a hypnotic. This worsening of the insomnia is often very unpleasant and anxiety provoking, but it is almost always temporary. If the patient is forewarned about the rebound insomnia they are more likely to be able to endure it until their sleep recovers. Further reading Bélanger L, Belleville G, Morin C. Management of hypnotic discontinuation in chronic insomnia. Sleep Medicine Clinics 2009 Dec;4(4):583–92. Hall-Porter JM, Curry DT, Walsh JK. Pharmacologic treatment of primary insomnia. Sleep Medicine Clinics 2010 Dec;5(4):609–25. Riemann D, Perlis ML. The treatments of chronic insomnia: a review of benzodiazepine receptor agonists and psychological and behavioral therapies. Sleep Medicine Reviews 2009 Jun;13(3):205–14.

Case 55 My body clock cannot keep up Mr V is a 36-year-old news editor who works for a 24-hour news TV station. He was referred to the sleep clinic by his employer’s occupational health department after he started falling asleep at work. He worked a shift pattern that involved one of three shifts: 8.00 a.m. to 4.00 p.m. (early shift), 2.00 p.m. to 10.00 p.m. (late shift) and 9.00 p.m. to 9.00 a.m. (night shift). He had been working in his post for seven years and initially had performed very well, rapidly advancing to a more senior position. However, approximately a year before his presentation he started to have difficulty concentrating during night shifts. He made a number of uncharacteristic mistakes which led his managers to express their concern about his performance and it was agreed that they would monitor his work more closely. It was during this monitoring period that he was found asleep at his desk on three separate occasions. Mr V admitted that he was finding night shifts increasingly difficult, primarily because he was unable to sleep during the day between shifts. This had never been a problem before, but he was now struggling to get adequate sleep, which left him feeling fatigued and sleepy at night. He was referred to occupational health who initially wondered if he was depressed, but a psychiatric consult found no evidence of a mood disorder, though they commented that he had an anxious disposition. The matter escalated when he started to have difficulty sleeping at night as well, leading to daytime fatigue. When he was found asleep at his desk twice during day shifts he was advised to take a month’s leave and ‘sort himself out’. Mr V decided the stress of his job was getting to him and so went to visit his parents in France for the month. He noticed that his sleep improved fairly quickly and he was able to sleep well at night and feel alert during the day. On returning to work he went on to day shifts

348 OXFORD CASE HISTORIES IN SLEEP MEDICINE for two weeks and his sleep remained good. He was therefore confident that the problem had been resolved. However, when he rotated on to night shifts he had trouble sleeping during the day again and, even when he rotated back to day shifts, his sleep remained poor. Within a month he was falling asleep at work again and was suspended from his job.

Case 55 349 1 What is the likely diagnosis? 2 Can you design shift patterns to minimize the risk of shift work disorder (SWD)? 3 How would you treat Mr V’s SWD? Questions

350 OXFORD CASE HISTORIES IN SLEEP MEDICINE Answers 1. What is the likely diagnosis? SWD, a disorder which may affect over one-fifth of night workers and workers on rotating shifts. This is a circadian rhythm disorder leading to insomnia and/or excessive sleepiness, particularly during work shifts, leading to occupational or other dysfunction. Humans have an internal circadian clock which is one of the major determinants of when we feel awake and when we feel sleepy. As diurnal creatures we are naturally predisposed to sleep at night and be awake during the day. This obviously makes it difficult to work nights, and most night workers will report periods of intense sleepiness and fatigue during night shifts that do not occur during the day. In addition to the difficulty of working at a time when the body expects to be asleep, it is also difficult to sleep at a time when the body expects to be awake. Therefore, despite being tired from a night shift (which is often longer than the day shift, as was the case for Mr V, and most doctors), the person may find it very difficult to go to sleep when they get home from work. Another complication is that when the worker is going home they may be exposed to bright morning light, which may have an alerting effect on the person and potentially confuse the body clock further. Finally, it is often more difficult to sleep during the day than during the night. There is usually more light and noise during the day, which is likely to disrupt their sleep. There are also social factors such as the fact that they may need to sacrifice some of their sleep time to make phone calls to companies that are only open during the day, go to the bank, fetch the kids from school, etc. Night work presents enough difficulties of its own. But when the person works rotating shifts an additional layer of complexity is added. Not only does the person have to cope with working unsociable hours, but these hours keep changing, usually at a pace too fast for the body clock to keep up. As a result, they may also find that they are sleepy at work when working day shifts and have difficulty sleeping at night.

Case 55 351 SWD is not only problematic for the patient, but can have serious consequences for society as a whole. For example, pilots, truck drivers, doctors and nurses, police, air traffic controllers, train drivers and taxi drivers are all at high risk of SWD. As their alertness is adversely affected by the SWD it is concerning that it is so rarely recognized. 2. Can you design shift patterns to minimize the risk of SWD? There is some controversy about which shift patterns are least likely to induce SWD. If the person does only a few days on each shift they will struggle to settle into the new schedule and, as soon as they do, they will rotate to a different schedule. On the one hand, doing a month of earlies, a month of lates and a month of nights gives the person’s circadian rhythm a sporting chance of catching up with the work schedule. However, a month of nights can be gruelling, particularly if their daytime sleep is disturbed by environmental stimuli, and has a significant impact on their social lives. Most jobs use fairly rapidly rotating shifts, spending a few days on each shift. There are three ways these shifts can be organized: ◆ Anti-clockwise rotation—the person works progressively earlier shifts, e.g. four days late, four days early, four days nights, four days off. ◆ Clockwise rotation—the person works progressively later shifts, e.g. four days early, four days late, four days nights, four days off. ◆ Random shifts where there is no clear pattern. This pattern is often found even when the rota uses one of the above patterns, as people swap shifts to meet social commitments. As a rule, the clockwise rotation is the best shift pattern. As most people have an inherent circadian rhythm that is slightly longer than 24 hours, it is easier to delay your circadian rhythm to advance it. Therefore, it is easier to adjust to a progressive delay in the shift pattern. It also means that when you move from one shift to another you have a longer break between the shifts. For example, if Mr V

352 OXFORD CASE HISTORIES IN SLEEP MEDICINE moves clockwise from an early to a late shift, there is a 22-hour break between the end of the early shift and the start of the late shift. But if he moves from the late to the early shift there are only ten hours between shifts. This would give him less time to sleep between shifts, so he may start the early shifts sleep deprived! 3. How would you treat Mr V’s SWD? There are four approaches to treating SWD: improving sleep between shifts, improving alertness during shifts, shifting the circadian rhythm to match the shift and designing the shift pattern to minimize the risk of SWD. Improving sleep between shifts: The first interventions to put in place are the common sense things such as ensuring their environment is conducive to sleep, especially when they are sleeping during the day. This will often require the cooperation of their family. They should avoid caffeine for approximately six hours prior to the desired time of sleep onset. If their sleep is adversely affected by anxiety, then using cognitive behaviour therapy can be helpful. Some patients benefit from using hypnotics to establish their new sleep pattern when they change shifts and particularly when they are trying to sleep during the day. Improving alertness during shifts: Timed naps are particularly helpful here. Naps can be timed to occur just prior to the start of the shift, in quiet periods during the shift and during periods when the circadian rhythm strongly predisposes one to sleepiness, e.g. at around 5.00 a.m. It should be noted that, as some people have an element of sleep inertia on waking from sleep, they should not nap if they may need to respond to emergencies immediately on waking. Judicious use of caffeine can be surprisingly effective and it can be used prior to the time they habitually feel sleepy to prevent the sleepiness occurring. Another possibility is to get exposure to bright light during the shift, as light has an alerting effect, and some patients find physical exercise to be helpful as well. In some cases stimulant medications such as modafinil are warranted and their use is supported by trial data.

