Medium/longer-term management \200\224 if the patient continues to have swallowing problem s, then a PEG or radiologically inserted gastros- tomy (RIG) tube can be inserted. Patients on long-term feeding should be reviewed regularly as swallow can return many months later and oral feeding can gradually be introduced and sometimes tubes can be removed. 2It is imp ortant to understand that arti \201 cial feeding by any method does not prevent aspiration and in some cases can aggravate it. See b \200\230The ethics of clinically assisted feedi ng \200\231, p.360, for discussion of the ethics of feeding. 190 CHAPTER 8 Stroke Stroke units De \201 nition Geographically de \201 ned unit staffed by a coordinated MDT with expertise in stroke. The gold standard is to admit stroke patients directly and con- t inue care through to discharge \200\224 known as a comprehensive stroke unit. Some units d eal with acute admissions only, others with the post-acute rehabilitation phase only. There is evidence for stroke-speci \201 c early sup- ported discharge schemes reducing death or dependency. Bene \201 ts Stroke units when compared with general ward care result in lower rates of de ath, dependency, and institutional care, without lengthening hospital stay. The number need ed to treat in a stroke unit to prevent one death or dependency is 18. Rationale The majority of improvement seems to occur in the \201 rst 4 weeks, and the mec hanism is unclear. Key components of stroke units include: Meticulous attention to physiological homeostasis \200 Attention to prevention of complic ations (such as thromboembolic disease and pressure sores) Early mobilization \200 Coordinated MDT care \200 Interest, expertise, and motivation o f staff \200 The individual impact of each of these is unknown, but combined they confer signi \201 cant bene \201 ts to the stroke patient Further reading Stroke Unit Trialists Collaboration, Cochrane Review online : M www2.cochra ne.org/reviews/en/ ab000197.html. STROKE UNITS 191 HOW TO Estimate prognosis after stroke After \201 rst-ever stroke, death occurs in 12 % by a week, in 31 % at 1 year, and in 60 % at 5 years. Indicators of a poor prognosis i nclude: \200 Impaired consciousness \200 Gaze preference \200 Dense weakness \200 C ardiac comorbidity \200 Urinary incontinence \200 Pupillary abnormalities The risk of r ecurrent stroke among survivors is 10 \200\22316 % at 1 year, there- after falling to about 4 \200\2235 % per annum. The risk is higher with increasing number of risk factors. Recovery is usually slow, and a clear time-frame established early on in the disease with t he patient and the relatives is helpful. Recovery is most rapid in the \201 rst 3 months, and this tends to be \200\230front loaded \200\231 so the most dramatic improvements occu r in the early weeks. Recovery then tends to slow, but may continue for up to 2 years. 2Eac h patient is different \200\224 recovery may be delayed by infections, depression etc., an d this time-frame should be a guide only. The risk of not returning to independence varies with stroke type. Overall, about 20 \200 \22330 % of survivors are dependent at a year, and 40 \200\22350 % are independent. 192 CHAPTER 8 Stroke Thrombolysis Rationale In acute ischaemic stroke, an artery becomes occluded by thrombus in situ or embolus, and blood supply is compromised. Death of surrounding brain tissue result s in de \201 cits in function associated with that part of the brain. Early recanalization of the vessel by lysing thrombus may limit the extent of brain injury. The agent used is i v recombinant tPA (r-tPA). Risks Treatment with thrombolysis leads to an excess in death due to intracra- nial hemorrh age (a \201 vefold increase compared with placebo). Bene \201 ts Despite early excess of deaths due to hemorrhage, treatment with thrombolysis leads to 44 fewer dead or dependent patients per 1000 treated with r-tPA within 6hr, and 1 26 fewer dead or dependent patients per 1000 treated with r-tPA within 3hr. Imaging This should be done prior to giving thrombolysis to exclude hemorrhage. Perfusion- and diffusion-weighted MR scans may give more information than CT. CT perfusion is being us ed more frequently. All need to be inter- preted by someone with the appropriate experience prior to thrombolysis. Plain axial CT remains the mainstay of imaging prior to thrombolysi s. Use Thrombolysis is recommended in centers with suf \201 cient expertise in stroke, and wi th facilities to deal with complications. In these centers, iv r-tPA is considered in all p atients with de \201 nite ischaemic stroke who present within 3hr of the onset of symptoms . Where this expertise doesn \200\231t exist, the service may still be provided via telemed icine links with stroke \200\230hubs \200\231. Careful discussion with the patient and fam ily of risks and bene \201 ts is required. Exclusion