Linked to frightening dream RSBD Wake/REM Acting out of dreams Linked to dream content Nocturnal paroxysmal dystonia All sleep stages (esp. N2) Bipedal automatisms, twisting of trunk/pelvis, vocalizations, posturing of head/limbs Accidental or related to hyperkinetic features Epileptic nocturnal wandering All sleep stages (esp. N2) Like sleepwalking, but more directed violence possible Accidental or when approached/ restrained Confusional states Awake Variable Variable Dissociative disorder Awake or wake/sleep Variable, frequently wandering, amnesia Self-harm, thrashing, assaults Malingering Awake Variable (evident primary or secondary gain) Variable 1 Mahowald MW, Bundlie SR, Hurwitz TD, et al. (1990) Sleep violence \200\224forensic scienc e impli- cations: polygraphic and video documentation. J Forensic Sci 35: 413 \200\22332. 1 Howell MJ, Schenck CH, and Crow SJ (2009) A review of nighttime eating disorders. Sleep M ed Rev 13: 23 \200\22334. 2 Schenck CH, Milner DM, Hurwitz TD, et al. (1989) Dissociative d isorders presenting as som- nambulism: polysomnographic, video and clinical documentation ( 8 cases). Dissociation 2: 194 \200\223204. 3 Rice E and Fisher C (1976) Fugue states in sle ep and wakefulness: a psychophysiological study. J Nerv Ment Dis 163: 79 \200\22387. 4 Sicl ari F, Khatami R, Urbaniok F, et al. (2010) Violence in sleep. Brain 133: 3494 \200\223509. 11_Semple_Chap11.indd 449 12/10/2012 6:29:02 PM CHAPTER 11 Sleep disorders 450 Sleep-related movement disorders Essence Usually relatively simple, stereotyped movements disturbing sleep, and causing inso mnia and EDS (see Table 11.9). Can also be a cause of sleep-related violence (see b p. 449) and lead to harm to self or others. Restless legs syndrome (Ekbom \200\231s syndrome)1 Unpleasant, often painful sensations in the legs, particularly on sleep onset. Signi \201 cantly interferes with the ability to ge t to sleep. Usually idiopathic or familial. Exacerbated by caffeine, fatigue, or stress. \200 \200 10% general population, 4 = 5, greater in the elderly. PLMS, pregnancy, uraemia, rheumatoi d arthritis, iron Prevalence: Associations: de \201 ciency anemia, folate de \201 ciency, hypothyroidism, p oliomyelitis, peripheral neuropathy (e.g. diabetes), chronic myelopathy, Parkinson \200\231 s disease, drug-related (e.g. antidepressants; phenothiazines; lithium; Ca2+ channel blocke rs; withdrawal from barbiturates, other sedatives and opiates). Differential diagnosis: Inv estigations: (polysomnography rarely needed). Management: General \200 or stimulation of the legs (rubbing, squeezing, hot showers, hot packs, ointments). Medication \200\224possi ble agents include: clonazepam, cabergoline, levodopa, ropinirole, rotigotine (patch), pram ipexole, opiates (oxycodone), clonidine, gabapentin (possibly other anti-epileptics), eithe r alone or in combination. \200 antipsychotic-induced akathisia, ADHD. full history, examination, routine blood tests \200\224treat any secondary causes. Movement (walking, stamping) Periodic limb movement (in sleep) disorder (PLMS)1 Periodic episodes of repetitive, stereot yped limb movements. Rare in children, common in over 60s (734%). May be a feature in up to 15% of patients with insomnia. Movements usually reported by bed partner. Associated dayti me somnolence. Polysomnography may aid diagnosis. \200 sleep starts (b p. 452), drug-related exacerbation Differential diagnosis: (e.g. TCAs, lithium). Management: levodopa. reassurance, remove exacerbating factors, clonazepam, Sleep-related leg cramps Sensations of painful muscular tightness or tension, in the calf ( or the foot), occurring during sleep, which awaken the sufferer. \200 Prevalence: elderly. Associated problems: arthritis, pregnancy, and Parkinson \200\231s dis ease. Differential diagnosis: following stroke, other neurological causes of muscle spastic ity. up to 16% of healthy individuals, more common in the excessive muscular activity, dehydration, diabetes, PLMS (painless), muscle spasm due to spasticity 11_Semple_Chap11.indd 450 12/10/2012 6:29:02 PM SLEEP-RELATED MOVEMENT DISORDERS 451 Management: muscle stretching; quinine sulfate (300mg nocte). only for severe, recurrent symptoms \200\224heat, massage, Sleep-related bruxism Clenching and grinding of the teeth during sleep that can result in a rousals. The activity may be severe or frequent enough to result in symptoms of temporomand ibular joint pain, wearing down of the teeth, or severe injury to the tongue and mouth. \200 Management factors, occlusal splints/night-time bite guard, use of clonazepam. General sleep hygiene measures, removal of exacerbating Sleep-related rhythmic movement disorder Stereotyped, repetitive movements involving large muscles, usually head and neck, typically immediately prior to sleep, sustained into light sleep. Common forms: head banging (jactatio capitis nocturna), head rolling, body rocking \200\224 movements may result in head injury. \200 Polysomnography: sleep, without evidence of epileptiform activity. Prevalence: (25% at 18mt hs, 8% at 4yrs). More frequent in boys. Associated problems: children). Management: in the majority of infants the disorder will resolve by around the age of 18 months. If injury or social disruption occurs, medication may be used (e.g. low-dose BDZ or antidepressant). rhythmic movement artifacts during light non-REM common in young children (60% at 9mths), decline with age developmental problems/psychopathology (older unnecessary in most cases. Parents can be reassured that Table 11.9 Classi \201 cation of sleep-related movement disorders with diagnostic codes ICSD-2 ICD-10 DSM-IV-TR Restless legs syndrome G25.81 Periodic limb movement disorder G47.61 Sleep-related leg cramps G47.62 Sleep-related bruxism G47.63 Sleep-related rhythmic movement disorder G47.69 Other sleep-related movement disorder, unspeci \201 ed G47.60 Sleep-related rhythmic movement disorder due to a drug or substance F10 \200\22319 292.85 Sleep-related rhythmic movement disorder due to a medical condition 1 Vignatelli L, Billiard M, Clarenbach P, et al. (2006) EFNS guidelines on management of re stless legs syndrome and periodic limb movement disorder in sleep. Eur J Neurol 13: 1049 \200\22365. 11_Semple_Chap11.indd 451 12/10/2012 6:29:02 PM CHAPTER 11 Sleep disorders 452 Isolated symptoms, apparently normal variants, and unresolved issues Essence Conditions that sit on the borderline between normal and abnormal sleep (see Table 11.10). Rarely pathological, they may nonetheless become a focus of anxiety and a reason fo r consultation. Long sleeper Sleep is normal in architecture and quality, but lasts longer than normal (i.e . >10hrs). The person may complain of EDS if they do not get their usual amount of sleep. Short sleeper Someone who requires 5hrs or less of sleep/day. In children, short sleepers n eed 73hrs less than the norm for their age. Snoring Respiratory sounds that are disturbing to the patient, bed partner, or others, but not associated with either insomnia, EDS, or other sleep disorder (e.g. OSA). Sleep-talking (somniloquy) The common uttering of words or sounds during sleep, without sub jective awareness, and speech generally devoid of meaning. Rarely, emotionally charged long \200\230tirades \200\231 occur with content related to the person \200\231s occupa- tion or preoccupation. \200 brief partial arousal during non-REM sleep is usually Polysomnogra phy: seen on EEG in about 60% of cases. Less commonly, somniloquy may occur during REM slee p, if related to dream content or in association with another disorder of REM sleep. Associ ated disorders: related eating disorder. unless the problem is leading to disruption of sle ep in Management: a bed partner, or is a secondary symptom of other sleep pathology, treatm ent is rarely necessary. confusional arousals, sleep terrors, RSBD, sleep- Sleep starts (hypnic jerks) Occur at sleep onset and present as sudden abrupt contractions of muscle groups, usually the legs, but sometimes also involving the arms, neck, or even th e entire body. When wakened by jerks, an individual may have the feeling of falling in spac e ( \200\230siderealism \200\231). Sometimes this feeling is so intense and frightening tha t it can lead to fear of going to sleep with subsequent sleep-onset dif \201 culties. \200 Polysomnography: contraction. Prevalence: onset process). Differential diagnosis: epi leptiform activity on EEG), fragmentary myoclonus (during non-REM sleep), nocturnal leg myo clonus/PLMS (often associated with restless legs syndrome), and the rare \200\230startle d isease \200\231 or \200\230hyperekplexia \200\231. occasional vertex waves, associated with muscular 60 \200\22370% (essentially a universal component of the sleep- nocturnal myoclonic jerks (with evident 11_Semple_Chap11.indd 452 12/10/2012 6:29:02 PM ISOLATED SYMPTOMS, NORMAL VARIANTS, AND UNRESOLVED ISSUES 453 syndrome (myoclonus occurs following minor stimuli both during wakefulness and sleep). Mana gement: interference with sleep \200\224general measures (e.g. avoidance of stimulants such as caffeine, nicotine) or low-dose clonazepam at night. treatment usually unnecessary. If there is signi \201 cant Benign sleep myoclonus of infancy A disorder of myoclonic jerks that occur during sleep in infants, typically from birth to 6mths, resolving spontaneously. Hypnagogic leg muscle foot tremor and alternating activation Occurs at the transition betwe en wake and sleep or during light NREM sleep. PSG shows recurrent EMG potentials in one or both feet that are longer than the myoclonic range (>250ms). Propriospinal myoclonus at sleep onset Recurrent sudden muscular jerks in the transition fr om wakefulness to sleep, which may be associated with severe sleep-onset insomnia. Excessive fragmentary myoclonus Small muscle