Note: in \200\230atypical \200\231 cases, one or more of these features may be absent. Physical signs \200 \200 b p. 400), but less severe. May be similar to anorexia nervosa ( Speci \201 c problems related to \200\230purging \200\231 include: \200 \200 \200 Arrhythmias Cardiac failure (sudden death) Electrolyte disturbances ( [laxatives] or alkalo sis [vomiting]) Oesophageal erosions Oesophageal/gastric perforation Gastric/duodenal ulcer s Pancreatitis Constipation/steatorrhoea Dental erosion Leukopenia/lymphocytosis dK+, dNa+, dCl \200\223, metabolic acidosis \200 \200 \200 \200 \200 \200 Investigations As for Anorexia nervosa (b p. 402). Differential diagnosis \200 \200 \200 \200 \200 Upper GI disorders (with associated vomiting) Brain tumors Personality disorder Depressive disorder OCD 10_Semple_Chap10.indd 406 12/7/2012 3:34:41 PM BULIMIA NERVOSA 407 \200 b p. 930) Drug-related increased appetite (see Other causes of recurrent overeating (e.g. menstrual-r elated syndromes \200\224 b p. 464, Kleine \200\223Levin syndrome \200\224 b p. 434) Comorbidity \200 \200 Anxiety/mood disorder \200\230Multiple dyscontrol behaviors \200\231 e.g.: \200 \200 \200 \200 \200 Cutting/burning Overdose Alcohol/drug misuse Promiscuity Other impulse disorders ( b pp. 408 \200\22311) Treatment \200 General principles \200 \200 \200 b p. 402). Full assessment (is for anorexia nervosa \200\224see Usually managed as an outpatient. Admi ssion only for suicidality, physical problems, extreme refractory cases, or if pregnant (du e to increased risk of spontaneous abortion). Combined approaches improve outcome. Pharmacological \200 Most evidence for high-dose SSRIs ( \202 uoxetine 60mg) \200\224long-term treatment necess ary (>1yr). Psychotherapy \200 \200 \200 Best evidence for CBT. IPT may be as effective long-term, but acts less quickly. Guided sel f-help is a useful \201 rst step (e.g. bibliotherapy), with education and support often i n a group setting. Prognosis Generally good, unless there are signi \201 cant issues of low self-esteem or ev idence of severe personality disorder. Box 10.7 The SCOFF1 questions These questions are useful as a screening tool for eating disorders (both anorexia and buli mia nervosa) in primary care. They have low sensitivity, and a score of 2+ \200\230yes \200\231 answers indicates that a further more detailed history is indicated, before consid ering treatment or referral. \200 \200 \200 \200 \200 Do you make yourself Sick because you feel uncomfortably full? Do you worry you have lost C ontrol over how much you eat? Have you recently lost more than One stone in a 3-month perio d? Do you believe yourself to be Fat when others say you are too thin? Would you say that F ood dominates your life? 1 Morgan JF, Reid F, and Lacey JH (1999) The SCOFF questionnaire: assessment of a new scree ning tool for eating disorders. Br Med J 319: 1467 \200\2238. 10_Semple_Chap10.indd 407 12/7/2012 3:34:41 PM CHAPTER 10 Eating and impulse-control disorders 408 Impulse-control disorders 11 Impulse-control disorders (ICDs) are disorders in which a pers on acts on a certain impulse, that is potentially harmful, but they cannot resist. There is usually an increasing sense of arousal or tension prior to committing or engaging in the a ct and an experience of pleasure, grati \201 cation, or release of tension at the time of committing the act (Note: this distinguishes these disorders from OCD where acts are not in themselves pleasurable). Intermittent explosive disorder (IED)1 Although not speci \201 cally recognized in ICD-10 and often subsumed under Emotionally Unstable PD, DSM-IV distinguishes IED for individuals who have extreme explosive behaviors out of proportion to the actual trigger (e.g. a person who feels insulted by a coworker may go into the lunch area and rip down the cabinets and throw the chairs, only to later feel very guilty and embarrassed). IED may have a lifetime prevalence up to 2 \200\22311%, and occurs most often in young men. Episodes are typically infrequent (not a personality trait per se) in occurrence, and last only 20mins or less. Ot her symptoms may include tingling, tremor, palpitations, chest tight- ness, head pressure, hearing an echo. Clinical features \200 Several discrete episodes of failure to resist aggressive impulses that result in serious a ssaultive acts or destruction of property. The degree of aggressiveness expressed during th e episodes is grossly out of proportion to any precipitating psychosocial stressors. Not du e to another disorder or substance use. Differential diagnosis ADHD, bipolar disorder, conduct disorder, personality disorder. Treatment Evaluate and treat comorbid disorders. IED is challenging to treat, and most effo rts are focused on minimizing aggression. There is some evidence for the use of mood stabil izers (lithium, semisodium