criteria There is a very long list of exclusions but the following are the common est reasons to withhold treatment: \200 Previous hemorrhage or active bleeding site \200 Seizure at onset \200 Impaired coagulation \200 Caution with very severe stroke This page intentionally left blank 194 CHAPTER 8 Stroke Ongoing management Should involve all of the MDT: Dietician Calculate food and \202 uid requirements for each individual patient; adapt die t for speci \201 c needs (eg diabetic, weight loss); develop regimens for NG or PEG feeds; advise on provision of modi \201 ed diets for stages of swallow recovery (thickened, pure ed, etc.); review nutrition as recovery alters needs. Doctors Diagnosis; manage medical complications; establish therapies. Nurses Monitor patient continuously; assist with basic care (physiological and physical); o ngoing bowel and bladder management; ongoing skin care; facilitate practice of skills acqui red in therapy; promote functional inde- pendence; \201 rst point of call for relatives. Occupational therapist Optimize functional ability (usually begin with upper limb work, coo rdi- nating with the physiotherapist); speci \201 c assessments of certain tasks (washing and dressing, kitchen safety, occupational tasks, etc.) as recovery continues; adaptation t o home environment by a series of home visits, with and without the patient, and the supply of aids (rails, bed levers, toilet raises, bath boards, etc.), provision of wheelchairs wh ere needed. Pharmacist Review charts; promote safe prescribing. Physiotherapist Assess muscle tone, movement and mobility; maximize functional independ- en ce by education and exercise; monitor respiratory function; initial bed mobility, then work on sitting balance, then transfers and \201 nally standing and stepping; help prevent co mplications such as shoulder pain, contrac- tures and immobility associated problems (press ure sores, DVT/PE). Psychologist Assess psychological impact of stroke on patient and family; allow the patient to talk about the impact of the illness; monitor for depression and other mood disorder, h ighlighting the need for medication; document cognitive impairment; assist in retraining wh ere neglect is prominent. Social worker Psychosocial assessment of patient and family; support with \201 nancial ma tters (accessing pension, arranging power of attorney, \201 nancing place- ment etc.); ad vice and support for patient and family on accommodation needs, especially \201 nding a c are home placement; link to community services (care package, community rehabilitation, day centers, etc.) ONGOING MANAGEMENT 195 Speech and language therapist Assess swallow (bedside video swallow testing) and establish plan for safe oral intake; reassess, and plan nutritional route during recovery; lan- guage screening (dysarthria, dysphasia and dyspraxia) with intervention to improve de \201 cits . HOW TO Protect your patient from another stroke Ensure that the following are address ed: \200 Lifestyle issues \200\224 smoking, diet and exercise \200 Antiplatelet therap y : Aspirin reduces relative risk of further event by about 25 % . Dose probably not important \200\224 generally use 75 \200\223300mg. Events that occur on aspirin ( \200\230aspirin failures \200\231) do not necessarily imply that aspirin is inadequate, but there may be an argument for increasing the dose (may be dose-dependent aspirin resistance), adding another antiplatelet agent (eg dipyridamole) or changing the agent (eg to clopidogrel) Adding clopidogrel to aspirin increases antiplatelet activity, but has been shown to increase the risk of cerebral hemorrhage and is no longer recommended for secondary prevention Lower blood pressure \200\224 choice of agent debated. The important thing is probably just to lower the blood pressure, but there is some evidence for the use of ACE inhibitors and thiazide diuretics as \201 rst line. If there are no contraindicati ons, lowering blood pressure per se is likely to be bene \201 cial, but aim for <130/85. Lower cholesterol \200\224 known for some time that lowering cholesterol is useful secondary prevention in coronary disease, but only recently in the He art Protection Study, bene \201 t has also been shown in stroke, speci \201 cally in olde r patients. The cut-off for treatment in this trial was 3.5, and so, as with BP, it may be the lower the better. Anticoagulation for AF \200\224 ( see b \200\230Atrial \201 brillation \200\231, p.276) . In infarction, likely to be safe to start warfarin after 2 weeks. With hemorrhage, judge each case individually (probably wait several months for haemorrhagic transformation; may n ever be appropriate in primary bleed) Carotid endarterectomy \200\224 > 70 % symptomatic stenosis carries a stroke risk of about 15 % per year, and is an indication for endarterectomy where there i s good recovery and the patient is \201 t for surgery (which can be done with local anest hesia). Perform early for greater bene \201 t See also b \200\230Vascular secondary prevention \200\231, p.308. 