Dementia Flashcards
Outline the differences in onset, duration, attentino, psychomotor activity, affect, and psychotic features of delirium, dementia and depression. What tests would you use for these illnesses?
delirium: 4AT, CAm
Dementia: MMSE, mini-Cog
5 broad neurocognitive domains
Learning and memory
Executive function
Language
Perceptual-motor function
Complex attention
Social cognition
Definition of MCI (Mild COgnitive Impairment):
Modest cognitive decline from previously level of performance in 1+ cognitive domains based on both:
Concern of the individual, knowledgeable informant or the clinician
Subjective cognitive impairment: the stage where the patient knows but the doctor doesn’t. 27% convert to MCI, 14% convert to dementia.
- Represents an opportunity to assess for reversible causes of cognitive impairment
Modest impairment in cognitive performance (preferably on documented on tested)
Cognitive deficits DO NOT interfere with independence in everyday activities
Cognitive deficits DO NOT occur exclusively in the context of a delirium or better explained by another mental disorder (depression, schizo)
T/F Mild cognitive impairment is actually normal in people 70+
False
Normal Cognitive Decline Definition: normal age-related changes in cognition. Usually mild and not noticeable until 70yo+
Symptoms: challenges with complex tasks, difficulty focusing, slower cognitive speed, slower reaction time, decline in memory (blocking, tip-of-the-tongue) well-practice skills & recall of familiar information not affected
-MCI is a deficit that is MORE than expected for age. Can be amnestic MCI or non-Amnestic MCI.
- considered a transitional stage between normal aging and dementia
- associated with an increased risk of dementia (10-15% per year, compared with 1-2% per year for those with normal cognition)
key test for MCI
management for MCI
complications?
invevstigations: MCI-MOCA; functional, affect/behavioural, and safety assessments
management: treat underlying/contribution causes, advance planning, healthy lifestyle, consider cognitive training
complications: 10-15% per year of progressivev to dementia
“Reversible” causes of Cognitive impairment
Alcohol, Hepatic dysfunction, Medications, Autoimmune and inflammatory disorders, Endocrine disorders, Infections – HIV, syphilis, cryptococcus, TB, Subdural haematoma, Normal pressure hydrocephalus, B12 deficiency, Neoplastic and paraneoplastic, Obstructive sleep apnoea
Difference in the definition between MCI and Dementia
Definition of Dementia: substantial cognitive decline from previous level of performance in 1 or more cognitive domains based on both:
Concerns of the individual, knowledgeable informant, or the clinician
Substantial impairment in cognitive performance (documented on testing)
In dementia, these cognitive deficits are SUFFICIENT TO INTERFERE with independence in everyday activities (as a minimum, assistance with comlex instrumental tasks are required)–> UNLIKE MCI, where the deficits are not significant enough to impair basic independence
These cognitive deficits DO NOT occur exclusively in the connect of a delirium
The cognitive deficits are not primarily attributable to another mental disorder.
Overall, dementia and MCI both require cognitive impairment, but differ based on the presence of absence of functional impairment. These are syndromes, not diseases– therefore, they have an underlying etiology although we don’t always find out what it is.
Epi of dementia: prevalence ___ every 5 years from 65-85, with 60% being women
Etiology:
Cognitive tests that can be used to look for dementia?
Epi of dementia: prevalence doubles every 5 years from 65-85 (>1/3 at 90-95), >60% are women
Etiology: Alzheimer’s disease (40-50% of cases), vascular disease, frontotemporal dementia, dementia with Lewy bodies, traumatic injury, substance/med usage, HIV, prion disease, Parkinson’s, Huntington’s
Investigations:
Brief cognitive testing (for dementia– MMSE and mini-Cog)
Lab investigations: CBC, electrolytes, Ca2+, albumin, creatinine, glucose, TSH, B12
Neuroimaging: primairly to detect cerebrovascular disease, space-occupying lesions
Indications for neuroimaging: rapidly progressive, short duration, head trauma, history of cancer that mets to the brain, anti-coag usage, bleeding disorders, focal neurologic signs, early gait abnormalities, autonomic signs, less than 65 yo.
neuroimaging is good to do to look for cerebellar lesions or an explainaition for someone’s dementia. What are the indiciations for neuroimaging/
Neuroimaging: primairly to detect cerebrovascular disease, space-occupying lesions
Indications for neuroimaging: rapidly progressive, short duration, head trauma, history of cancer that mets to the brain, anti-coag usage, bleeding disorders, focal neurologic signs, early gait abnormalities, autonomic signs, less than 65 yo.
methods of prevention for dementia
: promoting education (primary and secondary education), increase physical activity, prevent hypertension, healthier diets, adequate sleep, preventing depression/social isolation, no smoking/airpollution/support smoking cessation, management of medical problems, prevent/manage hearing loss, stay socially and mentally active, head protection, [*cardiovascular protection*– reasonable blood pressure management, reasonable glucose management, Antiplatelt for secondary prevention, specific stroke reduction, exercise, cognitive engagement, social engagement]
T/F generally speaking, cholinesterase inhibitors can be used to treat dementia or MCI
false.