valproate, maybe carbamazepine), phenytoin, SSRIs, -blockers ( best evidence if brain damage is present), 2-agonists (clonidine), and antipsychotics. Kleptomania1,2 Failure to resist impulses to steal items that are not needed for their per- sonal use or monetary value. Usually women, mean age 36, mean duration of illness 16yrs (o ften childhood onset). Accounts for about 5% of stealing in USA. Clinical features \200 Recurrent failure to resist impulses to steal objects that are not needed for personal use or for their monetary value. Increasing sense of tension immediately before committing the theft. Pleasure, grati \201 cation, or relief at the time of committing the theft. The ste aling is not committed to express anger or vengeance and is not in response to a delusion o r a hallucination. \200 \200 10_Semple_Chap10.indd 408 12/7/2012 3:34:41 PM IMPULSE-CONTROL DISORDERS 1 409 The stealing is not better accounted for by conduct disorder, a manic episode, or antisocia l personality disorder. Differential diagnosis Shoplifting (actions are usually well-planned and motivated by need or monetary gain), antisocial personality disorder, OCD, depression. Comorbidity Eating disorders, substance abuse, depression. May be precipitated by major str essors (e.g. loss events). Treatment SSRIs (e.g., \202 uoxetine); psychotherapy (e.g. CBT, family therapy). Pyromania3 The presence of multiple episodes of deliberate and purposeful \201 re- settin g, leading to property damage, legal consequences, and injury or loss of life. It is rare i n children; more common in male adolescents, particularly those with poor social skills and learning dif \201 culties. Clinical features \200 \200 Tension or affective arousal before the act. Fascination with, interest in, or attraction t o \201 re and its situational contexts. Pleasure, grati \201 cation, or relief when sett ing \201 res, or when witnessing or participating in the aftermath. Evidence of advance p reparation. Indifference to consequences on property or life. Not for \201 nancial gain, to express sociopolitical ideology, to conceal criminal activity, as an expression of anger or vengeance, to improve one \200\231s living circumstances, due to delusions or hallucina tions, or as a result of impaired judgment. \200 \200 Differential diagnosis Conduct disorder, ADHD, adjustment disorder, other major affective o r psychotic disorder. Comorbidity Substance misuse, past history of sexual or physical abuse, antisocial personal ity disorder. Treatment Should address any underlying or comorbid psychiatric disorder. Psychotherapeutic intervention may be helpful (e.g. CBT). 1 Dell \200\231Osso B, Altamura AC, Allen A, et al. (2006) Epidemiologic and clinical updat es on impulse control disorders: a critical review. Eur Arch Psychiat Clin Neurosci 256: 46 4 \200\22375. 2 McElroy SL, Pope HG Jr, Hudson JI, et al. (1991) Kleptomania: a report of 2 0 cases. Am J Psychol 148: 652 \200\2237. 3 Puri BK, Baxter R, Cordess CC (1995) Characteri stics of \201 re-setters. A study and proposed multiaxial psychiatric classi \201 cation . Br J Psychiat 166: 393 \200\2236. 10_Semple_Chap10.indd 409 12/7/2012 3:34:42 PM CHAPTER 10 Eating and impulse-control disorders 410 Impulse-control disorders 2 Pathological gambling disorder1 Persistent and recurrent malada ptive patterns of gambling behavior that may lead to signi \201 cant personal, family, and occupational dif \201 culties. The disorder is felt to start in adolescents, where the pr evalence is 4 \200\2237%. Prevalence in adults is reported around 1 \200\2233%, whereas aro und 80% of the general population consider themselves \200\230recreational gamblers \200 \231. Diagnostic criteria \200 Preoccupation with gambling (thinking of past gambling experiences, planning the next exper ience, or thinking of ways to get money to gamble). Needing to gamble with larger amounts o f money to get the same feeling of excitement. Unsuccessful attempts to stop gambling or to cut down. Restlessness or irritability when trying to cut down or stop gambling. Gambling to escape from problems or to relieve feelings of anxiety, depression, or guilt. Chasing lo sses (return after losing to get even). Lying to family or friends about gambling. Committi ng illegal acts to \201 nance gambling. Has lost or jeopardized a signi \201 cant relati onship, job, career, or educational opportunities because of gambling. Relies on family or friends for money to relieve \201 nancial problems caused by gambling. The gambling behav ior is not better accounted for by a manic episode. \200 \200 \200 \200 \200 Comorbidity Highly comorbid with mood disorders (both depression and bipolar), substance ab use or dependence. Other associations seen with ADHD, other impulse control disorders, pers onality disorders (esp. clus- ter B DSM-IV). Treatment Exclusion and treatment