Dementia Flashcards
Dementia is defined as a decline from prior functioning, interfering with ADLs when it isn’t better explained by _______ or __________ ________
Delirium or psychiatric disorder
T/F To be considered cognitively impaired you need 4/5 symptoms.
F. You need 2
What are the 5 diagnostic symptoms associated with dementia
- Visuospatial skills
- Language skills
- Memory
- Judgment, reasoning, or handling complex tasks
- Personality/ behavior changes
DDx for most dementias
(Alzheimer’s, Lewy Body, Vascular, Frontotemporal) Dementia/ CJD/ normal pressure hydrocephalus/ hypothyroidism/ depression/ Wernicke’s encephalopathy/ delirium/ Hepatic encephalopathy/ drug or EtOH intoxication/ Brain tumor or metastasis/ Pseudodementia/ Uremia/ Syphilis/ Intracranial hemorrhage
What is the MC type of dementia?
Alzheimer’s disease (AD)
What is the biggest risk factor for AD?
Older age (6th-7th decade)
Old people get AD: what are other risk factors?
FH (autosomal dominant genetic mutations - Down Syndrome), lower education level, being a woman
The Pathophys of AD is caused by what 2 proteins? What formations do they make?
Beta-amyloid - Neuritic plaque Hyperphosphorylated tau (p-tau) - neurofibrillary tangles
What neuro transmitter is decreased in AD?
Acetylcholine
What part of the brain is first to be affected by AD?
Hippocampus
What is the hippocampus involved in?
Memories, learning, emotions
explicit (declarative) memory declines first in AD
The ability to make an egg or ride a bike is a certain kind of memory. What is it?
Implicit (procedural) memory. This is spared in AD
AD patients present with declines in their executive function, especially when out of their safe, predictable environment. What are these deficits?
Les motivated, organized, and abstract thinking
Finances
Driving, shopping, housekeeping
Following instructions on the job
Memory is tricky because how do you know if you have lost it? And if you do know, will you remember? What is it called when you aren’t aware of your own deficits?
Anosognosia
Most patients are aware of their memory loss
T/F Behavioral/ neuro psychiatric abnormalities are common in mild, moderate, severe, and end stage AD
F: it isn’t common in mild. They only have slight recent memory issues
The common first behavioral/ neuropsychiatric symptoms of AD are what 3 things?
Apathy, irritable, socially disengaged
The common later behavioral/ neuropsychiatric symptoms of AD are what 4 things?
Overt agitation, aggression, psychosis, wandering
Define dyspraxia/ apraxia
difficulty/ inability to execute a motor task
What are the 6 main clinical presentations of AD?
Dyspraxia/ apraxia Olfactory dysfunction Sleep disturbances Visuospatial deficits (read a clock) Seizures Destabilization caused by changes
AD is a progressive disease. It starts mild and eventually will progress to death. What is the MCC of death?
Aspiration
From mild it first goes to Mod. What are the main deficits of AD that show up here?
Impaired language Easily lost and confused Not able to work Apraxia emerges Visuospatial ADL deficits become more prominent
From Mod the obvious progression is to Severe. What marks this stage of AD?
Either wandering away or stuck in bed since they can't walk. Delusional Disinhibited Disturbed sleep cycle Withdrawn
The definitive diagnosis is histological so we have to do it before the patient dies. What labs and imaging would you get to rule out other diagnosis?
CBC, CMP, TSH, B12, RPR, UA C&S
CT or MRI
You can get labs and imaging, but what else should you do to diagnose AD clinically?
Cognition assessment
What are three Cognition assessments?
MMSE, MoCA, SLUMS
There are 2 main drug treatments, 2 mixed drug treatments, and 2 treatments with no shown benefits. What are they?
Cholinesterase inhibitors and NMDA receptor antagonist
Vitamin E and Selegiline (antidepressant)
Anti-inflammatory drugs, Ginkgo biloba
Cholinesterase inhibitors work by slowing the progression of AD by increasing the amount of ACh in the CNS so it would benefit what stages of people with AD?
Mild- Mod
What are the 3 Cholinesterase Inhibitors from most to least common?
Donepezil (Aricept), Rivastigmine( Exelon), Galantamine (Razadyne)
What 2 side effects do every cholinesterase have?
N/V
What drug is used on patients with mod-severe AD?
NMDA receptor antagonists
Memantine (Namenda)
The drug name on this one is nice if you remember NMDA - N(a)M(end)DA
T/F Pts with AD could have delirium; you should consider other causes before you treat their neuropsychiatric symptoms.
True.
Consider medical causes, medication side effects, or pain they can’t express.
What are the 4 medication classes used to treat neuropsych symptoms in AD?
Antidepressants - Citalopram (Celexa)
Anti-seizure - Carbamazepine (Tegretol), Valproate (Depakote) Gabapentin (Neurontin)
Dextromethorphan-quinidine (Nuedexta)
When do you need to give antipsychotics to AD pts? Why should you be careful about using them?
Increases mortality. Not approved for treatment of behavioral disturbance in those with dementia.
Safety of caregiver necessitates use.