twitches in the \201 ngers, toes, or corner of the mouth that do not cause actual movements across a joint. Often an incidental \201 nding during PSG. Usually asymptomatic, but sometimes associated with EDS or fatigue. Table 11.10 Isolated symptoms, apparently normal variants, and unresolved issues with diagn ostic codes ICSD-2 ICD-10 DSM-IV-TR Long sleeper R29.81 307.47 Short sleeper R29.81 307.47 Snoring R06.5 Sleep-talking R29.81 Sleep starts, hypnic jerks R25.8 Benign sleep myoclonus of infancy R25.8 Hypnagogic foot tremor and alternating leg muscle activation R25.8 Propriospinal myoclonus at sleep onset R25.8 307.47 Excessive fragmentary myoclonus R25.8 307.47 11_Semple_Chap11.indd 453 12/10/2012 6:29:03 PM CHAPTER 11 Sleep disorders 454 Sleep disorders related to psychiatric disorders 1 Although unusual for psychiatric patient s to present with a p sleep disor- der, it is not uncommon for psychiatrists to have to dea l with secondary problems of insomnia (not getting enough sleep or feeling \200\230unrefre shed \200\231) or hypersomnia (feeling excessively sleepy during the day or sleeping too mu ch), in the context of a p psychiatric disorder, or as a consequence of medication. Equally , sleep deprivation may have its own psychological con- sequences, or may precipitate the o nset of a psychiatric illness, particularly a manic episode. Major affective disorders Alterations in sleep are central symptoms in the mood disorders. Initial insomnia, frequent waking (for often prolonged periods), early morning waking, vivi d or disturbing dreams, and daytime fatigue are frequently seen in major depressive disorde r. These features are associated with changes in sleep architecture: shortened REM sleep-on set latency, increased REM density, reduced total sleep time, reduced sleep ef \201 ciency , increased awakenings, decreased N3 sleep (SWS), and a shift of N3 from the \201 rst NRE M cycle to the second. Occasionally, hypersomnia may be a feature in atypical cases, bipola r affective disorder, and seasonal affective disor- der. Episodes of mania may be character ized by marked insomnia and a decreased need for sleep associated with a much reduced total sleep time, reduction in N3 sleep and no consistent change in REM sleep. Management \200 \200 Treat the primary disorder. Initial insomnia trazodone, nefazodone, mirtazapine, agomelatin e). Hypersomnia bupropion, MAOI, RIMA). : use a more sedating antidepressant (e.g. TCA, : use a more \200\230activating \200\231 antidepressant (SSRI, reboxetine, Note: most antidepressants are REM-suppressant and may exacerbate underlying primary sleep disorders (e.g. parasomnias and sleep-related movement disorders) either on commencement or cessation. Anxiety disorders Anxiety disorders commonly disrupt the normal sleep pattern leading to in somnia, which may be triggered by an acute stressful event. Symptoms include: initial insom nia, frequent waking, reduced total sleep time, and early morning waking. Generalized anxiety Typically prolonged sleep-onset latency, increased stages N1 and N2, le ss N3, a smaller percentage REM, and increased or normal REM sleep latency. Panic disorder Sleep-related (nocturnal) attacks may occur with associated intense fear, fe elings of impending doom, autonomic arousal, somatic symptoms, and fear of going to sleep ( leading to avoidance behavior, which may present as \200\230insomnia \200\231), see b p. 4 43. As many as 70% of patients with 11_Semple_Chap11.indd 454 12/10/2012 6:29:03 PM SLEEP DISORDERS RELATED TO PSYCHIATRIC DISORDERS 1 455 panic disorder have dif \201 culty with sleep-onset and maintenance insomnia, and often re port sleep paralysis and hypnagogic hallucinations. Studies in non-depressed patients with panic disorder report normal sleep-onset latency and modestly reduced total sleep time and sleep. However, stud- ies in patients with panic and comorbid major depression have report features typical of major depression, with substantially prolonged sleep onset latency, red uced total sleep time, sleep disruption, reduced N3, and early REM sleep onset. PTSD Sleep complaints almost universal in individuals diagnosed with PTSD; indeed, recurren t distressing dreams related to a traumatic event are a core feature of the disorder. Compl aints include: nightmares, dif \201 cul- ties initiating and/or maintaining sleep (in 70 \200\22390%), sleep paralysis, RSBD. Sleep disturbance soon after the traumatic event is a risk factor for PTSD and more severe sleep symptoms in PTSD are associated with depression severity, suicidal tendencies, anxiety, and substance use. Studies report increased sleep-o nset latency, decreased sleep ef \201 ciency, increased wake- fulness after sleep onset, d ecreased total sleep time, reduction in N2 sleep, increased N1 sleep, and variable effects on REM (normal parameters vs. reduced REM latency and increased REM density). Social