of any comorbid psychiatric disorder. Proposed speci \201 c treatments to control addictive behavior include SSRIs (e.g., \202 uoxetine, \202 uvoxamine, paroxetine, citalopram), lithium, clomipramine, and naltrexone. CBT may als o help reduce preoccupation with gambling. Trichotillomania2 Recurrent pulling of one \200\231s own hair, exacerbated by stress or rel axation (e.g. reading, watching TV). Feelings of tension are relieved by pulling hair. Usua lly involves the scalp, but may include eyelashes, eyebrows, axillae, pubic, and any other body regions. In children, 5 = 4, often with a limited course. In adults, 5 3.4% > 4 1.5%, with a chronic or episodic course. Lifetime prevalence rate of 1 \200\2232%. Clinical features \200 \200 Recurrent pulling out of one \200\231s hair resulting in noticeable hair loss. An increasin g sense of tension immediately before pulling out the hair or when attempting to resist the behavior. 10_Semple_Chap10.indd 410 12/7/2012 3:34:42 PM IMPULSE-CONTROL DISORDERS 2 411 \200 Pleasure, grati \201 cation, or relief when pulling out the hair. The disturbance is not b etter accounted for by another mental disorder and is not due to a general medical conditio n (e.g., a dermatological condition). The behavior causes clinically signi \201 cant distr ess or impairment in social or occupational functioning. Associated features Examining hair root, pulling strands between teeth, trichophagia (eatin g hairs), nail biting, scratching, gnawing, excoriation. Differential diagnosis OCD, Tourette \200\231s syndrome, pervasive developmental disorder ( e.g. autism), stereotyped behavior, factitious disorder. Comorbidity Depressive disorder, generalized anxiety disorder, OCD, personality disorder. Treatment Address any comorbid disorder. CBT/behavioral modi \201 cation (substitution, po sitive/negative reinforcement) is key to treatment. There is some evidence for use of SSRIs , clomipramine, pimozide, risperidone, and lithium. 1 Grant J, Potenza E, Marc N (2004) Impulse control disorders: clinical characteristics and pharma- cological management. Ann Clin Psychiat 16(1): 27 \200\22334. 2 Walsh KH and McDou gle CJ (2001) Trichotillomania. Presentation, etiology, diagnosis and therapy. Am J Clin De rmatol 2: 327 \200\22333. 10_Semple_Chap10.indd 411 12/7/2012 3:34:42 PM This page intentionally left blank 413 Chapter 11 Sleep disorders Introduction 414 Normal sleep: stages and cycles 418 Assessment of sleep disorders 420 Inso mnia 1: overview 424 Insomnia 2: general management strategies 426 Sleep-related breathing disorders 428 Hypersomnia 1: overview 430 Hypersomnia 2: narcolepsy 432 Hypersomnia 3: othe r causes 434 Circadian rhythm sleep disorders 1: overview 436 Circadian rhythm sleep disord ers 2: management 438 Parasomnias 1: overview 440 Parasomnias 2: disorders of arousal/NREM sleep 442 Parasomnias 3: sleepwalking and associated disorders of NREM sleep 444 Parasomnias 4: disorders associated with REM sleep 446 Parasomnias 5: other presentations 4 48 Sleep-related movement disorders 450 Isolated symptoms, apparently normal variants, and unresolved issues 452 Sleep disorders related to psychiatric disorders 1 454 Sleep disorders related to psychiatr ic disorders 2 456 Psychiatric medication and sleep 458 11_Semple_Chap11.indd 413 12/10/2012 6:28:55 PM CHAPTER 11 Sleep disorders 414 Introduction Disorders of sleep and wakefulness are a somewhat marginalized concern to most psychiatrists. Even taking a look at ICD-10 or DSM-IV reveals a disappointing paucity of c linical interest, which belies the advances which have taken place in sleep research in rec ent decades and their relevance to psychiatric training and practice. This is partly due to the fact that sleep research had focused on the physical causes of insomnia, such as obstr uc- tive sleep apnoea (see b p. 428) \200\224which is more the remit of respiratory physici ans \200\224or the neurological presentations, such as narcolepsy \200\224which have yielde d interesting genetic and neurobiological \201 ndings (see b p. 432). Having ventured dow n the cul-de-sac of dream/psychosis research in the 1960s and \200\23170s, few psychiatric units in the UK or Ireland still have facilities to conduct inpatient sleep monitoring. As a result we have to rely on good relations with our physician colleagues in order to appro priately investigate possible sleep disorders (see Box 11.1 for a brief history). Relevance to psychiatric practice Aside from the common-sense notion that \200\230getting a good night \200\231s sleep \200\231 is good for mental health, it is vital that mental he alth professionals under- stand the effects that mental disorder and treatment may have on the normal sleep \200\223wake cycle (see b pp. 454 \200\2239). Perhaps even more impor- tan t is the need to recognize that disorders of sleep and