Random Geri Lectures Flashcards
(156 cards)
1
Q
what are the two components of long term memory
A
explicit/declarative
implicit/non-declarative
2
Q
what are the two components of explicit/declarative long term memory
A
episodic
semantic
*are interrelated
3
Q
what is episodic memory
A
explicit long term memory that records BIOGRAPHICAL events
4
Q
what is semantic memory
A
explicit long term memory that records WORDS, IDEAS and CONCEPTS
5
Q
what are the components of implicit/non declarative memory
A
procedural (skills) and emotional conditioning
also priming effect and conditioned reflexes
6
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
memory impairment
A
normal aging–> retrieval deficit type
AD–> amnestic-type
7
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
semantic memory
A
normal aging–> IMPROVES
AD–> worsens
8
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
insight
A
normal aging–> normal
AD–> decreased
9
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
ADLs
A
normal aging–> normal
AD–> worsens
10
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
word finding
A
normal aging–> minor delay
AD–> major/anomia
11
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
visuospatial function
A
normal aging–> normal
AD–> worsens (i.e clock drawing)
12
Q
how does the following component of memory/function change with NORMAL AGING vs ALZHEIMERS type dementia:
social engagement
A
normal aging–> normal
AD–> apathy/decrease
13
Q
what is the prevalence of MCI above age 65
A
10-20%
*5-10% of those in community progress to dementia per year
*reversion to normal in up to 25-30%/year
14
Q
how should you approach management of MCI
A
- dont level as early dementia
- look for and treat depression
- screen for and treat vascular RFs
- promote healthy lifestyle both cognitive and physical
- yearly follow up on IADLs and cognition
- cholinesterase inhibitors, physical training unclear if decrease risk
15
Q
what are the 3 cortical dementias
A
AD
FTD
vascular dementia*
16
Q
what are the 3 subcortical dementias
A
parkinsons dementia
LBD
vascular dementia*
17
Q
what is the key feature of cortical vs subcortical dementia
A
cortical–> loss of ABILITY
subcortical–> loss of COORDINATION OF ability
18
Q
how are the following domains affected in the cortical vs subcortical dementias:
cognition
A
cortical–> true amnesia (recall/recognition failure)
+aphasia, agnosia, apraxia
subcortical–> forgetfulness (recognition > recall, so cuing helps)
+inattention
19
Q
how are the following domains affected in the cortical vs subcortical dementias:
executive functioning
A
cortical–> LATER executive impairments in proportion to other deficits
subcortical–> affected EARLY and SEVERELY
20
Q
how are the following domains affected in the cortical vs subcortical dementias:
motor
A
cortical–> decline in LATER stages
subcortical–> EARLY gate trouble, SLOWED
21
Q
how are the following domains affected in the cortical vs subcortical dementias:
speech
A
cortical–> articulate
subcortical–> dysarthric
22
Q
how are the following domains affected in the cortical vs subcortical dementias:
psychiatric
A
cortical–> personality changes, apathy (esp. with FTD)
subcortical–> affective changes, psychosis, apathy
23
Q
how does the risk for dementia change with age
A
risk DOUBLES every 5 years after age 65
24
Q
what is the prevalence of dementia in all canadians over age 65
A
8%
25
rank the dementias from most to least commonly seen in canadian dementia clinics
AD (47%)
AD + vascular (19%)
Vascular (9%)
FTD (5%)
AD + LBD (3%)
LBD and FTD+AD equal (2%)
26
what is the average amount of time from onset of AD symptoms to death
7-10 years
27
list risk factors for AD
age
sex (females 2x more than males)
low education
vascular RFs
hx depression
down syndrome
EOAD based on genetics (i.e PSEN1)
28
how much higher is your risk of AD if one of your relatives had it
4x higher risk
29
late onset AD is associated with what gene
APOE gene (chromosome 19)
--> helps clear deposits from parenchyma of the brain
--> allele E4 increases risk
*40% of those with late onset AD have allele E4 therefore is RF but NOT causative
30
is screening for APOE E4 recommended
no--> low sens/spec and low PPV/NPV
31
what type of plaques are found in the brains of people with AD
beta-amyloid plaques/senile plaques
--> insoluble, builds up
neurofibrillary tangles (made of Tau protein)
--> stops transport within neuron
32
what are the two neurotransmitter changes in AD
depletion of acetylcholine
hyperactivity of glutamate (causes neuronal toxicity)
33
what parts of the brain are affected in early AD
hippocampus (plaques and tangles begin, short term memory changes start)
parietal lobe (apraxia, agnosia, perceptual-motor abn)
34
what parts of the brain are affected in late AD
frontal lobe--> DLPFC
limbic
35
what parts of the brain are affected in end stage AD
brainstem
36
what do you see on CT head in AD
cortical atrophy
medial temporal lobe atrophy
37
what do you see on MRI in AD
parietal atrophy
hippocampal atrophy
38
what do you see on PET/SPECT in AD
bilateral temporoparietal hypometabolism
39
when does FTLD usually start
age 45-65
40
which type of FTLD is more common in males? females?