phobia Increased sleep-onset latency, awakening after sleep onset, and reduced total sleep time. OCD Sleep can become restricted due to engagement in compulsive behaviors. Sleep studies sh ow decreased total sleep time, increased awakenings, shortened REM latency, reduced N3 slee p, and reduced sleep ef \201 ciency. Management \200 Treatment of the primary anxiety disorder will generally improve the patient \200\231s abil ity to initiate and sustain sleep. Most anxiolytics tend to be sedating, and it is usual to prescribe a higher dose at night. When less sedating drugs such as the SSRIs are used, add itional treatment may be necessary to target persistent sleep problems (e.g. cognitive beha vioral techniques, short-term use of hypnotics, or a small dose of a more sedating antidepr essant at bedtime). Behavioral sleep interventions are effective in reducing night-time sym ptoms in PTSD, e.g. imagery rehearsal for chronic nightmares, stimulus control/sleep restri ction for insomnia (see b p. 427). Prazosin, an promising treatment of PTSD-related sleep d isturbance, including both nightmares and insomnia symptoms. 1-adrenergic receptor antagonist, has emerged as a Borderline PD Sleep architecture changes very similar to those seen in depresssion: reduced total sleep time, reduced sleep ef \201 ciency, reduced N3, increased N2, reduced REM lat ency, and increased REM density. 11_Semple_Chap11.indd 455 12/10/2012 6:29:03 PM CHAPTER 11 Sleep disorders 456 Sleep disorders related to psychiatric disorders 2 Schizophrenia Patients with schizophreni a demonstrate increased nocturnal wakeful- ness and daytime somnolence. PSG shows sleep con tinuity disturbance, reduced N3, decreased REM latency, and increased REM sleep. It is ofte n dif \201 cult to disentangle the effects of medication, active positive symptoms, persis tent negative symptoms, and disorganized behavior and some stud- ies show relatively little change in sleep. Research has suggested an inverse relationship between SWS (N3)/sleep mai ntenance and brain ventricle size/negative symptoms in schizophrenia. Management \200 EDS dosage. Insomnia behavioral approach when \200\230disorganization \200\231 is central feature; judicious use of hypnotics or higher dose of sedating antipsychotic nocte. : monitor effects of antipsychotic medication; adjust timing and : general sleep hygiene measures, with emphasis on Eating disorders Patients with bulimia may report EDS, but sleep studies show very little c hange in sleep parameters. Studies in anorexia nervosa have been more contradictory due per haps to the high rates of comorbidity with affective disorders and frequent family history of affective disorders in anorexia patients (hence, PSG similar to depression). In severe o r untreated cases of anorexia nervosa, insomnia and frequent waking very common. Sleep stud - ies show reduced total sleep time, decreased sleep ef \201 ciency, increased wakefulness after sleep onset, shortened REM latency, increased N1, and decreased N3 sleep, which norm alize after weight is gained. Management \200 Treatment of the primary eating disorder to establish better eating behaviors and re-establ ish normal BMI. General principles for insomnia and EDS (see Possible use of SSRI or altern ative antidepressant. \200 b p. 426). Dementia Normal ageing is associated with increased sleep latency, reduced total sleep time , loss of NREM sleep, frequent arousals leading to fragmentation of nocturnal sleep, and an increase in daytime napping. \200 Some sleep disorders (e.g. sleep apnoea syndromes, PLMS) occur more frequently in the elder ly population. Dementia generally causes further increases in sleep latency, further reduct ions in total sleep time, and increased fragmentation of nocturnal sleep, in proportion to the severity of the illness. Disorders of normal circadian rhythm are also commonly seen, w ith a characteristic \200\230sundown syndrome \200\231 of confusion and agitation at bedti me (nocturnal agitated wandering). 11_Semple_Chap11.indd 456 12/10/2012 6:29:03 PM SLEEP DISORDERS RELATED TO PSYCHIATRIC DISORDERS 2 457 Management \200 General sleep hygiene measures (with an emphasis on establishing and reinforcing a normal 2 4-hr circadian cycle through the use of environmental cues, daily routine, avoidance of day time napping, and regular activities). \200\230Sundown syndrome \200\231 may respond to lo w-dose antipsychotics (e.g. haloperidol, risperidone) or antidepressants (e.g. trazodone). Alcohol use Alcohol most probably exerts its sedative effects through a combination of GABA facilitation and glutamate inhibition. The acute effects of alco- hol lead to reduced slee p latency, increased total sleep time, increased N3, mild suppression of REM sleep in \201 rst half of the night, and subse- quent increased REM sleep in second half, associated with sleep disrup- tion, intense dreaming, and even