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 gns: rhabdomyolysis, respiratory or cardiac failure, BP \200\201, arrhythmias, seizures, co ma, sudden death. Re-feeding syndrome is very rare when with home re-feeding. Acute gastric 3 \200\223 dilatation can occur if a poorly nourished patient binges. Monitor serum PO4 (s top re-feeding if falling). Also watch for glucose \200\200, K+ \200\201, and Mg2+ \200\200 .200,208,209 Prognosis: 43% recover completely, 36% improve and 20% develop a chronic eati ng disorder. 5% die (mostly from suicide or direct medical complications, eg K+ \200\201 an d prolonged Q \200\223T interval predisposing to arrhythmias). Median time between diagnosi s and death is 11 years.210 Mortality is higher if: aged 20 \200\22329 at presentation, de layed access to treatment, binging and vomiting. Binge eating disorder/bulimia De \201 nit ion: 1 Recurrent episodes of binge eat- ing characterized by uncontrolled overeating; 2 Pre occupation with control of body weight 3 Regular use of mechanisms to overcome the fattenin g eff ects of binges, eg starvation, vomit-induction, laxatives, over-exercise 4 BMI >17.5. 211 Epidemiology: \200 : \200 \211\210 9 : 1. Prevalence (rising in developed countrie s) \211\210 0.5 \200\2231.0% in young women. Social class distribution: even. In Britain, young Muslim Asian women are at \200\200risk.212 Homosexuality/bisexuality may be a speci \201 c risk factor for bulimia in males (asexuality is more typical in \200 anorexia ner vosa).213 Cause/associations: Urbanization (not a risk factor for anorexia); premorbid obes ity. Commoner in \200 relatives of anorectics, suggesting a shared familial li- ability. Genetic contribution of 54 \200\22383%. Natural history: Age of onset: 18yrs. Symptoms: Fa tigue, lethargy,4 feeling bloated, constipation, abdominal pain, oesophagitis, gastric dila tation with risk of gastric rupture, heart conduction abnormalities, cardiomyopathy (if lax ative use), tetany, occasional swelling of hands and feet, irregular menstruation, erosion of dental enamel, enlarged parotid glands, calluses on the back of the hands (Russell \200 \231s sign, from tooth marks during induction of vomiting), oedema (use of laxatives and di uretics), metabolic alkalosis, hypochloraemia, hypokalaemia, metabolic acidosis (if laxativ e use), less commonly hyponatraemia, hypocalcaemia, hypophospha- taemia, hypomagnesaemia, a bnormal EEG, abnormal menstrual cycle, blunted response of TSH and growth hormone to thyroi d releasing hormone. Treatment: Mild symptoms: support, self-help books and food diary simi larly to anorexia. Referral to CMHT or EDU (above) in case of no response, moderate or seve re symptoms, and to a medical unit if medical complications.214 Anti- depressants have the most robust evidence at usual doses but \202 uoxetine may be needed at up to 60mg/day.215 Cognitive therapy can help (p370 \200\2231).216 Prognosis: In 2 \200\22310yrs, 50% improve , 20% show no change.217 349 y r t a i h c y s P 3 Parents describe parent-to-parent consultations as an intense emotional experience that h elps them to feel less alone, to feel empowered to progress, and to re \202 ect on changes in family interactions. 4 If hypersomnia, hyperphagia, and hypersexuality are features, su spect the Kleine \200\223Levin syndrome. Organic reactions (delirium; dementia) Acute organic reactions (Acute confusion, delirium) The key feature is im- paired consciousness with onset over hours or days. It is diffi cult to describe; take any opportunity to be shown it. You have the sense when trying to com- m unicate that your patient is not with you. He is likely to be disoriented in time (doesn \200\231t know day or year) and, with greater impairment, in place. Some- times he is quiet or drowsy; sometimes agitated, and you are called when he is disrupting the ward. Or he ma y be deluded (for example, accusing staff of plotting against him/her) or hallucinating. If there is no past psychiatric his- tory, and in the setting of a physical illness or post-s urgery, a confusional state is particularly likely \200\224especially if symptoms are worse at the end of the