Geri One Pagers (Harrison/Bennett) Flashcards
there is a big spike in dx alzheimer’s disease after what ageq
after age 75
what is the prevalence of alzheimer’s after 60s
above 25%
what two brain areas are most affected in early alzheimer’s
hippocampus
parietal lobe
what is the usual function of tau? how is tis changed in alzheimer’s
normal tau–> supports microtubules for function, transport within neuron
abnormal tau–> tau separates from microtubules, tau fragments form tangles and therefor transport within the neuron ceases
how much is your risk increased if you have a first degree relative with alzheimer’s
4x increased risk
why do people with down syndrome develop alzheimer’s
have extra chromosome 21, which means they have an extra copy of the amyloid precursor protein and thus high risk of developing alzheimer’s if survive to midlife
alzheimer’s is “early onset” if occurs before what age
55
what is the strongest risk factor for alzheimer’s
age
list 6 risk factors for alzheimer’s
age
sex (female higher risk)
vascular
hx depression
low education
TBI
what are two areas of life which are often the first to be affected in alzheimer’s
ability to drive
ability to handle finances
*good to screen for these
what two areas of functioning are classically affected in alzheimer’s
- amnestic memory loss/learning–> hippocampus
- perceptual/motor dysfunction–> parietal
(i.e do you get lost?)
what area of functioning is often preserved until late in course in alzheimer’s
social cognition
what 3 areas are often first affected when undergoing neuropsych testing in alzheimer’s
memory
language/fluency
executive function
what two things would you look for in CT head if suspecting alzheimer’s
cortical atrophy
medial temporal lobe atrophy
what two things would you look for on MRI is suspecting alzheimer’s
parietal atrophy
hippocampal atrophy
what would you look for on PET/SPECT if suspecting alzheimer’s
bilateral tempoparietal hypometabolism
what are the 3 hallmarks of alzheimer’s on postmortem exam of the brain
cortical atrophy
amyloid-predominant neuritic plaques
tau-predominant neurofibrillary tangles
what are two ways to look for amyloid early in pathophysiological cascade for alzheimer’s
PET amyloid imaging
CSF amyloid beta-42 (low levels)
what is the gene with the greatest known effect on the risk of developing late onset alzheimers
APOE (chromosome 19)
what are the two genes associated with EOAD
PSEN 1 or 2–> PSEN 1 causes up to 80% of all familial alzheimer’s cases
APP gene
what medication can be used for apathy in alzheimer’s
methylphenidate was only agent with benefit, according to cochrane review (small benefit only)
what is a mnemonic for the symptoms of the behavioural variant of frontotemporal dementia
HADES
Hyperorality and dietary changes
Apathy or inertia
Disinhibition of behaviour
Empathy or sympathy loss
Stereotyped, perseverative or compulsive/ritualistic behaviour
needs 3/5
what area of functioning is most prominently affected in behavioural variant of frontotemporal dementia
prominent decline in SOCIAL COGNITION or EXECUTIVE ABILITIES
what is relatively spared in FTD
learning and memory
perceptual-motor function
*relevant because these are the areas most affected in alzheimers
what is required for “probable” (instead of possible) FTD
evidence of a causative genetic mutation from either fam hx or GENETIC TESTING
OR
evidence of disproportionate frontal and/or temporal lobe involvement from NEUROIMAGING
what % of people with FTD have family hx of early onset NCD
about 40%
–10% show autosomal dominant inheritance pattern
list 3 genes that may be associated with FTD
MAPT
GRN
C9ORF72
why dont you treat FTD with cholinesterase inhibitors
because the cholinergic system is INTACT in these patients
treating with cholinesterase inhibitors can make behaviours WORSE
(serotonin is mostly affected, maybe some dopamine)
what % of those with FTD are diagnosed before age 65
75%
what is the classic presentation for FTD
progressive development of behavioural and personality change, language impairment
describe symptoms of behavioural variant of FTD
impaired insight
apathy, disinhibition
decreased socialization, self care, personal responsibilities, social appropriateness
changes in social style, religious/political beliefs, hyperorality
COGNITIVE DECLINE IS LESS PROMINENT
how do language variants of FTD typically present
primary progressive aphasia with gradual onset
list the 3 subtypes of FTD language variant
logopenic
semantic
nonfluent (agrammatic)
what is the earliest sign of FTD semantic variant
word finding
what is the most prominent symptom in FTD semantic variant
impaired single word comprehension and object naming
(preserved fluency, repetition, grammar)
what is the most prominent symptom in nonfluent/agrammatic FTD variant
motor speech deficit, articulatory difficulty
(can understand simple words)
what is the most prominent symptom in logopenic FTD
impaired single word retrieval, repetition, naming (vague)
*spared grammar
*more linked to alzheimers
what would you expect to see on CT/MRI in the behavioural variant of FTD
atrophy in frontal lobe (especially medial)
atrophy in anterior temporal lobe
what would you expect to see on CT/MRI in the semantic variant of FTD
atrophy in middle, inferior and anterior temporal lobe
–> bilateral but more left sided
what would you expect to see on CT/MRI in the nonfluent variant of FTD
atrophy in left posterior frontal-insular
what would you expect to see on CT/MRI in the logopenic variant of FTD