nightmares. Chronic effects of alcohol abuse include the loss of N3, sleep disruption, and signi \201 cant insomnia. Withdrawal from alcohol is also associated with insomnia. Sleep architec- ture is disrupted, with incr eased sleep latency, reduced total sleep time, loss of N3, increased REM density and/or amo unt. \200\230Delirium tremens \200\231, with marked agitation, confusion, and hallucinatio ns, is characterized by intense REM rebound. Use of other recreational drugs \200 Nicotine: with sleep disruption and increased REM sleep. Use of nicotine patches has been a ssociated with vivid dreams and nightmares. Cannabis: Appear to be similar to the effects o f benzodiazepines and alcohol, increasing NREM and suppressing REM sleep. Cessation may lea d to problems of initial insomnia, sleep disruption and REM rebound. Opiates: therapeutical ly for pain relief or in the treatment of restless legs, misuse is associated with generali zed sleep disruption. Changes in sleep architecture include decrease in sleep ef \201 cien cy, total sleep time, N3, and REM sleep. Withdrawal symptoms include insomnia, with fragmen tation of sleep and disruption of normal sleep architecture, related to increased arousal a nd REM rebound. Stimulants: REM sleep, and increased sleep and REM latency. Xanthines (caff eine, theophylline) have similar effects, acting through adenosine receptors, directly inte rfering with the generation of sleep. Amfetamine derivatives, e.g. fen \202 uramine and MD MA (ecstasy) have a pharmacological action that is primarily serotonergic which may lead to both daytime sedation and disturbed sleep (due to periods of drowsiness and wakefulness), as well as a reduced duration of REM sleep. SWS may be increased during the withdrawal phas e as a rebound phenomenon. this tends to cause initial insomnia, and may be associated hypnotic effects modulated by cannabinoid-1 receptors. although sleep is improved when opiates are used the effects of amfetamine and cocaine include reduced 11_Semple_Chap11.indd 457 12/10/2012 6:29:03 PM CHAPTER 11 Sleep disorders 458 Psychiatric medication and sleep Antidepressants Sedating \200 TCAs are usually sedative due to their anticholinergic effects. Amitriptyline, trimipramine , doxepin, imipramine, clomipramine are the most sedating and nortriptyline is the least se dating. Tetracyclic antidepressants (mianserin) and trazodone also have marked sedating pro perties, although these are less related to their anticholinergic properties and may be due to their 5-HT2 and histamine antagonism \200\224properties shared by some of the newer ant idepressants (e.g. mirtazapine) Agomelatine may promote sleep through melatonin (MT1/MT2) a gonism. Alerting MAOIs, SSRIs, NARIs (reboxetine), DARIs (bupropion), SNRIs (venlafax- ine, duloxet ine) all tend to have alerting effects which may be useful in the treatment of hypersomnole nce associated with \200\230atypical \200\231 depression, and should be taken in the morni ng or early afternoon. Antipsychotic drugs Most antipsychotics cause drowsiness and impaired performance. There is a great degree of variability even within groups of antipsychotics (see Table 11.11). Table 11.11 Sedative effects of antipsychotics Marked sedation Moderate sedation Mild sedation Minimal sedation Chlorpromazine Asenapine Flupentixol Amisulpiride Clozapine Benperidol Haloperidol Aripiprazole Levomepromazine Droperidol Paliperidone Pericyazine Fluphenazine Pimozide Loxapine Pipotiazine Olanzapine Quetiapine Perphenazine Risperidone Promazine Sulpiride Thioridazine Tri \202 uoperazine Zuclopenthixol Mood-stabilizing drugs \200 \200 Lithium: Carbamazepine: dose is being increased, but this is usually a transient effect. So dium valproate: mildly sedating (increasing N3 and reducing REM). may cause drowsiness at start of treatment or when mild effects on sleep \200\224less than carbamazepine. 11_Semple_Chap11.indd 458 12/10/2012 6:29:03 PM PSYCHIATRIC MEDICATION AND SLEEP 459 Benzodiazepines and associated hypnotics By de \201 nition, BDZs and barbiturates are seda ting. Problems arise due to withdrawal insomnia on discontinuation, tolerance to the bene \201 cial hyp- notic effects after long-term use, and problems of dependence Newer hypnotic s, such as the z-drugs, share the sleep-enhancing properties of the benzodiazepines, but ma y be less likely to cause rebound or dependence (see Table 11.12). Table 11.12 Polysomnographic (PSG) effects of hypnotics Drug Acute effects Withdrawal \206\221TST, N2, spindles \206\223WASO, REM \206\224 \206 \221TST, N2, spindles \206\223SL, WASO, REM, Comments \206\223TST Barbiturates Rapid development of tolerance, withdrawal insomnia, daytime sedation \206\223TST BDZs Wide variation in onset and duration of action (see Table 11.2, b p. 427) Long Thalf : EDS Short Thalf : tolerance, withdrawal insomnia \206\221TST \206\223SL \206\224 , REM \206\224 or \206\221 WASO Z-drugs No typical alteration of sleep architecture or withdrawal effects BDZ = benzodiazepine; TST = total sleep time; WASO = waking after sleep onset; SL = sleep l atency; = N3/slow wave sleep; EDS = excessive daytime somnolence Psychostimulant drugs Although very useful in the treatment of hypersomnia (particularly in nar- colepsy), ADHD, and to suppress appetite, this group of drugs all tend to cause insom nia with fragmented sleep due to frequent awakenings (e.g. dexamfetamine, methylphenidate, methamfetamine, mazindol, pemoline, and moda \201 nil) and should not be taken in the even ing. Cessation, with the notable exception of moda \201 nil, leads to increases in total s leep time and REM rebound. 