day. Differential diagnosis: If agitated, consider anxiety (usually read ily distin- guished on history-taking). If onset uncertain, consider dementia. Causes: (BOX 1)Infection; drugs (benzodiazepines, opiates, anticonvulsants, digoxin, L-dopa); U&E \200 \200 \200\201; hypoglycaemia; PaO2 \200\201; PaCO2 \200\200; epilepsy; alcohol with- drawal ; trauma; surgery (esp. if pre-op Na+ \200\201 or visual or hearing loss).218 Tests: U&E, F BC, blood gasses, glucose, cultures (blood, MSU), LFT, ECG, CT, CXR LP. Management: Find the cause. Optimize surroundings and nursing care. Exam- ine with above causes in mind; do tests; start relevant treatment, eg O2. \200 If agitation is distressing the patient, an d non-drug methods fail, consider haloperidol 1 \200\22310mg IV/IM/PO219 or risperidone 0.5 \200\2234mg/24h PO (smallest dose possible, esp. if elderly).220 Monitor BP. Wait 20min to judge IM eff ects. Amne- sia and cognition may worsen221 (SE: BP \200\201 \200\200, stroke ,220 insomnia, dyspepsia). Mu- sic, muscle relaxation, and massage (MMM) is a better approa ch to agitation. \200 Nurse ideally in a moderately lit quiet room with same staff in att endance. Reassure and re-orientate often. A compromise between a quiet room and a place whe re staff can keep under surveillance has to be made. Monitor BP. Chronic organic reactions (dementia) 6% of those \200\20665yrs. Cardinal signs: Global intellectual deterioration wi thout impairment of consciousness \200\224plus memory loss. Get a history from friends/rela tives. Exclude depression (may need a drug trial). Behavior: restless; no initiative; repet itive, purposeless ac- tivity; sexual disinhibition; social gaff es; shoplifting; rigid rou tines. \200 Speech: syntax errors; dysphasia; mutism. \200 Thinking: slow, muddled; del usions. Poor memory. No insight. \200 Perception: illusions, hallucinations (often visual ). \200 Mood: irritable, depressed; aff ect blunt; emotional incontinence (much crying). Tests: \200 FBC; B12; folate (MCV \200\200 suggests alcoholism, or low B12 or folate); ES R (malignancy); U&E, LFT, \200 GT, Ca2+ (renal/hepatic failure, alcoholism, malignancy, en docrinopathy (Ca2+ \200\200 or \200\201). TSH (hypothyroidism). \200 Serology: syphilis (OHCM p419) HIV. \200 CT/MRI excludes tumors, hydrocephalus, subdural, stroke etc. Vo lumetric MRI to subtype the dementia, eg medial temporal (MTL) and hip- pocampal atrophy \211\210 Alzheimer \200\231s disease (AD); in frontotemoral dementia tem- poral lobe atroph y is more inferior, and there may be marked asymmetry. In Lewy-body dementia, MTL is relati vely spared.222 DaT may help.1 FLAIR MRI ( \202 uid attenuated inversion recovery) for isc haemic damage (often co-exists with AD). Management: \200\207Involve the patient in her ow n therapy. Exclude the treat- able. Relatives may feel unable to look after the immobile, i ncontinent, ag- gressive, patient who keeps wandering. Good palliative care, walking frames , catheters, day care, holiday admission, an attendance allowance, electronic tagging 2 an lasting power of attorney can help. If not, long-stay institu- tional care may be needed . Agitation: MMM before drugs, as above.223 Protective agents (possibly): Statins (relative risk 0.29); antioxidants.224 n=1364 350 \200 y r t a h c y s P i 1 DaTSCAN comprises io \202 upane labeled with radioactive iodide. It is injected during S PECT imaging to detect loss of dopaminergic neuron terminals in the striatum. Speci \201 c ity in Lewy body dementia: 100%. 2 Supported by the Alzheimer \200\231s Soc. (if it \200 \231s not a substitute for 1st class care); restraint is unacceptable. 