Mild cognitive disorders and Dementia in Elderly Flashcards
Diagnosis of dementia needs evidence of:
impairment in ADLs and progression of cognitive decline
mild cognitive impairment
impaired cognition with preserved function and independence of daily activities of living.
Pts with amnestic MCI subtype are increased risk for developing dementia
Characteristics of normal aging
slight decrease in fluid intelligence (ability to process new information quickly)
normal functioning in all daily activities.
Mild neurocognitive disorder means
mild cognitive impairment
Mild neurocognitive disorder is
mild decline in one or more cognitive domains
normal functioning in activities of daily living with compensation.
Major neurocognitive disorder is
dementia
Major neurocognitive disorder definition
significant decline in one more cognitive domains
irreversible global cognitive impairment
marked functional impairment
chronic and progressive months to years
major depression
reversible mild to moderate cognitive impairment and features of depression and this can be episode to weeks and months.
what is true about PEG tubes in advanced dementia?
feeding tubes do not prolong survival with dementia, nor do they provide comfort, afford adequate nutrition or help with prevent pressure ulcer or aspiration pneumonia.
what are complications of having a feeding tube in elderly pt?
cellulitis, leakage, ileus
can see worsening of urinary and fecal incontinence, increased oral and pulmonary secretions and GERD
Also can increase risk for aspiration pneumonia and pressure ulcer infection.
what is the proper way to care for patients who have advanced dementia and failure to thrive?
caretakers should encourage hand feed pts if possible and maintain aspiration precautions. They should try to stimulated by providing favorite foods, varying flavors, amounts, consistencies and increasing availability of food. If this fails, make them aware that this is a terminal dx and they should have realistic goals for PEG tube (hydration, nutrition or meds for comfort care).
normal pressure hydrocephalus clinical features
gait instability (wide based) w/ frequent falls cognitive dysfunction urinary urgency and incontinence depressed affect (frontal lobe compression), and upper motor neuron signs in lower extremities
Diagnosis of normal pressure hydrocephalus
marked improvement in gait and spinal fluid removal
Miller Fisher lumbar tap test
enlarged ventricles out of proportion to underlying brain atrophy on MRI
treatment of normal pressure hydrocephalus
ventriculoperitoneal shunting
what is the pull back test?
stand behind patient and pull back on shoulder so as to unbalance them. Normal response is to fall 2-3 steps backward and regain stability. PTs with extrapyramidal symptoms (Parkinsons) needs more steps to regain stability or may fall backwards).
idiopathic Parkinson’s Disease is a
slowly progressive neurodegenerative disorder seen with bradykinesia, cogwheel rigidity and resting tremor.
When to use dopamine agonists for idiopathic Parkinson’s dx?
mild to moderate symptoms and patients who are <65 yrs old,
dopamine agonists are: bromocriptine, pramipexole or ropinirole. Don’t use carbidopa/levodopa in the young due to motor symptom fluctuations that can occur in 10 yrs time
carbidopa/levodopa is most effective in idiopathic Parkinson’s for motor symptoms
when do we use deep brain stimulation for treatment of idiopathic Parkinson’s dx?
when it’s medically refractory resting tremor, levodopa induced dyskinesias or significant motor fluctuations
What does donepezil do?
it’s a acetylcholinesterase inhibitor that increases acetylcholine levels of frontal lobes for pts who have dementia
Do we use propranolol for treatment of Parkinsonian tremor
no propranolol is used for treatment of essential tremor (typically symmetrical high frequency and worsens with action)
parkinsonian tremor is
better or worse with rest?
asymmetrical, low frequency, and worsens with rest. See with bradykinesia and rigidity
pill rolling
cardinal findings of idiopathic Parkinson’s dx?
