Elderly psych, dementia and delirium Flashcards
clinical features of dementia?
cognition: poor memory
impaired attention
aphasia-global, word finding difficulties, perseverance, decreased vocabulary, agnosia-impaired recognition of sensory stimuli not result of impaired language or sensory loss, apraxia-inability to perform previously learned purposeful movements despite normal coordination and strength e.g. problems dressing and using utensils
disorientation-get lost, impaired driving
personality change
loss of executive functions-problem solving, judgement, planning, abstraction
behaviour: odd and disorganised restless, wandering,aggressive self-neglect disinhibition social withdrawal
mood: anxiety
depression
thinking: slow, impoverished
delusions
perseveration
perception: hallucinations, often visual
illusion
impaired insight
severity classification of AD?
mild-forgetfulness, recent memory defecit, normal AODL
moderate-significant memory loss with personality and behavioural changes, difficulties in orientation and starting language, impaired AODL.
severe-dysphasia with disordered and fragmented speech, aggression, restlessness and wandering, hallucinations and delusions e.g. of poverty, incontinence, immobility, rigidity and recurrent falls and general physical deterioration.
common types of dementia?
Alzheimer’s (60%)
Vascular (20%)
Lewy Body (10%)
Others (10%) e.g. AIDS dementia, CJD-Creutzfeldt-Jakob Disease
potentially reversible types of dementia?
metabolic and endocrine disorders e.g. hypothyroidism, Cushing’s syndrome
Vit deficiencies e.g. thiamine, Vit B12, folic acid
neurological: normal-pressure hydrocephalus
IC tumour e.g. frontal lobe tumour
chronic subdural haematoma
chronic alcohol abuse
infection-syphilis-treponema pallidum-neurosyphilis treat with doxycycline.
epidemiology of dementia?
850,000 in the UK (10-15% prevalence)
4 times more common in men than women
how to distinguish between dementia and the pseudodementia associated with depression?
pseudodementia: evidence depressed mood preceded memory problems e.g. from another informant
memory testing shows improved poor performance when interest aroused
patient retarded and unwilling to cooperate in interview, whereas dementia pts usually willing to reply to qns but make mistakes.
quicker onset of depressive features
biological symptoms present
consistent mood and behaviour
admit to poor memory
normal orientation
normal MMSE
respond to antidepressants
a good insight into low mood suggests depression
irreversible causes of dementia?
primary degenerative conditions: Alzheimer's disease Lewy body dementia frontotemporal dementia (Pick's disease) Huntington's disease-chromosome 4* Wilson's disease MS MND
vascular (multi-infarct) dementia traumatic head injury encephalitis toxins e.g. alcohol anoxia- cardiac arrest, CO poisoning metabolic-hepatic encephalopathy, DM
RFs for dementia?
FH-genetic-apolipoprotein E (APOE)-15-20% of AD cases can be attributed to this risk
vascular-smoking, HTN, hypercholesterolaemia, DM, alcohol, obesity, CVS and CV disease, also all assoc. with AD.
psychosocial-isolated, lack of social engagement, poor education
also nutritional-diet rich in saturated fats and cholesterol
protective factors in dementia for delaying onset and reducing risk of cognitive impairment and dementia?
diet-antioxidants-Vit E and C, diet with plenty of fish and vegetables, fruit, and polyunsaturated FA
physical activity-sports, walking
mental activity e.g. reading, playing a musical instrument, dancing, engaging in social and cultural activities, gardening, knitting.
more complex work- high level of complex mental work over lifespan correlated with reduced hippocampal atrophy.
memory problems in AD?
commonest presenting symptom
initially inability to recall new info
remote memory declines with disease progression
disorientation to time and place is closely related to memory impairment
what is paraphrenia?
a mental disorder charactersied by an organised system of paranoid/persecutory delusions with or without hallucinations without deterioration of intellect or personality.
what is an encapsulated delusion?
A belief which is separate from the rest of the patient’s beliefs e.g. A pt may believe that his sexual fantasies and practices being widely discussed by strangers but his remaining beliefs are not influenced by this conviction, nor is his social or work life affected.
lab investigations in diagnosing dementia?
FBC-normochromic normocytic anaemia of malignancy, raised WCC with delirium secondary to infection, and infections causative of dementia e.g. syphilis, HIV-lymphopenia, CRP/ESR, Us and Es, TFTs-hypothyroid potentially reversible cause, LFTs-hepatic encephalopathy, vit B12, folate, thiamine, calcium, glucose-DM.
HIV and syphilis testing if strong clinical suspicion from history and exam.
drug tment of dementia?
AChesterase inhibitors e.g. donepezil, rivastigmine, galantamine-can improve cognitive function and behaviour, but no evidence for delaying or halting disease progression. Used if AD and MMSE score 10-20points, or those with agitation not controlled by non-drug measures or antipsychotics. Stop after 6mnths if no clinical benefit.
Memantine-glutamate NMDA receptor antagonist, improves mood, cognition and behaviour in moderate to severe AD.