Which is not an antipsychotic used to help in AD?
a. Seroquel
b. Risperidone
c. Gabapentin
d. Zyprexa
c. Gabapentin is an anti-seizure med.
When antipsychotics are used with AD, what are some side effects and how would you prevent them?
Tapering helps lessen S/E
EPS/TD, somnolence, Increased risk for: CVA, MI
AD is a progressive, incurable disease: what is the typical course from diagnosis?
8-10 years
What are the 5 most common causes of death in AD?
Aspiration (MCC), malnutrition, secondary infections, PE, heart disease
What is the second most common form of dementia?
VaD - Vascular Dementia
T/F There is a significant overlap of VaD with AD.
True. 15-20% have both
Men over the age of 65 get VaD the most. What are 5 other risk factors?
Cardiovascular disease, high glucose levels, DM, HTN, afib
The prognosis is fair for AD (8-10 yrs). Is it better or worse for VaD, and how much?
Worse. Survival ~ 5 years
Severe likelihood for CVA/ MI
VaD is caused by atheroslerotic plaques in the vasculature. These can grow and/or break and cause multiple infarctions of the brain. What are the three kinds of infarcts?
Large infarct, Lacunar infarct, chronic subcortical ischemia
Where is a large infarction?
At the level of major cerebral vessels (usually cortical)
Where is a lacunar infarct?
In a small artery infarction (subcortical)
Where is a chronic subcortical ischemia?
In distribution of small arteries of periventricular white matter
The clinical presentation of a patient with Cortical VaD is dependent on and specific to what?
The specific area affected
What are some common clinical presentations of Cortical VaD?
Speech difficulty Trouble preforming routine tasks Sensory interpretation difficulty Confusion Amnesia Executive dysfunction (Stepwise of fluctuant course common)
What are some common clinical presentations of Subcortical VaD?
Gait dysfunction Personality & mood changes Urinary frequency, urgency, or symptoms not from urologic disease Cognitive dysfunction (Gradual or stepwise)
What shows VaD infarcts the best? a. CT w/o b CT w/ c. CTA d. MRI
MRI
VaD has associated risk factors, what can be done to alleviate these?
Antihypertensive, DM management, Statins, Antiplatelet agents, smoking cessation, diet/ exercise
What are the three classifications of meds you can give to help with symptoms of VaD?
Acetylcholinesterase inhibitors
NMDA antagonists (Memantine)
Calcium Channel blockers (looks promising, more trials needed)
Name 3 acetylcholinesterase inhibitors used on VaD.
Donepezil
Galantamine
Rivastigmine
What is Pseudodementia and what patient population is it seen in?
It is a psychiatric illness who appears to be demented
It is commonly seen in an episode of major depression. (dementia syndrome of depression)
Think about the differences between depressed and demented patients. What were three differences given to us?
(Dementia/ Depression)
Answering questioning (confabulation/ “I don’t know” or correct)
Accomplishments (Delight in/ emphasizes failures)
Memory (tried to cover up/ complains)
[see slides for table]
What are the treatments for Pseudodementia?
Antidepressants (SSRI’s preferred)
ECT
What should you avoid giving to Pseudodementia patients?
Acetylcholinesterase inhibitors
NMDA antagonists
What is the umbrella term for a group of neurodegenerative diseases that result in degeneration of the frontal and/ or temporal lobe?
Frontotemporal dementia (FTD)
What is Frontotemporal dementia characterized by changes in?
Personality, language, and behavior
FTD is caused by degeneration of the frontal and/or temporal lobes: what 4 diseases are associated with these areas?
Pick disease, dementia associated with ALS, coritcobasal degeneration, and genetic mutations.
If you look at some brain under a microscope of someone with FTD, what are you going to see?
Neuronal loss, loss of myelin, astrocytic gliosis, and abnormal protein inclusions in neuronal or glial cells.
FTD as a 2 variants and 3 subtypes. What are they?
Behavioral (MC)
Primary Progressive Aphasia (PPA)
PPA has three subtypes: nonfluent, semantic, logopenic
The behavioral subtype of FTD is marked by what?
Disinhibition, apathy, loss of empathy, hyperorality, compulsive behaviors
Primary Progressive Aphasia (PPA) is a language impairment varient of FTD: what is brain functions are preserved in these patients?
Episodic memory and other cognitive functions.
Nonfluent variant PPA
Motor speech deficit - effort to produce words/ articulate
Effortful, halting speech
Distortions
Agrammatism (not grammatically correct)
Semantic variant PPA
Impaired: single word comprehension, object naming, spelling, word finding (earliest symptom)
Preserved: fluency, repetition. and grammar
Mispronouncing/ misspelling words with irregular spelling is called what?
Surface dyslexia or surface dysgraphia
Logopenic variant PPA
Impaired: single word retrieval, repetition, speech/naming errors
Preserved: single word comprehension, object knowledge, motor speech
“Empty” patients - vague stories w/o detail
Motor syndromes happen in conjunction with FTD and are correlated with what?
Shorter survival
What are the three main motor syndromes associated with FTD?