196 CHAPTER 8 Stroke Complications Contractures Longer-term complication. See b \200\230Contractures \200\231, p.485. Fecal incontinence May be due to immobility, cognitive problems, or neurological impair- me nt. Regulate bowel habit where possible with high- \201 bre diet and good \202 uid intak e and toilet regularly. If all else fails then deliberately consti- pating the patient with codeine and using regular enemas can work. See b \200\230Fecal incontinence: management \200\231, p.544. Infection Commonly chest or urine. Think of it early if a patient becomes drowsy, confused or appears to deteriorate neurologically. Prompt screening for sepsis and treatment with an tibiotics, oxygen and hydration are indi- cated in the majority of patients in the acute ph ase (stroke outcome very unclear initially) but may be withheld in a more established strok e where the prognosis can more con \201 dently be assessed as dismal (decision made with t he family). Muscle spasm Very common on affected side. Arthritic joints are exacerbated by spasm, and a ntispasmodics may need to be used alongside analgesia for effective pain relief. Try baclof en 5mg, or tizanidine. Increase dose slowly after a few days if needed but watch out for dr owsiness and loss of tone in the affected side that can hinder therapy. Pain Commonly shoulder pain in a paralyzed arm. Usually multifactorial, eg joint subluxatio n (treat with physiotherapy to strengthen muscles and arm support) interacting with muscle spasm and shoulder arthritis. Central post-stroke pain tends to affect all of the affected side and can be treated with amitriptyline (start low, eg 10mg at night). Pressure sores Should be avoidable in the majority of patients (see b \200\230Pressure sor es \200\231, p.502). Psychological problems Low mood is extremely common post-stroke (at 4 months, 25 % will be depressed, and over half of these remain depressed at a year). This is unrelated to the str oke type, but is associated with a worse outcome (perhaps because of lower motivation in th erapy). It should be actively sought (the screening question \200\230Do you think you are depressed? \200\231 is quick and effective; it may also be noticed by nurses, therapists or family; tools such as the GDS can also be used, but may be confounded by dysphasia). Treat ment is with psychosocial support and antidepressants (eg citalo- pram 20mg). Anxiety is al so very common, and often responds to expla- nation and empowerment. COMPLICATIONS 197 Thromboembolism Very common post-stroke especially if very immobile. Mobilize early. Low-do se low molecular weight heparin is sometimes used after the acute stage (when risk of hemor rhage into brain diminishes). Have a low threshold for investigating a leg that becomes swo llen or painful. HOW TO Manage urinary incontinence after stroke This is very common, more so after se vere stroke. It does, however, improve over time, and a \202 exible approach is required to ensure that a patient does not get catheterized and remain so. \200 Initially, try to manage with pads and regular toileting \200 If the skin starts to break down, or if the b urden on carers is heavy, then a catheter can be inserted for a limited time span Once mobility improves, try removing the catheter \200\224 ensure this is seen by all as a positive and exciting step back towards independence, as it can cause considerable anxiety If this fails, check for and treat UTI then try again \200 If this fails, then replace th e catheter and use bladder stabilizing agents for about 2 weeks (eg tolterodine 2mg bd) before removing it again If all this fails, consider sheath catheter devices or bottles (with non- return valves for use in bed) in men; commodes next to the bed for women 2The need for a permanent catheter post-stroke should be reviewed regularly as the conditio n is likely to improve. See b \200\230Urinary inconti- nence: causes \200\231, p.532. 198 CHAPTER 8 Stroke Longer-term issues Return to the community Best coordinated by the stroke MDT. Early suppor ted discharge may be useful if the patient can transfer, and there is a specialist communit y stroke team available. Later discharges are planned by the team, usually after careful as sessment of needs (home alterations, care packages, etc.) The general practitioner should b e alerted to continue medical moni- toring, in particular optimizing secondary prevention. Community teams (district nurses, community rehabilitation teams, home carers, etc.) should be aware of the patient \200\231s needs (continence, diabetic monitoring, ongoing therapy needs, etc.) and ideally be involved in the discharge planning. The patient and family shou ld have adequate information