341 SSRI issues SSRIs are under a cloud as a 2008 meta-analysis shows their eff ects in depres- sion may be no greater than placebo.131 Also, in one cohort study in the elderly (n=60,746 ) SSRIs had the highest hazard ratios for falls (1.66) and hyponatrae- mia (1.52). All-caus e mortality was also higher vs tricyclics.132 There is also the question of suicidal behavi or. In adults, research using the UK GP research database for 1993 \200\2239 found risk of suicidal behavior wasn \200\231t signi \201 cantly greater with SSRIs than vs tricyclics ( but strong suicidal drive is reported).133 Venlafaxine is also problematic.134 In teenagers , the position is complex, and prescribing bodies tend to recommend that no antidepressants be used \200\224but this is unworkable for those many teenagers with formidable mental hea lth problems where there is lack of availability of cognitive therapies, or they are not wo rking. Here the small risk of suicide ( \200\2051 : 4000 ) may be the least bad option.135 Before prescribing: get informed consent from the teenager and the parent/carer. Ensure met iculous follow-up, and ensure that it really is a major depression you are treating, using detailed questionnaires to aid diagnosis. A patient-centered approach to depression We can feel perplexed with antidepressants; it can feel like trial and error when prescribing them . What works well in one person may not help another. There seems to be an ever increasing choice of drugs and con \202 icting information on safety. In this context, the following may be helpful: Advice to give a patient when treating depression \200 Discuss choice of drug and non-pharmacological therapy. Cognitive thera- py is known to be as eff ective as a ntidepressants in mild to moderate de- pression.136 Combined use is better than either trea tment alone. 137,138 \200 Discuss side eff ects, not all side eff ects are undesirable (S SRIs may help pre- mature ejaculation). Warn that there may be an initial worsening of symp - toms in the \201 rst weeks so persevere before therapeutic eff ects are seen. \200 As sess after 4 \200\2236 weeks. If eff ective continue for at least 4 \200\2236 months after recovery, if stopped too soon 50% relapse. 139 If no eff ect, increase dose and review in 2 weeks. If still no response, increase dose if it is safe to do so (un- less poorly tolerat ed), review in 2 weeks. If no response or poor tolerability, switch to an alternative class of antidepressant (special method, p369). y r t a i h c y s P Recurrent depression: of those who have one episode of major depression 50 \200\22385% will have further episodes. Continuing antidepressants lowers the odds of relapse by 65%, whic h is about half the absolute risk. 140 Theories of antidepressant action 8 pharmacological actions are known, and over 20 antidepr essants exist. How do all they lead to a similar response? Why is there a delay? 2 theories : The neurotransmitter receptor hypothesis: Postulates that a change in receptor sensitivit y by desensitization and down- regulation of diff erent receptors (not just \200\200neurot ransmitter at the synapse) leads to clinical eff ects after a few weeks. The monoamine hypo thesis of antidepressants on gene expression: This suggests the eff ect of increased neurot ransmitter at the synapse initiates a sequence of events to give the anti- depressant respo nse. This includes up and down regulation of various genes with subsequent varying expressi on of receptors and critical proteins. 141 Have a non-pharmacological arm to every treatmen t plan Exercise (in wild Nature, eg on or near water ), tai chi (p753), Yoga, social int eraction, psychotherapy (p370), counseling (p380), reading clubs, medita- tion, poetry (rea ding/writing). Join a club, eg Ramblers. Rest from work. People may not want drugs, equatin g them with moral failure? If still unconvinced, an alternative therapy, eg St John \200 \231s wort, may be acceptable? 142 Electroconvulsive therapy (ECT) Mechanism There is MRI evidence for the idea that ECT inter rupts the hyper- connectivity between the various areas of the brain that maintain depressi on.143 Indications NICE recommends ECT is used only to gain rapid (if short-term) improveme nt of severe symptoms after an adequate trial of other treatments has proven ineff ective a nd/or when the condition is considered to be poten- tially life-threatening, in individuals with: \200 Severe depression \200 Catatonia (eg associated with schizophrenia. 