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.) Other evidence of vascular pathology, eg AF, peripheral vascular disease Neuroimaging shows either: Multiple large vessel infarcts \200 A single critical infarct (eg thalamus) \200 White matter infarcts or periventricular white matter changes \200 Microvascular disease, too \201 ne to be seen on neuroimaging, may cause a signi \201 cant proportion of vascular de mentia, apparent only post-mortem DEMENTIA: COMMON DISEASES 213 Differentiating between Alzheimer \200\231s and vascular dementia The importance of differentiating between Alzheimer \200\231s and vascular dementia can be overemphasized. Their presentations overlap, and pathologies commonly coexist. Increasingly it is believed that much Alzheimer \200\231s disease pathology has a vascular component. Pragmatically: \200 In cases where vascular risk factors and/or signs exist, treat vascular risk factors aggressively, whether or not there is signi \201 cant cerebrovascula r pathology on brain imaging A trial of acetylcholinesterase inhibitors (effective in Alzheimer \200\231s but much weake r evidence in vascular dementia), is probably worthwhile where vascular risk factors and/or pathology exists, but Alzheimer \200\231s may be contributing to the presentation 214 CHAPTER 9 Psychiatry Dementia and parkinsonism Dementia with Lewy bodies and Parkinson \200\231s disease with de mentia may be considered as extremes of a continuum. In the latter, motor impair- ments pre cede cognitive impairments and are more severe. In dementia with Lewy bodies, cognitive and behavioral impairments precede motor phenomena and are more severe. There are frequently a dditional contri- butions from Alzheimer \200\231s or vascular pathology. There are believe d to be common pathological processes in all these dementia syndromes. Dementia with Lewy bodies \200 A gradually progressive background dementia, with insidiou s onset \200 Shorter-term \202 uctuations in cognitive function and alertness \200 Pr ominent auditory or visual hallucinations, often with paranoia and delusions Parkinsonism is commonly present, but often not severe \200 Typical antipsychotics (eg ha loperidol) are very poorly tolerated, leading to worsening confusion or deterioration of pa rkinsonism. Atypical antipsychotics (eg risperidone, and especially quetiapine) may be bett er tolerated, but great caution is advised in their use Levodopa or dopamine agonists may worsen confusion \200 Anticholinergics (eg rivastigmine ) are effective, especially for hallucinations and behavioral disturbance Note that several features are common to both dementia with Lewy bodies and delirium, eg \202 uctuations, effect of drugs, perceptual, and psy- chotic phenomena. When comparing the two, the following is true of dementia with Lewy bodies: \200 Onset is insidious and pro gression gradual \200 No precipitating illness (eg infection) is found \200 Hallucinati ons are complex and not the result of misperception of stimuli \200 Delusions (commonly c omplex auditory or visual) are well-formed and may be persistent Syncope frequently occurs \200 Antipsychotics worsen status (not indicated as a diagnosti c trial) Parkinson \200\231s disease with dementia \200 People with Parkinson \200\231s disease ar e much more likely to develop dementia, especially older people, those in the later stages of the disease and those who become confused on Parkinson \200\231s medication \200 Typic al motor features of Parkinson \200\231s disease are present, and may be severe The presentation and neuropathology is variable, and may resemble Alzheimer \200\231s disease, vascular dementia, or dementia with Lewy bodies By de \201 nition, if features of Parkinson \200\231s precede dementia by more than a year, then the diagnosis is of Parkinson \200\231s disease with dementia, not dement ia with Lewy bodies. This applies even if the dementia syndrome is otherwise typical of dem entia with Lewy bodies \200 Multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration also present with both parkinsonism and dementia DEMENTIA AND PARKINSONISM 215 Minimal cognitive impairment in Parkinson \200\231s disease Many patients with PD have subt le impairments of cognition, too mild to justify a diagnosis of dementia. Slowed thinking a nd de \201 cits in visuospatial, attention and executive function are commonly seen. 216 CHAPTER 9 Psychiatry Normal pressure hydrocephalus Normal pressure hydrocephalus (NPH) classically presents with the triad: \200 Gait disturbance (wide-based) \200 Incontinence of urine \200 Cognit ive impairment (psychomotor slowing, apathy, appear depressed) 2Most patients with this triad have other (unrelated) causes, or have diffuse