left posterior perisylvian or parietal atrophy
what medications are used for FTD
SSRIs, trazodone, AAPs as alternatives
in what areas are the most effects noted in vascular dementia
complex attention (including processing speed) and frontal-executive function
what is CADASIL
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
genetic condition
in vascular dementia, if there is more of a picture of worsening executive function, where is the stroke more likely to have occurred
subcortical
in vascular dementia, if there is more of a picture of worsening complex attention, where is the stroke more likely to have occurred
cortical
describe 4 features of “vascular depression”
late onset depressive symptoms
psychomotor slowing
executive dysfunction
progressive small vessel ischemic disease
what gene anomaly causes CADASIL
NOTCH3 mutation
what should you do in patients with a stroke history in order to reduce the risk of post stroke depression
lower BP
does LBD have more or less of a cholinergic defecit than alzheimers
LBD has a MORE PROFOUND cholinergic deficit than in alzheimers
thus they RESPOND BETTER to cholinesterase inhibitors
how is the hippocampus affected in LBD compared to AD
hippocampus relatively preserved in LBD vs AD
what is a major risk factor for LBD
presence of REM sleep behaviour disorder
at what age do most LBDs present
mid 70s
what often occurs before diagnosis of LBD
prodromal delirium precipitated by illness or surgery
what are the 4 cardinal symptoms of LBD
- fluctuating cognition with variations in attention and alertness
- recurrent well formed visual hallucinations (or in other modalities; “feeling of presence” in up to 15%)
- REM sleep behaviour disorder (acting out dreams)
- parkinsons symptoms like bradykinesia, tremor, rigidity
what might you see on EEG in LBD
prominent slow wave activity
temporal lobe transient waves
what might you see on SPECT/CT perfusion scan in LBD
reduced occipital activity
generalized low uptake
low dopamine transporter uptake
which NCD population sees the MOST benefit from use of cholinesterase inhibitors
LBD–have even more cholinergic deficit than AZ
what is the preferred agent for treating hallucinations in LBD
quetiapine but often doesnt work (clozapine is best results)
what to use in REM sleep behaviour disorder
melatonin up to 12mg
trazodone is a good place to start
gabapentin or pregabalin
clonazepam later option with caution in LBD pop
list the 4 types of NONfluent aphasias
global aphasia
mixed transcortical aphasia
broca’s aphasia
transcortical motor aphasia
list the 4 types of FLUENT aphasias
wernicke’s aphasia
transcortical sensory aphasia
conduction aphasia
anomic aphasia
list the 4 types of aphasia where people CAN repeat words or phrases
mixed transcortical aphasia
transcortical motor aphasia
transcortical sensory aphasia
anomic aphasia
list the 4 types of aphasia where people CANNOT repeat words or phrases
global aphasia
broca’s aphasia
wernicke’s aphasia
conduction aphasia
list the 4 types of aphasia where someone CAN understand spoken messages
brocas aphasia
transcortical motor aphasia
conduction aphasia
anomic aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
fluent + comprehends spoken messages + can repeat words or phrases
anomic aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
non fluent + cannot comprehend spoken messages + cannot repeat words or phrases
global aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
fluent + cannot comprehend spoken messages + can repeat words
transcortical sensory aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
fluent + cannot comprehend spoken messages + cannot repeat words
wernicke’s aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
non fluent + can comprehend spoken messages + cannot repeat words
broca’s aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
fluent + can comprehend spoken messages + cannot repeat
conduction aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
non fluent + can comprehend + can repeat
transcortical motor aphasia
if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?
non fluent + cannot comprehend + can repeat
mixed transcortical aphasia
what is the most severe form of aphasia
global aphasia
can someone with global aphasia read or write
no
can someone with broca’s aphasia read or write
may be able to read
limited in writing
can someone with wernicke’s aphasia read or write
often reading and writing is severly impaired
“inability to grasp meaning of spoken words”
can someone with anomic aphasia read or write
read well
same trouble finding words in writing as in speaking
what is the clinical picture of anomic aphasia
people who are left wiht a persistent inability to supply the words for the very things they want to talk about (esp. significant nouns and verbs)
speech is full of vague circumlocutions and expressions of frustration
understand speech well
what is primary progressive aphasia
neurological syndrome in which language capabilities become slowly and progressively impaired
caused by neurodegenerative diseases (unlike other forms of aphasia which are susually caused by stroke or TBI)
results from deterioration of brain tissue responsible for speech and language
why does pseudobulbar affect occur
due to disconnect between the frontal lobe (which regulated emotions) and the cerebellum and brainstem (which is where basic reflexes are mediated)
LOSS OF INHIBITION from limbic motor neurons in the brain may also be involved