behavioural and semantic--> men
nonfluent variant--> women
41
how long from diagnosis to death in FTD
6-8 years
42
what neurotransmitters are implicated in FTLD
post synaptic serotoning deficit
some evidence foe dopamine depletion
**cholinergic system is INTACT**
43
what do you see on MRI for FTLD
specific atrophy patterns for behavioural FTD and language variants
44
what do you see on PET/SPECT for FTD
frontal anterior hypoperfuson
45
which has a more profound cholinergic deficit--> AD or LBD
LBD
46
how do you distinguish between parkinsons dementia and LBD
for parkinsons dementia, must have parkinsons disease for at least ONE YEAR before onset of cognitive changes
in LBD:
--more ATTENTION deficits
--more POSTURAL INSTABILITY and GAIT issues
--SEVERE reaction to antipsychotics
--2/3 of LBD patients have parkinsons disease and it is ususally SYMMETRICAL
47
what are the protein aggregates (lewy bodies) seen in parkinsons and LBD made of
neurofilaments and alpha-synuclein
48
how does the pathology of PDD and LBD differ
think that maybe PDD is "bottom to top" spread of lewy body pathology and LBD is "top to bottom"?
49
what neurotransmitters are affected in LBD/PDD
cholinergic and dopaminergic
50
what are the two major domains affected in vascular dementia
complex attention and frontal executive funcion
51
what % of people are diagnosed with dementia within 3 months of stroke
20-30%
52
are men or woman more affected by vascular dementia
men
53
what is Binswangers disease
slowly progressive decline in cognition, gait and early urinary incontinence
ddx = NPH vs Binswangers--> diffuse ATROPHY, confluent white matter changes on imaging
vascular RFs present but no hx of CVA/TIA
54
what causes the cognitive changes seen in Binswangers disease
due to damage within the frontal-subcortical projections in the cortex
55
what other dementia can be mimicked by Binswangers disease
FTD
(i.e executive dysfunction without language impairment, mild memory problems, psychomotor slowing)
56
what are the psychiatric manifestations of Binswangers disease
late life depression
apathy
"emotional incontinence"
57
what is the "frontal gait"
feet stuck to floor
58
which one dementia is more common in women than men
AD
(the rest are more common in med than women)
59
what are the basic ADLs
"DEATH"
Dressing
Eating
Ambulation
Toilet, Transferring
Hygiene, grooming
60
what are the IADLs
"M-SHAFT"
Medication
Shopping
Housework, Hobbies
Accounting
Food prep
Transportation and Telephone
61
What are some questions to ask to assess the various cognitive domains?
62
MMSE has limited sensitivity to what types of dementia
frontal and subcortical changes
63
what is the sensitivity for a MoCA score of 25/26 for dementia
100%
(specificity is 87%)
64
which is more sensitive--MMSE or MoCA
MoCA
65
what are the 3 steps of the mini-cog screen
register 3 words
clock drawing test
recall of the 3 words
(+ screen if abnormal clock and 1-2 recall words or zero recalled words)
66
are there any biomarkers that increase accuracy of diagnosis of dementia over clinical assessment
no
67
what are the first changes seen in alzheimers
mood
learning and memory
perceptual-motor
68
what are the first changes seen in FTD
language variant--> language
behaviour variant--> social cognition
69
what are the first changes seen in NCD secondary to parkinsons
executive function
70
what are the first changes seen in LBD
perceptual-motor
executive function
complex attention
71
what are the first changes seen in vascular dementia
complex attention
72
list the pathophysiology of alzheimers disease
APOE4
PSEN1/2
amyloid plaques
reactive glia
neurofibrillary tangles
amyloid angiopathy
loss of cholinergic neurons in forebrain
73
list the pathophysiology of FTD
TAUopathy
post synaptic serotonin deficit
cholinergic is relatively SPARED
about 10% has a causative gene on chromosome 17
74
list the pathophysiology of NCD secondary to parkinsons dementia
alpha-synnuclein
brainstem lewy bodies
75
list the pathophysiology of LBD
alpha synuclein
limbic/cortical lewby bodies
76
list the pathophysiology of vascular dementia
chronic small vessel disease (insidious)
77
which dementia is associated with the following pathology:
tauopathy
FTD
78
which dementia is associated with the following pathology:
APOE4
alzheimers
79
which dementia is associated with the following pathology:
alpha synuclein
FTD and PDD
80
which dementia is associated with the following pathology:
brainstem lewy bodies
NCD due to parkinsons
81
which dementia is associated with the following pathology:
chronic small vessel disease
vascular
82
which dementia is associated with the following pathology:
post synaptic serotonin deficit
FTD
83
which dementia is associated with the following pathology:
reactive glia
alzheimers
84
which dementia is associated with the following pathology:
loss of cholinergic neurons in the forebrain
alzheimers
85
which dementia is associated with the following pathology:
SPARED cholinergic neurons
FTD
86
which dementia is associated with the following pathology:
limbic/cortical lewy bodies
LBD
87
which dementia is associated with the following pathology:
causative gene on chromosome 17
FTD
88
which dementia is associated with the following pathology:
neurofibrillary tangles
alzheimers
89
which dementia is associated with the following pathology:
amyloid angiopathy
alzheimers
90
what do you see on SPECT for alzheimers
bilateral tempoparietal hypometabolism
91
what do you see on SPECT for FTD
more frontal
92
what do you see on SPECT for PDD
loss of dopamine uptake
93
what do you see on SPECT for LBD
functional impairment of primary visual cortex
loss of dopamine uptake
94
what do you see on CT for alzheimers
atrophy
95
in FTD, what part of the brain is most affected if the deficit is:
executive function
dorsolateral
96
in FTD, what part of the brain is most affected if the deficit is:
social deficit
orbitofrontal
97
in FTD, what part of the brain is most affected if the deficit is:
apathy
medial frontal
98
in FTD, what part of the brain is most affected if the deficit is:
nonfluent/agrammatic aphasia
left post frontotemporal
99
in FTD, what part of the brain is most affected if the deficit is:
semantic aphasia
anterior temporal
100
treatment for alzheimers disease
cholinesterase inhibitor
memantine (if severe)
101
how might you treat irritability in FTD
trazodone
102
how do you treat PDD
cholinesterase inhibitor
memantine sometimes
quetiapine or clozapine
103
how do you treat LBD
cholinesterase inhibitor sometimes used, memantine sometimes used
RIVASTIGMINE CAN DECREASE HALLUCINATIONS
AVOID APs
104
how do you treat vascular dementia
cholinesterase inhibitor
105
what are the two types of working memory
verbal/phonologic
spatial
106
where is semantic memory stored in the brain
inferolateral temporal lobes
107
list the core features of the classical amnestic syndromes
anterograde amnesia for explicit memory (autobiographical memory)
retrograde amnesia following Ribots law (retrograde gradient with most remote memories least affected)
preservations of SEMANTIC KNOWLEDGE
relative preservations of some types of IMPLICIT LEARNING
preserved attentional, linguistic, sensorimotor skills
108
what is prosopagnosia
"face selective" visual amnesia
109
what is the only prominent clinical deficit in Korsakoffs syndrome
memory impairment
persists after WKS resolves
severe impairment of recent memory vs remote memory
110
what is the most common features Wernicke Korsakoff syndrome
confusion and/or stupor
*severe impairment of attention, concentration, orientation, memory
*apathy and/or drowsiness
*distractability, perseveration
111
what % of people with Korsakoff syndrome NEVER (or only minimally) improve
50%
(25% improve but still have deficits over months to years, 25% recover completely)
112
when does transient global amnesia typically first appear
late in life--> after age 40, but usually around 60
113
when might provoke an episode of transient global amnesia
extreme physical stress (i.e cold shock, hot shower, orgasm) or psychological stress
angiography
driving or riding in a motor vehicle
114
what is typically IMPAIRED in transient global amnesia
anterograde and retrograde memory (but anterograde memory is worse)
115
what is generally PRESERVED in transient global amnesia
preserved insight--> great concern over their disorientation
preserved attention and "immediate" memory
116
how long does it usually take for transient global amnesia to recover
about 24 hours, with an island of memory loss for the ictus
117
list risk factors for transient global amnesia
migraine
temporal love epilepsy
CV risk factors
valsalva maneuver
118
do you ever see severe retrograde amnesia in the absence of anterograde amnesia in an "organic" amnesia
no--> except in delirium or severe dementia
so basically, if someone is not delirious, not demented, and has ONLY severe retrograde amnesia, this is likely FUNCTIONAL amnesia
in functional amnesia, personal identity is often lost (vs. preserved in organic amnesia)
119
what does the Trails Making test (Trails B) test assess
visuospatial and motor tracking
conceptualization
set shift
120
what does the Wisconsin Card Sorting test look at
attention
working memory
visual processing
abstract thinking
set shifting
L>R hemisphere
121
list some of the diseases that can affect the frontal lobes
TBI
frontal lobe seizures
vascular disease
tumours
MS
degenerative diseases (i.e Picks disease, Huntingtons)