and training, as well as a contact point in case of problems ( stroke coordinators often take this role). Voluntary agencies (eg the Stroke Association) a re helpful, and the patient should be informed about them. Driving regulations with cerebrovascular disease \200 TIA/stroke with full neurological r ecovery \200\224 1 month off driving \200 Recurrent TIAs \200\224 3 months off driving following last TIA \200 Stroke with residual neurological de \201 cit after 1 month \200\224 the patient must notify the DVLA, and the decision is made on a case-by-case basis , with evidence from medical reports Hemianopia, inattention, and impaired cognition are de \201 nite markers of lack of \201 tness to drive (can be decided by a GP, or hospital physician). \200 Dysphasia is harder \200\224 cognitive state is dif \201 cult to assess and associated impairments (such as problems reading street signs or misinterpreting the environment) are not readily identi \201 ed out of context. Pure limb weakness can often be safely managed with car adaptation. If there are any doubts and the patient wishes to drive then they should be seen in a driving assessment center (t he patient will have to pay). Stroke with seizure \200\224 this is treated as a provoked seizure. May be <1 year ban, depending on circumstances. See M www.dft.gov.uk/dvla/medical/ataglance.aspx. Follow-up Some follow up should be offered to all stroke survivors. The intensity and durat ion of inpatient care can contrast sharply with home. The reali- ties of living with disabi lity begin to sink in, and many questions and anxi- eties arise. Even minor strokes or TIAs require a further point of contact, as they will have been committed to lifelong medicatio n and will need monitoring of risk factors. In addition, stroke recovery continues (albeit at a slower pace) for up to 2 years (or even longer) and management plans made at discharge may need to be adapted. The Stroke Association Helpline: 0303 303 3100. M www.stroke.org.uk. Checklist for follow-up (Usually 2 \200\2234 months after discharge) Secondary prevention C heck drugs, blood pressure, diabetic control and cardiac rhythm Continence \200 Are there continence problems? \200 If a catheter is in situ, has mobility improved to a point at which trial removal can be done? If the patient was discharged on bladder stabilizing drugs, and has remained continent, can these be tailed off? Nutrition \200 Is nutrition adequate? (if not, refer to dietician) \200 If a PEG tube i s in place, is it still required? \200 Does the patient warrant another assessment of swa llowing (by SALT) to allow oral nutrition to begin? Communication and speech \200 Are there problems still? \200 Is there a need for a SALT review? Mood \200 Is the patient depressed? \200 Do they need referral to a psychologi st or (rarely) psychiatrist? \200 If discharged on an antidepressant, can it be discontin ued? Physical progress \200 Is there ongoing physical therapy? \200 If not, is there co ntinued improvement? If there has been deterioration then refer back for assessment for further therapy (Royal College of Physicia ns \200\231 guidelines) Contractures \200 Are there any contractures developing? (If so, refer to physiotherapy) Muscle spasms \200 Have these developed, or lessened since discharge? \200 Review need for anti-spasmodic medication \200\224 titrate down if no longer required Pain \200 Commonly in shoulder, or post-stroke pain \200 Has this developed, or lessene d? \200 Review need for medications Daily living \200 Are there any issues in managing day to day? \200 Is all the necessary equipment in place? (and is it still needed, eg a c ommode can be returned when the patient is able to mobilize to the toilet alone) Is there anything that they would like to be able to do that they cannot? (eg read a book, take a bath) Would a further review by a therapist be helpful? \200 Do they wish to drive? ( See b \200\230Longer-term issues, p.198) Support \200 Are they in contact with a community stro ke coordinator (if available)? \200 Are they aware of voluntary organizations? 200 CHAPTER 8 Stroke Transient ischaemic attack clinics Rapid outpatient assessment of TIA and minor stroke, to establish diagnosis, commence secondary prevention and lower risk of subsequent event. How fast? This depends on how high a risk the patient is. Use the ABCD 2 score (see Table 8 .3 ) and if the score is (cid:116) 4, the patient should be seen within 24hr \200\224 in s ome services these patients are admitted to hospital but larger centers may provide 7 day/w eek outpatient services. Patients who have recurrent symptoms within a week or those in AF should also be seen urgently. Those at lower risk should still be seen within 7 days. Currently early antiplatelet agents, antihypertensives, and statin use have been shown to s ubstantially reduce the chances of stroke