bradykinesia PLUS 4-6 Hz resting tremor OR cogwheel rigidity, excellent response to dopaminergic therapy (levodopa/carbidopa)
suggestive findings in Parkinson’s dx
unilateral onset, craniofacial (masked fascies, decreased blink rate, hypophonia)
visual (blurred vision, impaired upward gaze)
MSK (micrographia, dystonia, myoclonus)
shuffling stooped gait, postural instability
autonomic dysfunction
neuropsychiatric (depression, psychosis disturbed sleep and dementia
non motor (constipation, anosmia, and fatigue)
when do you use anticholinergics?
can be used in pts age<70 with tremor and no significant akinesia or gait disturbance.
when geriatric pt presents with cognitive impairment and mood and affects should be watched to see
if depression is playing a role. Things like social withdrawal, fatigue, and sleep disturbance in setting of bereavement raise concern for major depression
late life depression presents as
reversible cognitive impairment (pseudodementia) and neurovegetative features rather than subjective report of mood changes
what is an abnormal Mini mental state exam?
<26/30 and 24/30 or less is highly specific and sensitive for dementia
risk factors for delirium
advanced age neurological disorder (dementia and stroke) sensory impairment (hearing loss)
precipitating causes for delirium
central nervous system insult (seizure, stroke)
infection (pneumonia, UTI)
Medications (sedatives)
metabolic disturbances (electrolytes and uremia)
clinical features of delirium
acute onset, fluctuating mental status changes
disturbance in attention
sleep wake changes (sundowning)
management of delirium
avoid polypharmacy physical restraints
maintain normal sleep wake cycle
provide frequent reorientation
treat underlying cause (antibiotics)
Care giver distress signs
sleep disturbance, depression, irritability, anxiety and if untreated can cause caregiver burnout
what are negative effects of caregiver burnout
increased risk for mental and physical illness and increased likelihood of early nursing home placement for those with dementia.
Treatment of caregiver distress?
recognition of caregiver burden and providing assistance with obtaining support services including respite care services, adult day care centers, overnight care, and allows caregivers to take a break or have vacation.
Getting in touch with support groups
what is parkinson-plus syndrome?
this is 10-15% of cases of parkinsonism that is not the same as idiopathic Parkinson’s dx because of RAPID onset of symptoms, SYMMETRIC neurological findings (bradykinesia and rigidity) and ABSENT tremor and early autonomic dysfunction (urinary incontinence and orthostatic hypotension.
Also responds poorly to dopamine agonists.
3 most common Parkinson-plus syndromes are:
multiple system atrophy
progressive supranuclear palsy
corticobasal degeneration
multiple system atrophy diagnosis
clinical and incorporation of core findings like akinetic rigid parkinsonism, autonomic failure, cerebellar ataxia (wide based and unsteady gait)
Brain MRI will show nonspecific atrophy of putamen and middle cerebellar peduncle and pons but MRI is mainly used to exclude infarction or tumor.
dementia with lewy bodies is
cognitive impariment, parkinsonism, and autonomic dysfunction
see visual hallucinations, fluctuating cognition and alertness
frontal temporal lobe atrophy
frontotemporal dementia. seen in 50’s
see social disinhibitio nand emotional blunting and changes in personality and behavior.
rapidly progressive dementia with myoclonus
Sporadic spongiform encephalopathy (Creutzfeldt Jakob Dx)
Characteristic findings of Parkinson’s dx
slow progression of symptoms, neurological symptoms of tremor and bradykinesia are asymmetrical.