144) \200 A prolonged or severe manic episode. Emergency ECT is possible, eg in some elderly pa tients, but rarely used (but the success rate is good, eg 80%).145 Carry on antidepressants when ECT ends: this may prevent recurrences.146 Typical course length: 6 sessions (2 per w eek). Contraindications Recent subdural/subarachnoid bleed; no consent (p402; in- volve rel atives, but they cannot consent for an adult). Cautions Recent stroke MI, arrhythmia, CNS v ascular anomalies. SE: Anesthetic problems; amnesia; delirium/agitation (may respond to don epezil).147 Parkinsonism may improve. 148 Technique Check the patient \200\231s identity an d that \200\230nil by mouth \200\231 for >8h. \200 Ensure a detailed medical history and physical examination has been done, and any illnesses investigated and treated as far as p ossible. High anaes- thetic risk? \200\224See p614; seizure threshold \200\200 if on concu rrent benzodiazepines or anticonvulsants; also \200\200risk of heart complications if on t ricyclics. Liaise between psychiatric and anesthetic staff . Do bene \201 ts outweigh risk s? 342 y r t a h c y s P i ECT is frightening; give calm reassurance away from the site where ECT is go- ing on. (Patients should not witness other patients having ECT.1) Are the consent forms in order (p402; see below)? In the rare instances in the UK where ECT is given without consent, a second opinion from the Mental Health Commission must state th at the treatment is necessary (p402). Ensure that fully equipped resuscitation trolleys are present including a functioning de \201 brillator, suction apparatus, and pulse oximeter. \200 Ensure anesth etist (senior & ECT trained) knows of allergies drugs inter- fering with GA. For counter ing ECT-induced vagal stimulation, she may use at- ropine before using an ultra-short-actin g anesthetic agent with muscle re- laxation (eg suxamethonium) to minimize the seizure \200 \231s muscular component. \200 The ECT machine: checked recently? Reserve machine to hand ? What charge/ energy is to be given? Which waveform will be used (bidirectional or modi- \201 ed sinusoidal, or unidirectional)? See manufacturer \200\231s information. Put jelly on the electrode sites (not enough to allow shorting). See \201 g 1. \200 Whe n the anesthetist gives the word, give the shock. Be prepared to re- strain the patient if paralysis is incomplete. While the current passes, the muscles will contract. This will cea se as the current ceases. After 10sec, further clonic spasms occur, lasting 1min. The onl y sign may be lid \202 utter- ing. Clonus is probably needed for ECT to be fully eff ecti ve. Then coma position and BP/pulse, etc until conscious. Ask the anesthetist to try IV midazol am for those (few) who get very agitated during recovery. Consent for today \200\231s shock is suspect if yesterday \200\231s ECT has made you unable to remember your basic biography (am I divorced?).149 Re \202 ect on the blogs OP- POSITE, and on Hay \200\231s paradox: t he organ giving consent is the organ affected. As in all metaphysical paradoxes, don \200 \231t get overly wound up by the lack of any way out: remember that humans are quite good a t this sort of thing, your- self included. Start from the basic principle that if your pati ent \200\231s wishes are known, comply with them. Hay \200\231s paradox is partial because the organ giving consent is not uniformly aff ected, and decision-making may be rational. B ut if the deluded patient says \200\234I want ECT because it fries the transmitter the Pop e put in my head \200\235 you may need legal backing to endorse consent. But don \200\231t be too intellectually arrogant in dismissing a patient \200\231s reasoning: after all, none of us knows how ECT works, and all are entitled to an opinion. 343 What is the correct \200\230dose \200\231 of unilateral ECT? There is no universal answer, but there is evidence that therapeutic eff ects of ECT are proportional to seizure length. Be sure that you have adequate training on this issue by the consultant in charge of the s ession. Dose is better measured in millicou- lombs (mC) than milliamps. It depends on seizu re threshold, which varies 40-fold among patients. A moderately \200\230suprathreshold \200\231 dose (eg 200% above seizure threshold) usually gives seizures of ad- equate durati on, while aiming to minimize cogni- tive side eff ects \200\224according to the Royal Colle ge of Psychiatrists ECT Handbook. Fig 1. Electrode position: A \200\223B =10cm; A is 4cm from the green dotted line. y r t a i h c y s P Doses need to change depending on response, and dose of propofol150 in the anesthetic: also , seizure threshold rises by 80% as courses progress. A \200\230good \200\231 seizure is one which is of adequate duration ( 15sec during early ses- sions; duration is less importa nt later), with both a tonic and a clonic phase. Some machines allow EEG monitoring \200 \224useful as anesthesia renders seizure analysis diffi cult. If the seizure lasts >2min, t ell the anesthetist, who will give a bolus of diazepam, or GA agent. The frequency and speed of response of ECT varies according to indica- tion, eg bipolar dep ression patients show more rapid improvement and need fewer treatments than unipolar patien ts.151N=228 One retrospective study has found that female patients respond better to ECT th an male patients.152 Quotes from the blogsphere: \200 \200\234There is no treatment in psychiatry more fright ening than ECT \200 There is also no treatment in psychiatry more eff ective than ECT. \200 \235153 \200 \200\234Nighty-night \200\235 says the blue mask with piercing green eyes, and an in- stant later, I feel myself falling into yummy unconsciousness. When I awake from the treatment, I am back in my hospital room. My brain feels very foggy. I can \200\231t r emember what day it is or anything that happened that morning. I try to call my husband at home, but I can \200\231t remember my phone number and have to look it up in an address boo k I \201 nd in my nightstand. Waves of excruciating pain surge through my head, and I beg for pain medicine \200 This whole scenario repeats itself each day for the next week and a half. As the days pass, the headaches grow more and more unbearable, but life in general g rows surprisingly more toler- able \200 Gone are the days \201 lled with inescapable agon y, misery, despair and a desperate determination to die. In short, I have my life back \200 \200\235154 \200 \200\234My memory seems pretty bad. I forget lots of common easy thin gs that have no reason to be forgotten. This never happened prior to electro- convulsive tr eatment. My memory was picture perfect before. I have a mix of depression and anxiety. I \201 nd that with the ECT I also like 10mg Prozac It \200\231s strange how these meds al ways did me a little bit of good by themselves, but that with ECT they work so much better. \200\235155 \200 \200\234I \200\231ve always had a super good memory. It is unreal how poor it is now. But I don \200\231t mind. It \200\231s almost comical. \200\235155 \200 \234After you recover from depression, people encourage you to rebuild your life but [aft er ECT] I couldn \200\231t even remember what my life was. \200\235149 ( \211\210 \200\201r etrograde autobiographical memory.) What \200\231s it like to have ECT? ) L M J ( \200\235 . o g a t i e v i g t h g i m I d n a \200\224 s k r o w t i d n a , k c i u q s \200\231 t i , g n i n e t h g i r f s \200\231 t I \200\234 \200\207 1 Had Rockland asylum banned witnessing ECT, the greatest poem extolling the humanity of me ntal illness VS military-industrial greed could not have arisen. Carl Solomon \200\231s pos t-ECT babble \202 owed directly into Allen Ginsberg \200\231s Howl: \200\234I saw the be st minds of my generation destroyed by madness, starving hysterical naked, dragging themsel ves through the negro streets at dawn looking for an angry \201 x, / Angelheaded hipsters burning for the ancient heavenly connection to the starry dynamo in the machinery of night \200 I \200\231m with you in Rockland in my dreams you walk dripping from a sea-journey o n the highway across America in tears. \200\235 Anxiety neurosis/generalized anxiety disorder GAD Anxiety is a universal experience ( \200 : \200 \211\210 2 : 1); it is, according to some reckonings, the chief factor limiting hu man potential; it causes much suff ering, costing the UK \200\206 5 billion/yr. Neurosis refers to maladaptive psychological symptoms not due to organic causes or psychosis, and us ually precipi- tated by stress. Apart from free- \202 oating anxiety and depression, such symptoms are: fatigue (27%), insomnia (25%), irritability (22%), worry (20%), ob- sessions, compulsions, and somatization (p640) \200\224 all more intense than the stress precipitati ng them would warrant. Symptoms are not just part of a patient \200\231s normal personality , but they may be an exaggeration of personality: a generally anxious person may become eve n more so, ie develop an anxiety neurosis, as a result of job loss. The type of neurosis is de \201 ned by the chief symptom (eg anxiety, obsessional, depressive). Before diagnosing neurosis, consider carefully if there is underlying depression needing antidepressants.156 Symptoms of anxiety: Tension, agitation; feelings