at 1 week. Warfarin for patients with AF and earl y endarterectomy are also known to be bene \201 cial for a subset of patients. Function \200 Con \201 rm diagnosis \200\224 very variable, but up to a third of referr als to a TIA clinic are non-cerebrovascular. Main alternatives are migraine, epilepsy, card iac dysrhythmias, orthostatic hypotension, or rarely brain tumor \200 Arrange investigati ons \200\224 to aid diagnosis (eg CT brain) or investigate risk factors (eg FBC, ESR, gluc ose, cholesterol, ECG, carotid Doppler, 24hr tape and echocardiogram) Modify risk factors \200\224 ( see b \200\230HOW TO Protect your patient from anoth er stroke \200\231, p.195) set targets for blood pressure and glucose control, advise about antiplatelet agents (there is signi \201 cant regional variation in the therapy chosen in cluding aspirin alone, aspirin with modi \201 ed release dipyridamole, or clopidogrel alon e) and anticoagulation in AF, advise about statin use, refer for carotid endarterectomy urg ently, advise about smoking cessation Education \200\224 of patients, relatives, primary care doctors. Discuss stroke disease an d its modi \201 cation, time-frame for recovery, psychological aspects of stroke, driving restrictions Structure Varies enormously. Ideally would have: \200 Rapid referral protocol \200\224 p erhaps a standard referral sheet and fax number for GPs, perhaps via a single phone call to an answering machine Stroke specialist nurse \200\224 can take history including standardized risk factor analy sis, measure BP, provide education (lea \202 ets, individual action plans), coordinate inv estigations and follow-up. Role can be extended into community \200\224 point of access fo r patients Time for explanation \200\224 many patients will feel overwhelmed by the amount if informa tion they are being given. The specialist nurse can be very helpful in clarifying things, a nd information lea \202 ets allow the information to be revisited at home. There are often several new tablets, or even suggesting surgery for a patient who feels well. Comprehensio n is vital for concordance TRANSIENT ISCHAEMIC ATTACK CLINICS 201 Rapid access to investigations \200\224 particularly carotid Doppler, CT scanning, and echocardiography. Many clinics run a \200\230one-stop \200\231 service, wher e all assessments, investigations, and conclusions are completed at a single visit Prompt communication to GP \200\224 advice about risk reduction must be relayed promptly to the GP for maximum bene \201 t. Ideally same day by fax or delivered b y the patient Table 8.3 The ABCD 2 Score for TIA Score A Age (cid:116) 60 1 B BP (cid:116) 140/90mmHg 2 C Clinical features Unilateral weakness 2 Speech disturbance without weakness 1 D1 Duration (cid:116) 60min 2 10 \200\22359min 1 <10min 0 D2 Diabetes Diabetes 1 ABCD 2 score \200\224 risk of stoke at 2 days: 0 \200\2233 \200\224 1 % ; 4 \200\2235 \200\224 4 % ; 6 \200\2237 \200\224 8 % . Further reading Johnson SC , Rothwell PM , Nguyen-Huynh MN , et al . ( 2007 ). Validation a nd re \201 nement of scores to predict very early stroke risk after transient ischemic att ack . Lancet 369 ( 9558 ): 238 \200\223 92 . This page intentionally left blank 203 Chapter 9 Psychiatry Cognitive ageing 204 Impairments in cognitive function without dementia 205 Dementia: overv iew 206 HOW TO Distinguish delirium from dementia 207 Dementia: assessment 208 HOW TO Investigate a patient with dementia 210 Dementia: common diseases 212 Dementia and parkinsonism 214 Normal pressure hydrocephalus 2 16 Dementia: less common diseases 218 Dementia: general management 220 HOW TO Manage the driver who has dementia 221 Dementia: risk management and abuse 222 Dementia: prevention 223 Dementia: acetylcholineste rase inhibitors 224 HOW TO Treat with acetylcholinesterase inhibitors 225 Dementia: other drug treatments 226 HOW TO Manage patients with dementia in hospital 227 Dementia: managing behavioral problems 228 Compulsory detention and treatment 230 HOW TO Manage the older person refusing treatment 231 Psychosis 232 Delirium: diagnosis 234 Delirium: causes 236 Delirium: clinical assessment 23 8 Delirium: treatment issues 240 Delirium: non-drug management 241 Delirium: drug treatment s 242 HOW TO Prescribe sedating drugs in delirium 243 Confusion and alcohol 244 Squalor syndrome 245 Depression: presentation 246 HOW TO Distinguish dementia from a depressive pseudodementia 247 Depression: clinical features 248 HOW TO Assess depression 249 Depression: non-drug management 250 Depression: drug tre atments 252 Suicide and attempted suicide 254 204 CHAPTER 9 Psychiatry Cognitive ageing Cognitive, or thinking, ability is the product of: \200 \200\230Fixed i ntelligence \200\231, the result of previous thinking, which often increases with age, ie \200\230wisdom \200\231 \200\230Fluid intelligence \200\231, ie real-time information