Old age psychiatry (dementia and delirium) Flashcards

Question

DDs of delirium?

Answer 1

Dementia. Mood disorders: depression or mania (bipolar). Late onset schizophrenia. Dissociative disorders. Hypothyroidism and hyperthyroidism (may mimic hypo- and hyperactive delirium respectively).

Answer 2

Person centred care Identify and manage the possible underlying cause or combination of causes. Ensure effective communication and reorientation

Answer 3

Clear communication – explain what you are doing slowly and clearly, remember their STM is impaired so they might not remember. Try to use questions that need a ‘yes or no’ rather than asking them questions that rely on their memory as this can be distressing. Reminders of the day, time, location and identification of surrounding persons. Have a clock available. Have familiar objects from home, especially glasses, walking aids and hearing aids. Staff consistency - both doctors and nurses. Try not to move beds/wards. Involve the family and carers. Remove catheters etc where possible. Quiet environment with low lighting. Uninterrupted sleep – do they really need obs overnight? Mobilise regularly with physio – NICE recommends no cot side, encourage walking/motion exercises 3x daily

Answer 4

1. Age? (1) 2. Time to the nearest hour? (1) 3. Recall address at end: ‘42 West Street’ (1) 4. ‘What year is it?’ (1) 5. ‘Where are you right now?’ (1) 6. Identify two people. (1) 7. ‘What is your date of birth?’ (1) 8. ‘Date of First World War?’ (1) 9. ‘Who is the current monarch?’ (1) 10. ‘Count backwards from 20 to 1.’ (1) ≥8 → cognitive impairment unlikely

Answer 5

The Confusion Assessment tool (CAM) involves assessing a patient for four features. The diagnosis involves the presence of 1 and 2 + either 3 or 4: 1. Acute onset and fluctuating course. 2. Inattention (e.g. using the serial 7s test where 7 is subtracted from 100 and then 7 is taken from each remainder, i.e. 100, 93, 86, 79, 72…). 3. Disorganized thinking (e.g. incoherent speech). 4. Alteration in consciousness.

Answer 6

Treat underlying cause - Treat infections, correct electrolytes, stop potential offending drugs, Laxatives for faecal impaction Reassurance and re-orientation Provide appropriate environment - Quiet, well-lit side room, consistency in care and staff, reassuring nursing staff Managing disturbed, violent or distressed behaviour - encourage oral intake and continence, verbal and non- verbal de-escalation, oral low dose haloperidol (0.5-4mg) or olanzapine (2.5-10mg), avoid benzos

Answer 7

Antipsychotics and benzodiazepines are never first-line for managing delirium and unfortunately this is a misconception amongst many clinicians. Treating the underlying cause, providing reassurance and re-orientation and an appropriate environment are the main means for treating delirium as recommended by NICE guidelines. Low dose antipsychotics should only be used as a last resort in cases of violent or severely distressed behaviour and when other ways of calming the patient have failed.

Answer 8

Full recovery 18-22% Functional impairment Increased costs Institutionalization Death 30-40% Prolonged hospitalisation Psychological stress Long term cognitive impairment

Answer 9

Dementia is a syndrome of generalized decline of memory, intellect and personality, without impairment of consciousness, leading to functional impairment.

Answer 10

Neurodegenerative: Alzheimer’s disease, frontotemporal dementia, Pick’s disease, dementia with Lewy bodies (DLB), Parkinson’s disease with dementia, Huntington’s disease. Infections: HIV, encephalitis, syphilis, CJD. Toxins: Alcohol, barbiturates, benzodiazepines. Vascular: Vascular dementia, multi-infarct dementia, CVD. Traumatic head injury

Answer 11

Neurological: Normal pressure hydrocephalus, intracranial tumours, chronic subdural haematoma. Vitamin deficiencies: B12, folic acid, thiamine, nicotinic acid (pellagra). Endocrine: Cushing’s syndrome, hypothyroidism.