- Motor neuron disease (upper&lower)
- Corticobasal syndrome
- Progressive supranuclear palsy
How do you diagnose FTD?
Neuroimaging (SPECT, PET, Perfusion MRI, others…)
Many will show focal frontal or temporal atrophy
Functional imaging shows hypoperfusion or hypometabolism
Imaging is helpful for FTD, but you can also clinically diagnose. Name the 6 criteria.
T/F: You need 5/6 to be considered FTD
F: 3/6 required Disinhibition Apathy/ inertia Loss of sympathy/ empathy Perseverative/ compulsive behaviors Hyperorality Dysexecutive neurological function (have an idea, don't memorize)
What are the diagnostic criteria for the PPA subtype of FTD?
1-3 inclusion criteria must be answered positive
1-4 exclusion criteria must be answered negatively
(have an idea, don’t memorize)
What is the main treatment of FTD and the last resort med used?
SSRI trial - Paroxetine (Paxil) 10 mg PO daily
Atypical atipsychotic trial (last resort) - Seroquel 12.5 mg PO daily
Cholinesterase inhibitors no evidence, but reasonable if nothing else
(No effective disease modifying treatments exist - symptoms treated)
What is the prognosis for FTD pts?
8-10 yrs from onset-death (slightly more rapid than AD)
2 years from onset for pts with Motor Neuron Disease
(Paulson noted a 3 yr average)
Lewy Body Dementia (LBD or DLB) is characterized by dementia with or preceding _________ ___________
Parkinsonian symptoms
What Parkinsonian symptoms are seen in LBD?
Hallucinations Fluctuations in cognition/ alertness Dysautonomia (ANS nerves dysfunction) !Parkinsonism (Parkinson's has Lewy Bodies)!34 Disordered sleep
T/F: When you get PD before dementia it is considered PD, and when you get dementia before PD it is considered LBD.
True
VaD is the 2nd most common form of dementia. What is the 2nd most common form of degenerative dementia?
LBD
What kind of picture do you have in your mind of a typical LBD patient?
A 75 y/o male with a FH of PD, does NOT drink caffeine, has gone to college, and is a monozygotic twin.
What plays a role in developing LBD as a monozygotic twin?
Environment/ epigenetics and triplication of SNCA gene, and autosomal dominant inheritance of LBD.
(Didn’t talk about but is on slides)
Lewy bodies are round, ________ ____________ neuronal inclusions.
Eosinophilic intracytoplasmic
Where in the brain is LBD most commonly found?
Deep cortical layers, especially: Anterior frontal and temporal lobes Cingulate gyrus Insula Substantia nigra Locus Ceruleus
LBD - 3 Neuro-transmitter deficits
Acetylcholine
Dopamine
Serotonin
(probably play a pathological role)
LBD has dementia before PD, what comes before dementia in LBD?
Cognitive dysfunction, often presenting symptom
(Impaired: attention, exec. fxn., visuospation fxn.
What are the 2/3 core clinical features needed in LBD?
Cognitive fluctuations (Course of a day/seconds from lucid-comatose/ pleasant-difficult) [60-80%] Visual hallucinations (can be auditory) PD-ism
Feature of LBD that lasts seconds to days and happens in 60-80%% of cases. Can be subtle or quite dramatic
Cognitive fluctuations
PD symptoms
Bradykinesia Limb rigidity Shuffling gait Resting tremor Postural instability [70-90% of those with LBD]
There are 2 other clinical features than the main 3 in LBD. What are they?
REM sleep disorder (REM=dreams. looks purposeful) Neuroleptic Sensitivity (aka. anti psychotic sensitivity. Severe state, Dopamine is inhibited)
Supportive features of LBD
Falls Syncope, LOC ANS dysfunction Hallucinations Delusions Depression
T/F Imaging is necessary for LBD
False. Only a clinical diagnosis
LBD - treatment
Cholinesterase inhibitors.
First line - Rivastigmine (Exelon)
Donepezil (Aricept)
Melatonin or clonazepam (REM sleep disorder)
Levodopa
Rivastigmine (Exelon)
Treatment for LBD. PO or patch.
Less anxiety, delusions, hallucinations AND better performance on neuropsych testing
S/E: nausea, vomiting, dizziness, HA, diarrhea, falling
LBD - Prognosis
Progressive, Variable (generally faster than AD)
The last dementia! This is associated with a progressive virus.
HIV-Associated Dementia (HAD)
HAD is mostly in untreated patients with advanced HIV. What are the Sx/Ssx?
Subacute onset that may wax/wane Attention concentration Memory deficits Behavioral/ mood changes Impaired psychomotor speed/precision
What is the expected finding on the brains scan of HAD?
Cerebral atrophy
Mainly basal ganglia and white matter
T/F HAD can be explained by other conditions or pre-existing causes other than HIV.
F
HAD - management
Antiretroviral (get one that goes into CNS)
If they are compliant - LP and investigate
Do you think cerebral atrophy from a pt not taking their meds is a marker for increased mortality among HIV pts?
Duh
Is this the 100th card?
Yes!