processing, which declines modestly in older age There are structural changes in the brain with age (see b \200\230The ageing brain and ner vous system \200\231, p.152) but these correlate poorly with cognitive changes. Broadly, in tellectual function is maintained until at least 80 years, but processing is slower. Non-cr itical impairments include forgetfulness, modestly reduced vocabulary, and slower learning of, eg, languages. These changes are to be expected, their consequences can be managed, and they do not cause signi \201 cant reduction in functional level. Three factors support a diagnosis of normal ageing rather than disease: The ability to maintain function in normal life through aids (eg aides- memoire: lists or calendars) or adaptations (of one \200\231s environment or of one \200 \231s expectations) Very long time scale of decline: 10 \200\22330 years, compared with months or a few years in disease Relative decline, eg the academic who no longer holds his own at the graduates \200\231 reunion IMPAIRMENTS IN COGNITIVE FUNCTION WITHOUT DEMENTIA 205 Impairments in cognitive function without dementia Age-associated memory impairment (AAMI) or benign senescent forgetfulness Older people learn new information and recall information more slowly, but given time their performance is unchanged. This is distinct from the impa irment in dementia, in that in AAMI, overall function is unimpaired, and usually only less important facts are forgotten. It is often more both- ersome to the patient than a concern to relatives (compare dementia, when often the family are much more concerned than the pati ent). AAMI can present early (age 40s \200\22350s) when high achievers become frustrated by modes t deterioration in speed of new learning. It may be exacerbated by performance anxiety, cre ating a vicious cycle, and is often helped by psychological strategies to assist memory. Minimal cognitive impairment(MCI) or cognitive impairment no dementia (CIND) Impairments ar e more broad than memory alone, and are felt to be patho- logical (eg secondary to cerebrov ascular disease), but the full criteria for a diagnosis of dementia are not met \200\224 e g because there is not yet signi \201 cant impact on day-to-day functioning. Progression to dementia occurs in between 5 % (community studies) and 10 % (memory clinic s tudies) annually. Thus with time, many patients do develop dementia, but many do not, and i n some there is no deterioration. Diagnosis is important in order to: Reassure the patient (by distinguishing from dementia) \200 Modify risk factors for progr ession \200 Monitor deterioration such that intervention can begin promptly if progression occurs 206 CHAPTER 9 Psychiatry Dementia: overview Dementia is: \200 An acquired decline in memory and other cognitive fu nction(s) \200 In an alert (ie non-delirious) person \200 Suf \201 ciently severe to a ffect daily life (home, social function) All three elements must be present in order to mak e the diagnosis. Prevalence increases dramatically with age: 1 % of 60 \200\22365 year olds, > 30 % of over 85s. Over 50 % of nursing home residents have dementia. Major dementia syndromes (and proportion of cases in older people) include: \200 Mixed pathology \200\224 (especially Alzheimer \200\231s and vascular) is the commonest type in postmortem studies Dementia of Alzheimer type (60 % ) \200 Vascular dementia (30 % ) \200 Other neurodegen erative dementias (15 % ), eg dementia with Lewy bodies, Parkinson \200\231s disease with d ementia, frontotemporal dementia Reversible dementias (<5 % ), eg drugs, metabolic, subdural, normal pressure hydrocephalus Diagnostically, there are many false-positive and false-negative cases. Mild to moderate de mentia is easy to miss on a cursory, unstructured assess- ment. Patients labeled incorrectl y as having dementia may be deaf, dys- phasic, delirious, depressed, or under the in \202 uence of drugs. Triggers for considering a dementia diagnosis \200 Delirium (much commoner with underlyin g dementia) \200 \200\230Unmasking \200\231 of poor cognition after spouse \200\231s dea th \200 Social withdrawal \200 Request for social services help \200 Poor concordance with prescribed drug therapy \200 Domestic crisis (eg \201 re, road traf \201 c accid ent) \200 Spouse/family disproportionately in control or speaking for patient UK National Dementia Strategy This was published by the UK government in 2009 and promises a greater focus on acceleratin g the pace of improvement in dementia care, through local delivery of quality outcomes and local accountability for achieving them. This re \202 ects an increasing interest in demen tia management across the NHS See M www.dh.gov.uk/en/SocialCare/NationalDementiaStrategy DEMENTIA: OVERVIEW 207 HOW TO Distinguish delirium from dementia The most common issue in diagnosing the older patient with confusion ( \200\230brain failur e \200\231) is whether the patient has delirium alone, dementia alone, or a delirium superi mposed on a pre-existing dementia. Achieve this by combining information from the history with a physical and mental state examination. 