cerebrovascul ar disease. Assessment Neuroimaging \200 Shows ventricles that are enlarged disproportionately compar ed with the degree of cerebral atrophy Neuroimaging for unrelated reasons (eg TIA) may reveal ventricular enlargement that appears disproportionate to the degree of cerebral atrophy, suggesting possible NPH. In the absenc e of clinical features of NPH, the diagnosis cannot be supported, and the patient may be re assured. Lumbar puncture \200 Diagnostic and therapeutic procedure \200 Usually performed if cli nical and radiological \201 ndings suggestive of NPH \200 Before the procedure, assess baseline gait (eg timed walk) and cognition (eg MMSE, clock-drawing test) Opening pressure is normal in NPH \200 Remove 20 \200\22330mL of cerebrospinal \202 uid (CSF) \200 Check for improvement in gait and cognition after 1 \200\2232hr Treatment Ventriculoperitoneal shunting is effective for some, but many do not bene \201 t . Gait is more likely to improve than is cognition. It is a major procedure, and complications are common, eg infection and subdural haematoma. Decision to proceed requires: \200 A con \201 dent diagnosis (ma y require specialist neurological review) \200 Support of patient and carer for the proce dure \200 An assessment that the likelihood of bene \201 t is high Bene \201 t is more likely in those who: \200 Have a short history (days or weeks) \200 Have a known cause \200\224 usually trauma or subarachnoid hemorrhage \200 Have normal brain substance on n euroimaging \200 Have no signi \201 cant comorbidities. Cerebrovascular disease is espec ially relevant Bene \201 t from lumbar puncture and large volume CSF removal Further reading Juss JK , Keong N , Forsyth DR , et al. ( 2008 ). Normal pressure hydroceph alus. CME Geriatr Med 10 ( 2 ): 62 \200\223 7 . This page intentionally left blank 218 CHAPTER 9 Psychiatry Dementia: less common diseases Frontotemporal dementia \200 Neurodegenerative disease, wi th insidious onset and slow (several years) progression Family history is positive in 50 % of cases \200 Onset is often early (age 35 \200\22375) , and either behavioral or language dif \201 culties dominate the clinical picture. Forgetfulness is mild. Insight is lost ear ly. Dif \201 culties at work may be the \201 rst sign Commonly used assessment tools (eg MMSE) do not test frontal lobe function, so do not be put off the diagnosis by \200\230normal \200\231 cognitive scr eening tests Behavioral problems are most common and include disinhibition, mental rigidity, in \202 ex ibility, impairment of executive function, decreased personal care, and repetitive behavior s Language dysfunction may include word- \201 nding dif \201 culty, problems naming or understanding words, lack of spontaneous conversation or circumlocution Later, impairments become more broad, similar to severe Alzheimer \200\231s \200 Primitiv e re \202 exes (eg grasp, palmar-mental) may be found \200 Neuroimaging usually demonstr ates frontal and/or temporal atrophy \200 Frontotemporal dementia presents as a clinical spectrum. More speci \201 c conditions within that spectrum include: \200 Frontal lobe degeneration . Frontal greater than temporal degeneration Pick \200\231s disease . Similar to frontal lobe degeneration, but uncommon. Classical \200\230Pick bodies \200\231 seen postmortem Motor neuron disease (MND) with dementia. Usually late in the progression of MND (see b \200\230Motor neuron disease \200\231, p.170) \200 Progressive non- \202 uent aphasia an d semantic dementia . Temporal degeneration Dementia and infection \200 Neurosyphilis is becoming more common again. Serological test s for syphilis should be performed if a dementia syndrome has atypical features (eg seizure s) or risk factors for sexually transmitted disease (STD) (including mental illness, histor y of other STD, drug/alcohol abuse). Beware false-positive serological tests in African Car ibbeans with a history of yaws. If neurosyphilis seems possible, sample CSF and seek microb iology advice with a view to penicillin treatment HIV-associated dementia generally affects younger people, re \202 ecting the epidemiology of HIV infection. It occurs late in HIV, rarely if at all at presentation CJD is a prion-mediated, rapidly progressive cortical dementia. Myoclonus is found on physical examination. Psychosis occurs early DEMENTIA: LESS COMMON DISEASES 219 Vasculitis \200 Suggested by elevated CRP/ESR without other cause or characteristic CT/MRI (periventricular lesions) Heterogeneous presentation, including as delirium or dementia \200 Examine the patient fo r evidence of systemic vasculitis \200 Perform serology (eg anti-nuclear antibody) and lu mbar puncture with CSF tests to exclude infection/neoplasm