Other DSM-IV criteria (see Box 9.10) Epidemiology Risk of developing PTSD after a traumatic event 8 \200\22313% for men, 20 \200 \22330% for women. Lifetime prevalence estimated as 7.8% (4:5 = 1:2).1 Cultural differences exist. Some types of stressor are associated with higher rates of PTSD (e.g. rape, torture , being a prisoner of war). Etiology \200 \200 see b p. 384. Psychological/biological: Neuroimaging: reduced hippocampal volume (may relate to appreciat ion of safe contexts and explicit memory de \201 cits). Dysfunction of the amygdala, hippo campus, septum, and prefrontal cortex may lead to enhanced fear response. High arousal appe ars to be mediated by anterior cingulate, medial prefrontal cortex, and thalamus; dissociat ion by parietal, occipital, and temporal cortex. Genetic: higher concordance rates seen in MZ than DZ twins. Risk factors \200 Vulnerability factors: low education, lower social class, Afro-Carribbean/ Hispanic, female gender, low self-esteem/neurotic traits, previous (or 09_Semple_Chap09.indd 390 12/7/2012 3:34:10 PM PTSD 1: DIAGNOSIS 391 family) history of psychiatric problems (esp. mood/anxiety disorders), previous traumatic e vents (including adverse childhood experiences and abuse). Peri-traumatic factors: traumati c emotions, peri-traumatic dissociation. Protective factors: psychopathic traits, chance to view body of dead person. trauma severity, perceived life threat, peri- high IQ, higher social class, Caucasian, male gender, Comorbidity (may be primary or secondary) Depressive/mood disorders, other anxiety disorder s, alcohol and drug misuse disorders, somatization disorders. Differential diagnosis Acute stress reaction/disorder, enduring personality change after a cata- strophic event (duration at least 2yrs, see b p. 380), adjustment disorder (less seve re stressor/different symptom pattern), other anxiety disorder, depressive/mood disorder, O CD, schizophrenia (or associated psychosis), substance-induced disorders. Box 9.10 Other DSM-IV criteria Traumatic event is persistently re-experienced in 1 (or more) of the following ways: \200 Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions (or repetitive play in which themes or aspects of the trauma are expressed in children). Recurrent distressing dreams of the event (or frightening dreams without reco gnizable content in children). Acting or feeling as if the traumatic event were recurring ( or trauma- speci \201 c re-enactment in children). Intense psychological distress at expos ure to internal or external cues that symbolize or resemble an aspect of the traumatic even t. Physiological reactivity at exposure to internal or external cues that symbolize or rese mble an aspect of the traumatic event. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiv eness (not present before the trauma), as indicated by 3 (or more) of: \200 Efforts to avoid thoughts, feelings, or conversations associated with the trauma. Efforts t o avoid activities, places, or people that arouse recollections of the trauma. Inability to recall an important aspect of the trauma. Markedly diminished interest or participation in signi \201 cant activities. Feeling of detachment or estrangement from others. Restricted range of affect. Sense of foreshortened future. \200 \200 \200 \200 1 Kessler RC, Sonnega A, Bromet E, et al. (1995) Posttraumatic stress disorder in the Natio nal Comorbidity Survey. Archives of General Psychiatry 52: 1048 \200\22360. 