290 likes | 582 Views
Cognitive ageing. Cognitive, or thinking ability is the product of fixed intelligence' , the result of previous thinking , which often increases with age i.e wisdomfluid intelligence i.e. real time information processing which declines modestly in old ageIntellectual function is maintained unt
E N D
1. DEMENTIA Dr. O.Martinovic, SpR to
Dr. Heller
2. Cognitive ageing Cognitive, or thinking ability is the product of ‘fixed intelligence’ , the result of previous thinking , which often increases with age i.e wisdom
‘fluid intelligence ‘ i.e. real time information processing which declines modestly in old age
Intellectual function is maintained until at least 80 years of age, but processing is slower.
Non critical impairments include: forgetfulness, reduced vocabulary, slower learning
3. Impairments in cognitive function without dementia Age-associated memory impairment: older people learn new information and recall information more slowly but their performance is unchanged
Minimal cognitive impairment: more broad that memory alone and felt to be pathological i.e. due to cerebrovascular disease, full criteria for dementia are not met. Progression to dementia occurs in 5-10% cases
4. DEMENTIA Acquired decline in memory and other cognitive functions in an alert( i.e. on-delirious person) that is sufficiently severe to affect daily life.
Prevalence increases dramatically with age 1% 60-65 year olds, > 30% of over 85 year olds
5. Major dementia syndromes Dementia of Alzheimer’s type( 60-70%)
Vascular Dementia ( 10-20%)
Other neurodegenerative dementias(5-10%) Dementia with Lewy Bodies( up to 20%), PDD, Frontotemporal dementia
Reversible dementias ( < 5%), drugs, metabolic, SDH,NPH
Mixed pathology
6. History Take from patient and informant
Note onset, speed of progression, symptoms
Careful Drug History
Progressive decline in cognitive function over the years, ending in complete dependency and death. Deterioration may be stepwise( suggesting vascular ethiology), abrupt (single critical CVA) or rapid ( weeks, months-structural, metabolic or drug cause)
7. Deterioration occurs in Retention of new information, short term memory loss with repetitive questioning
Managing complex tasks
Language
Behaviour
Orientation
Recognition
Ability to self care
Reasoning
8. Physical examination Look for peripheral stigmata of vascular disease, neuropathy, PD, Thyroid disease, liver disease, malignancy
Mental state:
R/O DELIRIUM: features include agitation, restlessness, poor attention and fluctuating conscious level
R/O DEPRESSION: features include low affect, poor motivation, negative perspective. Perform Geriatric Depression Scale
Measure cognitive function
Neurophysiological assessment
9. INVESTIGATIONS Screen for reversible causes:FBC,U+E, CRP,ESR,LFT’s, B12, Ca,TSH, glucose
Resting ECG, CXR
Neuroimaging:
Early onset < 60
Sudden onset or brisk decline
Focal neurology
High risk of structural pathology
CT, MRI, SPECT
10. DEMENTIA-COMMON DISEASES ALZHEIMER’S DISEASE (AD)
Most common cause of dementia syndrome
Insidious onset, slow progression over the years
Early profound short term memory loss, progresses to include broad , global cognitive dysfunction, behavioural change, functional impairment
Behavioural problems common
Early onset AD ( <65) is uncommon
11. VASCULAR DEMENTIA Suggested by Risk Factors: (DM, HTN, SMOKING)
Cognitive impairment may be patchy
Frontal lobe, pseudobulbar, extrapyramidal features, emotional lability common
Urinary incontinence and falls
Other features may be cortical mimicking AD, or subcortical( apathy depression)
Onset often associated with CVA or deterioration may be abrupt, stepwise
12. Physical examination often shows focal neurology, suggesting CVA or diffuse cerebrovascular disease( hyperreflexia, extensor plantars,abnormal gait)
Other evidence of vascular pathology:AF, PVD
Neuroimaging shows: multiple large vessel infarcts,single infarct( i.e. thalamus), periventricular white matter change
13. Differentiating between Alzheimer’s and Vascular Dementia Presentations overlap, pathologies commonly coexist.
Pragmatically: In cases where vascular RF's present, treat them aggressively whether or not there is significant cerebrovascular pathology on imaging
A trial of cholinesterase inhibitors
14. Dementia and Parkinsonism DEMENTIA WITH LEWY BODIES
PARKINSON’S DISEASE WITH DEMENTIA
15. Dementia with Lewy bodies Cognitive and behavioural problems precede motor symptoms
Gradual progression, insidious onset
Fluctuations in cognitive function and alertness
Prominent auditory and visual hallucinations, paranoia, dellusions
Haloperidol poorly tolerated, Quetiapine better
Levodopa or dopa agonists may worsen the confusion
16. Parkinson’s Disease With Dementia Typical motor features present
Presentation may resemble: AD, VD, DLB
Features of PD precede dementia for more than a year
Other conditions: MSA, PSP, Corticobasal degeneration may present with both PD and dementia
17. Less common diseases Frontotemporal dementia:
Neurodegenerative disease, insidious onset, slow progression,
Early onset behavioural change, language difficulties, mild forgetfulness, loss of insight
FTD spectrum: frontal lobe degeneration, Pick’s disease, MND with dementia
18. Normal pressure hydrocephalus Gait Disturbance
Incontinence of urine
Cognitive impairment
Neuroimaging:enlarged ventricles disproportionate to the degree of cerebral atrophy
LP: assess baseline gait and cognition, opening pressure normal, remove 20-30 mls and check for improvement in gait and cognition in 1-2 hrs.
Treatment: VP shunt- gait more likely to improve than cognition
19. Other Dementias Drug/toxin induced: alcohol, psychoactive drugs
Infections: neurosyphilis, HIV ( in the young)
Vasculitis
20. Dementia- non Drug Treatment Modify reversible RF’s ( constipation, anaemia, infection)
Encourage physical+ mental activity
Treat Depression
Simplify meds ( Dosett boxes)
Organise carers
Inform patient and family of legal issues : Driving, enduring power of attorney, Wills
Discuss end of life issues( artificial feeding, comfort v.s life prolongation
21. Risk management Falls
Wandering
Aggression
Self neglect
Financial Abuse
22. Role of cholinesterase inhibitors Donepezil
Galantamine
Rivastigmine
Variable response
Symptomatic benefit, the underlying cause continues to progress at the same rate
Of the dementias, AD,DLB,PDD have the greatest cholinegic deficit and they benefit most
Only in mild to moderate, not severe dementia
Effect on the cognitive function is modest. However, even a small improvement in cognition can translate to significant improvement in day-to-day function, reducing carer burden
23. Managing behavioural problems Agitation, anxiety, irritability
trazodone->risperidone->olanzapine
Benzodiazepines only for brief anxiety relief
Depression : citalopram
24. Prevention Lifestyle-physical and cognitive activity
HRT doubles dementia risk
NSAIDs may be protective
Antioxidants
Antihypertensives
Statins
25. Thank you