Treatment of dementia/MCI: There is no proven pharmacological intervention that reduces the risk of MCI progression to dementia (cholinesterase inhibitors, memantie, ginkgo biloba, testosterone may help for ALZHEIMERS ONLY).
Dementia red flags (FERND)
F= features of delirium (fluctuation, acute onset)
E= early onset (<65)
R= rapid progression
N= neurological feautes- new focal neurology or features of normal pressure hydrocephalus
D= disordered movements (chorea, hemiballismus, myoclonus)
Outline the globla deterioration scale
- used to characterize the progression of dementia
T/F the MMSE is more sensitive for MCI compared to MOCA
false. For MCI, use MOCA
for dementia, use ____ and __ ___ tests.
MMSE and Minicog tests
Dementia: use MMSE and Mini-Cog
mini-Cog: 3-word registration→ draw a clock; set the time at ten past 11 → 3-word uncued recall.
Not as influenced by education or language abilities
Positive mini-cog for dementia if:
Forget 1-2 words and can’t draw the clock
Forgets all 3, but normal clock.
MMSE: score of 30, only for more moderate dementia, provides a rough gauge of severity. Age and education influences the score.
If lower educational levels or less fluent english: RUDAS exam.
MMSE and Mini-Cog test is used to look for dementia. if there is a lower education level or less fluent in english, what exam can you use instead?
RUDAS
What is the mini-cog and what constitutes as a positive test?
mini-Cog: 3-word registration→ draw a clock; set the time at ten past 11 → 3-word uncued recall.
Not as influenced by education or language abilities
Positive mini-cog for dementia if:
Forget 1-2 words and can’t draw the clock
Forgets all 3, but normal clock.
T/F MMSE is less influenced by education and language abilities than Mini-COG
false. Mini-cog is less influenced by langiage abilities. if less fluent in english, consider substituting the MSSE with the RUDAS exam
When to obtain structural neuroimaging in MCI/Dementia
- Onset of cognitive impairment within the past 2 years
- Unexplained decline in a patient already known to have dementia
- Recent and significant head trauma
- Unexplained neurological manifestations
- History of cancer
- Risk for intracranial bleeding– on antiplatelet therapy/anticoagulants
- Symptoms compatible with normal pressure hydrocephalus
- Significant vascular risk factors.
Rapidly progressing
Key features of Alzheimer’s Disease
- What is the diagnostic criteria?
Key Features/Natural progression of Alzheimer’s Diseaase
- Classical form has prominent early and progressive memory loss, often with subtle language errors and visuospatial difficulties
- Later followed by difficulties with orientation and judgement, and eventually aphasia and agnosia
- Progressively dependent for ADLs
- Eventual loss of ability to ambulate and swallow.
Proabble AD: evidence of causative AD mutation (biomarkesr) or clear evidence of decline in memory and learning, PLUS ONE OTHER COGNITIVE DOMAIN/STEADY DECLINE in cognition/no evidence of missed etiology.
Outline the difference between preclinical AD, MCI due to AD, and dementia due to AD
preclinical: no cognitive symptoms, but AD pathology detected by biomarkesr
MCI due to AD: cognitive symptoms but not demented + evidence of AD biomarkesr
Dementia due to AD: dementia + biomarkers
Fluid Biomarkers for AD
- low CSF beta amyloid
- high CSF Tau and phospho-TAU
- Neuronal dysfunction: decrease metabolism in parietal-temporal lobes on FDG PET
- Neurodegeneration: temporal, parietal, and or hippocampal atrophy on MRI
single most important risk factor for AD
old age
List four or more non-pharmacological elements of management of AD and two drug classes that can be used to treat symptoms.
Drug Classes for AD Management
Cholinesterase inhibitors: donepezil, galantamine, rivastigmine (moderate)
- Slower decline in cognition on testing
- Adverse events: nausea, vomiting, diarrhea, anorexia, bradycardia, bronchospasm, urinary urgency, vivid dreams.
Memantine: NMDA receptor blocker that works in setting of overactivation.
- In AD, NMDA glutamate receptors get over-activated due to neuronal injury.
- There is a small effect on cognition, and can be used in combo with AChel.
- Adverse events: headache, constipation, dizziness.
Amyloid Binders
- Amyloid dysregulation is pathognomonic for AD: many think it may be the cause.
- Adacanumab binds to Ab aggregates, soluble oligomers and insoluble fibers.
- Not yet approved in canada.
- Adverse effects; amyloid related imaging abrnomalities, headaches, falls.