09_Semple_Chap09.indd 391 12/7/2012 3:34:10 PM CHAPTER 9 Anxiety and stress-related disorders 392 Post-traumatic stress disorder 2: management1 Psychological Meta-analyzes support the super ior ef \201 cacy of trauma-focused treatments,2 speci \201 cally trauma-focused CBT and E MDR. These are recommended as \201 rst-line treatments in all recent guidelines. \200 CBT: includes elements of: education about the nature of PTSD, self- monitoring of symptoms , anxiety management, breathing techniques, imaginal reliving, exposure to anxiety-producin g stimuli in a supportive environment, cognitive restructuring (esp. for complicated trauma ), anger management. Eye movement desensitization and reprocessing (EMDR): treatment using voluntary multi-saccadic eye movements to reduce anxiety associated with disturbing thought s and help process the emotions associated with traumatic experiences (see Box 9.11). Other psychological treatments: Psychodynamic therapy \200\224 \200 provoked by the stressful events, the goal being to understand the meaning of the event in the context of the individ ual. Stress management (stress inoculation) cope with stress, such as relaxation, breathing , thought stopping, assertiveness, positive thinking. Hypnotherapy hyperarousal and distres s, enabling recollection of traumatic event. Concern over possible induction of dissociativ e states. Supportive therapy exploring thoughts, feelings, and behaviors to reach clearer s elf- understanding. 3 novel focus on resolving unconscious con \202 icts \200\224teaching skills to help \200\224use of focused attention to enhance control over \200\224non-directive, non-advisory method of Pharmacological Medication may be considered when there is severe ongoing threat, if the pa tient is too distressed or unstable to engage in psychological therapy, or fails to respond to an initial psychological approach. \200 (e.g. paroxetine 20 \200\22340mg/day; sertraline 50 \200\223200mg/day) are SSRIs licensed f or PTSD, and their use supported by systematic review.4 Other unlicensed possibilities incl ude: \202 uoxetine, citalopram, escitalopram, and \202 uvoxamine. Other antidepressants : TCAs (e.g. amitriptyline, imipramine); MAOIs (e.g. phenelzine) may also reduce anxiety (o ver-arousal), intrusiveness, and improve sleep; venlafaxine; mirtazapine. although unlicensed there is some evidence for It may be helpful to target speci \201 c symptoms: \200 Sleep disturbance mirtazapine (45mg/day), levomepromazine, prazosin (mean dose 9.5mg/day), or speci \201 c hypnotics (e.g. zopiclone, zolpidem). Anxiety symptoms/hyperarousal: 4 \200\2235mg/day), buspirone, antidepressants, propranolol. (including nightmares): may be improved by consider use of BDZs (e.g. clonazepam 09_Semple_Chap09.indd 392 12/7/2012 3:34:10 PM PTSD 2: MANAGEMENT 393 Intrusive thoughts/hostility/impulsiveness: carbamazepine, valproate, topiramate, or lithiu m. Psychotic symptoms/severe aggression or agitation: antipsychotic (some evidence for olan zapine, risperidone, quetiapine, clozapine, aripiprazole). some evidence for use of may warrant use of an Outcome 7 \200 50% will recover within 1st year, 730% will run a chronic course. \200 \200 Outcome depends on initial symptom severity. Recovery will be helped by: good social suppor t; lack of \200\223ve responses from others; absence of \200\230maladaptive \200\231 copi ng mechanisms (e.g. avoidance, denial, \200\230safety behaviors \200\231, not talking abou t the experience, thought suppression, rumination); no further traumatic life events (s pro blems such as physical health, acquired disability, dis \201 gurement, disrupted relations hips, \201 nancial worries, litigation). XBox 9.11 EMDR controversy In 1987 Francine Shapiro, a California psychologist in private p ractice, whilst walking in the woods, preoccupied with disturbing thoughts, dis- covered he r anxiety improved during the walk. She realized that she had been moving her eyes back and forth, from one side of the path to the other, while walking. Shapiro tried out variants o f this procedure with her clients and found that they felt better, too. Her \201 ndings w ere published in 1989 and EMDR was born. Initially developed to help clients with PTSD and other anxiety disor- ders, therapists hav e since extended EMDR to other conditions, includ- ing depression, sexual dysfunction, schi zophrenia, eating disorders, and stress associated with illnesses such as cancer. Like