wakefulness may themselves manifest bizarre and dif \201 cult to explain psychiatric symptoms, such as hypnic hallucinations a nd REM-sleep behavior, which ought not to be labeled as \200\230psychotic \200\231 in natu re (see b p. 440 for cautionary notes). Psychiatrists also should be aware of principles of good sleep hygiene (see b p. 426) and not always be reaching for the prescription pad to s ort out sleeping dif \201 culties! The International Classi \201 cation of Sleep Disorders In 2005 the American Academy of Sl eep Medicine (AASM) published a revised form of its International Classi \201 cation of Sl eep Disorders (ICSD-2). Its stated goals were: \200 To describe all currently recognized sleep and arousal disorders, and to base the descripti ons on scienti \201 c and clinical evidence. To present the sleep and arousal disorders in an overall structure that is rational and scienti \201 cally valid. To render the sleep a nd arousal disorders as compatible with ICD-9 and ICD-10 as possible. In this chapter, we have adhered to the structure laid out in ICSD-2 for the clinical syndr omes, rather than the much broader categories of ICD-10 or DSM-IV (see b p. 1034) as not on ly does this provide a more valid way of conceiving the disorders but also it is likely tha t future classi \201 cations in ICD and DSM will follow the lead of the AASM. Key ICSD-2 g roupings include: \200 \200 \200 \200 Insomnias. Sleep-related breathing disorders. Hypersomnias of central origin not due other causes. Circadian rhythm disorders. 11_Semple_Chap11.indd 414 12/10/2012 6:28:55 PM INTRODUCTION 415 \200 \200 \200 Parasomnias. Sleep-related movement disorders. Isolated symptoms, apparently normal variant s, and unresolved issues. Other sleep disorders. Box 11.1 A brief history of sleep research Interest in disorders of sleep and wakefulness truly began when, in 1880, G lineau describ ed 14 cases of hypersomnia, distinguished p from s hypersomnia and coined the term \200 \230narcolepsy \200\231 (Gk. \200\230seized by somno- lence \200\231). In 1902, Loewenfeld noticed the common association between the sleep attacks and paralysis during bouts of lau ghter, anger, or other strong emotions. This was referred to as \200\230cataplectic inhibi tion \200\231 by Henneberg in 1916 and later as \200\230cataplexy \200\231 (Gk. \200\230s tupefaction \200\231 or liter- ally \200\230strike down \200\231) by Adie in 1926. The ter m \200\230sleep paralysis \200\231 \200\224a brief episodic loss of voluntary movement tha t occurs on falling asleep or awakening \200\224was introduced by Wilson in 1928, although Mitchell had previously described the phenomenon as \200\230night palsy \200\231 as early as 1876. In 1903, the work of Cajal and Tello on the morphological changes in reptilian brains durin g hibernation led to a number of neuronal theories of sleep. These culminated in von Econom o \200\231s work in patients dying from encephalitis lethargicans, following the 1917 epide mic. The idea that there were centers in the brain that controlled sleep caught the imagina tion of neuroscientists, focused attention on the hypothalamus, and laid the foundations fo r further neurophysiological and neuropatho- logical research. In 1924, Berger succeeded in recording the \201 rst human EEG. Filled with doubt, it took him 5 years to publish his \201 rst paper in 1929, but he was the \201 rst to show tha t cerebral electrical activity was different during sleep than arousal. It took some time f or EEG to be accepted, but, in 1937, Loomis documented the slow wave EEG patterns of non- R EM (NREM) sleep (SWS). The major breakthrough came in 1949 when Moruzzi and Magoun \201 r st investigated the neural components regulat- ing the brain \200\231s sleep-wake mechanism s, discovering the relationship between the reticular formation (RAS) and EEG activation du ring transi- tions between sleep and wakefulness. This was followed in 1953 by Kleitman and Aserinsky publishing a paper in Science that desc ribed the rapid eye movement (REM) stage of sleep and proposed a correlation with dreaming. With his student, Dement, Kleitman also described the \200\230typical \200\231 architectu re of sleep in 1957. Dement went on to show that REM sleep was characterized by a character istic desynchronized, \200\230active \200\231 pattern, a \201 nding con \201 rmed by Jo uvet in 1959. Jouvet described the controlling centers in the brainstem, clari \201 ed the role of the pontine centers, and in 1962, presented a clear neurophysiological framework f or the generation of REM sleep with associated muscle atonia. The \201 rst speci \201 c treatment for a sleep disorder came in 1959 when Yoss and Daly used methylphenidate (Ritalin) to treat narcolepsy and in 1965 Oswald and Priest began usi ng the sleep laboratory to evaluate 11_Semple_Chap11.indd 415 12/10/2012 