Potentially treatable, so pursue this diagnosis vigorously if necessary. Specialist referral usually indicated Dementia and drugs/toxins \200 Alcohol-associated dementia may occur after many years of heavy drinking, presenting with disproportionate short-term memory impairment (see b \200 \230Confusion and alcohol \200\231, p.244) Psychoactive drugs may cause a dementia-like syndrome that is substantially reversible 220 CHAPTER 9 Psychiatry Dementia: general management General \200 Modify reversible aggravating factors , commonl y multiple but minor (eg constipation, low-grade sepsis, mild anemia, drug side-effects) Treat depression . SSRIs are much preferred to tricyclics. Repeat cognitive assessment 2 \200\2234 months after treatment to determine if cognitive impairmen t remains Social \200 Encourage physical and mental activity, including social activities (eg social clubs, day centers, see b \200\230Day hospitals \200\231, p.22) Create a safe, caring environment, usually in the patient \200\231s own home. A predictable routine is helpful. OT home assessment identi \201 es hazards, provides visual safety cue s, etc. Organize carers to assist with ADLs, prompt medication, etc. \200 Support caregivers: Enquire about caregiver burden, and psychiatric symptoms \200 Caregiver support groups \200 Respite care \200\224 usually in care homes, for a few days to 2 weeks \200 Sittin g services \200\224 usually for 2 \200\2233hr once or twice weekly \200 Family Support V isitor \200\224 provides emotional and practical support \200 Educate patients and famil ies about the disease and how to cope with its manifestations. This includes appropriate mo di \201 cations to the home environment and learning to communicate and interact with the patient with dementia. Counseling and support delays admission to care homes Practical \200 Suggest simple interventions to improve coping (eg lists, calendars, alarms) Simplify medication, and provide dosette boxes or similar, to aid concordance. In the later stages, drugs such as antihypertensives may become pointless if n ot harmful (ie risk > bene \201 t) Support and educate patient and carers about legal and ethical issues including: \200 Driving (see b \200\230HOW TO Manage the driver who has dementia \200\231, p.221) Lasting power of attorney ( see b \200\230Making \201 nancial decisions \200\231, p.658) Wills (see b \200\230Making a will \200\231, p.678) \200 Discussion of end-of-life issue s (clinically assisted nutrition, comfort versus life prolongation) may be appropriate. Further reading NICE . Dementia ( 2006 ) online: M www.nice.org.uk/nicemedia/pdf/CG042NICEG uideline.pdf . DEMENTIA: GENERAL MANAGEMENT 221 HOW TO Manage the driver who has dementia Road traf \201 c accident and injury risk increase with the severity of dementia. In most countries it is mandatory for the driver to report important health factors to the licensin g authority, which will then request further information from the patient \200\231s medical team. Patients and carers should be reminded of this responsibility at diagnosis. Assessment of driving ability during a hospital outpatient or general practice consultation is often dif \201 cult. In some cases, whether a patient is safe to drive will be obvious \200\224 either in the very earliest stages of cognitive impairment, or in more severe de mentia. In other cases, usually of mild (to moderate) cognitive impairment, the following e vidence is useful: \200 Reports of driving problems, incidents (eg near-misses) or accide nts. Are relatives/friends concerned to get into the passenger seat? Have they tried but fa iled to limit or prohibit driving? Some evidence is of less value, eg getting lost is a poo r indicator of safety Reports of how driving patterns have changed, and why. Are journeys now brief, infrequent, and con \201 ned to quiet local roads? Clinical evidence of major impairment in visuospatial function, attention or judgment. Howe ver, a combination of modest impairments may be as important Presence of non-cognitive impairments (eg visual, joint function) or other conditions that affect driving safety (eg seizures, syncope) Each case should be reassessed intermittently, either at regular intervals or at points pro mpted by critical incidents. The best assessment of driving ability is by a professional dr iving assessor, in the patient \200\231s own vehicle on the public roads. Such professional s, often occupational therapists, can deliver the con \201 dent, robust opinion that is of ten required, as well as offering useful practical advice to the cognitively or physically impaired driver. In general: \200 It is preferable that the patient, family, and doctor s hould agree that stopping