Answer 12

Clinical Syndrome Exclude Differential Diagnoses Bloods (confusion screen) Imaging CT/MRI DaT/SPECT Formal cognitive testing - ACE-III

Answer 13

Assess 5 cognitive domains “Normal” score 82/100 Sub-scores just as imporant as total score Change in score is relevant over time “Normal” score doesn’t exclude dementia

Answer 14

Attention /18 Memory /26 Fluency /14 Language /26 Visuospatial /16

Answer 15

DEMENTIA Drugs (e.g. barbiturates), Eyes and Ears (visual/hearing impairment may be confused with dementia), Metabolic (Cushing’s, hypothyroidism), Emotional (depression can present as a pseudodementia), Nutritional deficiencies/Normal pressure hydrocephalus, Tumours/Trauma, Infections (e.g. encephalitis), Alcoholism/Atherosclerosis

Answer 16

Alzheimer's (50%) Vascular dementia (25%) Lewy Body dementia (15%) Fronto-temporal dementia (<5%) Other causes of dementia (<5%)

Answer 17

In Alzheimer’s disease there is degeneration of cholinergic neurons in the nucleus basalis of Meynert leading to a deficiency of acetylcholine. Other pathophysiological changes can be divided into microscopic (Fig. 10.2.3) and macroscopic: Microscopic → Neurofibrillary tangles (intracellularly) and β-amyloid plaque formation (extracellularly). Macroscopic → Cortical atrophy (commonly hippocampal). Widened sulci and enlarged ventricles.

Answer 18

Vascular dementia (VaD) occurs as a result of cerebrovascular disease, either due to stroke, multi-infarcts (multiple smaller unrecognized strokes) or chronic changes (arteriosclerosis) in the small vessels

Answer 19

Onset: Step-wise Fluctuations: Sometimes Hallucinations: Sometimes Progressive: Yes Personality changes: Yes Insight: Varies

Answer 20

In Lewy body dementia (DLB), there is abnormal deposition of a protein (Lewy body) within the neurons of the brainstem, substantia nigra and neocortex. Outside the brainstem LBs are associated with more profound cholinergic loss than in AD. Within the brainstem, they are associated with dopaminergic loss and parkinsonian-like symptoms

Answer 21

there is specific degeneration (atrophy) of the frontal and temporal lobes of the brain. One type of fronto-temporal dementia is Pick’s disease, where protein tangles (Pick’s bodies) are seen histologically

Answer 22

Alzeheimers Fronto-temporal

Answer 23

Memory loss Severe Mood Normal Speech and language Early aphasia Personality Indifferent Coordination Normal Praxis Apraxia Motor speed Normal

Answer 24

Memory loss Moderate Mood Low Speech and language Can be dysarthria Personality Apathetic Coordination Impaired Praxis Normal Motor speed Slow

Answer 25

There are currently 800 000 people with dementia in the UK and it is estimated that there will be over one million by 2021. Dementia increases with age (rare if <55 years; 5–10% if >65 years; and 20% if >80 years). Overall prevalence is similar in ♂ and ♀, but AD is more common in ♀, whereas vascular and mixed dementias are more common in ♂. See Table 10.2.3 and Key facts 1 for risk factors and genes associated with AD.

Answer 26

Advancing age The incidence of AD increases with advancing age. Family history The lifetime risk of AD in first degree relatives of those affected is 25– 50%. Genetics See Key facts 1. Down’s syndrome The mutations in trisomy 21 are associated with the development of pre-senile AD. Low IQ Lower educational attainment and lower IQ scores are associated with higher risks of developing dementia. Cerebrovascular disease Strong risk factor for vascular dementia which can co-exist with AD. Vascular risk factors E.g. Past stroke/MI, smoking, hypertension, diabetes and high cholesterol are risk factors for both AD and vascular dementia.

Answer 27

Presenilin 1 (chromosome 14), Presenilin 2 (chromosome 2) and amyloid precursor protein (chromosome 21) are genes associated with early onset AD. ApoE-4 (chromosome 19) is a susceptibility gene that contributes to late onset AD. The ApoE-2 variant is thought to be protective.

Answer 28

A. Evidence of the following: 1. A decline in memory, which is most evident in the learning of new information, although in more severe cases, the recall of previously learned information may also be affected. 2. A decline in other cognitive abilities, characterized by deterioration in judgement and thinking, such as planning and organizing, and in the general processing of information. B. Preserved awareness of the environment for a period of time long enough to demonstrate (A). C. A decline in emotional control or motivation, or a change in social behaviour, manifested by one of the following: (1) Emotional lability; (2) Irritability; (3) Apathy; (4) Coarsening of social behaviour. D. For a confident diagnosis (A) must have been present for at least 6 months.