Case 55 353 Shifting the circadian rhythm to match the shift: This is often quite difficult, particularly in rapidly rotating shifts. As a rule of thumb, melatonin is given a few hours prior to the desired sleep period (though it should not be taken before driving home, as it is mildly sedative). Light exposure is timed to occur when the person first wakes up and they avoid light prior to going to bed (if necessary using dark glasses or welder’s glasses). Mr V had already taken the common sense steps of ensuring his sleep environment was dark and quiet, and he unplugged his phone to ensure he was not disturbed while sleeping during the day. He tried using hypnotics to help him sleep between shifts, and while this improved his sleep it did not particularly improve his alertness, especially during night shifts. He was also anxious about using hypnotics in the long term. We noted that his shift pattern was fairly random and wrote to his employers asking them to consider putting Mr V on a clockwise rotating shift pattern. We also advised them to facilitate timed naps during work. They initially agreed to the clockwise rotating shift but this fell apart after a month, as it required significant changes to everyone else’s shifts and they were not willing to do this. They were not willing to facilitate planned naps, but said that all workers had a 45-minute break in the middle of their shift for ‘lunch’ and Mr V could use the bed in the first aid room to nap then instead of eating. We gave Mr V melatonin 2 mg to be taken immediately on getting home from his shift and a light box to use immediately on waking. Although his shifts were too chaotic for us to have any realistic hope of shifting his circadian rhythm quickly enough to match his work pattern, we felt it was worth trying. He found the melatonin did improve his sleep and the light box had an alerting effect, so he started each shift feeling more awake than he had before. Mr V also used caffeine prior to the start of each shift and then again an hour prior to the times he felt most sleepy. These interventions helped to a certain extent but he was still struggling, so our next step was to prescribe modafinil to help him stay awake during the shifts. This was initially very effective and he

354 OXFORD CASE HISTORIES IN SLEEP MEDICINE was coping much better at work. Unfortunately, after a few months he started to develop headaches from the modafinil and had to stop it. He was not keen on trying any other stimulants and had decided that he needed to change his lifestyle to fit his body clock, rather than the other way around. Therefore, with our support, he asked his employers to take him off night shifts permanently. They were not willing to do this unless he took a demotion and a significant cut in his salary. After much soul-searching he decided his health was more important than the job and, with the help of his union, negotiated a severance package which he used to set himself up as a freelancer. He set himself very regular working hours and both his symptoms resolved completely. He was therefore discharged from the clinic. Learning points Shift work creates some unique problems for a person’s sleep–wake cycle. Some people cope with this well, but many will develop SWD. Designing shift patterns to better match the workers’ circadian rhythms is a sensible intervention. In practice this means rotating the shifts clockwise, i.e. rotating to later shifts rather than earlier shifts. Interventions involve improving sleep between shifts, improving alertness during shifts and shifting the circadian rhythm to better match the shift pattern. Some patients will not improve despite the above interventions and therefore there are circumstances where the best treatment is to stop doing shift work. Further reading Crowley SJ et al. Complete or partial circadian re-entrainment improves performance, alertness, and mood during night-shift work. Sleep 2004 Sep;27(6):1077–87. Owens JA, Veasey SC, Rosen RC. Physician, heal thyself: sleep, fatigue, and medical education. Sleep 2001 Aug;24(5):493–5. Wright KP, Bogan RK, Wyatt JK. Shift work and the assessment and management of shift work disorder (SWD). Sleep Med Rev 2013 Feb;17(1):41–54.

Section 1: Snoring and sleep-disordered breathing 1. Snoring and witnessed apnoea in a 70-year-old thin man 2. An obese post-menopausal woman snored like a tank 3. Severe OSA in an overweight Chinese man—craniofacial features 4. Unable to throw a cricket ball and could not breathe at night 5. A sleepy bus driver 6. Rapid onset daytime sleep presenting as transient loss of consciousness 7. Unexplained breathlessness and pulmonary arterial hypertension in an obese man 8. Post-operative apnoeas and hypoxia due to undiagnosed OSA 9. Polycythemia got better with CPAP 10. Hyperphagia and sleep disorder in Prader–Willi Syndrome 11. Shot in the head—acquired hypothalamic syndrome 12. Collapsed in a café: acute respiratory failure 13. Overlap syndrome—COPD and OSA 14. Neuropsychological impairment in a psychoanalyst with post-polio syndrome 15. Nocturnal choking in a patient with a goitre and retrosternal extension 16. OSA persists despite removal of a pituitary tumour causing acromegaly 17. CPAP transformed my life 18. Persistent daytime sleepiness despite CPAP 19. CPAP intolerance and non-compliance treatment with MAS 20. Will not use CPAP—ends up with tracheostomy 21. Bariatric surgery cures sleep apnoea 22. Sleep disturbance and daytime sleepiness persists in a snorer despite CPAP—PLMS 23. Worrying pauses in breath without choking and snoring—CSA 24. Irresistible daytime sleepiness in a young obese woman List of cases by diagnosis

356 LIST OF CASES BY DIAGNOSIS Section 2: Snoring and OSA: role of dental and ENT surgeons 25. Contribution of facial skeletal pattern to sleep apnoea 26. MAS therapy for severe OSAHS 27. Effectiveness, compliance and side effects of MAS therapy 28. Allergic rhinitis 29. Nasal polyposis 30. Septoplasty 31. UARS 32. Laser Assisted Uvulopalatoplasty (LAUP)/tonsillectomy 33. Epiglottic trapdoor 34. Tracheostomy Section 3: Neurological sleep disorders 35. Sleep groaning 36. Nocturnal punch and fight 37. Jumpy legs 38. Episodic weak legs in a sleepy man 39. Just sleepy all the time 40. Moving and thrashing around during sleep 41. Panic attacks during sleep 42. Frozen in sleep 43. Confused, irritable and sleepy young man 44. Chattering teeth during sleep 45. Sexsomnia Section 4: Insomnia and circadian rhythm disorders 46. I keep falling asleep at family dinners 47. I have not slept in years 48. Spending too long in bed

List of cases by diagnosis 357 49. A sleep cycle that keeps moving 50. My body is in London but my body clock is in New York 51. A very, very long day 52. Sleep and alcohol abuse 53. Choosing and using hypnotics 54. Please see this patient who is addicted to sleeping pills 55. My body clock cannot keep up

Case numbers are in italics abnormal speech, 43 airflow obstruction, 8 alertness problems, 52 allergic rhinitis, 19 amnesia, 43 anosmia, 29 anxiety, 48, 52, 55 asthma, 24, 29 attention difficulties, 13 brady–tachycardia, 6 breathing problems, 7, 9, 11, 23, 30 cataplexy, 24 chattering teeth, 44 Cheyne–Stokes/periodic breathing, 23 choking, 12, 15, 33 confusion, 43 constant sleepiness, 39 cough, 14 cramp, 37 daytime sleepiness, 4, 8, 9, 10, 11, 12, 13, 15, 16, 17, 18, 19, 22, 23, 24, 26, 27, 29, 31, 33, 35, 37, 38, 39, 40, 43, 46, 49, 50, 55 delusions, 43 depression, 43, 45, 50, 53 derealization, 43 dream enactment, 38 List of cases by principal clinical features at diagnosis

360 LIST OF CASES BY PRINCIPAL CLINICAL FEATURES AT DIAGNOSIS eating disorders, 43 EDS (excessive daytime sleepiness), 1, 6, 39 fascio-mandibular myoclonus, 44 fatigue, 54 foreign body in throat, 34 frozen in sleep, 42 globus, 34 groaning, 35 hallucinations, 38, 43 headaches, 37, 40 heart rate, 6 hypersexuality, 43 hyperventilation, 23 hypnogogic hallucinations, 38 hypnopomic hallucinations, 38 hypocapnia, 23 hyposmia, 28 hypoventilation at night, 14 hypoxia, 8, 12 hypoxia at night, 11 inability to move, 42 incontinence, nocturnal, 40 insomnia, 46, 47, 48, 49, 50, 55 insomnia, rebound, 54 irritability, 43, 53 irritation, 43 kicking, 40 lack of sleep, 51 limb pains, 37 morning headaches, 40 morning tiredness, 50