351 Causes of organic reactions ! t s e t Acute (delirium) Chronic (dementia) \200\226Alzheimer \200\231s; Huntington \200\231s (OHCM p694); \200 \226Lewy-body (OHCM p478), CJD & Pick \200\231s (p650) Tumors; subdural haematoma; multiple sclerosis; Parkinson \200\231s; normal pressure hydrocephalus Late syphilis; chronic or su b- acute encephalitis; CNS cysticer- cosis; cryptococcosis; HIV Thromboembolic multi-infarc t (arteriosclerotic) dementia Liver and kidney failure non-metastatic or metastatic cancer T4 \200\201; Addison \200\231s; hypoglycaemia hypopituitarism; hypo-/hyper- parathyroidism2 25 \200\226 \200\230Alcohol dementia \200\231; barbitur ate abuse; too much manganese or c arbon disul \201 de Degenera- tive e l b i s s o p Other CNS Cerebral tumor or abscess; sub- dural haematoma; epilepsy; acute post-trauma psyc hosis y r e v e Infective \200\226 Many, eg meningoencephalitis; septicaemia; cerebral malaria; trypanosomi asis Vascular Stroke (or TIA); hypertensive g n i r e d r o y b encephalopathy; SLE U&E \200\200 \200\201; \200\226hypoxia; \200\226liver and kidney fail ure; non-metastatic cancer; porphyria; \200\226alcohol withdrawal y r t a i h c y s P t n e i t a p Metabolic \200\226 r u o y Endocrine Addisonian or hyperthyroid crisis; diabetic pre-coma; hypoglycaemia; hypo/hyperpa rathyroidism \200\226Alcohol; many drugs (check data- sheet/statement of product charac- t eristics); lead; arsenic; mercury t s u a h x e Toxic t \200\231 n o D De \201 ciency Thiamine; B12; folate; nicotinic acid Thiamine; B12; folate; nicotinic acid \200\226 denotes a leading cause. Example of advice addressed to relatives/carers of deme nted people 1 Alzheimer \200\231s disease is progressive, but some problems, eg aggression, may improve in time. Both rate of change and length of life vary greatly. Should you try t o explain to your relative what the diagnosis is? There is no easy answer. The advantage of frank talking is that he can par- ticipate in his care (the vexed issue of stopping drivin g may be easier to handle). Also, in the early stages, he can consent to plans. Most would want to be informed if they got Alzheimer \200\231s. 2 Take opportunities to talk of your predicament with other people in the same position. Th is is often just as useful as talking to doctors. The Alzhei- mer \200\231s Disease Society exists to put you in touch: UK tel: 020 7306 0606. 3 Accept off ers of help, eg with carer programs, and of daycare and res- pite care:1 you certainly deserve, and need, a break from time to time. 4 Help for carers:uk \200 Carers Allowance (> 58/wk2) \200 Attendance Allowance \200 Council tax rebate from Social Services \200 Local voluntary organizations \200 Annual health checks to look after the emotional/physical lives of carers \200 Direct payments \200 Help in balancing work and care. There are 6 million carers in the UK. 50% give 20h care a week; >1 million give more than 50h/ wk. We all need to be aware of this huge burde n being carried by carers.226 5 Lock up any rooms in the house which you do not use. Your r elative will not notice this restriction \200\224and this may make your life much easier. 6 Lock drawers which contain important papers or easily spoiled items to prevent him storing odd things in them, such as compost, or worse. 7 Remove locks from the lavatory \200\224so he/she cannot get locked in. 8 Sexual activitie s may stop; spouses should try not to fall into the trap of asking \200\234What \200\231s the matter with me? \200\235 (NB: SSRI or cyproterone acetate titr- ated to 50mg/12h help \200 hypersexuality3 and other aggressive problems).227 9 Prepare yourself psychologically for the day when he/she no longer recog- nizes you. This can be a great blow, unless you prepare for it. 1 Social ServicesUK often refuse 24h help saying that needs aren \200\231t complex enough; Courts may reverse this. 2 Ineligible if: receiving state pension; <35h of care/wk; income > 95/wk after tax; a full-time student. 3 Real hypersexuality (libido \200\200) is rare. M ost inappropriate sexual behaviors are related to disinhibition or lack of taking into acco unt contextual environment and feelings of others. Psychiatric aspects of Alzheimer \200\231s disease (AD) NICE A common scenario. \200\234Do ctor, I think my memory is failing. I go into a room full of people I know and cannot remem ber a single name: the only name to come is Alzheimer \200\235 Is this mild cognitive i mpairment (and relatively static) or is it AD? (progressive). What most doctors do is some sort of memory test, but a better approach is to get a history from a friend/spouse ( \200 \234Does he ever get lost in familiar