Dementia: risk factors
- Age
- Family Hx
- Vascular disease/ Diabetes
Dementia: protective factors
Education, continuing intellectual stimulation
Dementia: patient
Over 60 yo, w/ risk doubling every 5 years after that.
Differentiate delirium from dementia
Delirium: acute confusional state that often occurs in response to an identifiable trigger. (eg, drugs, infection, metabolic disturbance, sleep deprivation, or other neurologic disease.
Delirium will have a fluctuating level of arousal including drowsiness or agitation that improves with removal of precipitating factor.
Word-finding difficulty (def and lesion location)
a dementia symtom- refers to difficulty recalling the names of people, places, or objects (low-frequency first), resulting in speech laden with pronouns and circumlocations. NO problems with articulation, fluency, or word meaning.
Suggests lesion in temproparietal junction of L hemisphere.
Visuospatial dysfunction (def and lesion location)
Symptom of dementia: results in poor navigation and getting lost in familiar places, inability to identify familiar faces or buildings, or trouble discerning object from background.
Suggests lesion in R parietal lobe.
Short-term memory loss (def and lesion location)
It is what it sounds like. Suggests lesion in hippocampus.
Executive dysfunction (def and lesion location)
easy distractability, impulsivity, mental inflexibility, slowed processing, impaired judgement, poor planning.
Suggests lesion in frontal lobe or subcortical areas (basal ganglia, white matter).
What are some other Sx of dementia (not including short term memory loss, word-finding difficulty, visuospatial dysfunction, executive dysfunction)? Where do they suggest lesions?
Apathy- damage to frontal lobe, basal ganglia, or white matter.
Apraxia- loss of learned motor behaviors- damage in frontal or parietal (esp L) lobes.
Why is it so important to have a baseline assessment of functional status (ADLs, IADLs) for geriatric patients?
Cognitive and functional decline may ONLY be noticeable when compared to pt’s baseline.
What are the limitations of mini-mental status exams (including Folstein MMSE and Montreal Cog Assessment)?
They are insensitive to mild cognitive impairment, may be biased negatively by language/attention problems, does not correlate with functional capacity.
Dementia screening guidelines for asymptomatic older patients:
There aren’t any! Current suggests for patients >70: Test registration (apple, book, car), clock test (hands at 11:10), short term memory (repeat 3 words after clock test). If there is any abnormality (remember <3 words or have a weird clock), then do a full MMSE.
For whom is brain imaging indicated? What are you looking for?
Any patient with a new, progressive cognitive complaint. Goal is to rule out occult cerebrovascular disease, tumor, or other structural abnormality (not provide positive evidence of disease). MRI is preferred.
When is a PET scan useful?
When you are trying to distinguish between several dementia causes (eg, Alzheimer and frontotemporal dementia). Specifically, PET imaging with a radiolabeled ligand for beta-amyloid is sensitive to amyloid pathology and provides positive evidence of Alzheimer).
Alzheimer pathology
Plaques containing beta-amyloid peptide and neurofibrillary tangles containing tau protein occur throughout neocortex.
Alzheimer: clinical features
Most common age-related neurodegenerative disease. Short term memory impairment is prominent w/ variable deficits in executive function, visuospatial function, and language
Vascular dementia pathology
Multifocal ischemic changes
Vascular dementia: clinical features
Progressive accumulation of cognitive deficits in association with repeated strokes. Specific sx are specific to location of strokes.
Normal pressure hydrocephalus: clinical features
Gait apraxia (magnetic gait- feet stuck to floor), urinary incontinence, and dementia.
What do you order to R/O normal pressure hydrocephalus? What are you looking for?
CT or MRI- showing enlarged ventricles disproportionate to sulcal widening and overall brain atrophy
What lab tests should you order when working up suspected dementia? What are they for?
Serum B12 (r/o B12 neuropathy); free T4 (thyroid function); TSH. Get these in ANY pt with cog sx. RPR if worried about latent syphillis.
ApoE- get this in a young patient with cognitive impairment to raise index of suspicion for Alzheimer.
What are some non-pharmacologic treatments for dementia?
Aerobic exercise (45 mins for most days of week) and frequent mental stimulation reduce the rate of functional decline.
Mental stimulation= maintaining an active role in the community (if possible) and emphasizing activities in which the patient feels confident. Note that memory improvement programs etc show little effect and that once a pt loses the ability to do something competently, they won’t recover it. Avoid frustrating activities.
Dementia with Lewy bodies- what is it (super basic)
Cognitive dysfunction with Parkinson’s sx. May include psych disturbance w/ fluctuating delirium.
First line treatment for Alzheimer’s-related cognitive decline:
Mild-moderate (MMSE > 17) Cholinesterase inhibitors (donepezil, rivastigmine). Start low and titrate dose up. Symptomatic tx for cognitive Sx. Not disease altering.
CI: frontotemporal dementia
What is frontotemporal dementia
Complex disease that peaks in 6th decade. Behavioral variant (mainly behavioral sx- disinhibition, apathetic w/ relatively preserved memory); Semantic- deficits in word-finding, single word comprehension (may be combined with behavioral type); Progressive nonfluent aphasia: speech effortful with dysarthria, weird sounds, bad grammar.
Not on our objectives, but important because cholinesterase inhibitors, used for Alzheimer, will worsen frontotemporal dementia.
First line treatment for dementia w/ Lewey bodies:
Cholinesterase inhibitors. Not disease-altering.
2nd Line for Alzheimer’s and Dementia w/ Lewey bodies:
Memantine (NMDA antagonist). Not disease altering. Better for moderate-severe dementia.
First line for depression associated w/ dementia:
SSRIs (not paroxetine due to anticholinergic effects)
Tx for agitation and impulsivity in dementia (for patient safety):
1: Behavioral interventions- reorientation, avoid anxiety-provoking stimuli. Ensure adequate activity during day and sleep at night.
2. Make sure pt has appropriate pharmacologic tx for cognitive decline
3. LAST resort- low dose atypical antipsychotic (eg quetiapine)- use w/ caution if fall risk, parkinsonism present.
When should a patient stop driving?
Any patient with mild dementia or worse should stop driving.
Rapidly progressive dementia
Dementia that develops quickly with obvious decline over weeks to months. Consider atypical etiologies, including infectious.
How should you work up rapidly progressive dementia?
MRI of brain w/ contrast, labs (B12, free T4, TSH, RPR, HIV, Lyme serology, rheumatologic tests, anti-thyroglobulin, anti-thyroperoxidase, paraneoplastic autoimmune antibodies, CSF studies). CSF studies include: cell count/diff, protein electrophoresis for oligoclonal IgG, PCR for Whipple’s, CMV, HSV, varicella zoster.
What are some etiologies of rapidly progressive demantia?
Can be due to typical causes, but also: HIV, Lyme, Syphillis, rheumatic disease, neoplasims, Hashimoto encephalopathy, antibody-mediated paraneoplastic syndrome, Jakob-Creutzfeldt disease (cortical ribboning and restricted diffusion to caudate/ anterior putamen on diffusion-weighted MRI).