othe r serendipitous discoveries the claims for EMDR were treated with a healthy dose of skeptic ism, esp. when its proponents tried to explain \200\230how \200\231 it worked, using erron eous theories of memory, right \200\223left brain imbalance, and REM-sleep-like processing. It became associated with alternative thera- pies, such as Roger Callahan \200\231s Though t Field Therapy and Gary Craig \200\231s Emotional Freedom Therapy. These therapies have al l the hallmarks of pseudoscience (see b p. 20). Although the mechanism of action of EMDR is not fully understood, it has been shown that th e eye movements are not a necessary compo- nent of the therapy. In fact, well-established p sychological principles of attention, imaginal exposure, and methods of relaxation are prob ably suf \201 cient to explain the ef \201 cacy of the EMDR procedure. 1 NICE (2005) PTSD: the management of PTSD in adults and children in primary and secondary care. Clinical guideline CG26. Available at: M http://www.nice.org.uk/CG26 2 Bisson J, Ehle rs A, Matthews R, et al. (2007) Systematic review and meta-analysis of psychological treatm ents for post-traumatic stress disorder. Br J Psychiat 190: 97 \200\223104. 3 Shapiro F (19 95) Eye movement desensitization and reprocessing: basic principles, protocols, and procedu res. New York: Guildford Press. 4 Stein DJ, Ipser JC, and Seedat S (2006) Pharmacotherapy f or posttraumatic stress disorder (PTSD). Cochrane Database System Rev Issue 1. 09_Semple_Chap09.indd 393 12/7/2012 3:34:11 PM CHAPTER 9 Anxiety and stress-related disorders 394 Depersonalization (derealization) syndrome Essence A rare disorder, characterized by persis tent or recurrent episodes of a dis- tressing feeling of unreality or detachment. This may be in relation to the outside world (derealization) or the person \200\231s own body, thoug hts, feelings, or behavior (depersonalization). It is viewed as a dissociative disorder (DS M-IV) or an anxiety/stress-related disorder (ICD-10). Clinical features \200 Patients may \201 nd it dif \201 cult to describe their experiences, often reporting fee ling \200\230as if \200\231 they are a passive observer of what is going on around them or their own actions. This may be accompanied by an emotional numbness (inability to experien ce feelings) and the impression of being in a dream- or trance-like state. There may also b e the experience of alterations in the perception of objects or people, appearing unfamilia r or different in respect to usual color, shape, distance, or size. Insight tends to be pre served (unlike \200\230passivity phenomena \200\231 in psychoses): the patient recognizes the experiences as abnormal, and often \201 nds them unpleasant, distressing, and anxiety -provoking. Epidemiology1 Up to 50% of \200\230normal \200\231 individuals may experience depersonaliz ation in their lifetime (usually in the context of psychological distress) with 1 \200\2232 % having more chronic symptoms. In psychiatric populations it is a very com- mon experience (lifetime prevalence 780%), with persistent symptoms (and associated functional impairment ) in 712%. In clinical populations 4:5 = 1:2 whereas in the general population 4 = 5. Age o f onset usually ado- lescence/early adulthood (may go undetected in children). Etiology \200 Psychoanalytical: impulses, or affects; usually rooted in childhood trauma.2 adaptive respo nse to overwhelming stress, allowing Psychological: continued function by protecting agains t potentially overwhelming anxiety. Speci \201 c precipitant(s) may not be readily identi \201 able. Biological: of information in the brain (with functional localization in the pa rietotemporal and limbic areas), where serotonergic mechanisms play a key role.3 Appears to be a role for the effects of illicit drugs with 10 \200\22320% of patients describing symp toms \201 rst occurring in the context of drug use (especially cannabis). ego defense against painful and