Answer 29

Early stages - memory lapses, difficulty finding words, forgetting names of people/ places Disease progression - Apraxia, confusion, language problems, difficulty with executive thinking, Later stages - Disorientation to time and place, wandering, apathy, incontinence, eating problems, depression, agitation

Answer 30

Onset: Gradual Fluctuations: No Hallucinations: Sometimes Progressive: Yes Personality changes: Yes Insight: Varies

Answer 31

MRI scan showing clear evidence of hippocampal atrophy and enlarged ventricles in Alzheimer’s disease (right side) compared to control subject (left side).

Answer 32

AD can be classified into early onset or pre-senile (<65 yrs, familial) and late onset or senile (>65 yrs, sporadic), but it usually occurs after the age of 65. It has an insidious onset over years.

Answer 33

Executive functions: Problem solving, abstract thinking, reasoning, decision making, judgement, planning, organization and processing. Visuospatial abilities: Getting lost, impaired driving, copying figures. Language disturbances (dysphasia): Word finding difficulties, decreased vocabulary, perseveration (uncontrollable repetition of a particular response, such as a word, phrase, or gesture), global aphasia (impairment of language, affecting the production or comprehension of speech and the ability to read or write). Apraxia: Inability to carry out previously learned purposeful movements despite normal coordination and strength, e.g. dressing, unbuttoning shirt. Agnosia: Impaired recognition of sensory stimuli not attributed to sensory loss or language disturbance, e.g. object agnosia, auditory agnosia.

Answer 34

Perception (hallucinations), thought content (delusions), emotion (depression, apathy), behaviour (wandering, aggression, restlessness).

Answer 35

A. The general criteria for dementia A–D must be met. B. No evidence for any other possible cause of dementia or systemic disorder. Early onset Alzheimer’s disease A. General criteria for Alzheimer’s met and age of onset is <65. B. At least one of the following must be met: (1) relatively rapid onset and progression; (2) in addition to memory impairment there is aphasia, agraphia (↓ ability to communicate through writing), alexia (↓ ability to read), acalculia (↓ ability to perform mathematical tasks) or apraxia. Late onset Alzheimer’s disease A. General criteria for Alzheimer’s met and age of onset is >65. B. At least one of the following must be met: (1) slow, gradual onset and progression; (2) predominance of memory impairment over intellectual impairment.

Answer 36

Usually presents in the late sixties or early seventies. Stepwise rather than continuous deterioration, i.e. stepwise increases in severity of symptoms. Memory loss. Emotional (depression, apathy) and personality changes (earlier than memory loss). Confusion is common. Neurological symptoms or signs (e.g. unilateral spastic weakness of the limbs or increased tendon reflexes, an extensor plantar response or pseudobulbar palsy). On examination there may be focal neurology (often upper motor neurone signs) and signs of cardiovascular disease elsewhere

Answer 37

Features of both Alzheimer’s disease and vascular dementia.

Answer 38

Day to day fluctuations in cognitive performance. Recurrent visual hallucinations. Motor signs of parkinsonism (tremor, rigidity, bradykinesia). Recurrent falls, syncope, depression. Severe sensitivity to neuroleptic drugs. People with Parkinson’s disease who develop dementia after 12 months are diagnosed as having Parkinson’s disease with dementia as opposed to DLB where dementia and parkinsonian features within 12 months of one another.

Answer 39

Usually occurs between the ages of 50 and 60 and develops insidiously. Family history is positive in 50% of cases. Early personality changes: e.g. disinhibition (reduced control over one’s behaviour), apathy/restlessness (see Key facts 4 for frontal lobe tests). Worsening of social behaviour. Repetitive behaviour. Language problems: e.g. difficult to find word, problems naming/understanding words. Memory is preserved in early stages whereas insight is lost early.

Answer 40

Autosomal dominant, therefore strong family history. Abnormal choreiform movements of face, hands and shoulders and gait abnormalities. Dementia presents later.

Answer 41

Average age of onset after 70. Triad of dementia with prominent frontal lobe dysfunction, urinary incontinence and gait disturbance (wide gait).

Answer 42

Onset usually before 65. Rapid progression with death within 2 years. Disintegration of virtually all higher cerebral functions. Dementia associated with neurological signs (pyramidal, extrapyramidal, cerebellar).