11_Semple_Chap11.indd 459 12/10/2012 6:29:04 PM This page intentionally left blank 461 Chapter 12 Reproductive psychiatry, sexual dysfunction, and sexuality Introduction 462 Menstrual-related disorders 464 Premenstrual disorders 466 Disorders assoc iated with pregnancy 468 Disorders related to childbirth 470 Sexual dysfunction 1: general principles 472 Sexual dysfunction 2: problems common to men and women 474 Sexual dysfunction 3: problems speci \201 c to women 476 Sexual dysfunction 4: problems sp eci \201 c to men 478 Disorders of sexual preference 1: general aspects 480 Disorders of s exual preference 2: assessment and management 482 Transsexualism 1: diagnosis 484 Transsexualism 2: management 486 12_Semple_Chap12.indd 461 12/7/2012 3:42:30 PM CHAPTER 12 Reproductive psychiatry and sexuality 462 Introduction Of necessity this chapter is an amalgam of a number of areas in psychiatry tha t overlap but which are important subspecialties in themselves. They intersect with other m edical specialties including gynecology, obstetrics, urology, and general practice. Most se rvices will be integrated with their medical counterparts as the assessment process necessi tates a more holistic approach, even to the point where psychiatrists are employed in obste tric departments and offer a perinatal service for pregnant and post- partum women. It is t rue to say that research has formerly focused more on female reproductive psychiatry. This does not mean that men do not have their share of problems in this area, rather that the re search base is relatively lacking at this point in time. Mental health problems can arise at various milestones in an individual \200\231s physiolog ical, psychological, and social development. It is important to include issues relating to normal physiological changes, hormonal factors, sexual orientation and its expression, and sexual function when consider- ing associated predisposing, precipitating, and perpetuating factors. Other important considerations relate to side-effects and risks of the medications we presc ribe for the treatment of mental disorders. These are covered in the therapeutic section of this Handbook \200\224e.g. prescribing during pregnancy (b p. 968), prescribing during lac tation (b p. 970). It is also vital that psychiatrists are involved in assessing the presence or absence of ps ychiatric disorder when it comes to major life decisions, such as those generated by disord ers of gender identity (b p. 484). The taboo associated with many of the topics covered in this section, even in the twenty- \201 rst century (and despite \200\224or perhaps because \200\224of the popular media) means that psychiatrists will often have an educative role. There are still many myths that need to be dispelled. Equally, many psychiatrists have neither the theoretical framework nor the experience to de al competently with reproductive or sexual issues. Whilst this text can serve as an introdu ction to the topic and offers some signposts to management, there is no substitute for seek ing expert advice when confronted with complex problems. 12_Semple_Chap12.indd 462 12/7/2012 3:42:30 PM This page intentionally left blank CHAPTER 12 Reproductive psychiatry and sexuality 464 Menstrual-related disorders Premenstrual symptoms Characteristic physical signs and symptom s affect up to three-quarters of women with regular menstrual cycles. The most common prese ntations are abdominal bloating (present in 90% of women with any symptoms), breast tendern ess, and headaches. These mild symptoms do not usually interfere with a woman \200\231s abi lity to function. Management Premenstrual symptoms that do not meet premenstrual syndrome (PMS) or premenstru al dysphoric disorder (PMDD) criteria are initially managed conservatively unless there is signi \201 cant psychiatric comorbidity. This management involves a diet low in salt, fat, caffeine, and sugar; restric- tion of alcohol and tobacco; exercise; and measures to reduc e stress. If there is failure to adequately respond to conservative management after 2 \200 \2233mths, a trial of an SSRI may be considered. Premenstrual syndrome (PMS) or tension (PMT) For further details