2The history is key. The duration of symptoms is most important. Information from medical r ecords, carers, and family will help determine whether dementia was present before onset of delirium. \200\230When was his memory last as good as yours? \200\231 (Table 9.1 ) Table 9.1 Features distinguishing delirium from dementia Feature Delirium Dementia Mode of onset Acute or subacute Chronic or subacute Reversibility Often reversible Rarely reversible Generally little diurnal variation, although some deteriorate during the evening; \200\230 sundowning \200\231. Day-to-day \202 uctuation more common in Lewy Body dementia Fluctuation Diurnal or hour- to-hour \202 uctuation common Poor attention Yes (but variable hour-to-hour) In severe dementia Normal Conscious level Usually affected but may be subtle and variable Hallucinations and misinterpretations Common Usually occurs late in the disease. Visual hallucinations earlier in the disease, especiall y when symptoms \202 uctuate, suggests in Lewy Body dementia Fear, agitation, aggression Common Uncommon in early stages Common Late. Often poverty of thought Disorganized thought, unreal ideas Motor signs Tremor, myoclonus, asterixis common Late only Speech May be dysarthric, dysnomic Normal Dysgraphia Often present Usually late Short and long term memory Poor Long-term memory often normal until late 208 CHAPTER 9 Psychiatry Dementia: assessment The most important component of assessment. Obtain information from bo th patient and family/friends. Note onset, speed of progression, symp- toms. Take a careful drug history, including over-the-counter drugs and recreational drugs (especially alcohol) . Also ask about a family history of early dementia and a personal psychiatric history of, eg, depression. Usually there is a progressive decline in cognitive function over several years, ending wit h complete dependency and death (usually due to dehydration, malnutrition, and/or sepsis). Deterioration may be Insidious and gradual (eg Alzheimer \200\231s) \200 Stepwise (suggesting stroke/vascular etiology) \200 Abrupt (after a single critical stroke) \200 Rapid over weeks/months, su ggesting a drug, metabolic, or structural cause (eg tumor, subdural) Abnormalities occur in: \200 Retention of new information (eg appointments, events, worki ng a new household appliance); short-term memory loss is often severe, with repetitive ques tioning Managing complex tasks (eg paying bills, cooking a meal for family) \200 Language (word- \201 nding dif \201 culty with circumlocution, inability to hold a conversation) Behavior (eg irritability, aggression, poor motivation, wandering) \200 Orientation (eg g etting lost in familiar places) \200 Recognition (failure to recognize \201 rst acquain tances, then friends or distant family, then close family, eg spouse) Ability to self-care (grooming, bathing, dressing, continence/toileting) \200 Reasoning: poor judgment, irrational or unaccustomed behaviors \200 Ability to recognize familiar ob jects, people, and places (agnosia) \200 Ability to carry out complex, coordinated moveme nts (apraxia) Physical examination \200 To determine possible causes of a dementia syndrome, including reversible factors Look for vascular disease (cardiovascular, peripheral vascular and cerebrovascular), neuropathy, parkinsonism, thyroid disease, malignancy, dehydration, ( alcoholic) liver disease In advanced dementia of any type primitive re \202 exes (eg grasp, suckling, palmar-mental ) and global hyperre \202 exia with extensor planters may occur DEMENTIA: ASSESSMENT 209 Mental state \200 Exclude delirium . Features include agitation, restlessness, poor atten tion and \202 uctuating conscious level ( see b Appendix, \200\230CAM \200\231, p.692) \200 Exclude depression . Features include low affect, poor motivation and a negative perspecti ve. Perform a GDS (see b Appendix, \200\230Geriatric Depression Scale \200\231, p.687) Measure cognitive function . Serial testing may be helpful in borderline cases \200\224 is there evidence of progression? Many measurement tools are available, eg MMSE, Mini-Cog, number of animals named in 1min, clock- drawing test (see b \200\230Measur ement instruments \200\231, p.78, b Appendix, \200\230The abbreviated mental test score \200\231, p.690, and b Appendix, \200\230Clock- drawing and the Mini-Cog \204 \200\231, p .693) Full neuropsychological assessment (detailed, prolonged assessment by a specialist psycholo gist) may be helpful in: \200 Distinguishing between dementia and depression \200 Disti nguishing between different subtypes of dementia \200 Distinguishing between AAMI and