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Old Age Psychiatry

Dementia

 Syndrome of progressive, chronic, global cognitive defects sufficient to impair


activities of daily living, no clouding of consciousness
 Diagnosis based on the significant impairment of normal function of daily living,
problems should have been present in clear consciousness for at least 6 months
 ICD-10 criteria
o Decline in:
 Memory
 Other cognitive abilities – planning, organising, problem solving
 Absence of clouding of consciousness
 Change in emotion, personality or behaviour
 6% of those over 65
 20% of those over 80
 Clinical features
o Memory impairment – forgetfulness from short term to long term
o Anxiety and depression
o Disorientation from time, place and then person
o Personality change – social withdrawal, mood lability, disinhibition, reduced
self-care, apathy, fatigue, deteriorating executive function
 Executive function – involves frontal lobe
 Planning, verbal reasoning, problem solving, multi-tasking, initiation
and monitoring of actions
o Wandering, sleep disturbance, delusions, hallucinations, shouting,
inappropriate behaviour – sexual disinhibition, aggression
o Dyspraxia
o Visuospatial agnosia
o Anxiety and depression
o BPSD – behavioural and psychological symptoms of dementia
 Ix
o Collateral history
o Physical assessment
o FBC, LTFs U&Es, glucose, ESR, TFTs, calcium, magnesium, phosphate, HIV,
syphilis (VDLR), B12, folate, CRP, blood culture
o LP, EEG, CXR, ECG, CT, MRI
o MMSE, ACE-III, cognitive examination
o Septic screen – MSU, CXR, blood culture, wound swabs, sputum/stool sample
o MRI scan/CT head, DAT scan, UDS
o Assess activities of daily living
 Personal care, nutrition, continence, mobility, driving
 Management
o Adaptations for patients
 Carry ID, address and contact number in case they get lost
 Dossett boxes to aid medication compliance
 Change gas to electric (to avoid leaving the gas on)
 Reality orientation – clocks, calenders
o Social support
 Personal care, meal preparations or medication prompting
 Day care centres to provide social and daytime activities
 Day hospitals for psychiatric care
o Support carers
 Emotional support
 Educate patient
 Train to manage common problems
 Provide respite care
o Optimize physical health
 Treat sensory impairment e.g. glasses
 Exclude superimposed delirium
 Treat underlying risk factors e.g. statin
 Review all medication
o Psychological therapies
 Behavioural approacbes
 Identify and modify underlying triggers for risk behaviour e.g.
wandering due to boredom etc.
 Reminiscence therapy
 Talking about past reinforces identity and builds confidence
 Validation therapy
 Reassure and validate
 Multisensory therapy
 Cognitive stimulation therapy
 Memory training and relearning
o Psychotropic medications
 Treat comorbidities e.g. antidepressants
 Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine,
galantamine
 Increases Ach to compensate for loss
 Trazodone – sedative antidepressant
 Sodium valproate, BDZ, low-dose antipsyhotics
 Anti-oxidants – vitamin E, ginkgo biloba
 Memantine
 Carbamazepine – sedating, induces metabolism of other drugs
o MDT led care
 GP, social worker, community nurse, old-age psychiatrist,
psychologist, geriatrician, occupational therapist, admiral nurse
 DDx
o Delirum
o ‘reversible’ dementias e.g. endocrine, vit def, space occupying lesion, normal
pressure hydrocephalus, subdural haematoma
o Psuedodementia – severe depression
o Rule out any organic underlying cause
o Minimal cognitive impairment (Age-related memory impairment)
o Learning disability
o Dysphasia
 Prognosis
o 2/3rd will live at home alone or with carer
o Nursing home is never first line management, only in accordance to
increasing needs
o GP and MHOA in reach support important in nursing homes
o Elder abuse in forms of neglect or abuse more likely in elderly female
patients, living alone with the abuser
o Life expectancy 8 years after diagnosis

Alzheimer’s disease

 Insidious onset, progressive cognitive decline where delusions are common


 Aeitology
o Age
o Genetics
 Familial early-onset AD due to rare autosomal dominant gene causing
increased B-amyloid
 Presenilin 1 (chr. 14) and Presenilin 2 (chr. 1)
 B-amyloid precursor protein gene (chr 21)
 Late onset > 65 years AD
 Apolipoprotein E4 allele (chr 19)
o Vascular risk factors e.g. hypertension
o Low IQ/poor educational level
o Head injury
o FHx of parkinsons, downs, alzheimers
o Down’s syndrome or hypothyroid
 Pathology
o Atrophy
 Due to neuronal loss
 Hippocampus needed for new learning and visuospatial skills affected
early
o Plaque formation
 Amyloid plaques become insoluble lumps
o Intracellular neurofibrillary tangles
 Severity of dementia associated to number of these
o Cholinergic loss
 Clinical presentation
o Amnesia – recent memories lost first
o Aphasia – word finding problems occur
o Agnosia – recognition problem
o Apraxia – inability to carry out skilled task despite motor function
o Early – failing memory, wandering, irritability
o Middle – dysphasia, personality changes, impaired executive function
o Late – gait abnormalities, full dependence, extra-pyramidal signs, tremor
o Psychiatric – delusions, hallucinations, depression
o Behavioural disturbances – aggression, sexual disinhibition
 Gold standard – MRI with atrophy of grey matter

Vascular dementia

 Due to infarcts by thrombo-embolus or ateriorsclerosis – ‘stroke-related dementia’


 Abrupt onset with stepwise deterioration, fluctuating course and patchy deficits
 Risk factors
o Old age
o Male
o Smoking/alcohol
o Hypertension
o Diabetes
o High cholesterol
o Atrial fibrillation
o Previous MI or TIAs
 Pathology
o Arteriosclerosis, cortical ischaemia and infarctions
 Clinical presentation
o Sudden onset, step-wise progression – each step is a sudden deterioration as
an infarct occurs
o Symptoms reflect site of lesions so presentation may be patchy
o Personality changes with areas of cognition spared
o Neurological signs such as hemiparesis or aphasia present
o Episodes of confusion esp at night
 Tx – control risk factors e.g. stop smoking with DM/HTN control and daily aspirin to
delay course of disease progression
 NICE guidelines
o Specialist diagnosis and initial prescription
o MMSE 12 or greater when starting medication
o Clinician must be sure of compliance
o Patient assessed after 2-4 months and then every 6 months
o Stop if MMSE < 12
o Continue if MMSE does not fall
o Shared care protocols for GP prescribing
o

Dementia with Lewy Bodies

 Pathology
o Lewy bodies are eosinophilic intracytoplasmic neuronal structures
o Comprised of alpha-synuclein with ubiquitin
o Found in cingulate gyrus and neocortex and brainstem
o Parkinsons also has lewy bodies found in brain stem
 Clinical presentation
o Gradual decline
o Fluctuating confusion with variation in levels of alertness
o Vivid visual hallucinations
o Spontaneous (new) parkinsonian signs
o Repeated falls, syncope, transient loss of soncsiousness
o Can resemble delirium but never prescribe anti-psychotics as extreme
antipsychotic sensitivity in dementia with lewy bodies can cause death
o Depression
 Life expectancy 6 years from diagnosis

Fronto-temporal dementia – Pick’s disease

 Atrophy of fronto-temporal regions with usually earlier onset


 Insidious onset and gradual progression, early decline in social ability
 Behavioural disorder
o Neglect personal hygiene
o Distractibility
o Pressured speech
o Personality changes
o Sexual disinhibition
o Anti-social behaviour

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