voluntarily is advisable. Compulsory license withdrawal by the au thority generates great anger and distress The issue is best discussed early in the course of the disease, when the patient has best insight If driving is safe for the moment, encourage patient and family to think ahead, to a time w hen driving cannot be continued \200\224 is local public transportation suf \201 cient, o r will a spouse have to hone long-lost driving skills? Rarely, a patient continues to drive when clearly unsafe and having been informed that they must stop. In most cases, further clear statements of this, backed up by the threat of med ical reporting to the authorities, are suf \201 cient to prompt cessation. If driving cont inues, the clinician is ethically justi \201 ed in reporting this to the authorities, and will usually have the strong support of the family. Further reading Driver and Vehicle Licensing Agency online: M www.dft.gov.uk/dvla/medical/a taglance.aspx . 222 CHAPTER 9 Psychiatry Dementia: risk management and abuse Risk management is an essential part of care. \200 Is there a risk of harm to the patient or to others? \200 How great is the risk, over how l ong is the patient (or other person) exposed to it, and how severe are the consequences of the risk? 2There is no such thing as \200\230safe \200\231 only \200\230safer \200\231 and risk man agement demands careful balancing between autonomy/quality of life and safety. Common risks include: Falls. Moving from own home to institutional care is rarely the answer. Supervision is far from continuous in any institution, the environment is less familiar and the \202 oors ar e often uncarpeted and unforgiving \200 Wandering. Usually more distressing to carers tha n presenting risk to the patient Aggression by a patient towards carers or family . Usually verbal, but sometimes physical or sexual. May lead to carers refusing to work with patient Aggression towards a patient by carers or family. Less easy to identify, as the patient may not complain, through fear or due to cognitive problems. Be concerned if there are unexpla ined \200\230falls \200\231 or unusual patterns of bruising (see b \200\230Elder abuse \200\231, p.674) Self-neglect. Often with denial. May manifest as poor diet, poor hygiene etc Fire risk. May be easily modi \201 able, through removal or modi \201 cation of kitchen a ppliances, gas \201 res, etc. Cigarette smoking is more problematic Driving . ( See b \200\230HOW TO Manage the driver who has dementia \200\231, p.221) Financial abuse (see b \200\230Elder abuse \200\231, p.674) Theft or fraud \200 Modi \201 cation of wills \200 Misuse or transfer of a patient \200\231s money Having determined the nature and magnitude of a risk, consider \200\230Can the risk be red uced? \200\231 and \200\230Should it be reduced? \200\231 Consider whether the patient is competent to make their own decisions about risks or whethe r you are required to act in patient \200\231s \200\230best interests \200\231. If risk re duction can be done without impacting on the patient \200\231s independence or enjoyment of life, then go ahead. If reducing risk involves curtailing liberty or restricting enjoyable activity (walking, wandering, living alone), then consider: \200 If competent, what is the patient \200\231s attitude to risk? \200 If unable to express this, what was his/her premorbid a ttitude, and what would he/she now want? What is the view of carers? Commonly, discussions around risk occur when a patient is perce ived by some (carers, relatives, nursing or therapy staff) to have become unsafe to remain at home. This should prompt multidisciplinary assessment and discussion, including whether a move to institutional care would involve a change of risk patterns rather than a reductio n in overall risk. DEMENTIA: PREVENTION 223 Dementia: prevention Lifestyle interventions \200 Physical activity . Con \202 icting da ta. Physical activity may well not protect against dementia, but should be encouraged for other reasons Cognitive activity . Observational studies suggest that games, reading, etc. are protective , but these associations may not be causal, and there are no good randomized controlled stu dies (RCTs) Diet . Again, observational studies suggest bene \201 ts from a high \201 sh oil diet, but there is no high-quality prospective evidence Drugs \200 Hormone replacement therapy (HRT) . Con \202 icting data from epidemiological and prospective studies. In one large prospective study, HRT doubled dement ia risk. Cannot be recommended for prevention NSAIDs . Large prospective cohort studies suggest that long-term NSAID use is protective, especially when used several years before dementia onset. RCTs are ongoing. NSAIDs may