Tremor is common
postural instability is late in disease
dysautonomia is late in dx
responsive to levodopa
what differentiates Parkinsonian dx and Parkinson-plus dx?
progression is slow in Parkinson but fast in Parkinson plus
Neurological findings are asymmetric in Parkinson’s but symmetric in Parkinson-plus
Tremor is common in Parkinson’s but NOT seen in Parkinson-plus
Postural instability and dysautonomia are seen late in Parkinson’s dx but seen early in Parkinson-plus
Levodopa response is excellent in Parkinson’s but poor in Parkinson’s plus
advanced dementia is defined by:
profound memory deficits, total functional dependence, limited ability to ambulate and likely can qualify for hospice care
what does hospice care do for advanced dementia pts?
it improves end of life experiences for pts, lower rate of hospitalizations, increases chances of appropriate pain management, and provides bereavement for families
Side effect of donepezil
bradycardia, nausea, diarrhea and vivid dreams
does an appetite stimulant like megestrol helps with pts who have dementia
no
Medicaid qualifying reasons to enroll someone with ADVANCED dementia into hospice:
dependence on others for all activities of daily living,
lack of verbal communication
inability to ambulate
+ one medical condition (aspiration pneumonia, eating issues, pyelonephritis or upper UTI, septicemia, sacral decubitus ulcer stage 3 to 4, recurrent fever after abx, not eating enough to sustain life)
Risk factors for increased driving risk based on medical history:
- history of falls in the past 1-2 years
- recent accidents
- sedating medications (TCAs, benzos, anticholinergics)
- Hx of TIA, syncope, seizures, unstable ischemic heart dx and sleep disorders
- ETOH use
- inability to perform ADLs
- anxiety with driving
Risk factors for increased drinking risk based on physical exam:
visual deficits >20/40 acuity in at least one eye <120 of peripheral horizontal vision
cognitive impairment 15 seconds.
what does loss of driving do for older individuals?
loss of independence, self esteem, and qualtiy of life.
advance regarding driving competency must maintain careful balance between avoiding endangerment of the general public and patient autonomy.
most effective treatment for Parkison’s dx?
carbidopa/levodopa
relieves motor symptoms of tremor, rigidity and bradykinesia
Seen in about 50% of pts after taking levodopa for 5-10 years
motor fluctuations while on carbidopa/levodopa happens when
levodopa doses wears off and pts develop underlying Parkinson symptoms
happens after awakening or in a specific part of day or middle of night
what happens during these motor fluctuations or wearing off periods with carbidopa/levodopa?
can have dystonia or akathisia from levodopa withdrawal
how to prevent the wearing off period with carbidopa/levodopa?
get a long acting carbidopa/levodopa at night to ensure steadier levels.
Mild cognitive impairment (MCI) pts are at
increased risk for dementia with 10% progression per year
Rest either remain the same or improve.
Treatment of mild cognitive impairment
no FDA treatment. no supplement or medication has demonstrated cognitive decline prevention
what is the best way to help with mild cognitive impairment?
physical exercise- helps with global cognition, executive function, attention, and delayed recall.
Cognitively stimulating activities and active social engagement can help slow progression of Alzheimer’s dx in at risk pts.
Silent chronic lacunar infarcts lead to
increased risk for developing dementia in the 5 years after compared to normal brain imaging.
vascular dementia is also called
binswanger’s dementia
what are the neuropsychiatric symptoms of Alzheimer’s dementia?
agitation, aggression, paranoid delusions, hallucinations and wandering
very common
seen worse in the evening (called sundowning)
what is the most challenging thing for most pts and caregivers with the Alzheimer’s
sundowning or the neuropsychiatric symptoms
agitation, aggression, paranoid delusions, hallucinations and wandering
how to manage “sundowning” or Alzheimer’s dementia?
behavioral methods of structured routines, using distraction and redirection and identifying and avoiding environmental triggers that cause agitation (sudden change in surroundings)
environmental therapy: exercise, music therapy, touch therapy, removing offending stimuli) combined with caregiver education (teaching family members structured routines, providing reassuring responses) and help diminish agitation
when do we use pharmacology to control sundowning of Alzheimer’s
when agitated behavior poses a safety risk to self or others.
low dose antipsychotics can be used but noted there is an increased mortality with elderly pts with dementia.
early idiopathic Parkinson’s dx is seen in
<40 yrs
early idiopathic Parkinson’s dx features
non motor symptoms can be seen years before onset of motor symptoms (bradykinesia, rigidity, tremor) and these include:
sleep, excessive daytime somnolence, mood disturbance, anosmia, constipation
REM sleep behavior disorder is seen with
15-47% of PD and seen with dream enacting behaviors like talking, yelling, punching, kicking, jumping from bed.
anosmia, sleep disturbance disorder and excessive daytime sleepiness
early signs of idiopathic Parkinson’s dx.