con \202 icting memories, altered function in systems central to integrated processing Comorbidity Anxiety disorders (particularly phobias, panic disorder, OCD), depressive disor ders, personality disorders (anankastic/obsessional, BPD). Differential diagnosis Depersonalization may be experienced in the context of sleep or sen- sory deprivation, being in unfamiliar surroundings, or an acutely stressful/ 09_Semple_Chap09.indd 394 12/7/2012 3:34:11 PM DEPERSONALIZATION (DEREALIZATION) SYNDROME 395 traumatic situation. May also be a symptom in schizophrenia/psychosis (usually accompanied by a delusional explanation, e.g. Cotard delusion), mood or anxiety disorders, acute intoxi cation/withdrawal from alcohol, illicit substances (particularly cannabis or hallucinogens) , or medication, and in organic disorders (hyperventilation, hypoglycaemia, migraine and ep ilepsy, usually brief stereotyped episodes, or other neurological conditions). Management4 \200 5 Use of rating scales (e.g. The Cambridge Depersonalization Scale) may assist assessment of treatment response. Exclude organic causes with appropriate investigations, which may somet imes include brain imaging (CT/MRI) and EEG. Comorbid psychiatric conditions should be iden ti \201 ed and treated. Despite successful treatment, depersonalization may persist. Evide nce for successful management of depersonalization syndrome is poor. No drugs are licensed for use in the UK. Some evidence supports a role for SSRIs (usually citalopram or escitalop ram) alone or in combination with lamotrigine (up to 500mg/day). Where there is marked anxi ety, clonazepam (0.5 \200\2234mg/day) may be useful; anecdotal evidence supports clomiprami ne (if obsessional symptoms are marked), naltrexone, and bupropion. CBT is the only psychol ogical treatment shown to be bene \201 cial in an open trial, particularly in tackling anx ieties, ruminations, and avoidance behaviors relating to identi \201 able stressors. Other psychotherapeutic approaches: acceptance and understanding of symptoms; identi \201 catio n of \200\230putative \200\231 defense functions; identifying underlying psychopathology; integration of traumatic experiences and memories. Course \200 Onset is usually sudden, with symptoms persisting only for a brief period. Gradual onset do es occur and course is very variable \200\224both episodic and continuous. Occasionally sym ptoms may persist for hours, days, weeks, months, or even years (rare). Resolution tends to be gradual. Recurrent episodes generally occur in the context of recurring (perceived) str essful situations or fatigue. Chronic symptoms run a \202 uctuating course, and may be tr eatment- resistant. 1 Hunter ECM, Sierra M, and David AS (2004) The epidemiology of depersonalization and derea li- sation: a systematic review. Soc Psychiat Psychiat Epidemiol 39: 9 \200\22318. 2 Danger s of attributing present psychopathology to childhood events cannot be overstated. Recently illustrated by high-pro \201 le cases of alleged \200\230recovered memories \200\231 (se e Box 9.8). Regard unsubstantiated claims of childhood (or other) abuse with extreme cautio n. Psychodynamic notion of \200\230repression \200\231 is intellectually dubious, and sign i \201 cance of childhood trauma, even in empirical studies, \201 nds little support. Se e Pope HG (1997) Psychology astray: fallacies in studies of \200\230repressed memory \200 \231 and childhood trauma. Boca Raton: Upton. 3 As early as 1935, Mayer-Gross thought psych ological explanations to be of \200\230limited value \200\231, seeing depersonalization as \200\230an unspeci \201 c preformed functional response of the brain \200\231. Mayer-Gro ss W (1935) On depersonalization. Br J Med Psychol XV(2): 103 \200\22326. 4 Medford N, Sier ra M, Baker D, et al. (2005) Understanding and treating depersonalization disor- der. Adv P sychiat Treat 11: 92 \200\223100. 