of impending doom, trembling; a sense of collapse; insomnia; poor concentration; \200\230goose \202 esh \200\231; \200\230butte r \202 ies in the stomach \200\231; hyperventilation (so tinnitus, tetany, tingling, chest pains); headaches; sweating; palpitations; poor appetite; nausea; \200\230lump in the thr oat \200\231 unrelated to swallowing (globus hystericus); diffi culty in getting to sleep; excessive concern about self and bodily functions; repeti- tive thoughts and activities (p3 46). Children \200\231s symptoms: Thumb-sucking; nail-biting; bed-wetting; foodfads. Causes Genetic predisposition; stress (work, noise, hostile home), events (los- ing or gaining a spouse or job; moving house). Others: Faulty learning or sec- ondary gain (a husband \200 \230forced \200\231 to stay at home with agoraphobic wife). Treatment Symptom control: List ening is a good way to \200\201anxiety. Explain that headaches are not from a tumor, and t hat palpitations are harmless. Anything done to enrich patients \200\231 relationship with others may well help. Regular (non-obsessive!) exercise: Bene \201 cial eff ects appear to equal medita- tion or relaxation. Acute anxiety responds better than chronic anxiety.157 M editation: Intensive but time-limited group stress reduction intervention based on \200 \230mindfulness meditation \200\231 can have long-term bene \201 cial eff ects.158 Cogniti ve \200\223behavioral therapy (p373) and relaxation appear to be the best speci \201 c mea sures159 with 50 \200\22360% recovering over 6 months.160 N=404 Behavioral therapy employs graded exposure to anxiety-provoking stimuli. Drugs augment psychotherapy: 1 Benzodiazepine s (eg diazepam 5mg/8h PO for <4wks. SEs/withdrawal, p368, limit utility). 2 SSRI (p340, eg paroxetine in so- cial anxiety). 161 3 Azapirones (buspirone, 5HT1A partial agonist; 5mg/8 \200\22312h; ?less addictive/sedating than diazepam, and few withdrawal issues). 162 4 Old- style antihistamines (eg hydroxyzine).163 5 \200 -blockers.164 6 Others: pregabalin and ve nlafaxine. 165 Progressive relaxation training: Teach deep breathing using the diaphragm, a nd tensing and relaxation of muscle groups, eg starting with toes and work- ing up the body . Practice is essential. CDs aid learning; in some contexts, eg stress, relaxation is not a s good as cognitive restructuring.166 N=87 Hypnosis Initially the therapist induces progres sively deeper trances eg us- ing guided fantasy and concentration on bodily sensations, suc h as breathing. Later, some patients will be able to induce their own trances. It powerfull y reduces anxiety, and is useful, eg medical contexts (eg post-op). 167 N=32 Prognosis GAD often gets better by 50yrs (often replaced by somatization).168 344 \200 Classifying anxietyDSM-IV \200 Generalized anxiety dis- order (GAD): anxiety +3 somatic s ymptoms and present for \211 6 months \200 Panic disorder \200 Phobia, eg agoraphobia \200 Post-traumatic stress disorder Social anxiety disorder \200 Obsessive \200\223compulsive disorder y r t a h c y s P i 345 Some remarks on adolescent anxiety and mood swings Anxiety is the engine in us, and also ou r steering wheel, weaving us in and out of the fast or slow lanes of our lives. Some of us seek out anxiety as a way of feeling alive (the tightrope walker, or the falconer, placing the meat for his bird between his own eyes). The lives of others are dominated by the imper ative of minimizing anxiety, to the extent that some of us never leave home, either physica lly or metaphorically. Anxiety implies heightened awareness, which is why it is one of the dominant colors in the artist \200\231s metaphysical palette. The artist makes us anxious s o that we see familiar objects diff erently. Anxiety, up to a point, makes us sit up, and t ake note; beyond a certain level (diff erent in all of us, and diff erent at diff erent tim es) anxiety is counter-productive: we become preoccupied with the feeling itself, which cho kes our ability to act (angere =to choke gives us anxiety and angina). y r t a i h c y s P Anxiety is reduced by the chief CNS inhibitory neurotransmitter, GABA (gam- ma-amino-butyri c-acid) which counteracts excitatory limbic system eff ects of glutamate. Stress releases a llopregnanolone (THP) which increases GABA \200\231s calming eff ects in adults. But in ado lescents (at least in adolescent mice), THP has the opposite eff ect. THP has 2 roles: 1 in the limbic system it tranquilizes; 2 in the hippocampus of adolescents THP does the opposi te (the hippocampus is important for emotion regulation, as well as memory). This re \202 ects adoles- cents \200\231 enhanced expression of \200 4 \200 \200\210 GABAA receptors i n the hippocampus. This may explain why, in some adolescents, and maybe other individuals, calm- ness is unattainable (activating the break also activates the accelerator, so respons es are ampli \201 ed into unpredictable mood swings).169 Quotes from the blogsphere: what \200\231s it like to have panic attacks? \200 \200\234I worry about everything: from the detergent I use to the war in Iraq. I am just completely ridiculous with it. To the point where I experience pan- ic attacks, which are terrifying experiences. They feel like heart attacks. Worry steals every happy moment away. It takes away my drive, my ambi- tion, my se nse of adventure, my ability to relax, my ability to have fun. I \200\231m aware of it, and I cannot seem to stop it, nor control it \200 \200\235170 \200 \200\234I woke up in my bed, in the middle of the night. I was sweating, but I was cold. I was so scared that I li terally could not move \200\224all my muscles were locked in position. My heart was racing, and I was breathing so hard that anyone listening would have thought I had just run a mara thon \200 \200\235171 \200 \200\234I felt like I had a tennis ball wedged in the middle of my chest, below my breastbone and above my stomach. It was tight, made me breathe er- r atically \200 and caused me to panic \200 I couldn \200\231t drive like a normal human bei ng \200\224I had to stop every 20 minutes or so to let yet another panic attack pass. I usu ally had to get out of the car, walk around it a few times \200 \200\235172 \200 \200 \234The dentist was in a hell of a hurry \200 I tried to tell him I was not having any reac tion (to the anesthetic). I had a panic attack \200 his hand, scrambled out of the chair tr ailing hoses & drills, scuttled across \202 oor on hands and knees trying to escape. Then I had an asthma attack brought on by panic and it was touch and go for a while. Oh, did I mention that I wet myself? \200\235173 \200 \200\234It had been two years since my last panic attack (deep breathing, medi- tation, and generally better stress management eliminat ed even the tini- est hint of an attack) before I began to plan my trip home \200 \200\235 174 Immunizing ourselves against neurosis: one man \200\231s methodologies \200 Pretending to be a tree \200 Bagpipes \200 Playing with dolphins \200 Seneca (AD65)1 \200 Sea-ba thing Sur \201 ng Self-hypnosis \200 Exercise 1 \200\226 \200\234Men do not care how nobly they live, but only how long, but it is withi n the reach of every man to live nobly, but within no man \200\231s power to live long. \200\226Life without the courage for death is slavery. \200\226Most power- ful is he who h as himself in his own power. \200\226 Toil to make yourself remarkable by some talent or o ther. \200\226Fire is the test of gold; adversity, of strong men. \200\226There is no gre at genius without some touch of madness. \200\235 Other neurotic disorders Phobic disorders involve anxiety in speci \201 c situations only, and leading to their avoidance. These are labeled according to speci \201 c circumstance: agora- phobia (agora, Greek for market place) is fear of crowds, travel, or situations awa y from home; social phobias (where we might be minutely observed, eg small dinner parties); simple phobias, eg to dentists, intercourse, Friday the 13th (triskaidecophobia), spiders (arachnophobia, p372), beetles (paint them red with black spots on and they are charming la dybirds). There may also be free- \202 oating \200\230fear of fear \200\231, or fear of disgracing oneself by uncontrollable screaming. Elicit the exact phobic stimulus. It may be speci \201 c, eg traveling by car, not bicycle. Why are some situations avoided? If delud ed ( \200\234I \200\231m being followed/ persecuted \200\235), paranoia rather than phobia is likely. For panic attacks, try cog- nitive-behavior therapy175 (p373, eg paroxetine 2 0 \200\22350mg/day PO).176,177 Obsessive \200\223compulsive disorder (OCD) Compulsions are senseless, repeated rituals. Obsessions are stereotyped, purposeless words, ideas, or phras es that come into the mind. They are perceived by the patient as nonsensical (unlike delusi onal beliefs), and, although out of character, as originating from them- selves (unlike hal lucinations or thought insertion). They are often resisted by the patient, but if longstand ing, the patient may have given up resisting them. An example of non-verbal compulsive beha vior is the rambler who can never do a long walk because every few paces he wonders if