LIST OF CASES BY PRINCIPAL CLINICAL FEATURES AT DIAGNOSIS 361 mouth opening during sleep (MDSA), 26 movement problems, 42 movements at night, 36, 38, 40, 41, 45 moving during sleep, 40 muscle aches, 40 muscle jerks, 22 muscle weakness, 4 nasal itching, 28 nasal obstruction, 2, 4, 22, 28, 29, 30 nocturia, 29 nocturnal hypoventilation, 14 nocturnal hypoxia, 11 nocturnal incontinence, 40 nocturnal movements, 36, 38, 40, 41, 45 nocturnal tonic–clonic seizures, 40 nocturnal wakefulness, 48, 50, 51, 52, 53, 54 obesity, 1, 2, 3, 5, 6, 7, 9, 10, 11, 12, 15, 18, 24 oedema, 14 panic attacks, 41 paroxysmal arousals, 40 pauses in breath, 23 post-nasal drip, 28 pulmonary arterial hypertension (PAH), 7, 13 rebound alertness, 52 rebound insomnia, 54 respiratory effort related arousals (RERAs), 31 rhinitis, 30 rhinorrhoea, 28 sex during sleep, 45 short sleepers, 51 shouting in sleep, 41 sleep apnoea, 35 sleep disturbances, 6, 18, 19, 22, 24, 49, 50, 52, 55

362 LIST OF CASES BY PRINCIPAL CLINICAL FEATURES AT DIAGNOSIS sleep initiation problems, 48, 50, 51, 52, 53, 54 sleep paralysis, 38 sleep talking, 45 sleep-disordered breathing, 30 sleep, lack of, 51 sleep, movements in, 36, 38, 40, 41, 45 sleep, unsatisfactory, 25, 26, 35, 38, 40, 49, 53 sleepiness, 5 sleepiness during day, 4, 8, 9, 10, 11, 12, 13, 15, 16, 17, 18, 19, 22, 23, 24, 26, 27, 29, 31, 33, 35, 37, 38, 39, 40, 43, 46, 49, 50, 55 sleepwalking, 29, 40, 45 sneezing, 28 snoring, 1, 2, 4, 5, 6, 7, 8, 9, 10, 11, 15, 17, 18, 19, 21, 22, 24, 25, 26, 27, 29, 31, 34, 40 speech abnormalities, 43 talking in sleep, 45 tearfulness, 53 teeth chattering, 44 tiredness, 50 tongue biting, 40, 44 tongue swelling, 34 tonic–clonic seizures, 40 tonsil enlargement, 32 tonsillitis, 5 tracheo-cutaneous fistulae, 34 unexplained breathlessness, 7 unsatisfactory sleep, 25, 26, 35, 38, 40, 49, 53 upper airway obstruction, 9 urinary problems, 40 urination problems, 7 vasomotor rhinitis, 19 visceral obesity, 2 wakefulness after sleep onset (WASO), 48 wakefulness at night, 48, 50, 51, 52, 53, 54 witnessed apnoea, 1, 4, 5, 8, 11, 23, 33, 34, 35

Case numbers are in italics age, 1 alcohol abuse, 15 amyotrophic lateral sclerosis (ALS), 4 anaesthesia problems, 5, 8 anatomical problems, 1, 3, 6, 16, 25, 33 anxiety, 48 body clock problems, 55 cardiovascular conditions, 13, 17, 18, 20, 23 cerebrovascular stroke, 11 chronic obstructive pulmonary disorder (COPD), 12, 24 Coffin Lowry syndrome, 38 coronary artery disease, 18 craniofacial skeletal abnormalities, 1, 3, 16, 25 craniopharyngioma, 11 Cushing’s syndrome, 10 cystic fibrosis, 29 dementia, 22 diabetes insipidus, 11 diabetes mellitus, 7, 17 diaphragm weakness, 14 Duchenne muscular dystrophy, 4 encephalitis, 38 endocrine problems, 10 epilepsy, 41 List of cases by aetiological mechanisms

364 LIST OF CASES BY AETIOLOGICAL MECHANISMS fascioscapulohumeral dystrophy (FSHD), 4, 25 gastro-oesophageal reflux disease (GORD), 34 gender, 1, 2 growth hormone, 16 head trauma, 38 heart failure, 23 Huntington’s disease, 36 hypermotor phenomena, 40 hypersomnia, recurrent, 43 hypnotic addiction, 53, 54 hypothalamus disorders, 18 hypothyroidism, 10 inspiratory muscle weakness, 14 Kartagener’s syndrome, 29 laryngo-pharyngoreflux (LPR), 34 Lewy body dementia, 36 lifestyle problems, 10, 13, 15, 52 lymphoid hyperplasia, 34 micrognathia, 1, 3 Möbius syndrome, 38 motor neurone disease, 4 multisystem atrophy, 36 myasthenia gravis, 4 myotonic dystrophy, 4 narcolepsy, 11, 22, 36 neurological disease, 4, 18, 36 neuromuscular conditions, 4 Niemann–Pick disease, 38 nocturnal epilepsy, 41 Norrie disease, 38

LIST OF CASES BY AETIOLOGICAL MECHANISMS 365 occlusal changes, 27 oral cavity size, 1 palate size, 3 Parkinson’s disease, 22, 36 pituitary tumours, 16 pneumonia, 34 Prader–Willi syndrome, 38 prion diseases, 36 respiration problems, 12, 14, 24 retrognathia, 1, 3 seizures, 40 sleep cycle, 49 sleep deprivation, 51 sleep drunkenness, 39 smoking, 13, 15 surgical side-effects, 8, 16 syringomyelia, 4 teeth problems, 25 temporomandibular joints (TMJ), 25, 27 thyroid disease, 14, 15 tongue size, 3 tumours, 11, 38 vascular lesions, 38

Index A abdominal movement, OSA diagnosis 12 abdominal wall muscles, post-polio syndrome 98 acetazolamide, CSA treatment 155, 156 acoustic rhinometry, rhinitis 198 acquired hypothalamic syndrome case study 73–80 clinical features 79 CPAP 73 definition 79 EDS 73–74 nocturnal hypoxia 73 obesity 73–74 acromegaly case study 107–110 craniofacial abnormalities 108 growth hormone 108 insulin-like growth factor 108 MRI 109f OSA 108 treatment 108 see also pituitary tumours actigraphy ASPS diagnosis 272 DSPS investigations 309 non-24-hour sleep–wake syndrome 301–302, 301f acute hypercapnic respiratory failure (AHRF) case study 81–87 causes 85, 85t chest X-ray 81, 82f clinical features 84, 84t C-reactive protein (CRP) 81 CT 81 Glasgow Coma Scale (GCS) 81 OSA risk from 86–87 sleep study 81–82, 83f white cell count 81 adaptive servo-ventilation (ASV), CSA treatment 156 advanced sleep phase syndrome (ASPS) case study 271–276 diagnosis 272–273 treatment 273 aero-allergens 188 age, OSA 8 AHI see apnoea hypopnea index (AHI) AHRF see acute hypercapnic respiratory failure (AHRF) airflow obstruction 53 alcohol abuse case study 321–328 detoxification 322 effects on sleep 324 history 321–322 OSA 103, 105–106 treatment 324–326 see also alcohol-induced hypotonia alcohol-induced hypotonia 105–106 oximetry 106f allergen avoidance, allergic rhinitis 188–189 allergen-specific IgE blood tests 188 allergic rhinitis 129 allergen avoidance 188–189 case study 185–190 investigations 187–188 pharmacological treatment 189–190 skin prick testing 187, 187f ALS (amyotrophic lateral sclerosis), OSA 30 alternative remedies 329 American Academy of Sleep Medicine, sleep assessment 36 amphetamines, narcolepsy treatment 242 amyotrophic lateral sclerosis (ALS), OSA 30 Notes vs. indicates a comparison or differential diagnosis Page numbers suffixed with ‘t’ refer to details in table, ‘f ’ in figures.