Infectious disease
psychiatric illness
122
which areas of the brain are more vulnerable in the closed head injury (and resultant stretching/shearing of fibers and resultant diffuse axonal injury)
orbitofrontal and temporal lobes
123
what usually causes frontal lobe seizures
usually secondary to trauma
124
what area of the brain is damaged in an ACA infarction
medial frontal area
125
what area of the brain is damaged in MCA territory infarction
dorsolateral frontal lobe
126
what might you see clinically if a patient has had an Anterior Communicating artery aneurysm rupture
personality change
emotional disturbance
confabulation--> combination of damage to forebrain and frontal damage
127
what types of brain tumour might result in profound personality changes and dementia
subfrontal and olfactory groove meningiomas
128
where in the brain has the second highest number of plaques int he brain of someone with MS
frontal lobes
can result in mood lability, memory problems, cognitive and behavioural affects
129
what infectious diseases may result in frontal symptomrs
neurosyphillis
HSV encephalitis (frontal and temporal)
130
what is the main excitatory neurotransmitter in the frontal lobe
glutamate
131
what is the main inhibitory neurotransmitter in the frontal lobe
GABA
132
what is the main neurotransmitter in the basal ganglia
serotonin--5HT1
133
what do you use for decreasing the elevated sex drive that can be seen in frontal lobe syndromes
SSRI (HIGH DOSE)
134
list some medications that can be used in management of frontal lobe syndromes
SSRIs
beta blockers
antipsychotics
mood stabilizers
benzos--> lecture says "dont be afraid!" of using these
cannabinoids
anti-androgen (cyproterone acetate, cimetidine)
*these are symptomatic treatments only
135
why might you use antipsychotics in treating frontal lobe syndromes
behavioural control
136
why might you use SSRIs in treating frontal lobe syndromes
agitation
high dose for decreasing sex drive
137
what are the core features of LBD
fluctuating cognition, varying attention/alertness
recurrent visual hallucinations, well formed, detailed
spontaneous features of parkinsonism
**2 for probably, 1 for possible
138
list 3 LBD indicative biomarkers
1. LOW DOPAMINE transporter uptake in BASAL GANGLIA on SPECT or PET
2. low uptake Iodine-MIBG myocardial scintigraphy
3. polysomnogram confirmed REM sleep WITHOUT ATONIA
*possible LBD if just 1 biomarker
*probable if 1 core feature + 1 biomarker
139
which areas of the brain are relatively preserved on MRI/CT in LBD
temporal lobes
140
which cholinesterase inhibitor has the best evidence in PDD/LBD
rivastigmine
141
what is the preferred parkinsons disease med to maintain mobility in patients with PDD/LBD
L-dopa
*avoid dopamine agonists, amantadine, selegiline
142
which antipsychotic has the best results for PDD/LBD psychotic symptoms
clozapine
but QUETIAPINE is a "reasonable first choice"
abilify is uncertain
143
what antipsychotics should be AVOIDED in PDD/LBD
risperidone
olanzapine
typical antipsychotics
144
what is an antidepressant that can be used an as alternative for sleep/nonspecific agitation in PDD/LBD
trazodone
145
what is the underlying pathology of Multiple System Atrophy
synucleinopathy like PDD/LBD
146
what is the course of evolution of symptoms of Multiple System Atrophy
rapid--4-7 years
147
what are the features of Multiple System Atrophy
autonomic failure with POSTURAL HYPOTENSION
ataxis and parkinsonian subtypes
cognitive impairment is MILDER
FRONTAL-CORTICAL
148
what is the underlying pathology of progressive supranucleur palsy (PSP)
tauopathy
149
what type of aphasia is associated with progressive supranucleur palsy
progressive NONfluent aphasia
150
what is the pattern of cognitive changes seen in progressive supranucleur palsy
frontal subcortical
151
what physical symptoms are characteristic of progressive supranucleur palsy
impaired vertical gaze doe voluntary saccades
swallowing difficulties
falls
axial rigidity
NO tremor
152
what medication might be considered in progressive supranucleur palsy
small % respond to L-dopa
153
what is the underlying pathophysiology of Corticobasal Degeneration
tauopathy
154
what is the type of aphasia associated with Corticobasal Degeneration
progressive NONfluent aphasia
155
what physical symptoms are associated with Corticobasal Degeneration
UNILATERAL rigidity
myoclonus
apraxia
"ALIEN LIMB"
speech apraxia
swallowing problems
156
list some of the "parkinsons like dementias"
Corticobasal Degeneration
Multiple system atrophy
progressive supranuclear palsy
normal pressure hydrocephalus
valproate induced cognitive impairment and gait disorder
vascular parkinsons
idiopathic calcification of the basal ganglia