5 M http://www.iop.kcl.ac.uk/iopweb/blob/downloads/locato r/l_911_Scale3.pdf 09_Semple_Chap09.indd 395 12/7/2012 3:34:11 PM This page intentionally left blank 397 Chapter 10 Eating and impulse- control disorders Anorexia nervosa 1: overview 398 Anorexia nervosa 2: physical consequences 400 Anorexia ner vosa 3: assessment 402 Anorexia nervosa 4: management 404 Bulimia nervosa 406 Impulse-contr ol disorders 1 408 Impulse-control disorders 2 410 10_Semple_Chap10.indd 397 12/7/2012 3:34:40 PM CHAPTER 10 Eating and impulse-control disorders 398 Anorexia nervosa 1: overview Essence Condition most commonly seen in young women in which t here is marked distortion of body image, pathological desire for thinness, and self-induced weight loss by a variety of methods. Signi \201 cant mortality: 10 \200\22315% (2/3 physi cal complications, 1/3 suicide). Epidemiology 4:5 = 1:10; mean age of onset: 5 16 \200\22317yrs (rarely >30yrs); 4 7 12yrs. Incidence 70.5% of adolescent and young women. Community samples suggest equal distribution across the social classes, but clinic samples show excess of upper/middle classes. Diagnostic criteria \200 Low body weight 10.1 for calculation). Self-induced weight loss purging, excessive exercise, use of appetite suppressants. Body image distortion low weight threshold. Endocrine disorders interest/impotence, raised GH levels, raised cortisol, alte red TFTs, abnormal insulin secretion. Delayed/arrested puberty \200\22415%+ below expected, BMI 17.5 or less (see Box \200\224avoidance of \200\230fattening \200\231 foods, vomiting, \200\224 \200\230dread of fatness \200\231: over-valued idea, imposed \200\224HPA axis: e.g. amenorrhoea, reduced sexual \200\224if onset pre-pubertal. Note: in \200\230atypical \200\231 cases one or more of these key features may be absent, or all are present but to a lesser degree. Etiology \200 Genetic 6 \200\22310%. Adverse Life events (compared to psychiatric control s). Psychodynamic models \200 Concordance rates MZ:DZ = 65%:32%, female siblings: No excess of childhood physical or sexual abuse Family pathology \200\224enmeshment, rigidity, over-protectiveness, lack of con \202 ict r esolution, weak generational boundaries. Individual pathology \200\224disturbed body image (due to dietary problems in early life, parents \200\231 preoccupation with food, lack of a sense of identity). Analytical model \200\224regression to childhood, \201 xation on the oral stage, escape from the emotional problems of adolescence. Biological \200 \200 Hypothalamic dysfunction \200\224? cause or consequence. Neuropsychological de \201 cits \200\224reduced vigilance, attention, visuospatial abilities, and associative memory (corre ct with weight gain). Brain imaging CT: \200\230pseudoatrophy \200\231/sulcal widening and ventricular enlargement (corrects with weight gain). Functional imaging: unilateral tempor al lobe hypoperfusion perhaps related to visuospatial problems/body image distortion. 10_Semple_Chap10.indd 398 12/7/2012 3:34:40 PM ANOREXIA NERVOSA 1: OVERVIEW 399 Differential diagnosis \200 \200 \200 \200 \200 Chronic debilitating physical disease. Brain tumors. GI disorders (e.g. Crohn \200\231s dis ease, malabsorption syndromes). Loss of appetite (may be secondary to drugs, e.g. SSRIs, am fetamines). Depression/OCD (features of which may be associated). Box 10.1 BMI (body mass index)* BMI is a ratio between weight and height, which correlates with body fat, and is used to ev aluate if a person is at an unhealthy weight (given a certain height). BMI value is more us eful for predicting health risks than the weight alone (for adults aged 18+ yrs). To calculate BMI the following formulas are used: Weight (in kilos) Height (in meters)2 BMI = or Weight (in pounds) \227 704.5 Height (in inches)2 BMI = Range Women Men Interpretation Risk to health <19.1 <20.7 Underweight The lower the BMI, the greater the risk 19.1 \200\22325.8 20.7 \200\22326.4 Ideal weight Normal, very low risk 25.8 \200\22327.3 26.4 \200\22327.8 Marginally overweight Some risk 27.3 \200\22332.2 27.8 \200\22331.1 Overweight Moderate risk 32.3 \200\22344.8 31.1 \200\22345.4 Very overweight or obese High risk >44.8 >45.4 Morbid obesity Very high risk Note: BMI is less reliable for: children and teenagers (ranges are based on adult heights), competitive athletes and bodybuilders (muscle weight may skew the results), pregnant or nu rsing women, and people over 65. The formula for BMI was developed by the Belgian statistician Adolphe Quetelet in the ninet eenth century and is sometimes referred to as \200\230Quetelet \200\231s formula \200\231. 