territory/at home? trouble with shopping, and countin g out cash etc) and then do some visuo-spacial tasks, eg \200\234Draw a house with a door, a side, a chimney and a few windows \200\235 or \200\234draw a clock face and put the num - bers in and set to time to 2 : 30. \200\235 A drawing is useful because it is a permanant snapshot of an unfolding process, and can be compared over time. Clock draw- ing is also p art of systematic diagnostic methods \200\224the TYM test (Test Your Memory, OHCM p85). Se e BOX 1 for a brief memory test. Cause It is not clear if the problem is amyloid plaques an d neuro \201 brillary tan- gles (are they epiphenomena?). Selective loss of temporal lobe synapses may be more important228 loss of whole neurons in the hippocampus, amygdala, te mporal lobe and subcortical nuclei (OHCM p492). Treatment doesn \200\231t focus on any of t hese areas, but assumes that what is important is loss of cholinergic function (?one reason why drugs often disappoint in AD). Vascular eff ects may trump any of the above (95% of AD patients show CNS ischaemia). Risk factors 1st-degree relative with AD; Down \200\231s syn drome; homozygosity for the apolipoprotein (Apo) E e4 allele; PICALM, CL1 and CLU gene muta tions; vas- cular risk factors such as \200\200BP, diabetes, dyslipidaemia, \200\200homoc ysteine,1 atrial \201 brillation; \200\201physical and cognitive activity; depression. E vidence on smoking and alcohol is inconsistent: \200\2062U/day of alcohol accelerated onse t of AD by 5yrs in one study (others say red wine may be protective); \200\20620 cigarette s/day \211\210 2yrs; ApoE e4 genotype \211\210 3yrs. \200\207Delaying onset by 5yrs woul d \200\201prevalence by 50%. Presentation In STAGE I of AD there is amnesia and spatial d isorientation. In STAGE II (some years later): personality disintegration, eg with aggressi on, psy- chosis, agitation, depression, and focal parietal signs, eg dysphasia, apraxia, ag nosia, and acalculia. Parkinsonism may occur. She may use her mouth to examine objects (hyp erorality). STAGE III Neurovegetative changes with apa- thy (or ceaselessly active \200\224 akathisia), wasting, immobility, and incontinence, seizures and spasticity. Mean surviva l: 7yrs from clinical (overt) onset. Drugs Get expert help to increase CNS acetylcholine by inhibiting the enzyme causing its breakdown (donepezil; rivastigmine; galantamine). Memant ine, a NMDA (N-methyl-D-aspartate) receptor antagonist, may help moderate to severe AD. Cau tions: creatinine \200\200; epilepsy. SE: confusion, headache, hallucina- tions, tiredness; rarer: vomiting, anxiety, hypertonia, cystitis, \200\200libido. Dose: initially 5mg each morning; \200\200 in steps of 5mg at intervals of 1wk to 10mg/12h. Practical help \200 \207p351. Exclude treatable dementias (B12, folate, syphilis serol- ogy, T4, HIV). CT/MRI ( p352). Treat concurrent illnesses (they worsen dementia). Avoid sedatives and neuroleptics (longevity, \202 uency, and cognition all suff er). In most, dementia progresses. Involve relatives and relevant agencies. Prevention B vitamins to lower homocysteine;1 long-chain omega-3 fatty ac- ids/N-3 PUFAs, eg eicosapentaenoic acid (EPA+DHA), in \202 ax, walnuts, tuna, mack- erel, and herring oil show promise.229,230 More fruit (?risk \200\201 by \205\223);231 cognitively stimulating hobbies (a 1-point \200\200in cognitive activity sco re can \200\201risk by \205\223). 352 2010 \200 y r t a h c y s P i A cohort study of 678 nuns showed that education and use of syntactically and imaginatively rich language at 18yrs old predicts onset of AD 50yrs later.232 + 20mg vit B6 /day PO \200\201mild cognitive impairment (MCI) if baseline homo- 1 0.8mg fo lic acid, 0.5mg vit B12 cysteine >11 mol/L. B vitamins also \200\201 rates of MRI brain a trophy in MCI (Celeste de Jager s VITACOG trials).233 353 =10 ) & other tests Hodgkinson \200\231s Abbreviated Mental Test Score (max Check that he is fully awake and not in pain. 1 2 Name of your country \200\231s 1 president, ruler or premier 1 Memorize address (42 West St, Hull) 1 1 1 Date of world war (I or II) 1 1 Count backwards from 20 to 1 234Alternative : TYM test, OHCM p85; Mini-mental State cannot be printed for copyright reasons Present year and own age Time to nearest hour Recognition of people Name of place Birthday (day & month) Temporal lobe function is tested by memory tests (above); scores of \211 6 sug- gest confu sion or dementia (correct in 80%).235 Serial changes mean more than a one-off value. Other illness can lower scores (eg \200\201cardiac output). 