he h as really locked the car, and has to return repeatedly to ensure that this has, in fact, be en done. Cleaning (eg hand-washing), counting, and dressing rituals are other examples. Pat hophysiology: CNS imaging implicates the orbitofrontal cortex178 and the caudate nucleus. S uccessful treatment is re \202 ected by some normalization of metabolism in these areas.17 9 Treatment: Behavioral (or cognitive) therapy (p372). Clomipramine (start with 25mg/day PO ) or SSRIs (eg \202 uoxetine, start with 20mg/day PO) really can help (even if patients a re not depressed): see p340. What \200\231s it like to have OCD? Quotations from the blogsp here: \200\234That afternoon, I found that when I got home from school, I couldn \200\231t get around the house or do normal things without performing rituals to cancel out bad thou ghts over and over again. It was weird and I didn \200\231t want to do it, but if I didn \200\231t I would feel a lot of anxiety and panic like something was very wrong. I kept hav ing to enter and re-enter through the front door. I ended up spending about 3 or 4 hours in the bathroom because I couldn \200\231t get out of there because every time I tried to do the perfect ritual, my body would itch or something else would go wrong and I had to redo t he rituals over again. After a few hours, I wanted to get out of there bad, I felt like a p risoner in my own bathroom! \200\235180 Depersonalization This is an unpleasant state of di sturbed perception in which people, or the self, or parts of the body are experienced as be ing changed ( \200\234as if made of cotton wool \200\235), becoming unreal, remote, or auto ma- tized ( \200\234replaced by robots \200\235). There is insight into its subjective natu re, so it is not a psychosis, but the patient may think he is going mad. Depersonalization may be primary, or part of another neurosis. CNS imaging shows that it is as- sociated with functional abnormalities in the sensory cortex in areas where visual, auditory, and somato sensory (cross-modal) data integrate.181 Derealization These are psychosensory feelings (ak in to depersonalization) of detachment or estrangement from our surroundings. Objects appea r altered: buildings may metamorphose in size and color. The patient acknowledges the unrea lity of these ideas, but is made uneasy by them. 346 \200 y r t a h c y s P i (Our isolation in an alien or unreal universe, and our estrangement from our- selves, are major themes of leading novelists such as Albert Camus.)182 Dissociation (forme rly hysteria) Clinical details: p334. Example of mass hyst- eria spread by TV \200\224Pokem an induced \200\230seizures \200\231: see \200\230the Pokeman contagion \200\231. 183 \201\227: Behavior therapy (p372 antidepressants) if he really wants to change. 347 Near-death; war; rape; earthquake; torture; crimes of passion; shipwreck Stress and post-traumatic stress disorder Relieving stress Smoking, alcohol, and chat- teri ng are popular methods. If drugs must be used, propranolol 10mg/8h PO may \200\201autonomi c failure; heart symptoms (CI: asthma; heart block). Alternatives: exercise, singing, progr es- sive rel axation (p344),counseling (p380). Post-traumatic stress disorder Suspect this if symptoms (BOX) become chronic, with these signs (may be delayed years): diffi culty modu lat- ing arousal; isolated-avoidant modes of living; alcohol abuse; numb to emotions and re lation- ships; survivor guilt; depression; altered world view in which fate is seen as unta mable, capri- cious or absurd, and life can yield no meaning or pleasure. 185 NB: some peop le have this with no known stressor: DSM-IV wrongly calls this adjustment disorder, whereas it is a form of existentialism that only the healing power of story-telling can transform \200\230by serving as an axe for the frozen sea inside us. \200\231Franz Kafka Acute stress reactions \200 Fearful; horri \201 ed; dazed \200 Helpless; numb, detache d \200 Emotional responsiveness \200\201 \200 Intrusive thoughts \200 Derealization (p346) \200 Depersonalization \200 Dissociative amnesia \200 Reliving of events \200 Avoidance of stimuli184 \200 Hypervigilance \200 Concentration \200\201 \200 Restle ssness \200 Autonomic arousal: h t e b c a M \200\224 \200\235 s w o r r o s d e t o o r r e h t o y r t a i h c y s P d n a pulse \200\200; BP \200\200; sweating \200\200 \200 Headaches; abdo pains n i a r b e h t f o s e l b u o r t MRI implicates the anterior cingulate area, with failure to inhibit amyg- dala activation lowered amygdala threshold1 to fearful stimuli.186,187 Treatment: Debrie \201 ng may