368 INDEX anaesthesia 115 OSA problems 56–57 sleep apnoea 37–38 anatomy assessment in epiglottic trapdoor 212 EDS 44 anosmia, nasal polyposis 192 ANP (atrial natriuretic peptide) in nocturia 48 antidepressant drugs cataplexy treatment 242 insomnia 332 Kleine–Levin syndrome treatment 263 non-REM parasomnia treatment 256 see also specific drugs antiepileptic drugs Kleine–Levin syndrome treatment 263 PLMS/RLS 234 see also specific drugs antihistamines 189 anxiety, insomnia 285–286 apnoea definition 62 witnessed see witnessed apnoea apnoeagraph, UARS 203 apnoea hypopnea index (AHI) CSA 151 OSA 3 appetite control, hypothalamus 76 armodafinil 123 arterial blood gases, overlap syndrome 89 arterial hypertension, case study 47–51 Asian populations, OSA 22 ASPS see advanced sleep phase syndrome (ASPS) asthma 194 snoring 160 ASV (adaptive servo-ventilation), CSA treatment 156 atrial natriuretic peptide (ANP) in nocturia 51 at-risk population, OSA 8 audio-visual monitoring, OSA 53 auto-CPAP, OSA 13, 26 autosomal dominant inheritance, restless legs syndrome mnemonic 232 auto-titrating CPAP 128 azelastine 189 B baclofen 234 bariatric surgery benefits 142–143 case study 139–144 NICE guidelines 142 OSA prevalence 56–57 sleepiness 31–32 basal atelectasis 86 behavioural interventions ASPS treatment 275 see also cognitive behavioural therapy (CBT) behaviourally induced insufficient syndrome, idiopathic hypersomnia vs., 246 benign prostatic hypertrophy (BPH) 51 benzodiazepines non-REM parasomnia treatment 256 side effects 335 Berlin sleep questionnaire OSA prevalence 8 sleep assessment 36 betamethasone 189 bi-level positive airway pressure see BIPAP (bi-level positive airway pressure) bilio-pancreatic diversion (BPD) 142, 143 bimaxillary facial surgery 168, 170f BIPAP (bi-level positive airway pressure) CSA treatment 155–156 OSA 53 post-polio syndrome 97 bleeding, tracheostomy 218 body clock problems case study 347–354 see also shift work disorder (SWD) body mass index (BMI) septoplasty 198–198 see also obesity body temperature, sleep cycle 78–79, 79f body weight changes, Prader–Willi syndrome 67, 68f BPD (bilio-pancreatic diversion) 142, 143 BPH (benign prostatic hypertrophy) 51 brady–tachycardia, OSA 45f breath, pauses in 151–156 breathing pattern, CSA 154 breathlessness obesity 50 unexplained 47–51 bright light, ASPS treatment 273 bronchiectasis 47 bruxism, tongue biting 266

INDEX 369 C caffeine avoidance 352 idiopathic hypersomnia treatments 247 carbamazepine nocturnal epilepsy 253 non-REM parasomnia 256–257 PLMS/RLS 234 cardiovascular disease, OSA 136–137 cataplexy 161, 237–243 definition 240 narcolepsy with 240 signs and symptoms 240 treatment 242–243 catathrenia (sleep groaning) differential diagnosis 224 investigations 224–225 treatments 225 cat hair avoidance 188 CBT see cognitive behavioural therapy (CBT) central sleep apnoea see CSA (central sleep apnoea) cephalogram, OSA 21, 21f, 22t, 172 cephalometric skeletal evaluation 168, 168f cerebrovascular stroke, hypothalamic damage 79 cetirizine 189, 190 chattering teeth during sleep, case study 265–266 chemotherapy, DSPS treatment 310 chest wall movement, OSA diagnosis 12 chest X-ray acute hypercapnic respiratory failure 81, 82f post-polio syndrome 95 Cheyne–Stokes/periodic breathing 154 CSA 151, 152f chlordiazepoxide 322 choking at night 101–106 chronic intermittent nocturnal hypoxia, pulmonary arterial hypertension 50–51 chronic obstructive pulmonary disorder (COPD) clinical features 85 with OSA see overlap syndrome snoring vs., 160 circadian rhythm 78f, 350 ASPS 272 disorders see DSPS (delayed sleep phase syndrome); shift work disorder (SWD) citalopram 329 claustrophobia, CPAP non-compliance 130 clomipramine 163, 242 clonazepam half-life 334t non-REM parasomnia treatment 256 PLMS/RLS 234 REM sleep behavioural disorder 229 tongue biting 266 clonidine 234 codeine 234 Coffin Lowry syndrome, narcolepsy 242 cognitive behavioural therapy (CBT) 278–279 alcohol abuse 326 CPAP non-compliance 130 hypnotics, with 335, 343–344 paradoxical insomnia treatment 281, 282 shift work disorder treatment 352 short sleeper treatment 318 complex sleep apnoea 121, 155 compliance chart, CPAP 112f computed tomography (CT) acute hypercapnic respiratory failure 81 goitres 101, 102f nasal polyposis treatment 193, 193f post-polio syndrome 95 confusion, case study 261–263 continuous positive airway pressure see CPAP continuous sleepiness case study 245–247 see also idiopathic hypersomnia COPD see chronic obstructive pulmonary disorder (COPD) coronary artery disease 117 cough, post-polio syndrome 95 CPAP acquired hypothalamic syndrome 73 auto-titrating 128 CSA treatment 155–156 effects of 111–115 epiglottic trapdoor management 212 ESS therapy 190 goitres 101

370 INDEX CPAP (continued) insufficient pressure 121 mask displacement 129 OSAHS therapy 172 OSA therapy 4–5, 19, 53–54, 60, 117 overlap syndrome 89, 93 PLMS therapy 146 post-polio syndrome 96–97 post transsphenoidal surgery 109 respiration effects 64 side effects 6 sleep apnoea therapy 64, 73, 139 sleepiness 36 titration sleep study 128 CPAP compliance 6, 60, 118 case study 125–132 compliance chart 112f epiglottic trapdoor 211 improvement practices 206 non-compliance 205, 206 psychological barriers 129–130 reasons for 128–130, 128t refusal to use 133–138 suboptimal compliance 120 CPAP rhinitis 129, 199 cramp, restless legs syndrome vs., 232 craniofacial features acromegaly 108 OSA case study 19–24 craniofacial skeletal abnormalities clinical implications 23–24, 23f OSA clinical predictors 11 craniopharyngioma 79 C-reactive protein (CRP), acute hypercapnic respiratory failure 81 CRP (C-reactive protein), acute hypercapnic respiratory failure 81 CSA (central sleep apnoea) AHI 151 breathing pattern 154 case study 151–156 Cheyne–Stokes/periodic breathing 151, 152f CPAP 155–156 definition 154 heart failure 155 history 151 hyperventilation 155 hypocapnia 155 prevalence 154 pseudo CSA vs., 154 studies 151, 152t symptoms 154 treatment 155–156 Cushing’s syndrome 70 custom-made mandibular repositioning devices 126, 131, 146 facial skeletal problems 168 OSAHA 176 cystic fibrosis 194 D daytime naps, narcolepsy treatment 242 daytime sleepiness 25 assessment 157 case study 145–149, 237–243, 271–276 differential diagnosis 148 epiglottic trapdoor 211 ESS 157, 237 history taking 160 obesity case study 157–163 persistent see persistent daytime sleepiness rapid onset 41–45 reassessment 160 shift work disorder 347 see also upper airway resistance syndrome (UARS) delayed sleep phase syndrome see DSPS (delayed sleep phase syndrome) dementia 148 demyelination in narcolepsy 242 dental measurements 182 detoxification 345 alcohol abuse 322 dexamfetamine 247 diabetes insipidus 73 diabetes mellitus 51 diabetes mellitus type 2, 115 diaphragmatic function test 47 diaphragm weakness, post-polio syndrome 98 dim light melatonin onset (DLMO) test ASPS diagnosis 273 DSPS treatment 310 DLMO see dim light melatonin onset (DLMO) test dopaminergic medication 234 REM sleep behavioural disorder 229 dopamine transporter (DaT) scans 228, 229 dream enhancement 256 driver vehicle licensing agency (DVLA) nocturnal epilepsy 253–254 sleep apnoea information 111