Answer 43

Questions to ask the patient ‘Do you find yourself forgetting things? Can you give some examples? When did it begin?’ ‘Do you find yourself forgetting familiar people’s names?’ ‘Do you get lost more easily than you used to?’, ‘Are you able to handle money confidently?’ ‘Do you think being forgetful is stopping you from doing anything?’ Collateral history from informant (Also ask about functional status. See Key facts 2) ‘Are they repetitive in conversation?’ ‘Has their personality changed, for example, are they more irritable or anxious?’ ‘Have you noticed any change in their behaviour, for instance being more isolated?’ ‘Are their memory problems getting in the way of their daily life?’ ‘Do you have any concerns about their safety?

Answer 44

Appearance & Behaviour May appear unkempt with poor self-care. Behaviour may be inappropriate, e.g. in fronto-temporal dementia due to disinhibition. Uncoordinated or restless. Speech Slow, confused. Difficulty finding right word. Repetitive. Mood Low or normal. Disturbance of affect more common in VaD. Thought May have delusions. Perception Hallucinations are a core feature in DLB. May have illusions. Cognition Affected in all dementias but to varying degrees depending on the type and severity of dementia. Memory impairment is most severe in cortical dementias. There is usually impaired attention and disorientation. Insight May be preserved initially but is invariably lost in the latter stages of the disease.

Answer 45

Blood tests: FBC (infection, anaemia); CRP (infection, inflammation); U&Es (renal disease); calcium (hypercalcaemia); LFTs (alcoholic liver disease); glucose (hypoglycaemia); vitamin B12 and folate (nutritional deficiencies); TFTs (hypothyroidism).

Answer 46

1. Urine dipstick: Rule out UTI. 2. Chest X-ray: Pneumonia, lung tumour. 3. Syphilis serology and HIV testing: Only if there are atypical features or special risks. 4. Brain imaging: Imaging is only indicated for dementia if there is early onset (<60 years), sudden decline, high risk of structural pathology, focal CNS signs or symptoms (to rule out space-occupying lesions, e.g. subdural haematoma, abscess and tumour), or to monitor disease progression. CT scan: usual imaging modality. Can identify hippocampal atrophy. MRI: identifies posterior circulation vascular pathology with much greater sensitivity. SPECT: rarely used in specialist centres to reliably differentiate between Alzheimer’s disease, vascular dementia and fronto-temporal dementia. 5. ECG: If cardiovascular disease suspected. 6. EEG: If fronto-temporal lobe dementia or CJD is suspected, or where seizure activity is a possibility. 7. Lumbar puncture: If meningitis or CJD is suspected. 8. Genetic tests: For Huntington’s disease and familial dementia. 9. Cognitive assessment: Folstein Mini-Mental State Examination (MMSE, see Key facts 3), the Abbreviated Mental Test (AMT), the Addenbrooke’s Cognitive Examination (ACE), General Practitioner Assessment of Cognition (GPCOG) or the Montreal Cognitive Assessment (MOCA).

Answer 47

Normal ageing and mild cognitive impairment. Delirium. Trauma: Stroke, hypoxic or traumatic brain injury. Depression (‘pseudodementia’): Poor concentration and impaired memory are common in depression in the elderly. Identify whether the low mood or poor memory came first. Late onset schizophrenia. Amnesic syndrome: Severe disruption in memory with minimal deterioration in cognitive functioning. Learning disability. Substance misuse. Drug side effects: Opiate, benzodiazepine

Answer 48

Normal: MMSE 25–30 Mild: MMSE 21–24 Moderate: MMSE 10–20 Moderate–severe: MMSE 10–14 Severe: MMSE <10

Answer 49

Generally speaking, a quick and informal cognitive assessment can be carried out by recording the following: Orientation in time, place, and person Attention and concentration, e.g. serial sevens test. Record the time taken and the number of errors Memory: short-term memory recent memory remote memory Grasp, e.g. name the prime minister and reigning monarch If cognitive impairment is suspected, you can carry out the Folstein Mini-Mental State Examination (MMSE). The MMSE is scored out of 30. Scores of less than 22 are indicative of significant cognitive impairment, while scores of 22 to 25 are indicative of moderate cognitive impairment. The result is invalid if the patient is delirious or has an affective disorder. Due to recent copyright restrictions only some of the items on the MMSE can be reproduced here. Sample items from the Folstein Mini-Mental State Examination Orientation to time “What is the date?” Registration “Listen carefully. I am going to say three words. You say them back after I stop. Ready? Here they are … APPLE (pause), PENNY (pause), TABLE (pause). Now repeat those words back to me.” [Repeat up to five times, but score only the first trial.] Naming “What is this?” [Point to a pencil or pen.] Reading “Please read this and d