6:28:55 PM CHAPTER 11 Sleep disorders 416 sleeping pills. Also in 1965 Gastaut and colleagues in Marseilles and Jung and Lugaresi in Bologna independently described obstructive sleep apnoea (OSA) and a variety of surgical tr eatments was proposed. The publication of Rechtschaffen and Kale \200\231s Manual of standardized terminology, tec hniques and scoring system for sleep stages of human sub- jects in 1968, the identi \201 c ation of the suprachiasmatic nuclei (SCN) as the site of the biological clock in 1971, the \201 rst formal classi \201 cation of sleep disorders in 1979, and the introduction of C PAP to treat OSA by Sullivan and colleagues in 1981, were all signi \201 cant advances in the diagnosis, treatment, and neurobiology of speci \201 c sleep disorders and set the sta ge for the next generation of sleep researchers. 11_Semple_Chap11.indd 416 12/10/2012 6:28:55 PM This page intentionally left blank CHAPTER 11 Sleep disorders 418 Normal sleep: stages and cycles Sleep normally follows a typical pattern of stages and cycl es that can be objectively measured using electroencephalography (EEG; see Fig. 11.1).1,2 Non-REM (NREM) sleep stages3 N1 (light sleep) As wakefulness declines, posterior activit y (8 \200\22313Hz) disappears, with slow (4 \200\2237Hz) and (0.5 \200\2232Hz) activi ty emerging, plus occasional vertex waves. This stage lasts only a few minutes, but may rec ur brie \202 y during the night during sleep stage transitions or following body movements . Sudden twitches and hypnic jerks may be associated with the onset of sleep during N1. Hyp nagogic hallucinations may also be experi- enced during this stage. During N1, there is los s of some muscle tone and most conscious awareness of the external environment. N2 Characterized by sleep spindles (0.5s phases fast activity, maximal at the vertex) rangi ng from 11 to 16Hz (most commonly 12 \200\22314Hz) and K-complexes (symmetrical high-voltag e vertex waves) that arise both spon- taneously and in response to sudden stimuli. During t his stage, muscular activity as measured by EMG decreases, and conscious awareness of the e xternal environment disappears. This stage occupies 45 \200\22355% of total sleep in adults . This lasts 15 \200\22330min, followed by the gradual appearance of high- voltage waves (> 75 V) in the delta range in a semi-symmetrical distribution over both hemispheres occupyin g less than 20% of the EEG recording. N3 (deep or slow wave sleep [SWS]) De \201 ned by the presence of a mini- mum of 20% wa ves (0.5 \200\2232 Hz; peak-to-peak amplitude >75 V). This is the stage in which parasomni as such as night terrors, nocturnal enuresis, sleepwalking, and somniloquy occur. Other tex ts may still describe stage 3 sleep (S3) with 20 \200\22350% waves and stage 4 sleep (S4 ) with greater than 50% waves; these have of \201 cially been combined as stage N33. N3 lasts 30 \200\22345min, before reversion to N2. Theta waves N1 K complex Sleep spindle N2 N3 R Fig. 11.1 Sleep stages: characteristic EEG traces. 11_Semple_Chap11.indd 418 12/10/2012 6:28:55 PM NORMAL SLEEP: STAGES AND CYCLES 419 REM sleep (stage R) The end of the \201 rst sleep cycle is marked by a brief period of ar ousal before the onset of REM sleep. This has characteristic low-voltage, desyn- chronized EEG activity with associated muscle atonia (paralysis may be necessary to protect organisms from self-damage through physically acting out scenes from the often-vivid dreams that occ ur during this stage) and episodic rapid eye movements (REM). Occasional bursts of EMG acti vity (myoclonia) may be seen in association with the phasic eye movements. There are no sle ep spindles or K complexes and activity is rarely seen. Sleep cycles A typical night \200\231s sleep has 4 or 5 cycles of these sequential stages, each lasting 90 \200\223110min (see Fig. 11.2). As the night progresses, the amount of time spent in sleep decreases, with consequent increase in REM sleep. Hence, the \201 rst REM period may last 5 \200\22310min, while the last, just before waking, may last up to 40m in. Although the total amount of sleep needed varies between individuals and with age, tota l sleep time in adults is usually between 5 and 9hrs. Remarkably, REM sleep occupies 20 \200\22325% of the total sleep time in all ages. Awake Drowsy R N1 N2 N3 2300 0100 0300 Time 0500 0700 Fig. 11.2 Typical hypnogram. 1 Rechtschaffen A and Kales A (1968) A manual of standardized terminology, techniques and s coring system for sleep stages of human subjects. Washington, DC: US Government Printing Of \201 ce, Public Health Service. 2 Iber C, Ancoli-Israel S, Chesson A, et al. (eds) (2007) The AASM manual for the scoring of sleep and associated events: rules, terminology, and te chnical speci \201 cation. Westchester: American Academy of Sleep Medicine. 