Index 371 DSM, insomnia 316 DSPS (delayed sleep phase syndrome) 272 case study 305–311 diagnosis 308 history 305 investigations 309 morning tiredness 305, 309 treatment 310–311 Duchene muscular dystrophy 30 E von Economo, Constantin 76 EDS (excessive daytime sleepiness) acquired hypothalamic syndrome 73–74 anatomy 44 case study 41–45 causes 122t characterisation 41 EEG 41 epilepsy vs., 44 ESS assessment 120 idiopathic hypersomnia 245 Lamotrigine 41 MRI 41, 42f, 44 obesity 42 OSA 10–11 overnight PSG 167 road traffic accidents (RTAs) 137 sleep assessment 167 sleep studies 42 EEG catathrenia (sleep groaning) 224 EDS 41 epilepsy vs. EDS 44 non-REM parasomnia 257, 257f electroculogram (EOG), OSA 63 Embletta 202 EMG (electromyogram) OSA 63 PLMS 146, 147f Empey index, goitres 101 encephalitis, narcolepsy 242 endocrine problems, obesity 70 endoscopic polypectomy 193 endoscopy, UARS 203 EPAP (Expiratory Positive Airway Pressure), overlap syndrome 90 epiglottic trapdoor case study 211–213 CPAP compliance 211 daytime sleepiness 211 investigations 212 management 212 epiglottis wedge excision epiglottic trapdoor management 212 side effects 213 epilepsy EDS vs., 44 at night see nocturnal epilepsy parasomnia vs., 256 episodic nocturnal wanderings, nocturnal epilepsy 252 episodic weak legs, case study 237–243 Epworth Sleepiness Scale see ESS (Epworth Sleepiness Scale) ESS (Epworth Sleepiness Scale) CPAP 190 daytime sleepiness 157, 237 EDS 120 goitres 101 OSA 3, 10–11, 25 OSA prevalence 8 persistent daytime sleepiness incidence 120 polycythemia 59 Prader–Willi syndrome 67, 68f reduction of 190 sleepiness 33 excessive daytime sleepiness see EDS (excessive daytime sleepiness) exercise tolerance 54 Expiratory Positive Airway Pressure (EPAP), overlap syndrome 90 F facial photographic features, OSA diagnosis 20 facial skeletal pattern case study 167–173 OSA 172 radiography 168 facial skeletal problems bimaxillary facial surgery 169, 170f custom-made mandibular repositioning devices 168 falling asleep during day see daytime sleepiness family history narcolepsy 162 restless legs syndrome mnemonic 232 sexsomnia 267 fascio-mandibular myoclonus 266 9780199683956-Makker.indb 371 23/02/15 7:11 PM

372 INDEX fascioscapulohumeral dystrophy (FSHD) 25, 30 fentanyl 234 ferritin, PLMS 233 fistulation, tracheostomy 218 flexible nasendoscopy 186, 186f globus 216 flow limitation 202–203 flucasone nasal drops 190 fluoxetine 242 fluticasone 189 FRC (functional residual capacity), intra-operative atelectasis 38 frontal lobe epilepsy and parasomnias (FLEP) scale 252, 253t frozen in sleep 259–260 FSHD (fascioscapulohumeral dystrophy) 25, 30 functional residual capacity (FRC), intra-operative atelectasis 38 fungal allergies 189 G gabapentin 234 gastro-oesophageal reflux disease (GORD) 216 GCS (Glasgow Coma Scale) 81 gender, OSA 8, 16–17 Glasgow Coma Scale (GCS) 81 globus case study 215–219 causes 216 symptoms 216 see also tracheostomy goitres case study 101–106 CPAP 102 CT 101, 102f Empey index 101 ESS 101 Mallampati score 101 sleep study 101 snoring 101 GORD (gastro-oesophageal reflux disease) 216 granulomatous inflammation, hypothalamus 79 growth hormone, acromegaly 108 H head gunshot wounds case study 73–74 see also acquired hypothalamic syndrome head trauma, narcolepsy 242 heart failure CSA 155 treatment 155–156 heart rate, OSA 45, 45f Herbst appliance, removable 168, 169f history taking ASPS diagnosis 272 daytime sleepiness 160 DSPS investigations 309 insomnia 288, 333 nasal symptoms 186 non-24-hour sleep–wake syndrome 300 HLA, narcolepsy 241 HLADR2 162 house dust mite allergy 188–189 Huntington’s disease 228 hypoid bone, OSA diagnosis 21 hypermotor phenomena, nocturnal front lobe seizures 252 hyperphagia case study 67–71 hypothalamic dysfunction 70 Prader–Willi syndrome 70 hypersomnia idiopathic see idiopathic hypersomnia recurrent, case study 261–263 hypertension OSA 114–115 overlap syndrome 89 untreated sleep apnoea 115 hypertrophy, tonsil 125 hyperventilation, CSA 155 hypnotic(s) ASPS treatment 275 case study 329–337 choice of 333–336 with cognitive behavioural therapy 335 combination with other drugs 343–344 half-lives 334t paradoxical insomnia treatment 281 side effects 335 tolerance 343 see also specific drugs hypnotic addiction case study 339–346 diagnostic problems 343 history 339–340 risk of 335

INDEX 373 signs and symptoms 343–344 treatment 344–345 hypocapnia, CSA 155 hypocretin (orexin) 162 deficiency 162 narcolepsy 241 receptor mutation 241 hypoid muscles, OSA 28 hypopnoea 62 hyposmia 186 hypothalamus acquired damage see acquired hypothalamic syndrome appetite control 76 disorders of 122 sleep 76 hypothyroidism, obesity 70 hypoventilation at night see nocturnal hypoventilation hypoxia nocturnal 73 obesity 86 undiagnosed OSA case study 53–58 I ICD (International Classification of Diseases), insomnia 316 idiopathic hypersomnia case study 245–247 diagnosis 246 differential diagnosis 246 EDS 245 investigations 247 signs and symptoms 245 treatments 247 imaging UARS 203 see also computed tomography (CT); magnetic resonance imaging (MRI); X-rays (radiography) incontinence, nocturnal 252 insomnia aggression on contradiction 279–280 anxiety 285–286 case study 277–283, 285–294, 313–319 definitions 316 diagnosis 280–281 investigations 288, 333 paradoxical see paradoxical insomnia rebound 342, 345 shift work disorder 347 short sleep 317 short sleepers 316 signs and symptoms 313 sleep diary 280 time in bed 286 inspiratory muscle weakness, post-polio syndrome 98 Inspiratory Positive Airway Pressure (IPAP) 90 insulin-like growth factor, acromegaly 108 International Classification of Diseases (ICD), insomnia 316 International Classification of Sleep Disorders (ICSD 2), insomnia 316 intra-operative atelectasis 38 intubation difficulties 115 IPAP (Inspiratory Positive Airway Pressure) 90 ipratropium bromide 189 iron supplements 234 irritation, case study 261–263 isolated sleep paralysis case study 259–260 investigations 260 treatment 260 K Kartagener’s syndrome 194 Kleine–Levin syndrome case study 261–263 prognosis 262–263 signs and symptoms 262, 262t treatments 262–263 L lamotrigine EDS 41 nocturnal epilepsy 253 laryngo-pharyngoreflux (LPR) 216 laser assisted uvulopalatoplasty (LAUP) 125 case study 205–209 sleep studies 206, 207f snoring 10 UARS 203 lateral radiography, OSA diagnosis 21 LAUP see laser assisted uvulopalatoplasty (LAUP) Lewy body dementia 228 lifestyle alcohol abuse 325–326 obesity 70 snoring 10