Answer 50

There are a number of frontal lobe tests that are useful adjuncts when considering a diagnosis of fronto-temporal dementia. Verbal fluency and initiation: Ask the patient to recall as many words as possible in one minute starting with the letter ‘S’. Fewer than 10 words is abnormal. Should aim for >15. Cognitive estimates: Ask the patient to make educated guesses to questions which they are unlikely to know the specific answer to e.g. ‘what is the age of the oldest person in the country?’ Clock drawing test: Tests executive function. Ask the patient to draw a large clock face, put the numbers in and then make the clock show ten past five. Similarities (conceptualization): Ask in what way two objects are alike e.g. banana and orange (both fruits), table and chair (both items of furniture), tulip and rose (both types of flower). Motor sequencing (Luria’s 3 step test): Tell the patient you are going to show them a series of hand movements. Demonstrate fist, edge, palm 5 times without verbal prompts and ask them to repeat.

Answer 51

After a diagnosis of dementia is made, patients are legally obliged to contact the Driver and Vehicle Licensing Agency (DVLA). They may be able to continue driving subject to medical reports and annual review. Early discussions should take place to allow advance planning prior to cognition deteriorating. Topics include advance statements or decisions, lasting power of attorney and preferred place of care plans. In the later stages of the disease, if patients are not competent to make a decision, the requirements of the Mental Capacity Act 2005 should be adhered to. Vascular dementia is modifiable and preventable by targeting cardiovascular risk factors

Answer 52

1st line - Supportive treatment, environmental control measures, Acetylcholinesterase inhibitors Adjuncts - Antidepress, antipsychotics, insomnia mgmt, mgmt of behavioural and psychological symptoms, adding in or switching to memantine

Answer 53

Acetylcholinesterase inhibitors Donepezil, Galantamine, Rivastigmine Best for cognitive problems Side-effects include bradycardia, diarrhoea, headache NMDA Receptor Antagonists Memantine Severe impairment or unable to tolerate AChEI Better for neuropsychiatric impairment Can be added to AChEI Side-effects include confusion and dizziness

Answer 54

NMDA receptor antagonists (work on glutamate neurotransmitter) and affect glutamate-mediated toxicity of neurons - Excessive activation of iGluR (ionotropic glutamate receptors) which leads to loss of post-synaptic dendrites and cell bodies NMDA receptor antagonist (ketamine)

Answer 55

Vascular Prevent further damage Treat vascular risk factors Alcohol-related Prevent further damage Stop drinking alcohol Fronto-temporal Dementia No specific treatment Vascular risk factors, e.g. smoking, weight, hypertension, obesity, Diabetes etc Stopping drinking alcohol in Alcohol-related dementia can lead to improvement in symptoms

Answer 56

AChE inhibitors Treat agitation Treat low mood and insomnia Functional support Social support Support for carers

Answer 57

Social support including support groups such as Alzheimer’s Society. Increasing assistance with day-to-day activities Information and education Community dementia teams Home nursing and personal care Community services such as meals-on-wheels, befriending services, day centres, respite care and care homes. For non-cognitive symptoms or behaviour that challenges, aromatherapy, massage, therapeutic use of music or animal-assisted therapy may be considered.

Answer 58

The three acetylcholinesterase (AChE) inhibitors (donepezil, galantamine and rivastigmine) are recommended as options for managing mild to moderate Alzheimer’s disease. They can also be used in dementia with Lewy bodies, in cases where non-cognitive symptoms cause significant distress Memantine is an NMDA (N-methyl-D-aspartate) receptor antagonist and is an option for Alzheimer’s disease in the following circumstances: Moderate Alzheimer’s disease in those who are intolerant of or have a contraindication to AChE inhibitors. Severe Alzheimer’s disease. For behaviour that challenges, if non-pharmacological strategies have proved ineffective, a short course of an antipsychotic (e.g. risperidone) can be used. For low mood, antidepressants (e.g. sertraline) can be initiated.