see b p. 466. Clinically s igni \201 cant PMS occurs in 20 \200\22330% of women with severe impair- ment, in about 5% including associated premenstrual dysphoric disorder (PMDD). PMS is characterized by the p resence of both physical and behav- ioural symptoms that recur in the second half of the me nstrual cycle, and often the \201 rst few days of menses. Most common behavioral symptoms are fatigue, labile mood, irritability, tension, depressed mood, increased appetite, forge tfulness, and dif \201 culty concentrating (see Table 12.1). These symptoms must be severe enough to impair the patient \200\231s social and occupa- tional functioning. Most common criteria used: University of California San Diego (UCSD) criteria for PMS.1 Women with PMS have a higher incidence of affective and anxiety disorders and are at greater risk of havin g them in the future. The reason for this correlation is not yet known. Premenstrual dyphoric disorder (PMDD) For further details see b p. 466. PMDD is a research diagnosis in DSM-IV (coded as depressive disorder NOS) distinguished from PMS by the promin ent presence of one or more marked affective symptoms: notably depressed mood, anxiety, aff ective lability, and/or irritability or anger. PMDD occurs in 2 \200\2238% of women with re gular menstrual cycles. There is no evidence for cultural, ethnic, or socio-economic differ ences in prevalence. Note: the criteria require behavioral symptoms only; the presence of physical symptoms is n ot required. PMDD may occur in the presence of other psychiatric disorders if it is not an exacerbation of these disorders. Menopausal disorders There is an increased incidence of anxiety and depression in peri- or post- menopausal women. This is not related directly to hormonal changes. Rather, patients presenting with mood-related problems around the men- opause experience coincident psychoso cial stressors,2 and the changes in gonadal hormones may exacerbate pre-existing mood disor ders.3 12_Semple_Chap12.indd 464 12/7/2012 3:42:30 PM MENSTRUAL-RELATED DISORDERS 465 Assessment Exclude other causes of mood disturbance. Particular attention should be paid to past psychiatric history and current social history. Management Evidence for HRT is inconclusive, although if mood symptoms are secondary to phy sical symptoms this may have a role (HRT may also augment effects of antidepressants).4 Tre atment is with standard approaches for depression/anxiety. Table 12.1 Frequency of premenstrual symptoms1 Symptom Frequency, % of cycles Fatigue 92 Irritability 91 Bloating 90 Anxiety and/or tension 89 Breast tenderness 85 Mood lability 81 Depression 80 Food cravings 78 Acne 71 Increased appetite 70 Oversensitivity 69 Swelling 67 Expressed anger 67 Crying easily 65 Feeling of isolation 65 Headache 60 Forgetfulness 56 Gastrointestinal symptoms 48 Poor concentration 47 Hot \202 ushes 18 Heart palpitations 14 Dizziness 14 1Mortola JF, Girton L, Beck L, et al. (1990) Diagnosis of premenstrual syndrome by a simple prospective reliable instrument. Obstet Gynecol 72: 302. 1 Mishell DR (2005) Epidemiology, and etiology of premenstrual disorders. Managing the spec trum of premenstrual symptoms, a clinician \200\231s guide, pp. 4 \200\2239. San Antonio, D annemiller Foundation/Med Pro Communications. 2 Cooke DJ (1985) Psychosocial vulnerability to life events during the climacteric. Br J Psychiat 147: 71 \200\2235. 3 Sagsoz N, Oguztur k O, Bayram M, et al. (2001) Anxiety and depression before and after the menopause. Arch Gy necol Obstet 264: 199 \200\223202. 4 Birkhauser M (2002) Depression, menopause and estrogen s: is there a correlation? Maturitas 41 (Suppl. 1): S3 \200\2238. 12_Semple_Chap12.indd 465 12/7/2012 3:42:30 PM CHAPTER 12 Reproductive psychiatry and sexuality 466 Premenstrual disorders Etiology Evidence supports a genetic vulnerability conferring increa sed sensitivity to normal changes in hormone levels throughout the menstrual cycle. This ca uses alterations in the normal cyclic ovarian steroid interactions with central neurotransm itters and neurohormones. Cyclic changes in ovar- ian steroids alone do not lead to PMS/PMD D. Most evidence supports involvement of the serotonergic system, endorphins and GABA, and the renin \200\223angiotensin \200\223aldosterone system. The autonomic and peripheral nerv ous systems may be involved in certain symptoms. Minimal or no evidence for: trace vitamin and element de \201 ciencies, personality factors, and stress. Stress also has little effe ct on PMS severity, and PMS is more likely to cause stress than vise versa. Morbidity These disorders can extend over a woman \200\231s entire reproductive cycle, from approximately age 14 to 50. Symptoms are relatively constant between cycles, and can cause an aggregate total of years of disability over a lifetime. This negatively affects quality of life and can have both direct and indirect economic