374 INDEX light exposure, shift work disorder treatment 353 light sensitivity, Supra Chiasmatic Nucleus 77 light stabilization, non-24-hour sleep–wake syndrome treatment 302 lithium 263 loratadine 189 lower jaw see mandible LPR (laryngo-pharyngoreflux) 216 lung function tests 95 lymphoid hyperplasia 216 M MADs (mandibular advancement devices) 208 magnetic resonance imaging (MRI) acromegaly 109f EDS 41, 42f, 44 maintenance of wakefulness test (MWT) 37 Mallampati score goitres 101 OSA 3, 13 mandible micrognathia 11, 20, 21 OSA 20 mandibular advancement devices (MADs) 208 mandibular advancement splint see MAS (mandibular advancement splint) mandibular repositioning devices (MRD) 131 custom-made see custom-made mandibular repositioning devices MAS (mandibular advancement splint) 125–132 background 179 case study 179–182 customized vs. pre-fabricated 182 custom-made 126 follow-up measures 172 long-term side effects 180 nasendoscopy 172 occlusal changes 180, 181f OSA 130–131 OSAHS case study 175–178 sleep apnoea 67–68 snoring 10 mask displacement in CPAP 129 maxilla-facial surgery 172 maxilla size, OSA diagnosis 21 maximum expiratory flow volume (MEFV) 104 maximum inspiratory flow volume (MIFV) 104 MDSA (medical dental sleep appliance) 169–170 MDSA (mouth opening during sleep) 176, 176f medical costs, obesity 143 medical dental sleep appliance (MDSA) 169–170 MEFV (maximum expiratory flow volume) 104 melatonin ASPS treatment 273, 275 modified release, half-life 334t non-24-hour sleep–wake syndrome treatment 302 REM sleep behavioural disorder 229 shift work disorder treatment 353 methadone 234 methylphenidate 247 micrognathia, OSA 11, 20, 21 micro-sleeps 240 MIFV (maximum inspiratory flow volume) 104 Mmcal dental sleep appliance 171f Möbius syndrome 242 modafinil (Provigil) 162–163 idiopathic hypersomnia treatments 247 narcolepsy treatment 242 persistent daytime sleepiness 123 shift work disorder treatment 353–354 sleep apnoea 67–68 mometasone 189 mono-block mandibular advancement splint 6 morning headaches, nocturnal epilepsy 252 morning tiredness, DSPS 305, 309 mortality OSA 137 overlap syndrome 92 motor neurone disease 28 motor vehicle accidents (MVAs), sleep apnoea 38 mouth breathing 129 mouth opening during sleep (MDSA) 176, 176f

INDEX 375 moving during sleep case study 249–254 see also nocturnal epilepsy MRD (mandibular repositioning devices) 131 MRI see magnetic resonance imaging (MRI) multichannel sleep studies 202 OSA 4t, 5t, 11 multiple sleep latency time (MSLT) narcolepsy 241 sleep assessment 36–37 multisystem atrophy, REM sleep behavioural disorder 228 muscle aches, nocturnal epilepsy 252 muscle jerks 148 muscle weakness, OSA 25–26 MVA (motor vehicle accidents), sleep apnoea 38 MWT (maintenance of wakefulness test) 37 myasthenia gravis 30 myoclonus, nocturnal see periodic limb movement syndrome (PLMS) myotonic dystrophy 30 N narcolepsy 77, 149, 240 associated neurological conditions 242 case study 237–243 with cataplexy 240 causes 162, 241 diagnosis 161, 240 family history 162 HLA 241 idiopathic hypersomnia vs., 246, 246t investigations 241 prevalence 240 REM features 161, 161f REM sleep behavioural disorder 228, 240 signs and symptoms 240 treatment 162–163, 242–243 nasal inspiratory peak flow measurements 198 nasal obstruction 186 OSA 16 sleep-disordered breathing 194 tropical nasal steroids 189 nasal polyposis 192f anosmia 192 case study 191–194 CT 193, 193f definition 194 endoscopic polypectomy 193 oral steroids 193 systemic steroids 192 topical steroids 192 treatment 192–193 nasendoscopy 125 flexible see flexible nasendoscopy MAS 172 OSAHA 176 pre-tonsillectomy 209 UARS 203 National Institute of Clinical Excellence (NICE) bariatric surgery 142 MAS recommendations 131 natural sleep cycle 78 n-CPAP, OSAHS 175 neck size, OSA 8, 11, 13, 17, 20, 20f neurodegenerative diseases, REM sleep behavioural disorder 228 neurological conditions 121–122 OSA case study 25–31 neurological examinations, PLMS 233 neuromuscular conditions, OSA 29–30 NICE see National Institute of Clinical Excellence (NICE) Niemann–Pick disease 242 NIV (non-invasive ventilation), overlap syndrome treatment 90, 93 nocturia atrial natriuretic peptide (ANP) 51 OSA 48, 51 nocturnal choking, case study 101–106 nocturnal epilepsy case study 249–254, 255–258 diagnosis 252 differential diagnosis 252 driving 253–254 temporal seizure pattern 256 treatment 253 nocturnal front lobe seizures 252 nocturnal hypoventilation post-polio syndrome 98 sleep apnoea vs., 99 nocturnal hypoxia 73 nocturnal incontinence 252 nocturnal myoclonus see periodic limb movement syndrome (PLMS)

376 INDEX nocturnal punch and fight see REM sleep behavioural disorder (RBD) nocturnal tonic–clonic seizures 252 non-24-hour sleep–wake syndrome case study 297–303 diagnosis 300 high risk groups 300 investigations 301–302 signs and symptoms 297 sleep history 297 treatment 302–303 non-invasive ventilation (NIV), overlap syndrome treatment 90, 93 non-REM parasomnia 256 carbamazepine 256–257 case study 255–258 investigations 257–258 nocturnal epilepsy vs., 252 sexsomnia 267–268 treatment 256–257 triggers 268 non-REM sleep, OSA 63 non-steroidal anti-inflammatory drugs (NSAIDs) 136 Norrie disease 242 NSAIDs (non-steroidal antiinflammatory drugs) 136 nutrient deficiencies 142–143 O obesity acquired hypothalamic syndrome 73–80 basal atelectasis 86 breathlessness 50 causes of 70 Cushing’s syndrome 70 daytime sleepiness case study 157–163 EDS 42 endocrine problems 70 hypothyroidism 70 hypoxia 86 lifestyle 70 medical costs 143 OSA 8, 11, 13, 160 Prader–Willi syndrome 70 pulmonary restriction 50 respiratory infections 86 respiratory system 85–86 sleepiness 33 weight loss see weight loss obesity hypoventilation syndrome (Pickwickian syndrome) 82, 86 AHRF risk 86–87 obstructive sleep apnoea see OSA (obstructive sleep apnoea) obstructive sleep apnoea hypopnoea syndrome see OSAHS (obstructive sleep apnoea hypopnoea syndrome) occlusal changes, MAS 180, 181f oedema, post-polio syndrome 95 oesophageal manometers 202 opioids/opiates 136 PLMS/RLS 234 oral cavity size OSA 3 see also Mallampati score orexin see hypocretin (orexin) orlistat (Xenical) 157 oro-nasal airflow, OSA diagnosis 12 OSA (obstructive sleep apnoea) abdominal movement 12 acromegaly 108 age 8 AHI 3 AHRF risk 86–87 alcohol drinking 103, 105–106 amyotrophic lateral sclerosis 30 anaesthesia problems 56–57 Asian populations 22 associated risks 136–137 at-risk population 8 audio-visual monitoring 53 auto-CPAP 13, 26 bariatric surgery 56–57 benzodiazepine side effects 335 Berlin Questionnaire 8 brady–tachycardia 45f cardiovascular disease 136–137 cephalogram 21, 21f, 22t, 172 chest wall movement 12 chronic obstructive pulmonary disorder (COPD) with see overlap syndrome clinical predictors 11 co-existing conditions 121 craniofacial features case study 19–24 craniofacial skeletal abnormalities 11 EDS 10–11 effects on sleep 63–64 facial photographic features 20 facial skeletal pattern 172 fascioscapulohumeral dystrophy 25, 30 gender effects 8, 16–17 heart rate 45, 45f hyoid bone 21 hypertension 114–115