do more harm than good.188 Macbeth \200\231s \200\230sweet oblivious antidot e to cleanse the stuff ed bosom of that perilous stuff which weighs upon the heart \200\231 has yet to be found. Is the best advice to try to for- get or ignore the past? Macbeth \200\231s doctor asserts (Act V ) that such a pat- ient \200\230must minister to himself \200\231, when he had been unreasonably but royally commanded to \200\230raze out the writ ten troubles of the brain \200\231 \200\224and perhaps tragic literature can off er more th an medicine here, as demonstrated by the many soldiers who have bene \201 tted from Jonath an Shay \200\231s book Achilles in Vietnam.189 In narrative exposure therapy, adults or chi ldren are asked to describe what happened in great detail (what they saw, heard, smelled, f elt, the movements they recall and how they felt and thought at the time). Initial distress is marked, but as sessions are long, habituation ensues as more and more details are recal led. Emphasize integrating emotional and sensory memory within a detailed autobiographic na rrative. After 4 ses- sions, scores on intrusion and avoidance may drop markedly;190 but do n \200\231t expect despression to resolve.191 N=28 Eye movement desensitization and re- pro cessing (EMDR) may also have a role. n e t t i r w e h t t u o g n i z a r \200\234 \200 g n i n a e m h g u o r h t g n i l a e h After the 2004 Indian Ocean tsunamis, psychopathology was as common as physical injury: WHO advised practical outreach help, and to avoid mental health labels (contrary to NICE \200 \231s medicalizing approach to PTSD).192 d n a , e r a e p s e k a h S Amitriptyline, mirtazapine, paroxetine, and atypical anti-psychotics (p360) can help (warn of SEs and withdrawal phenomena, p340).193,194 Prevention: Rehearse t eamwork \200\224and techniques of stress inoculation (by exposure), and desensitization (by helping real casualties, eg if preparing for war). Keeping combatants in tight-knit groups cemented by the ties of mutual interdependency is recommended by military strategists. NB: mor- phine use at the time of injury may be protective. www.killology.com , y p a r e h t o g o L 1 The Papez circuit of emotion runs from the hippocampus to the amygdala and thence to sero tonergic pacemaker cells in the dorsal raphe nucleus (DRN). The DRN projects to the dentate gyrus directly and indirectly via pacemaker cells in the entorhinal cortex. The direct rou te promotes neurogenesis in the dentate; the indirect route has 2 purposes: to imprint ongo ing moments of consciousness onto new dentate cells for retention as memory, and to provide \200\223ve feedback for regulation. Pathologic overdrive of the DRN causes over- drive of the entorhinal cortex, which leads to excitotoxic cell death of neurons in the hippocampus involved in the \200\223ve feedback loop. The disinhibited amygdala and DRN then orchestr ate the syndromes of chronic stress. Recovery from chronic stress requires repopulating the dentate gyrus and restoring the feedback loop.195 Eating disorders: anorexia and bulimia nervosa Eating disorders are common \200\224don \200 \231t expect your patient to \201 t neatly into any category: \200\230Eating disorder no t otherwise speci \201 ed \200\231 is the commonest type; categories such as purging disor der and non-fat-phobic anorexia nervosa are newly proposed categories that may be appropria te to use. Anorexia nervosa \200\207The most fatal of all mental illnesses ( 20%, if sever e). There is a compulsive need is to control eating, as if worth equates with shape (a noto rious western cult). Low self-worth is common and weight loss becomes an over-valued idea e ven when weight is very low. This is achieved by over-exercising, induced vomiting, laxativ e abuse, diuretics, or appetite suppressants. Many also have episodes of binge eating, foll owed by remorse, vomiting, and concealment. Diagnostic criteria:196 1 Weight <85% of pre- d icted (taking into account height, sex, and ethnicity, p181), or BMI \211 17.5kg/ m2. 2 Fe ar of weight gain, even when underweight, leading to dieting, induced vomiting, or excessiv e exercise. 