Diagnostic features of dementia with Lewy Bodies:
progressive cognitive decline and dementia
fluctuating cognition, visual hallucinations (detailed and recurrent), spontaneous parkinsonism features
REM sleep behavior disturbance
Suggestive features: severe antipsychotic sensitivity, SPECT and EPT scan showing low dopamine transporter uptake in basal ganglia
Supportive findings: repeated falls, syncope or near syncope, severe autonomic dysfunction
delusions and depression or anxiety
what makes Dementia with lewy body less clear?
neuroimaging showing CVA
parkinsonism appearing first and dementia appearing later.
prion dx is seen with
behavioral changes
rapid progression
myoclonus and seizures
dementia with lewy body
visual hallucinations
spontaneous parkinsonism
fluctuating cognition
frontotemporal dementia findings:
early personality changes
apathy, disinhibition, compulsive behavior
frontotemporal atrophy in neuroimaging
vascular dementia
stepwise decline
early executive dysfunction
cerebral infarction or deep white matter changes on neuroimaging
normal pressure hydrocephalus changes
ataxia early in dx
urinary incontinence
dilated ventricles on neuroimaging.
normal mini mental status exam but pt shows cognitive dysfunction (memory loss, visuospatial impairment) and can’t manage his medications. Pt is highly educated
can have a false negative MMSE
MMSE<24 is 87% sensitive and 82% specific for dementia but individuals with mild dementia or those who are highly educated can have normal scores.
possible cut off for people who have gone to college is MMSE of 27 or lower.
Multiple system atrophy
parkinson’s plus syndrome
see combination of parkinsonism, cerebellar ataxia, and dysautonomica
symptoms suggestive of parkinson’s plus syndrome or multiple system atrophy:
anosmia and acting out in dreams
can trial levodopa
corticobasal degeneration
marked asymmetric parkinsonism and frequently seen with dystonia myoclonus and cortical sensory deficits and prominent cognitive dysfunction and apraxia (impaired motor function)
progressive supranuclear palsy
postural instability
impairment of vertical extraocular movements
Treatment of vascular cognitive impairment
treat with donepezil as off label use.
also treat underlying CVA risk factors.
how to treat severe apathy in pts who have vascular cognitive impairment?
methylphenidate
how to treat pseudobulbar symptoms ?
citalopram or other SSRI’s.
when to initiate ACh inhibitors Alzheimer’s
first line for mild to moderate to Alzheimer’s dx (mild cognitive impairment)
in an Alzheimer’s pt, after a ACH inhibitor (donepezil galantamine, rivastigmine) are started what do you do?
follow up with pt in 4 weeks and assess for side effects.
If cognitive impairment doesn’t improve switch to a different .
If it continues to deteriorate then can add memantine.
Memantine has been shown to improve cognitive and ability to function.
if pt with Alzheimer’s continues to decline despite combo therapy of ACH inhibitor and memantine, what to do?
stop the therapy as it can only increase risk for side effects.
when to add memantine in for someone who has Alzheimer’s dementia
add after acetylcholinesterase inhibitor
rapid onset of dementia <12 months, myoclonus and ataxia and increased DTR in upper extremities and decreased in lower extremities
Creutzfeldt Jakob dx prior dx
prion dx
no treatment for any prion dx and they are rapidly fatal.
labs associated with Creutzfeldt Jakob dx
see T-tau 14-3-3 in CSF
MRI shows classically the hockey stick sign
see spongiform changes with gliosis on brain biopsy