ear ly dementia \200 Distinguishing between focal impairments (eg aphasic or amnesic syndromes) and dementia Measuring progression and response to treatment Disclosure of dementia diagnosis Each case should be considered individually, but in genera l the diagno- sis should be revealed. Disclosure: \200 Is consistent with the patient \200\231s right to know (autonomy). Most older people say that they would want to know the diagnosis Facilitates medical, \201 nancial, and care planning, eg advance directives, powers of attorney, living arrangements Allows for consent to treatment and facilitates participation in research Facilitates discussion between patient and carer Arguments against disclosure include a pos sible depressive reaction, accentuated by a perceived lack of effective treatments. Such a reaction is minimized by sensitive multidisciplinary support that emphasizes the positive t herapeutic solutions available. 210 CHAPTER 9 Psychiatry HOW TO Investigate a patient with dementia Cases of reversible dementia are uncommon, but their identi \201 cation is important, as e ffective treatment may reverse the impairment and prevent progression. Therefore screen for them. Blood tests The following are generally considered useful: FBC, ESR, B 12 , folate, U,C + E , calcium, LFTs, TSH, CRP, random glucose Request syphilis and HIV serology only if there are atypical features or special risks. ECG and CXR (Evidence of heart disease, occult malignancy.) Neuroimaging It is arguable whether every person with dementia should undergo brain imaging . Imaging is indicated where there is: \200 Early onset (<60 years) \200 Sudden onset o r brisk decline \200 High risk of structural pathology (eg known cancer, falls with head injury) Focal CNS signs or symptoms In more typical cases suggestive of either Alzheimer \200\231s, vascular, or mixed (Alzheimer \200\231s-vascular) dementia, the diagnostic yield is very l ow. Thus, in most cases, imaging does not alter the clinical management based on history, e xamination, and lab tests alone. If a patient or carer is par- ticularly anxious (eg fear o f brain tumor), imaging may help allay fears, although of course dementia is a far from a b enign diagnosis. \200 CT is the usual imaging modality \200 MRI identi \201 es posteri or circulation vascular pathology with much greater sensitivity SPECT is used rarely, usually in specialist centers, to more reliably differentiate between Alzheimer \200\231s and vascular dementia Additional testing as clini cally indicated : EEG is used for suspected frontotemporal dementia or Creutzfeldt \200\223 Jakob disease (CJD), or where seizure activity is a possibility Lumbar puncture where CNS infection is considered This page intentionally left blank 212 CHAPTER 9 Psychiatry Dementia: common diseases Alzheimer \200\231s disease (dementia of Alzheimer type) \200 T he most common cause of a dementia syndrome \200 Diagnosis is made clinically, based on t he typical history, mental state examination, and unremarkable physical examination History \200\224 insidious onset, with slow progression over years. Early, profound short- term memory loss progresses to include broad, often global cognitive dysfunction, behaviora l change and functional impairment. Behavioral problems are common, usually occurring in mo derate to severe dementia, but sometimes preceding overt cognitive impairment Physical examination \200\224 normal \200 Neuroimaging \200\224 demonstrates no other c auses of dementia (eg tumor or infarct) and may show disproportionate medial temporal lobe atrophy Treatment with acetylcholinesterase inhibitors may be indicated (see b \200\230Dementia: acetylcholinesterase inhibitors \200\231, p.224) Early-onset Alzheimer \200\231s disease (<65 years) is uncommon, has a stronger genetic com ponent, and is more rapidly progressive Vascular dementia \200 The next most common cause \200 Suggested by vascular risk facto rs, eg diabetes mellitus, hypertension, smoking or other vascular pathology, with other sup porting evidence on history, examination, or tests History \200\224 cognitive impairment may be patchy, compared with the more uniform impairments seen in Alzheimer \200\231s disease. Onset is often associated wit h stroke, or the deterioration is abrupt or stepwise, however, using \200\230multi-infarct dementia \200\231 as a synonym for vascular dementia is imprecise and its use should be di scouraged. Frontal lobe, extrapyramidal, pseudobulbar features, and emotional lability are common. Urinary incontinence and falls without other explanation are often early features. Other features may be mostly cortical (mimicking Alzheimer \200\231s disease) or subcortica l (eg apathy, depression) Physical examination often shows: Focal neurology suggesting stroke or diffuse cerebrovascular disease (hyperre \202 exia, extensor plantars, abnormal gait, etc.)