10_Semple_Chap10.indd 399 12/7/2012 3:34:40 PM CHAPTER 10 Eating and impulse-control disorders 400 Anorexia nervosa 2: physical consequences Common problems Mainly due to the effects of star vation or vomiting: \200 \200 Oral Cardiovascular cardiomyopathy. Gastrointestinal altered antral motility, gastric atrop hy, decreased intestinal mobility); constipation. Note: prokinetic agents may accelerate ga stric emptying and relieve gastric bloating, which can accelerate resumption of normal eati ng habits. Endocrine and metabolic hypoglycaemia; hypothermia; altered thyroid function; hy percortisolaemia; amenorrhoea; delay in puberty; arrested growth; osteoporosis. Renal Repro ductive Dermatological downy) body hair. Neurological enlargement, sulcal widening, cerebra l atrophy (pseudoatrophy \200\224 corrects with weight gain). Haematologic Dental caries. Hypotension; prolonged QT; arrhythmias; Prolonged GI transit (delayed gastric emptying, Hypokalaemia; hyponatraemia; \200 \200 Renal calculi. Infertility; low birth-weight infant. Dry scaly skin and brittle hair (hair loss); lanugo ( \201 ne Peripheral neuropathy; loss of brain volume: ventricular Anemia; leukopenia; thrombocytopenia. Cardiac complications \200 \200 The most common cause of death (mortality rate 7 \200\22310%). Findings may include: \200 \200 \200 Signi \201 cant bradycardia (30 \200\22340bpm). Hypotension (systolic <70mmHg). ECG change s (sinus bradycardia, ST-segment elevation, T-wave \202 attening, low voltage, and right axis deviation) may not be clinically signi \201 cant unless there are frequent arrhythmia s (QT prolongation may indicate increased risk for arrhythmias and sudden death). Echocardi ogram may reveal decreased heart size, decreased left ventricular mass (with associated abn ormal systolic function), and mitral valve prolapse (without signi \201 cant mitral regurg itation). These changes re \202 ect physiological response to malnutrition and will recove r on refeeding. Amenorrhoea \200 Included in the diagnostic criteria, due to hypothalamic dysfunction (hypothalamic \200\223 pituitary \200\223ovarian axis) with low levels of follicle- stimulating hormone (FSH) and luetinizing hormone (LH), despite low levels of estrogen (reversion to the pre-pubertal sta te occurs with LH response to GnRH blunted leading to amenorrhoea). Consequences include re duced fertility, multiple small follicles in the ovaries, decreased uterine volume, and atr ophy. 10_Semple_Chap10.indd 400 12/7/2012 3:34:40 PM ANOREXIA NERVOSA 2: PHYSICAL CONSEQUENCES 401 Note: weight loss, excessive exercise, and stress are also important. However, amenorrhoea can persist (in 5 \200\22344% of cases) even after recov- ery and return to normal weight. Osteopenia Both cortical and trabecular bone are affected, and osteopenia persists despite estrogen therapy. Contributing to bone loss are low levels of progesterone and decreased IG F-1 levels. Treatment \200 No speci \201 c treatment exists; however, 1000 \200\2231500mg/d of dietary calcium and 40 0IU of vitamin D is recommended to prevent further bone loss and maximize peak bone mass. E xercise and HRT, although of bene \201 t in adult women, may be harmful for adolescents wi th anorexia nervosa (causing premature closure of bone epiphysis). Box 10.2 Physical signs \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 loss of