3 In 2007, the American Academy of Sleep Medicine (AASM) modi \201 ed the Rechtschaffen and Kales (R&K) standard guidelines for sleep classi \201 cation (1968). One of the major changes was a ch ange in terminology: in the AASM classi \201 cation, NREM sleep stages formerly called sta ge 1, 2, 3, and 4 (S1,S2,S3, S4) are referred to as N1, N2, and N3, with N3 re \202 ecting slow wave sleep (SWS, R&K stages S3 + S4); REM sleep is referred to as stage R. The new ma nual also clari \201 es the de \201 nition of the sleep \200\223wake transition, sleep sp indles, K-complexes, slow wave sleep, and REM sleep, as well as arousals and major body mov ements. 11_Semple_Chap11.indd 419 12/10/2012 6:28:57 PM CHAPTER 11 Sleep disorders 420 Assessment of sleep disorders Sleep history Always try to obtain a third-party account from the patient \200\231s bed partner, or from an informant such as a parent or carer. The mai n areas covered should include: \200 The presenting complaint(s): \200 \200 Onset, duration, course, frequency, severity, effects on everyday life. Pattern of symptoms , timing, \202 uctuations, exacerbating/relieving factors, environmental factors, relevan t current stressors. The usual daily routine: \200 \200 \200 Waking (time, method, e.g. alarm, natural), usual morning routine. Daily activities (start/ \201 nish times), any daily naps (when, duration). Bedtime (preparations for bed, time of going to bed, time of falling asleep, activities in bed, e.g. TV, reading, sex). Description of sleep: \200 \200 \200 \200 Daytime somnolence: \200 \200 Behavior whilst asleep. Dreams/nightmares. Episodes of wakening (and how they are dealed wi th). Quality and satisfaction with sleep. General level of alertness during the day. When/if sleep occurs (e.g. when active, mealtime s, walking, driving, operating machinery). Effects on work/social activities. Any periods o f confusion. Any episodes of collapse. \200 \200 Family history Past and current history of medical or psychiatric problems Drug and alcohol history \200 General review of regular medications (alerting/sedating effects), including timing of admi nistration. Speci \201 c questions regarding: caffeine-containing drinks (tea, coffee, sof t drinks), smoking, alcohol, other recreational drugs. Previous treatments \200 \200 Types of treatment tried. Bene \201 ts/problems/side-effects. Third-party/other information \200 \200 Breathing problems (snoring, gasping, choking, stopping breathing). Motor activity (muscle twitches, limb movements, unusual or complex behaviors, e.g. sleep-talking/sleepwalking/dre am enactment). Frequency of occurrence and any clear pattern. Any recent mood changes. Any recent change in use of drugs or alcohol. \200 \200 11_Semple_Chap11.indd 420 12/10/2012 6:28:57 PM ASSESSMENT OF SLEEP DISORDERS 421 Methods of further assessment Sleep diary To create a record of the sleep \200\223wake patt ern over a 2-wk period in order to clarify any pattern or particular factors that may be pr esent. Important information includes: daily activities, pattern of sleeping, mealtimes, co n- sumption of alcohol/caffeine/other drugs, exercise, and daytime sleepiness/ napping. Video recording A useful component of assessment, particularly for the parasomnias. Routine ly used in sleep laboratory studies; however, home videos of sleep-related behavior may be just as informative. Actigraphy A method of both quantifying circadian sleep \200\223wake patterns and identify- ing movement disorders occurring during sleep. Actigraphs incorporate a piezoelectric moti on sensor, often in a wristwatch-like unit, that collects data on movement over several day s, for later computer analysis. Indications Circadian rhythm sleep disorders, jet lag, pediatric sleep disorders, moni- tor ing leg movements (e.g. in \200\230restless leg syndrome \200\231 or periodic move- ments of sleep) or other movement disorders (e.g. Parkinsonian tremor). Polysomnography Detailed recording of a variety of physiological measures including EEG, el ectro-oculogram (EOG), and EMG. Other parameters may be added as required: ECG, respiratory monitoring (nasal/oral air \202 ow, diaphragm EMG), pulse oximetry, actigraphy, penile tu mescence, and oesophageal pH (for oesophageal re \202 ux). Audio and video recording help to assess nocturnal behaviors, vocalizations, and snoring. Time coding of all these measure s allows temporal correlations to be made of the various param- eters. In general, one nigh t of testing, followed by a daytime multiple sleep latency test (MSLT), is suf \201 cient to diagnose most conditions. Indications Hypersomnia (where common extrinsic causes, e.g. medication, shift work, have b een excluded; to diagnose suspected periodic limb movements of sleep, sleep apnoea, or narc olepsy), insomnia (where periodic limb move- ments of sleep or sleep apnoea are suspected a nd initial treatment has