consequences. Psychiatric consultation For already diagnosed premenstrual symptoms this is rare unless em o- tional symptoms are marked and/or there are vegetative symptoms, sui- cidal ideation, or a frequent inability to function. Differential diagnosis Up to 40% of women presenting to a physician with presumed PMS have another mood disorder; many meet the criteria for a depressive or anxi- ety disorder.1 PMDD can be a premenstrual exacerbation of an underlying psychiatric disorder or of a medical c ondition. Medical disorders such as migraine, chronic fatigue syndrome, and irritable bowel syndrome can have exacerbations prior to or during menses. Exclude perimenopause, gynae- c ological disorders (dysmenorrhoea, post-partum status, polycystic ovary disease, and endome triosis) and hypothyroidism and nutrient de \201 ciencies (e.g. manganese, magnesium, B vi tamins, vitamin E, and linoleic acid). Investigations \200 There are no speci \201 c tests diagnostic of premenstrual disorders. Prospective charting of daily symptoms for at least two menstrual cycles is essential to con \201 rm the cycli cal pattern. If menses are not regular and/or if they have length <25 days or >36 days refe rral should be made for a reproductive endocrine evaluation. For concomitant medical condit ions consultation with a general practitioner or gynecologist for a physical exam and exclu sion of medical disorders as well as appropriate routine blood tests including TFTs may be warranted. 12_Semple_Chap12.indd 466 12/7/2012 3:42:31 PM PREMENSTRUAL DISORDERS 467 Assessment tools Prospective Record of the Impact and Severity of Menstruation (PRISM), the Calendar of Premenstrual Experiences (COPE), and the Daily Record of Severity of Problems (DRSP). The DRSP is available online at M http:// www.pmdd.factsforhealth.org/have/dailyrec ord.asp. Treatment of PMS and PMDD First-line therapy \200 Antidepressants are effective for PMDD, with \202 uoxetine the most studied. At a dose of 20mg/day the overall response is 60 \200\22375%. Other SSRIs and venlafaxine have also sho wn ef \201 cacy in placebo-controlled trials. Luteal phase therapy: therapy in the luteal phase alone, starting 14d prior to the expected next menses, and terminating with the onset of menses. Second-line therapy \200 \200 Alprazolam (250 \200\223500mcg tid) for luteal phase depression. For severe PMDD, refractor y to other treatment, refer to a specialist. Potential treatments include medical oophoriec tomy with a GnRH agonist (e.g. leuprorelin, danazol). There are signi \201 cant side-effec ts related to hypoestrogenism (e.g. hot \202 ashes, long-term effects of estrogen de \201 ciency, osteoporosis, etc.). For patients who respond well, treatment can continue ove r the long term (>6mths) with continuous add-back of estrogen (+ progesterone when indicate d) to decrease and/or prevent these side-effects. For rare, refractory cases with severe di sabling symptoms, surgical bilateral oophoriectomy may be considered. Other promising possible treatments or adjuncts \200 RCTs initially failed to demonstrate the effectiveness of OCP in treating PMS or PMDD. Newe r placebo-controlled trials are showing that a 24-day (rather than 21-day) hormonal formula tion is ef \201 cacious for PMDD.2 Diuretics for severe oedema, e.g. furosemide, spironola ctone; danazol for mastalgia. There is some evidence for the ef \201 cacy of pyridoxine (v itamin B6) (no more than 100mg/day), vitamin E, calcium, vitamin D, and magnesium. No evide nce for multiple other treatment options including progesterone treatment, ginkgo biloba, e vening primrose oil, essential free fatty acids. 1 Keenan PA, Stern RA, Janowsky DS, et al. (1992) Psychological aspects of premenstrual syn - drome. I: Cognition and memory. Psychoneuroendocrinol 17: 179 \200\22387. 2 Yonkers KA, B rown C, Pearlstein TB, et al. (2005) Ef \201 cacy of a new low-dose oral contraceptive wit h drospirenone in premenstrual dysphoric disorder. Obstet Gynecol 106(3): 492 \200\223501. 12_Semple_Chap12.indd 467 12/7/2012 3:42:31 PM CHAPTER 12 Reproductive psychiatry and sexuality 468 Disorders associated with pregnancy Anxiety/mood symptoms in normal pregnancy Although ther e is usually an increase in symptoms of anxiety and depres- sion during pregnancy, these ar e quite normal and usually related to \200\230adjustment \200\231 in the 1st trimester and \200\230fears \200\231 in the 3rd trimester. Unless there is a past history of psychiatri c illness, there is no reported increase in the incidence of psychiatric disorders.1 Risk factors Family or personal history of depression; ambivalence about the pregnancy; hig h levels of neuroticism; lack of marital, family, or social supports. Treatment Usually will focus on psychosocial interventions; speci \201 c psychiatric disor ders should be identi \201 ed and treated appropriately (see Prescribing in pregnancy b p. 968).