muscle mass dry skin brittle hair and nails callused skin over interphalangeal join ts (Russell sign) anemia hypercarotinaemia (yellow skin and sclera) \201 ne, downy, lanug o body hair eroded tooth enamel peripheral cyanosis hypotension bradycardia hypothermia atr ophy of the breasts swelling of the parotid and submandibular glands swollen tender abdomen (intestinal dilatation due to reduced motility and constipation) peripheral neuropathy 10_Semple_Chap10.indd 401 12/7/2012 3:34:40 PM CHAPTER 10 Eating and impulse-control disorders 402 Anorexia nervosa 3: assessment Full psychiatric history (Box 10.3) \200 Establish the context in which the problems have arisen (to inform development of a treatme nt plan). Con \201 rm the diagnosis of an eating disorder. Assess risk of self-harm/suicid e. \200 Box 10.3 Commonly reported psychiatric symptoms \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Concentration/memory/decision-making problems Irritability Depression Low self-esteem Loss of appetite Reduced energy Insomnia Loss of libido Social withdrawal Obsessiveness regardin g food Full medical history (Box 10.4) \200 \200 b p. 400). Focus on the medical complications of altered nutrition ( Detail weight changes, dietary pa tterns, and excessive exercise. Box 10.4 Symptoms commonly elicited on systemic enquiry \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 General physical health concerns Amenorrhoea Cold hands and feet Weight loss Constipation D ry skin Hair loss Headaches Fainting or dizziness Lethargy Physical examination \200 \200 \200 \200 b p. 399). Determine weight and height (calculate BMI \200\224see Assess physical signs of starvation and vomiting ( Routine and focused blood tests (see Box 10.5). ECG (and echocardiogram if i ndicated). b p. 400). 10_Semple_Chap10.indd 402 12/7/2012 3:34:41 PM ANOREXIA NERVOSA 3: ASSESSMENT 403 Box 10.5 Blood tests FBC Hemoglobin (Hb) usually normal or elevated (dehydration); if anemic, investigate furthe r. Leukopenia and thrombocytopenia seen. ESR Usually normal or reduced; if elevated, look for other organic cause of weight loss. U&Es Raised urea and creatinine (dehydration), hyponatraemia (exces- sive water intake or s yndrome of inappropriate antidiuretic hormone secretion [SIADH] \200\224neurogenic diabetes insipidus, affecting 40%, may be treated with vasopressin, but is reversible following wei ght gain), hypokalaemic/hypochloraemic metabolic alkalosis (from vomiting), metabolic acido sis (laxative abuse). Other abnormalities may include hypocalcaemia, hypophosphataemia, hyp omagnesaemia. Glucose Hypoglycaemia (prolonged starvation and low glycogen stores). LFTs Minimal elevation. TFTs Low T3/T4, increased rT3 (euthyroid sick syndrome \200\224an a daptive mechanism; hormonal replacement not necessary; reverts to normal on refeeding). Albumin/total protein Usually normal. Cholesterol May be dramatically elevated (starvation) \200\224secondary to decreased T3 lev els, low cholesterol binding globulin, and leakage of int- rahepatic cholesterol. Endocrine Hypercortisolaemia, iGH levels, d luetinizing hormone releas- ing hormone (LHRH), dLH, dFS H, doestrogens, and dprogestogens. 10_Semple_Chap10.indd 403 12/7/2012 3:34:41 PM CHAPTER 10 Eating and impulse-control disorders 404 Anorexia nervosa 4: management General principles \200 \200 Most patients will be treated as outpatients. A combined approach is better: \200 Pharmacological ideas regarding food); previously TCAs or chlorpromazine used for weight ga in. Psychological individual therapy (behavioral therapy = CBT; may improve long- term outc ome). Education self-help manuals ( \200\230bibliotherapy \200\231). Fluoxetine (especially if there are clear obsessional Family therapy (more effective in early onset), Nutritional education (to challenge over-valued ideas), Hospital admission should only be considered if there are serious medical problems (see Box 10.6). \200 Compulsory admission may be