been ineffective), parasomnias (where the clinical history is uncl ear, initial treatment has been unsuccessful, and polysomnography is likely to aid the diag nosis, e.g. REM sleep behavior disorder or multiple parasomnias), to validate the accuracy of a sleep complaint (where a more objective measure is needed), to assess the bene \201 t s of treatment (e.g. continuous positive airway pressure [CPAP]), suspected nocturnal epile psy, serious cases of sleep-related violence. Multiple sleep latency test (MSLT) Devised to assess daytime somnolence, but also helps in identifying day- time REM sleep, for example in narcolepsy. The patient is put to bed at 2- h intervals starting at 8a.m. with the objective of measuring time to 11_Semple_Chap11.indd 421 12/10/2012 6:28:57 PM CHAPTER 11 Sleep disorders 422 sleep onset (sleep latency). In adults a mean sleep latency of 5min or less indicates a pat hological level of daytime somnolence; 5 \200\22310min is \200\230inde- terminate \200\231 but may re \202 ect a primary psychiatric disorder; over 10min is regarded as normal. The ICSD-2 suggests speci \201 c MSLT criteria for a diag- nosis of narcolepsy (see b p. 433) . 11_Semple_Chap11.indd 422 12/10/2012 6:28:57 PM This page intentionally left blank CHAPTER 11 Sleep disorders 424 Insomnia 1: overview Essence Persistent problems (at least 3 days/wk for 1mth) falling asle ep, maintain- ing sleep, or poor quality of sleep. Individuals are preoccupied and exces- s ively concerned with their sleep problems, distressed by them, and social or occupational f unctioning is affected. Insomnia may be primary \200\224caused by both extrinsic and intrin sic factors \200\224or secondary to medical or psychi- atric illness, other sleep disorders , or substance misuse. When it is dif \201 cult to determine the direction of the associat ion the term comorbid insomnia is preferred. Prevalence Common complaint (730% general population), 5 > 4, greater in the eld- erly. \200\230Clinically signi \201 cant insomnia \200\231 (causing marked personal distress or interference with social and occupational functioning) 9 \200\22312%. Primary causes (see Table 11.1) \200 Psychophysiological insomnia: with associated somatized tension anxiety: over-concern with inability to sleep, and learned sleep prevention. Paradoxical insomnia: also called \200 \230sleep state misperception \200\231: patient complains of little or no sleep without obj ective evidence of sleep disturbance. Adjustment sleep disorder: stress, con \202 ict, or environmental change, causing emotional arousal. Disorder usually resolves once the stresso r is no longer present. clinically signi \201 cant disruption of the normal Inadequate sle ep hygiene: sleep \200\223wake schedule due to a wide range of daily living activities (e.g . level of coffee consumption, frequent late nights) is inconsistent with the maintenance o f good-quality sleep and full daytime alertness. Understanding the contribution of each fac tor and taking steps to eliminate or minimize their effects usually sorts out the problem. Idiopathic insomnia: Behavioral insomnia of childhood: \200 dif \201 culty initiating and maintaining sleep, sleep disturbance temporally related to \200 Rare, lifelong inability to sleep adequately. includes two common subtypes: \200\224estimated prevalence 5 \200\22310% in children, Limi t-setting sleep disorder characterized by inadequate enforcement of bedtimes by a caregiver , with resultant stalling or refusal to go to bed at an appropriate time. Sleep-onset assoc iation disorder \200\224occurring mainly in children aged 6mths to 3yrs, sleep onset is im paired by the absence of a certain object (e.g. favorite toy) or set of circumstances (spec i \201 c routine, TV, night-light). Less commonly: childhood problem (prevalence 5% in chi ldren aged 6mths to 3yrs), with marked decrease after weaning, characterized by recurrent a wakenings and inability to return to sleep without eating or drinking. nocturnal eating (drinking) syndrome \200\224primarily a Other sleep disorders: \200 Environmental sleep disorder due to disturbing environmental factor(s) (e.g. heat, cold, no ise, \200\224common transient sleep disturbance 11_Semple_Chap11.indd 424 12/10/2012 6:28:57 PM INSOMNIA 1: OVERVIEW 425 light, excessive movement of bed partner, danger, allergens, hospitalization, unfamiliar su rroundings) leading to insomnia or excessive sleepiness. Altitude insomnia \200\224unusual form of acute insomnia, accompanied by headaches, loss of appetite, and fatigue, occuring at high altitudes in the absence of administered oxygen. Seen in 25% of individuals who asc end above 2000m above sea level, and in most individuals above 4000m. Food allergy insomnia sleep due to an allergic response to food allergens. \200\224a rare disorder of initiating and maintaining Secondary or comorbid