INDEX 377 lower jaw features 20 MAS 130–131 maxilla size 21 micrognathia 11, 20, 21 mortality 137 motor neurone disease 28 nasal obstruction 16 neck obesity 8, 20 neck size 11, 13, 17, 20f neurological disease case study 25–31 neuromuscular conditions 29–30 see also specific conditions nocturia 51 with nocturnal hypoventilation see obesity hypoventilation syndrome (Pickwickian syndrome) NREM sleep 63 obesity 8, 11, 13, 160 breathlessness, hypertension case study 47–51 oral cavity size 3 oro-nasal airflow 12 palate size 20 persistent daytime sleepiness see persistent daytime sleepiness PLMS with 148 post-menopausal women 8, 13–18 post-operative complications 136, 136t presenting features 9–11 prevalence 8 pre- vs. post-menopausal women 17–18 racial craniofacial features 8 REM sleep 63 respiration effects 64 Respiratory Distress Index 19 respiratory monitoring 12 retrognathia 11, 20, 21 risk factors 8–9 risk stratification 57f severity measurements 12 sex hormones 17–18 skull base 21 smoking 103, 105–106 snoring 9–10 snoring case study 3–12 surgical risks 57–58 syringomyelia 28 thyromental angle 20f thyromental distance 20f thyromental plane 20f tongue size 20 tracheal intubation 56 undiagnosed case study 53–58 upper airway muscles 28–29 visceral obesity 17 OSA diagnosis 53 confirmation 11–12 diagnostic criteria 62–63 EMG 63 EOG 63 ESS 3, 8, 10–11, 25 lateral radiography 21 Mallampati score 3, 13 multichannel sleep studies 4t, 5t, 11 oximetry 12, 13, 48, 51, 148 PSG 11–12 sleep questionnaire 8 sleep summary 4t, 5t OSA treatment bi-level positive airway pressure 54 CPAP 4–5, 19, 53–54, 60, 117 curative treatments 130 tracheostomy 130, 137, 217 see also tracheostomy weight loss 130, 143–144 OSAHS (obstructive sleep apnoea hypopnoea syndrome) background 175 clinical examination 175–176 CPAP 172 custom-made mandibular repositioning devices 176 MAS case study 175–178 mouth opening during sleep 176, 176f n-CPAP 175 partner-recorded snoring questionnaire 176 SF-36 quality of life 176 sleep nasendoscopy 176 symptoms 175 Osler test 37 overlap syndrome arterial blood gases 89 case study 89–94 CPAP 89 definition 92 Expiratory Positive Airway Pressure 90 hypertension 89 Inspiratory Positive Airway Pressure 90 mortality 92 non-invasive ventilation 90 pulmonary hypertension 92, 93 quality of life 92 sleep study 89

378 INDEX overlap syndrome (continued) smoking history 93 spirometry 89 suspicions of 92–93 treatment 93 overnight pulse oximetry 202 overnight sleep studies, insomnia 333 over-the-counter snoring remedies 9–10 oximetry alcohol-induced hypotonia 106f OSA 12, 13, 48, 51, 148 sleepiness 34f oxycodone 234 oxygen, CSA treatment 155, 156 oxygen saturation (SaO2) monitoring 60, 62f P PAH see pulmonary arterial hypertension (PAH) palatal muscles 28 palatal surgery, OSA risks 58 palate size 20 panic attacks case study 255–258 differential diagnosis 256 paradoxical insomnia case study 277–283 diagnosis 280–281 self-monitoring 280 treatment 281–282 Paradoxical Intent 282–283 parasomnia epilepsy vs., 256 non-REM see non-REM parasomnia Parkinson’s disease 148, 149, 228 paroxysmal arousals, nocturnal front lobe seizures 252 partner-recorded snoring questionnaire 176 pauses in breath 151–156 Periodic Limb Movement Index 36/ hour 146, 147f periodic limb movement syndrome (PLMS) 121–122 associated diseases/disorders 233 case study 145–149, 231–235 characteristics 233 CPAP 146 definition 148–149 EMG 146, 147f investigations 233 with OSA 148 PSG 146, 146f symptoms 145 treatment 146, 234 see also restless legs syndrome (RLS) persistent daytime sleepiness case study 117–123 clinical findings 117 co-existing conditions 121 incidence 120 incidence by ESS 120 treatment 120–121, 123 pharyngeal muscles 28, 29f physical exercise, ASPS treatment 275 Pickwickian syndrome see obesity hypoventilation syndrome (Pickwickian syndrome) Pittsburgh sleep questionnaire 36 pituitary tumours case study 107–110 see also acromegaly PLMS see periodic limb movement syndrome (PLMS) pneumonia 218 pollen avoidance 189 polycythemia case study 59–65 ESS 59 oxygen saturation (SaO2) monitoring 60, 62f respiratory monitoring 59 sleep monitoring 59–60 polysomnography see PSG (polysomnography) positional snoring treatments 10 post-menopausal women obesity case study 13–18 OSA 8, 13–18 pre- vs. in OSA 17–18 post-nasal drip 186 post-operative apnoeas 53–58 post-operative complications, OSA 136, 136t post-operative risks, sleep apnoea 37–38 post-polio syndrome abdominal wall muscles 98 BiPAP 97 case study 95–100 chest X-ray 95 cough 95 CPAP 96–97 CT 95

INDEX 379 definition 98 diaphragm weakness 98 inspiratory muscle weakness 98 lung function tests 95 nocturnal hypoventilation 98 oedema 95 repetitive oxygen desaturation 98–99 respiratory problems 98 sleep quality 96 sleep study 95–100, 96f post transsphenoidal surgery, CPAP 109 Prader–Willi syndrome body weight changes 67, 68f case study 67–71 ESS 67, 68f hyperphagia 70 narcolepsy 242 obesity 70 sleep apnoea 70–71 visilab sleep study (audio-visual recording with oximetry) 67 pramipexole 234 pregabalin 234 pre-menopausal women, post- vs. in OSA 17–18 pressure insufficiency, CPAP 121 prion diseases 228 promethazine 334t Provigil see modafinil (Provigil) pseudo CSA, CSA vs., 154 PSG (polysomnography) 202 insomnia 333 narcolepsy 241 non-REM parasomnia 257–258 OSA diagnosis 11–12 overnight, EDS 167 paradoxical insomnia treatment 282 PLMS 146, 146f REM sleep behavioural disorder 228–229 with respiratory monitoring 224 psychological barriers to CPAP 129–130 pulmonary arterial hypertension (PAH) case study 47–51 chronic intermittent nocturnal hypoxia 50–51 overlap syndrome 92, 93 pulmonary function tests 47 pulmonary restriction, obesity 50 pulse oximetry OSA 45f overnight 202 Q quality of life overlap syndrome 92 tracheostomy 218–219 questionnaires anaesthesia screening 56 OSA prevalence 8 partner-recorded 176 Pittsburgh sleep questionnaire 36 St George’s Respiratory Questionnaire 92 see also Berlin sleep questionnaire R racial craniofacial features 9 radioallergosorbent test (RAST) 188 radiography see X-rays (radiography) rapid onset daytime sleep 41–45 RAST (radioallergosorbent test) 188 RBD see REM sleep behavioural disorder (RBD) RDI (Respiratory Distress Index) 19 rebound alertness, alcohol abuse 324 rebound insomnia 342, 345 recurrent hypersomnia, case study 261–263 removable Herbst appliance 168, 169f REM sleep catathrenia (sleep groaning) 224–225, 224f narcolepsy 161, 161f OSA 63 REM sleep behavioural disorder (RBD) 256 associated conditions 228 case study 227–229 characteristics 256 diagnosis 228 investigations 228–229 nocturnal epilepsy vs., 252 treatment 229 see also narcolepsy repetitive oxygen desaturation, post-polio syndrome 98–99 RERAs (respiratory effort related arousals) 203 respiration CPAP effects 64 obesity effects 85–86 OSA 64 post-polio syndrome 98 Respiratory Distress Index (RDI) 19