3 Feeling fat when thin. 4 Amenorrhoea: 6 consecutive menstrual cycles absent u nless on the Pill (in women), or \200\201libido \200 . Epidemiology: \200 : \200 \200 \206 4 : 1197 (men are more likely to be undiagnosed; don \200\231t as- sume that a fragile sexual identity exists in these men).198 Typical age of onset is mid-adolescence \200\224b ut may be older than 60yrs.199 Prevalence: 0.7% in teen- age girls and no restriction to a particular ethnic group. Incidence in primary care: 20 : 100,000 in females aged 10 \200 \22339 (stable over the last 20 years).200 Cause: CRF hypothesis;1 55% concordance in monoz ygotic twins in some areas. Comorbidity/risk factors: Depression; anxiety; obsessive compul sive features (=anankastic); perfectionism;201 anxious \200\223avoidant \200\223dependent p ersonality; sub- stance abuse; TV (esp. soap-opera) watching; image-aware work (eg ballet); 202 past teasing or criticism for fatness.203 Adverse life events and diffi culties; most c ommonly in the area of close relationship with family or friends; low self-esteem; impulsiv ity; rarely dietary problems in early life; parents preoc- cupied with food; family relatio nships that leave the person without a sense of identity. There is scant evidence that the chief problem is psychosexual im- maturity (antecedent sexual abuse is not a speci \201 c risk factor). Other signs: Fatigue; cognition \200\201 (cerebral atrophy) altered sleep cyc le; sensitivity to cold; dizziness; psychosexual problems; dental caries; constipation; ful lness after eating; subfertility/amenorrhoea; \200\201WCC; anemia; \200\201platelets; glu cose \200\200 \200\201; \200\201K+; \200\201PO4 3 \200\223; \200\200bicarbonate; \200 \200LFT; \200\200amylase if binging/purging; \200\200T3/T4; normal or \200\201TSH; \200 \201LH; \200\201estrogen; \200\200GH; \200\200cortisol; \200\200CCK; normal prolactin; \200\201renal function; osteo- porosis if malnourished; BP \200\201; \200\200QT interval; amorphous ovaries. In early onset disease, functional MRI shows \200\201blood \202 ow t o the temporal lobe unilaterally. Also: \200\201visuo-spatial ability; \200\201visual mem ory; \200\200speed of information processing. SCOFF questionnaire: (can be used for preven tion)1 Do you ever make yourself sick because you feel too full? Do you worry you \200\231v e lost control over eating? Have you recently lost more than one stone in 3 months? Do you believe you are fat when others say you are thin? Does food dominate your life?204 \200 \200 : Depression, Crohn \200\231s/coeliac disease, hypothalamic tumors. Red \202 ags \200\223 \200\223risk \200\200 \200\200 if: <34.5 348 \200 y r t a h c y s P i T : Vascular: BP <80/50; pulse <40; SaO2 <92%; limbs blue and cold Skin: purpura BMI <13 or below 2nd centile Wt loss >1kg/wk Muscles: unable to get up without using arms for leverage. Blood (mmol/L): K+ <2.5; Na+ <13 0; \200\201PO4 ECG: long QT; \202 at T waves. 3 \200\223 <0.5. Treatment: 2 Aim to restore nutritional balance (eg weight gain of 1.5kg/week; \201 nal B MI 20 \200\22325). Treat complications of starvation. Explore comorbidity. In- volve family /carers. Address factors maintaining the illness. Severe anorexia 1 Anorexics possibly diff er from others in being unable to adapt to corticotrophin releasing factor (CRF) elevation s. Signs of CRF dysfunction and HPA-axis hyperactivity: \200\200physical activity, \200 \201reproductive hormones, \200\201sexual behavior, amenorrhea, hypotension, bradycardia, anxiety, \200\201social interaction, \200\200vigilance, \200\201immune system function, \200\201food intake, impaired weight gain, aff ecting both energy intake and utilization. 205 2 Screen if BMI \200\201; amenorrhoea; poor growth if >8yrs; unexplained vomiting; poor ly-compliant type 1 DM. (BMI <15kg/m2, rapid weight loss + evidence of system failure) requires urgent referral to eating disorder unit (EDU), medical unit (MU) or pediatric medical wards (P). Re-feeding is considered \200\230treatment \200\231 under the Mental Health Act 1983/Children Act 1989, and it may be needed if insight is lacking. In moderate anorexia (BMI 15 \200\22317.5, no evidence of system failure) routine referral can be to the local community mental health te am (CMHT)/adolescent unit or EDU if avail- able. In mild anorexia (BMI >17.5) focus on buil ding a trusting relationship and encouraging use of self-help books and a food diary.206 If there is no response within 8wks, consider referral to secondary care. No drug treatments for ano- rexia nervosa are validated by good randomized trials. Fluoxetine (20 \200\22360mg / day) prevents relapse in open trials. Monitor Q \200\223T interval. There is wide vari- a bility in the availability of psychological therapies and no uniform approach. Cognitive th erapies (p372), analytic, interpersonal, supportive, or family ther- apy ( parent-to-paren t consultations3) may be tried. In children and adoles- cents consider family therapy.207 O lanzapine may help (unlicensed use). Re-feeding syndrome: (On rapid intake of calories). Si