required: feeding is regarded as \200\230treatment \200\231 (N ote: ethical issue regarding patient \200\231s \200\230right to die \200\231 vs. their \200\230right to treatment \200\231). Box 10.6 Criteria for admission to hospital Inpatient management may be necessary for patients with signi \201 cant medical or psychia tric problems: \200 Extremely rapid or excessive weight loss that has not responded to outpatient treatment. Se vere electrolyte imbalance (life-threatening risks due to hypokalaemia or hyponatraemia). o C; fainting Serious physiological complications, e.g. temperature < 36 due to bradycardia ( PR <45bpm) and/or marked postural drop in BP. Cardiac complications or other acute medical disorders. Marked change in mental status due to severe malnutrition. Psychosis or signi \201 cant risk of suicide. Failure of outpatient treatment (e.g. inability to break the cyc le of disordered eating or engage in effective outpatient psychotherapy). Admission should not be viewed as punishment by the patient and the goals of inpatient therapy should be ful ly discussed with the patient (and their family): \200 \200 \200 \200 \200 Addressing physical and/or psychiatric complications. Development of a healthy meal plan. A ddressing underlying con \202 icts (e.g. low self-esteem, planning new coping strategies). Enhancing communication skills. 10_Semple_Chap10.indd 404 12/7/2012 3:34:41 PM ANOREXIA NERVOSA 4: MANAGEMENT 405 Risks of re-feeding With re-feeding, cardiac decompensation may occur, especially during th e \201 rst 2wks (when the myocardium cannot withstand the stress of an increased metaboli c demand). Symptoms include excessive bloating, oedema, and, rarely, congestive cardiac fai lure (CCF). To limit these problems: \200 \200 Measure U&Es and correct abnormalities before re-feeding. Recheck U&Es every 3 days for the \201 rst 7 days and then weekly during re-feeding period. Attempt to increase daily calo ric intake slowly by 200 \200\223300kcal every 3 \200\2235 days until sustained weight gain of 1 \200\2232 pounds/wk is achieved. Monitor patient regularly for development of tachyca rdia or oedema. Prognosis \200 If untreated, this condition carries one of the highest mortality \201 gures for any psyc hiatric disorder (10 \200\22315%). If treated, \200\230rule of thirds \200\231 (1/3 full r ecovery, 1/3 partial recovery, 1/3 chronic problems). Poor prognostic factors include: \200 \200 \200 \200 \200 \200 \200 \200 chronic illness late age of onset bulimic features (vomiting/purging) anxiety when eating w ith others excessive weight loss poor childhood social adjustment poor parental relationshi ps male sex. 10_Semple_Chap10.indd 405 12/7/2012 3:34:41 PM CHAPTER 10 Eating and impulse-control disorders 406 Bulimia nervosa Essence Characterized by recurrent episodes of binge eating, with compensat ory behaviors and overvalued ideas about \200\230ideal \200\231 body shape and weight. Oft en there is a past history of anorexia nervosa (30 \200\22350%) and body weight may be norm al. Epidemiology Incidence 1 \200\2231.5% of women, with mid-adolescent onset, and presentation in early 20s. Etiology Similar to anorexia nervosa, but also evidence for associated personal/ family his tory of obesity, and family history of affective disorder and/or substance misuse. Possible \200\230dysregulation of eating \200\231, related to serotoner- gic mechanisms (?supersen sitivity of 5-HT2C secondary to d5-HT). Diagnostic criteria (see Box 10.7) \200 Persisten t preoccupation with eating \200 Irresistible craving for food \200 \200\230Binges \200\231 \200\224episodes of overeating \200 Attempts to counter the \200\230fattening \200\231 effects of food (self-induced vomiting, abuse of purgatives, periods of starvation , use of drugs, e.g. appetite suppressants, thyroxine, diuretics) Morbid dread of fatness, with imposed \200\230low weight threshold \200\231 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.