380 INDEX respiratory effort related arousals (RERAs) 203 respiratory infections, obesity 86 respiratory monitoring OSA diagnosis 12 polycythemia 59 respiratory stimulants, CSA treatment 155 respiratory tract infections 133 restless legs syndrome (RLS) case study 231–235 cramp vs., 232 diagnosis 232–233 signs and symptoms 232 treatment 234 see also periodic limb movement syndrome (PLMS) retrognathia, OSA 11, 20, 21 rhinitis 198 topical nasal steroids 199 rhinorrhoea 186 ipratropium bromide 189 rimonabant 69 RLS see restless legs syndrome (RLS) road traffic accidents (RTAs) 137 ropinirole 234 rotigotine 234 Roux en Y gastric bypass (RYGB) 142 RTAs (road traffic accidents) 137 RYGB (Roux en Y gastric bypass) 142 S SAD see seasonally affective disorder (SAD) lamp sarcoidosis, hypothalamic damage 79 satiety control 76 SCN (Supra Chiasmatic Nucleus) 77–78 SE see sleep efficiency (SE) seasonally affective disorder (SAD) lamp DSPS treatment 310 non-24-hour sleep–wake syndrome treatment 302–303 seizures catathrenia (sleep groaning) vs., 224 nocturnal front lobe 252 tongue biting 266 septal deviation 196f case study 195–200 rhinitis 198 septoplasty 195–200 alternatives to 199 BMI 198–199 complications 199 sleep-disordered breathing effects 199–200 sex hormones 17–18 sexsomnia 267–268 SF-36 quality of life, OSAHA 176 shift patterns 351–352 shift work disorder (SWD) case study 347–354 daytime sleepiness/fatigue 347 diagnosis 350–351 insomnia 347 minimisation 351–352 treatment 352–354 short sleepers case study 313–319 causes 317 insomnia 316 need of 317 treatment 317–318 single-photon emission computerized tomography (SPECT) 229 skin prick testing 187, 187f sleep chattering teeth case study 265–266 disruption 148 disturbance of 145–149 duration in OSA 63 EDS assessment 167 environment 353 hypothalamus 76 mouth opening 176, 176f movement disorders 148 moving in 249–254 OSA effects 63–64 paralysis 148 persistent daytime see persistent daytime sleepiness polycythemia 59–60 short duration case study 313–319 very short, case study 313–319 sleep apnoea anaesthesia 37–38 catathrenia (sleep groaning) vs., 224 CPAP 64, 73, 139 diabetes mellitus type 2, 115 diagnosis lag time 114 driver vehicle licensing agency 111 mandibular advancement splint 67–68 modafinil 67–68 motor vehicle accidents 38 nocturnal hypoventilation vs., 99

INDEX 381 obstructive see OSA (obstructive sleep apnoea) post-operative risks 37–38 Prader–Willi syndrome 70–71 screening for 114–115 sleep study 139 untreated consequences 115 sleep cycle body temperature 78–79, 79f case study 297–303 sleep deprivation 317 sleep diaries ASPS diagnosis 272, 273, 274t DSPS investigations 309 insomnia 280, 288, 289t, 292 sleep-disordered breathing nasal obstruction 194 septoplasty 199–200 sleep drunkenness 246 sleep efficiency (SE) increase of 290, 292 insomnia 278, 290 sleep groaning see catathrenia (sleep groaning) sleep history, non-24-hour sleep–wake syndrome 297 sleep hygiene 278–279, 329 narcolepsy treatment 242 sleepiness assessment 36–37 bariatric surgery 33–34 case study 33–39 continuous, case study 245–247 CPAP 33 definition 36 ESS 33 obesity 33 oximetry 34f sleep studies 33, 34, 34f tonsillitis 33 sleeping pill addiction see hypnotic addiction sleeplessness for years case study 277–283 see also insomnia sleep onset latency (SOL) 278, 290 sleep quality OSA 63 post-polio syndrome 96 sleep rhythm generation and control 77–78 sleep schedules insomnia 290, 292, 294, 332–333 paradoxical insomnia treatment 282 sleep space separation 326–327 sleep state misperception case study 277–283 see also paradoxical insomnia sleep studies acute hypercapnic respiratory failure 81–82, 83f EDS 42 goitres 101 laser assisted uvulopalatoplasty 206, 207f overlap syndrome 89 post-polio syndrome 95–96, 96f sleep apnoea 139 sleepiness 33, 34, 34f sleep-talking 225 sleeve gastrectomy 142, 143 smoking OSA 103, 105–106 overlap syndrome 93 snoring asthma 160 case study 3–12, 13–18, 47–50 COPD vs., 160 goitres 101 laser assisted uvulopalatoplasty 10 lifestyle changes 10 mandibular advancement splint 10 natural history of 16 OSA 9–10 partner-recorded questionnaire 176 treatments 9–10 SOL (sleep onset latency) 278, 290 SPECT (single-photon emission computerized tomography) 229 spending too long in bed 285–294 spirometry 82, 103 overlap syndrome 89 upper airway obstruction 104–105, 104f steroids 193 systemic see systemic steroids topical see topical steroids St George’s Respiratory Questionnaire 92 substance misuse services 342 Supra Chiasmatic Nucleus (SCN) 77–78 surgery nasal polyposis treatment 192 OSA risks 57–58 risks in OSA 57 snoring 10 swallowing difficulties, tracheostomy 218 SWD see shift work disorder (SWD)

382 INDEX syringomyelia 28 systemic steroids allergy treatment 189 nasal polyposis treatment 192 T teeth problems 167–168 temazepam 334t temporomandibular joints (TMJ) 167–168 asymptomatic 182 theophylline 155 threshold time calculation 290, 292 thyroid disease 103, 105 thyromental angle 20f thyromental distance 20f thyromental plane 20f timed naps, shift work disorder treatment 352 time in bed (TIB) 278 titration sleep studies, CPAP 128 TMJ see temporomandibular joints (TMJ) tongue based surgery 58 OSA 28 size 20 swelling 216 tongue biting case study 265–266 nocturnal epilepsy 252 tonic–clonic seizures, nocturnal 252 tonsillectomy 125, 133 case study 205–209 disadvantages/side effects 209 pre-surgical assessment 209 UARS 203 tonsillitis 33 tonsils enlargement 208, 208f hypertrophy 125 topical steroids 192, 199 nasal obstruction 189 total sleep time (TST) 278, 290 tracheal intubation 56 tracheo-cutaneous fistulae 218 tracheostomy 134f care advice 217–218 case study 133–138, 215–219 complications 218–219 OSA treatment 130, 137 transsphenoidal surgery 108 Trib2 antibodies 241 TST (total sleep time) 278, 290 tumours hypothalamic damage 79 narcolepsy 242 U UARS see upper airway resistance syndrome (UARS) unexplained breathlessness 47–51 upper airway(s) assessment 56 obstruction see below oedema 108 surgery 58 upper airway muscles 28–29, 29f training 30–31 upper airway obstruction 62 spirometry 104–105, 105f upper airway resistance syndrome (UARS) 145–146 apnoeagraph 203 case study 201–203 investigations 203 tonsillectomy 203 treatments 203 URGE, restless legs syndrome mnemonic 232 urinary frequency 51 uvulopalatopharyngoplasty (UPPP) 130 V valproate 234 vascular lesions, narcolepsy 242 vasomotor rhinitis 129 venlafaxine 242 ventro-lateral pre-optic area (VLPA) 76, 77f very short sleep, case study 313–319 video-EEG telemetry 252 visceral obesity, OSA predictor 17 visilab sleep study (audio-visual recording with oximetry) OSA diagnosis 117 Prader–Willi syndrome 67 VLPA (ventro-lateral pre-optic area) 76, 77f vocal problems, post-tracheostomy 218 W wakefulness after sleep onset (WASO), insomnia 278, 290 WASO (wakefulness after sleep onset), insomnia 278, 290

INDEX 383 weight loss CPAP compliance 206, 208 OSA therapy 130, 143–144 white cell count, acute hypercapnic respiratory failure 81 witnessed apnoea 10 case study 3–12 X Xenical (orlistat) 157 X-rays (radiography) facial skeletal pattern 168 OSA diagnosis 21 see also chest X-ray Z zaleplon ASPS treatment 275 characteristics 335 half-life 334t zeitgebers 300 zolpidem addiction see hypnotic addiction characteristics 334–335 half-life 334t zopiclone 334 alcohol abuse 322, 326 half-life 334t