236 Other pointers to dementia Incr easingly, do you \201 nd that \200 You forget what you are saying or reading in mid- sentence? \200 You have to rely on lists whereas previously this was not necessary? \200 Thought is slow or imprecise, harmonizing poorly with motor control? \200 Mental agilit y is lacking, with powers of concentration declining? \200 Is there diffi culty executing fast movements of eyes or limbs, or diffi culty in walking? \200\224eg with spastic ataxic gait or quadriparesis of HIV \200\2231 asso- ciated cognitive/motor complex, or psychomoto r retardation, release re \202 exes such as a snout response, or hyperactive deep tendo n re \202 exes. NB: including an \200\230informant report questionnaire \200\231 improves the effi ciency of the mental test score as a screening tool for dementia.237 Bedside test s of frontal lobe function (eg executive function).238 \200 Verbal \202 uency and initi ation: Ask the patient to recall as many words y r t a i h c y s P as possible in 1 minute starting with \200\230S \200\231 ; fewer than 10 is abnormal. Cognitive estimates: Ask to give educated guesses to questions which they are unlikely to k now the answer, eg \200\234How old is the oldest person in the country? \200\235 \200\234 How many camels are there in Holland? \200\235 Abstract thinking: Proverb interpretation (however interpretation highly dependent on educa tional, cultural factors). Explain the linkage between pairs: eg poem & statue; praise & pu nishment; orange & banana. \200 Tests of \200\230response inhibition \200\231 and \200 \230set shifting \200\231 \200\224eg a triangle and square test: draw an alternating sequen ce of triangles and squares \200\224and ask the patient to copy what you are doing. Only th e grossly impaired will keep drawing just one of the shapes (perseveration). Clock drawing test: \200\230draw a large clock face, put the numbers in, put the hands in to show ten past \201 ve \200\231. Tests frontal (executive) and domi- nant parietal (pra xis) function, and is an adjunct to mental test scores. Quotes from the blogsphere. \200\234My mother has Alzheimer \200\231s \200 \200\235 \200 \234Each morning she wakes up smiling and walks out not knowing she has soiled herself \200 She doesn \200\231t know why she is being stripped and washed. It \200\231s like a daily physical and emotional rape. Her cries echo in my ears even when she is not crying. In her lucid moments she says, \200\234Anu, I don \200\231t know what I \200\231m doing. Why is t his happening to me? \200\235. . y l i m a f r e h & u n A \200\234My kids are petri \201 ed of old age and though they are very young, they keep as king me if I will become like my mother when I grow old. I have no time to spend with my hu sband \200 I can see my marriage getting aff ected, but after staying awake with my mother in her room for days and then dragging myself to work, not sleeping even four hours for wee ks, I \200\231m ex- hausted emotionally and physically. There are days I drive on the highw ay and wish a truck would crush me. \200\235 Would Anu consider a nursing home? \200\234My mother will die. Even though she is in an advanced stage of Alzheimer \200\231s she knows she is with family. In her lucid moments she asks, \200\234Tum mujhe chod to nahin dogey n a? \200\235 (You won \200\231t desert me will you?) \200\235 . 