Antipsychotics if severely distressed or agitated causing risk to self or others. Slight increase risk of cerebrovasc events in mild to mod dementia. atypical antipsychotics assoc. with greater risk of CVS events when used in alzheimer’s patients, notably ischaemic stroke
BZDs-IM lorazepam alternative to antipsychotic for extreme agitation.
in lewy body dementia, give L-DOPA for parkinsonism. avoid anticholinergics as can increase confusion and visual hallucinations. if antipsychotics needed, should give atypical 1st as this dementia has higher risk of neuroleptic malignant syndrome than other conditions-muscle rigidity always present-may be dyspnoea due to resp muscle rigidity, dysphagia or difficulty walking with a shuffling gait, hyperthermia, likely to be altered mental state with confusion or altered consciousness and may be tremor, tachycardia and pallor result of autonomic dysfunction. should stop causative drug, check airways and breathing, give BZDs if severely agitated, IV fluids, can use muscle relaxants and dopamine agonsits e.g. bromocriptine, cooling devices, antipyretics, dialysis if AKI.
pathological features of AD?
widened sulci, large ventricles
ATROPHY, cell loss, shrinkage of dendritic tree, astrocyte proliferation, increased gliosis.
histologically: beta amyloid plaques-dense insoluble beta amyloid peptide surrounded by abnormal neuritis, beta amyloid from APP protein, and neurofibrillary tangles-flame-shpaed helical filaments of Tau protein in a highly phosphorylated state throughout cortical and subcortical grey matter. initially both form in hippocampi, then spread more widely, occipital lobe and cerebellum tend not to be affected.
the 3 pathological hallmarks of AD?
beta amyloid plaque deposition
neurofibrillary tangles
neuronal loss-primarily cholinergic- led to cholinergic hypothesis that cognitive impairment due to defecit of cholinergic neurotransmission.
DSM-IV diagnostic criteria for AD dementia?
development of multiple cognitive deficits seen by both memory impairment and at least one of aphasia, apraxia, agnosia or disturbance in executive functioning e.g. planning, judgement, processing.
cognitive defecits cause significant impairment in social or occup. functioning and represent signif decline from prev level of functioning.
course characterised by gradual onset and continuing cognitive decline.
cognitive defecits not due to any of following: other CNS conditions causing progressive defecits in memory and cognition, systemic condition known to cause dementia, substance-induced conditions.
defecits do not occur exclusively during course on delirium.
disturbance not better accounted for by another Axis I disorder.
AD RFs?
age FH APP, presenilin, or apoE4 gene mutation carrier previous head injury Down's syndrome hypothyroidism Parkinson's disease CVD low level of education, lower IQ
most frequent cause of death in AD?
bronchopneumonia
clinical features of vascular dementia?
mores sudden onset than AD
may present post stroke or due to sudden unexplained decline in function
emotional and personality changes tend to occur early before memory loss in apparent
fluctuating symptoms, and episodes of confusion espec. at night
depression
fits, TIAs
focal neurology e.g. UMN defecits such as +ve Babinski test-extensor plantar reflexes, unilateral limb
signs of CVD elsewhere e.g. previous MI, IC.
stepwise progression
uneven distribution of defecits
more likely to have insight, and so more willing to accept help from family and treatment
vascular dementia RFs?
CVD history includ hypercholesterolaemia and HTN smoking DM FH of CVD or cerebrovasc AF coagulopathies polycythaemia sickle-cell anaemia carotid disease
what do pts with vascular dementia usually die of?
IHD
others-cerebral infarct or renal complications
clinical features of Lewy Body dementia?
fluctuating cognitive ability and level of consciousness, relative sparing of memory
parkinsonism-postural instability and shuffling gait
liliputian visual hallucinations
falls
depression
sleep disorders-daytime somnolence
if needed, why should atypical antipsychotics be used before typical in treament of Lewy body dementia?
disease carries higher risk of neuroleptic malignant syndrome
drugs that may cause cognitive impairment?*
TCAs
specific areas of neuronal tract decay in AD?
entorohinal cortex-part of medial temporal lobe
hippocampus
parietal lobe assoc. areas
symptoms of frontal lobe disease in AD?
irritability
disinhibition-social
religious delusions?
logoclonia may develop in advanced AD, what is this?
spasmodic repetition of words, often the last syllable
clinical course of AD?
gradual onset, slow progression
duration of less than 10yrs on average between diagnosis and death.
pathology of vascular dementia?
arteriosclerosis-hardening of walls of arteries and arterioles usually as result of HTN or DM. Smooth muscle hypertrophy, endothelial cell dysfunction and elastic fibre fatigue occur as result of elevated arterial pressure.
large and small vessels
occlusive neuronal death
mutliple infarctions and ischaemic lesions in white matter
atrophy of old infarcted areas
infarcts tend to be bilateral
lesions involve full thickness of white matter
changes in b.flow in unaffected regions
entire brain smaller and ventricles expanded
emboli, vasculitis, haemorrhage