causes \200 Sleep disorders classi \201 ed elsewhere: (b p. 428); circadian rhythm disorders (b p. 436); sleep-related movement disorders (b p. 450). Insomni a due to medical condition: headache), respiratory disorders (COPD, cystic \201 brosis, a sthma), diabetes, Parkinson \200\231s disease, endocrine disorders (Addison \200\231s disea se, Cushing \200\231s syndrome). Insomnia due to mental disorder Drugs and alcohol SSRIs, v enlafaxine, reboxetine); anti-Parkinsonian medication; bronchodilators (e.g. aminophylline, theophylline, pseudoephedrine); cardiovascular medication (e.g. -blockers, clonidine, hi gh-dose digoxin, verapamil); chemotherapy agents; corticosteroids/anabolic steroids; NSAIDs (high-dose); stimulants (e.g. dexamfetamine methylphenidate, amfetamine cocaine, caffeine, nicotine); levothyroxine withdrawal/ dependency (e.g. hypnotics, opiates, alcohol, or cann abis). sleep-related breathing disorders pain (arthritis, peptic ulcer, \200 (see b pp. 454 \200\2237). (see also b p. 458). Antidepressants (e.g. MAOIs, Table 11.1 Classi \201 cation of insomnia with diagnostic codes ICSD-2 ICD-10 DSM-IV-TR Psychophysiological insomnia F51.04 307.42 Paradoxical insomnia F51.03 307.42 Adjustment insomnia F51.02 307.42 Inadequate sleep hygiene Z72.821 307.42 Idiopathic F51.01 307.42 Insomnia due to mental disorder F51.05 327.02 Behavioral insomnia of childhood Z73.81 307.42 Insomnia due to a medical condition G47.09 327.01 Insomnia due to a drug or substance F11 \200\22319.x 291.85 Insomnia due to alcohol F10.x 291.82 Physiological (organic) insomnia, unspeci \201 ed G47.00 Insomnia not due to a substance or known physiological condition, unspeci \201 ed F51.09 11_Semple_Chap11.indd 425 12/10/2012 6:28:57 PM CHAPTER 11 Sleep disorders 426 Insomnia 2: general management strategies Education about sleep Many myths surround sleep and the clinician should be able to educate the patient about the stages of sleep, sleep cycles, changes in sleep patterns with age, a nd the nature of the particular sleep problem or disorder the patient presents with. Sleep hygiene Establishing good sleep habits Control environmental factors (noise, light, t emperature); \200\230wind down \200\231 time (71hr) before going to bed: distract from the day \200\231s stresses (reading, watching television, listening to music, having a warm ba th); avoidance of caffeine-containing drinks after about 16.00hr; not smoking for at least 1 hr before bed; regular exercise (not late at night); late \200\230tryptophan \200\231 sn ack (warm milk or other milky drink); avoid naps during the day (or con \201 ne naps to th e early afternoon, not longer than 740min); set aside time during the day to re \202 ect o n problems and stresses. Stimulus control Go to bed only when sleepy; avoid other activities (with the exception of sex) whilst in bed; if sleep does not occur, do not remain in bed for more than 10 \200\223 20min, get up and go to another room (without turning on all the lights), returning to bed only when sleepy; establish a regular time to get up, with no more than 1hr variation (even at weekends and during holidays). Relaxation training The regular practice of relaxation t echniques during the day (particularly progressive relaxation) may help to provide patients with the means to reduce general arousal, which can be used if necessary whilst in bed. Sleep restriction When sleep is fragmented, a sleep restriction strategy may help to reduce total time spent in bed and improve quality of sleep by \200\230consolidation \200\231. T here are a number of steps to sleep restriction, and to complete the program does require m otivation and encouragement (see Box 11.2). Medication Despite prevailing public perception that insomnia is best treated by use of a s leeping tablet \200\224prescribing should be last option, rather than \201 rst. Before a hypnotic is prescribed, cause of insomnia should be estab- lished, possible underlying fact ors addressed, and any primary medical or psychiatric disorder effectively treated. Should only be used to treat insomnia when it is severe, disabling, or subjects individual to extr eme distress. Ideally, hypnotics should be short-term adjuncts to other forms of therapy an d avoid prolonged administration. Interrupted courses (i.e. 5 nights with medication, 2 wit hout) for no more than 4wks may help avoid tolerance and reduce \200\230rebound insomnia \200\231 often accompanying ces- sation. Choices (see Table 11.2) include: benzodiazepines, the \200\230Z-drugs \200\231 11_Semple_Chap11.indd 426 12/10/2012 6:28:57 PM INSOMNIA 2: GENERAL MANAGEMENT STRATEGIES 427 (zopiclone, zolpidem, zapeplon \200\224usually \201 rst line), chloral hydrate, sedat- in g antidepressants (e.g. trazodone, mirtazapine), sedating antipsychotic, and possibly melat onin agonists. Box 11.2 Sleep restriction \200 