Answer 59

Acetylcholinesterase inhibitors are centrally acting agents that work by compensating for the depletion of acetylcholine in the cerebral cortex and hippocampus in AD. They are cautioned in arrhythmias (sick sinus syndrome and other supraventricular conduction abnormalities), peptic ulcer disease and asthma/COPD. Galantamine is contraindicated in severe renal or hepatic impairment. Side effects include gastrointestinal disturbances, bradycardia and muscle spasms. Rivastigmine may cause extrapyramidal side effects. Doses: donepezil (5–10 mg OD), rivastigmine (1.5–6 mg BD), galantamine (4–12 mg BD).

Answer 60

Cognitive impairment without functional impairment Aetiology similar to dementia Prognosis 1/3 will improve 1/3 will remain stable 1/3 will progress to dementia

Answer 61

Cognitive Impairment secondary to mental illness Most commonly depression “Don’t know” answers Impairments in executive functioning and attention Frontal lobe changes White matter hyperintensities on MRI

Answer 62

Alzheimer’s Dementia Lewy Body Dementia Hyperactive Delirium Delirium Tremens

Answer 63

Alzheimer’s Dementia Depression Delirium Delirium Tremens

Answer 64

23% lifetime risk of developing by 75years Prevalence ~3-15% in OA population Higher in care homes/hospital Higher rates of suicide in older adults Approx 1/3 comorbid harmful drinking Suicide tend to use more drastic measures in OA population.

Answer 65

Under-recognised and under-diagnosed “Depression without sadness” Biological symptoms thought of as physical illness Less likely to seek help Vague presentations Relationship with physical health Bidirectional relationship Higher physical morbidity and mortality Depression without sadness – more lethargy/apathy/physical complaints Larger burden of physical illness in OA group, so biological symptoms are thought of as being more likely to be linked to physical problems Don’t complain of symptoms or seek help for this Non-specific and vague symptomatology

Answer 66

Depression increases risk of physical disease Physical illness increases risk of depression High physical morbidity/mortality in depression

Answer 67

hanges to cortical circulation White matter hyperintensities on MRI Presentation associated with: Cognitive Impairment Psychomotor retardation and apathy Poor Insight Poor response to antidepressants Often considered to be “treatment resistant” Commonly prodromal to dementia

Answer 68

Drugs Beta-blockers/nifedipine/clonidine Opiods/antipsychotics/benzodiazepines Methyldopa/anti-parkinsonian medications Digoxin Metabolic Anaemia/B12 or folate deficiency Hypercalcaemia/Hypothyroidism/ hyper- or hypo- kalaemia or natraemia Infective Post-viral/neurosyphillis Intracranial Post-stroke/subdural haematoma/Parkinson’s Disease/SOL/Dementia

Answer 69

Same as for younger adults “Start low and go slow” with antidepressants Psychological therapies/social inclusion ECT Max doses of antidepressants sometimes the same as for younger adults Some specifics – sertraline in post-MI ECT more commonly used in older adults age group

Answer 70

Cerebrovascular changes major risk factor Good prognostic factors: Onset <70y Absence of physical illness Good previous recovery Religious beliefs Two-fold increase in risk of Alzheimer’s Disease

Answer 71

Capgras – Delusion that a close friend/relative/pet has been replaced by an identical imposter Fregoli – Delusion that a stranger is someone they know in disguise Cotard – Nihilistic delusion that body parts are missing/person is dead/parts are rotting De Clerambault – Erotomania (beliefs of another person being in love with the patient)

Answer 72

Secondary to delirium? Primary mental illness Schizophrenia Late onset schizophrenia Delusional disorder Affective disorder Dementia

Answer 73

Common psychotic elements include: Nihilistic delusions Hypochondriacal delusions Delusions of poverty Auditory hallucinations (second person derogatory) Treat with antidepressants +/- antipsychotics

Answer 74

AKA Paraphrenia Onset of symptoms >60 years old F>M Persecutory delusions classical Negative symptoms and thought disorder uncommon

Answer 75

Persistent delusions without hallucinations Often more distressing to other people than the patient Patients often reluctant to seek or accept help Common delusions include: Persecutory (being targeted by someone) Erotomania (someone is in love with them) – often dangerous! Theft Mistaken Identity

Answer 76

Visual hallucinations Simple repeated patterns Complex images of people/landscapes/objects Associated with visual impairment No role for antipsychotics/treatment Patient usually retains insight

Answer 77

Do patients need treatment? How much distress are symptoms causing? Treat underlying cause Dementia/Depression Antipsychotics Cardiovascular side-effects EPSEs Effect on cognition