239 Courtesy of o t d e t a c i d e d s i e g a p s i h T Kavita Chhibber Mania and bipolar aff ective disorder Quote from Zo \200\231s mother:240 \200\234 \200 \230There \200\231s been a fatality on the line \200 \200\231 Nei- ther of us guessed it w as you, even though you \200\231d tried to kill yourself before. We called it a nervous bre akdown when Bristol University sent you home for \200\230undisciplined behavior. \200\231 As our memories faded and you seemed set for a brilliant career, no one spoke about this \201 rst episode. \200\234I \200\231ve been to the bottom, \200\235 you used to say, \200 \234I \200\231m strong. \200\235 We put the horror behind us. It was over. Then when your c harisma and enthusiasms grew wild again, and ag- gressive, we said \200\234Zo is just be ing Zo \200\235. We were in denial and so were you. We followed your lead. You gave up yo ur job and against everyone \200\231s advice, went to Morocco \200\234to \201 nd myself \200\235. I loved the emails you sent in those \201 rst weeks, full of enthusiasm about I slamic culture, learning Arabic and meet- ing the love of your life. Then the emails grew w ilder, your projects more farfetched, but we suspected nothing until we arrived to \201 n d you in full blown mania: attacking the hotel staff , knocking my glasses off my nose, ref using to eat, hectoring everyone in earshot with grandiloquent schemes to save the universe \200 Perhaps you were too \201 ne for us? The beat of the drum you danced to didn \200 \231t \201 t with our drab, calculating world; or was it random mis \201 rings, turning your reactions from vivid to \202 orid? \200\235Letter to a Lost Daughter Prevalence may be increasing in those <19yrs old241 (0.25% in 1994; 1% in 2003). Signs of mania Mood: Irri tability (80%), euphoria (71%), lability (69%). \200 Cognition: Grandiosity (78%); \202 ight of ideas/racing thoughts (71%); distract- ibility/poor concentration (71%); confusion (25%), many con \202 icting lines of thought urgently racing in contrary directions; lack of insight. Behavior: Rapid speech (98%), hyperactivity (87%), \200\201sleep (81%), hyper sexuality (57%), extravagance (55%). Psychotic symptoms: Delusions (48%), hallucinations (1 5%). Less severe states are termed hypomania. If depression alternates with mania, the term bipolar affective disorder is used (esp. if there is a history of this). During mood swing s, risk of suicide is high. Cyclical mood swings without the more \202 orid features (as above) are termed cyclothymia. Causes Physical: Infections, hyperthyroidism; SLE; thromboti c thromocyto- penic purpura; stroke; water dysregulation/Na+ \200\201; ECT. Drugs: Amphetam ines, cocaine, antidepressants (esp. venlafaxine242), captopril, steroids, procyclidine, L- dopa, baclofen. Bipolar disorder: (Age at onset: <25.) In a 1st attack Ask about: Infection s, drug use, and past or family history of psychiatric disorders. Do: CT of the head, EEG, and screen for drugs/toxins.243 \200 Assess: Psychotic symptoms (p316); cycling speed; Tr eating acute mania suicide risk. \201\227 for acute moderate/severe mania: olanzapine 10mg PO, adjust to 5 \200\22320mg/day (SE: weight \200\200; glucose \200\200), or valproate sem isodium, eg 250mg/8h PO (Depakote ; may be \200\200 rapidly to 1 \200\2232g/24h). NB: som e people are most ful \201 lled and creative when manic and don \200\231t want to change; others recognize, in retro- spect, that use of mental health law (a last resort) was a turn ing point. Prophylaxis Those who have bipolar aff ective disorder after successful treat- m ent of the manic or depressive episode should have a mood stabilizer for longer-term contro l. If compliance is good, and U&E, ECG, and T4 normal, give lithium carbonate 125mg \200 \2231g/12h PO. Adjust dose to give a plasma level of 0.6 \200\2231mmol/L Li+, on day 4 \200\2237, 12h post-dose. A range of 0.4 \200\2231 may be equally valid; \200 Check Li+ levels weekly ( 12h post-dose) until the dose has been constant for 4wks; then monthly for 6 months; then 3-monthly, if stable; more often if on diuretic, NSAIDs, ACE-i (all \200 \200 Li+) or on a low-salt diet or if pregnant (?avoid Li+). \200 If Li+ levels are progr essively rising, suspect progressive nephrotoxicity. \200 U&E + TSH 6-monthly; Li+ SE: hy pothyroidism; nephrogenic diabetes insipidus). \200\207Avoid changing brands [Li+ \200\201 \200\200]. \200\207Ensure you can contact urgently if Li+ >1.4mmol/L. \200\207Toxic sign s: vision \200\201; D&V; K+ \200\201; ataxia; tremor; dysarthria; coma. 354 \200 D. Schwarz; Chipmonka y r t a h c y s P i consider a tighter range if elderly ( \200\200 sensitivity to Li+ neurotoxicity).244 355 Helping those with mania and a high risk of suicide \200\235 s s e n l l e w n i d a e d l e e f Risk of suicide is high if: \200 Previous suicide attempt \200 Family history of sui- c ide \200 Early onset of bipolar disorder \200 Extent of depressive symptoms (eg hopeles sness) \200 Increasingly bad aff ective signs \200 Mixed aff ective states \200 Rapid cycling \200 Abuse of alcohol or drugs.245 Lithium reduces risk of suicide.245 If contraindicated, olanzapine + \202 uox- etine may be better than lamotrigine (below).246 \200\207But don \200\231t rely on drugs. Often peop le with mania won \200\231t take them anyway. As one bipolar writer said \200\234I do not believe that a complex problem can be solved simply by pop- ping pills \200 I thrive in the extremes of my cycles, and the words pour from my mind and hand. All that evaporates in we llness,1 so I imagine it would dissolve completely if I chemically alleviated my malady. I will not dilute my intensity and drain my writing. I feel dead in wellness, so I fear that I would feel just as lifeless if I was \200\230cured. \200\231 My identity is also still s o blended with this disorder. It is a fundamental part of me and shapes my world. I accept this disorder as a forming force in my life and value how it has made me. It tested me; it made me stronger; it made me diff erent; it gave me my creativity \200 It is not just a dis ease to be remedied; it is a real part of me that I need to learn to cope with and adapt to . I need to discover how to control it, rather than allow it to dominate me so that I can l ive with it as a vital aspect of my life. \200\235247 Cognitive therapy (p373) is of great value in helping people (who retain some insight) ride their cycles without falling off .24 6 I \200\234 : e r u c d n a e s a e s i d f o s a e d i y r t a i h c y s P s t r e v b u s s g o l B When lithium does not give good control Note that abrupt cessation of lithium precipitates acute mania in up to 50% of patients. Discontinuation should be gradual over 2 \200\2234 we eks. Anticonvulsants: Semisodium valproate (SE: hyperandrogenism if \200 ) and carbamazepi ne (400mg/8h PO; swallow whole; do not chew) are next steps.248 Some authorities say most s peci \201 c indication may be in rapid cyclers ( \211 4 acute mood swings/yr). Lamotrigine may be as good as citalopram in bipolar depressive states.249 Antipsychotics: Olanzapine h as a role.250 In one meta- analysis, there was no diff erence in overall effi cacy of treat ment between haloperidol and olanzapine or risperidone. Some evidence suggests that halo- p eridol could be less eff ective than aripiprazole.251 Anticonvulsants such as lamotrigine, gabapentin and topiramate are po- tential mood stabilizers. Lamotrigine has the strongest evidence.252 Combination treatments : (Often tried). Lithium plus carbamazepine may be synergistic.253 Lithium (or valpoate) pl us an atypical antipsychotic, eg risperi- done or olanz apine may help if unresponsive to m onotherapy.254,255 Antidepressants with lithium Lithium (or an alternative mood stabilizer) reduces risk of mood \202 uctuations from mania to depression in people with bipolar aff ective disorder. For depression occurring during lithium treatment antidepressants can be used: selective serotonin reuptake inhibitors (SSRIs) bupropion, and venlafaxine are said b y expert committees to be best. Ta- per from 2 to 6 months after remission to minimize mani c relapse.256 Consider monoamine oxidase inhibitors for anergic (=lacking in energy) bipolar depression.2 57 ECT also has a role (p342),258 and meta-analyzes support use of omega 3 oils (only for w hen mood is low).259 \201\2011 A counter argument from the periodically depressed poet Thomas Krampf: \200\234 one can have a vision but no vision is worth anything if one is too sick to implement it \200\235 \200\224 and many writers have found their creativity \202 ourish more when treatment is underway. M Berlin 2008 Poets on Prozac, Baltimore.