function by reducing amyloid formation, and this may be speci \201 c to only some NSAIDs (eg ibuprofen). Side effects are considerable for long-term users \200 Antioxidants . High dietary intake of antioxidants (eg vitamins C and E) is associated with lower risk of dementia, but methodological concerns exist (eg does subcl inical cognitive impairment reduce recall during questionnaire surveys of diet). Extrapolat ing from in vitro studies, and some early positive studies in coronary heart disease (now l argely refuted), some recommend high dose ( > 400IU/day) vitamin E supplements Antihypertensives . Con \202 icting data. Dementia prevention is not in itself a reason to lower blood pressure Statins . Associated with a lower frequency of dementia, but this may be spurious, due to p rescribing bias (eg physicians less likely to prescribe to those with subclinical cognitive impairment) Overall, there are few high-quality RCTs of primary prevention in dementia, but many epidem iological studies. Usual practice is to encourage physical and mental activity ( \200\230us e it or lose it \200\231), to optimize blood pres- sure and to encourage low-dose aspirin i n those with or at high risk of cerebrovascular disease. Some physicians are treating patie nts at high risk of Alzheimer \200\231s disease with NSAIDs and antioxidants, but this is n ot generally advised because there are several examples where promising epidemiological evi dence was followed by evidence of harm when RCTs \201 nally reported (eg B -carotene, HRT ). In vascular dementia, there is little evidence for atheroma reduction, but it is usual p ractice to modify general vascular risk factors (see b \200\230Vascular secondary preventi on \200\231, p.308), and those with clear clinical or radiological evidence of TIA or strok e should have the usual measures. 224 CHAPTER 9 Psychiatry Dementia: acetylcholinesterase inhibitors Acetylcholinesterase inhibitors, released in 1997 , were the \201 rst drug class proven to improve cognition in some patients with dementia . They work by blocking acetylcholinesterase which breaks down acetylcholine, an important neurotransmitter for memory. Effectiveness Acetylcholinesterase inhibitors are far from miracle drugs, with very vari- a ble response. In general: \200 They offer symptomatic bene \201 t through a one-off incr ement in cognition. The underlying disease continues to progress at the same rate and patients stopp ing the drug revert to where they would have been without treatment Of the dementias, Alzheimer \200\231s disease, dementia with Lewy bodies and Parkinson \200 \231s disease with dementia have the greatest cholinergic de \201 cit, and these are the d ementia types known to bene \201 t most from acetylcholinesterase inhibitor treatment About half of patients show no bene \201 t, a signi \201 cant minority show moderate improvements ( \200\230clock turned back a few months \200\231) and for a small mi nority there is substantial improvement In some, there is a worsening in cognition, or onset of agitation that may be temporary or respond to a change in drug Early studies focused on effects on cognitive function, and these are overall modest. However, small improvements in cognition can translate into signi \201 cantly improved day-to-day function, reducing carer burden (by 730min daily in moderate de mentia) Some evidence that acetylcholinesterase inhibitors can reduce the requirements for home care, and can delay placement in nursing home \200 Bene \201 t has been demonstrated for mild to moderate dementia, not in severe dementia. Recent NICE guide lines (March 2011) supports their use in both mild and moderate disease Choosing a drug The three acetylcholinesterase inhibitors currently available are: \200 D onepezil 5mg od increased to 10mg od after 4/52 \200 Galantamine 4mg bd increased to 8mg bd after 4/52, 12mg bd after 8/52 \200 Rivastigmine 1.5mg bd increased to max 6mg bd with in 12/52 Selecting an agent is dif \201 cult, as there are few head-to-head comparisons. E ffectiveness seems broadly similar, and choice can be made based on costs, and the team \200\231s experience. There is most evidence for donepezil in Alzheimer \200\231s disease a nd it has fewer adverse events than rivastigmine which is probably better for Lewy body dem entia. Donepezil will be off- patent in the UK soon which will make its use more widespread . Overall, the evidence for acetylcholinesterase inhibitors is strongest in Alzheimer \200 \231s and Lewy body dementia, and weakest in vascular dementia. Further reading NICE . Donepezil, galantamine, rivastigmine and memantine for the treatment of Alzheimer \200\231s disease ( 2011 ) online: M http://guidance.nice.org.uk/TA217 .