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2. Geriatric Psychiatry + Neuroanatomy > Random Geri Lectures > Flashcards

Random Geri Lectures Flashcards

1
Q

what are the two components of long term memory

A

explicit/declarative

implicit/non-declarative

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2
Q

what are the two components of explicit/declarative long term memory

A

episodic

semantic

*are interrelated

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3
Q

what is episodic memory

A

explicit long term memory that records BIOGRAPHICAL events

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4
Q

what is semantic memory

A

explicit long term memory that records WORDS, IDEAS and CONCEPTS

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5
Q

what are the components of implicit/non declarative memory

A

procedural (skills) and emotional conditioning

also priming effect and conditioned reflexes

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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

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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

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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

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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

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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

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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)

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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

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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

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14
Q

how should you approach management of MCI

A
  1. dont level as early dementia
  2. look for and treat depression
  3. screen for and treat vascular RFs
  4. promote healthy lifestyle both cognitive and physical
  5. yearly follow up on IADLs and cognition
  6. cholinesterase inhibitors, physical training unclear if decrease risk
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15
Q

what are the 3 cortical dementias

A

AD

FTD

vascular dementia*

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16
Q

what are the 3 subcortical dementias

A

parkinsons dementia

LBD

vascular dementia*

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17
Q

what is the key feature of cortical vs subcortical dementia

A

cortical–> loss of ABILITY

subcortical–> loss of COORDINATION OF ability

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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

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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

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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

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21
Q

how are the following domains affected in the cortical vs subcortical dementias:

speech

A

cortical–> articulate

subcortical–> dysarthric

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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

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23
Q

how does the risk for dementia change with age

A

risk DOUBLES every 5 years after age 65

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24
Q

what is the prevalence of dementia in all canadians over age 65

A

8%

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25
Q

rank the dementias from most to least commonly seen in canadian dementia clinics

A

AD (47%)
AD + vascular (19%)
Vascular (9%)
FTD (5%)
AD + LBD (3%)
LBD and FTD+AD equal (2%)

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26
Q

what is the average amount of time from onset of AD symptoms to death

A

7-10 years

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27
Q

list risk factors for AD

A

age

sex (females 2x more than males)

low education

vascular RFs

hx depression

down syndrome

EOAD based on genetics (i.e PSEN1)

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28
Q

how much higher is your risk of AD if one of your relatives had it

A

4x higher risk

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29
Q

late onset AD is associated with what gene

A

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

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30
Q

is screening for APOE E4 recommended

A

no–> low sens/spec and low PPV/NPV

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31
Q

what type of plaques are found in the brains of people with AD

A

beta-amyloid plaques/senile plaques
–> insoluble, builds up

neurofibrillary tangles (made of Tau protein)
–> stops transport within neuron

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32
Q

what are the two neurotransmitter changes in AD

A

depletion of acetylcholine

hyperactivity of glutamate (causes neuronal toxicity)

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33
Q

what parts of the brain are affected in early AD

A

hippocampus (plaques and tangles begin, short term memory changes start)

parietal lobe (apraxia, agnosia, perceptual-motor abn)

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34
Q

what parts of the brain are affected in late AD

A

frontal lobe–> DLPFC

limbic

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35
Q

what parts of the brain are affected in end stage AD

A

brainstem

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36
Q

what do you see on CT head in AD

A

cortical atrophy

medial temporal lobe atrophy

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37
Q

what do you see on MRI in AD

A

parietal atrophy

hippocampal atrophy

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38
Q

what do you see on PET/SPECT in AD

A

bilateral temporoparietal hypometabolism

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39
Q

when does FTLD usually start

A

age 45-65

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40
Q

which type of FTLD is more common in males? females?

A

behavioural and semantic–> men

nonfluent variant–> women

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41
Q

how long from diagnosis to death in FTD

A

6-8 years

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42
Q

what neurotransmitters are implicated in FTLD

A

post synaptic serotoning deficit

some evidence foe dopamine depletion

cholinergic system is INTACT

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43
Q

what do you see on MRI for FTLD

A

specific atrophy patterns for behavioural FTD and language variants

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44
Q

what do you see on PET/SPECT for FTD

A

frontal anterior hypoperfuson

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45
Q

which has a more profound cholinergic deficit–> AD or LBD

A

LBD

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46
Q

how do you distinguish between parkinsons dementia and LBD

A

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

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47
Q

what are the protein aggregates (lewy bodies) seen in parkinsons and LBD made of

A

neurofilaments and alpha-synuclein

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48
Q

how does the pathology of PDD and LBD differ

A

think that maybe PDD is “bottom to top” spread of lewy body pathology and LBD is “top to bottom”?

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49
Q

what neurotransmitters are affected in LBD/PDD

A

cholinergic and dopaminergic

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50
Q

what are the two major domains affected in vascular dementia

A

complex attention and frontal executive funcion

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51
Q

what % of people are diagnosed with dementia within 3 months of stroke

A

20-30%

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52
Q

are men or woman more affected by vascular dementia

A

men

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53
Q

what is Binswangers disease

A

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

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54
Q

what causes the cognitive changes seen in Binswangers disease

A

due to damage within the frontal-subcortical projections in the cortex

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55
Q

what other dementia can be mimicked by Binswangers disease

A

FTD

(i.e executive dysfunction without language impairment, mild memory problems, psychomotor slowing)

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56
Q

what are the psychiatric manifestations of Binswangers disease

A

late life depression

apathy

“emotional incontinence”

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57
Q

what is the “frontal gait”

A

feet stuck to floor

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58
Q

which one dementia is more common in women than men

A

AD

(the rest are more common in med than women)

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59
Q

what are the basic ADLs

A

“DEATH”

Dressing

Eating

Ambulation

Toilet, Transferring

Hygiene, grooming

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60
Q

what are the IADLs

A

“M-SHAFT”

Medication

Shopping

Housework, Hobbies

Accounting

Food prep

Transportation and Telephone

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61
Q

What are some questions to ask to assess the various cognitive domains?

A
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62
Q

MMSE has limited sensitivity to what types of dementia

A

frontal and subcortical changes

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63
Q

what is the sensitivity for a MoCA score of 25/26 for dementia

A

100%

(specificity is 87%)

64
Q

which is more sensitive–MMSE or MoCA

A

MoCA

65
Q

what are the 3 steps of the mini-cog screen

A

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
Q

are there any biomarkers that increase accuracy of diagnosis of dementia over clinical assessment

A

no

67
Q

what are the first changes seen in alzheimers

A

mood

learning and memory

perceptual-motor

68
Q

what are the first changes seen in FTD

A

language variant–> language

behaviour variant–> social cognition

69
Q

what are the first changes seen in NCD secondary to parkinsons

A

executive function

70
Q

what are the first changes seen in LBD

A

perceptual-motor

executive function

complex attention

71
Q

what are the first changes seen in vascular dementia

A

complex attention

72
Q

list the pathophysiology of alzheimers disease

A

APOE4

PSEN1/2

amyloid plaques

reactive glia

neurofibrillary tangles

amyloid angiopathy

loss of cholinergic neurons in forebrain

73
Q

list the pathophysiology of FTD

A

TAUopathy

post synaptic serotonin deficit

cholinergic is relatively SPARED

about 10% has a causative gene on chromosome 17

74
Q

list the pathophysiology of NCD secondary to parkinsons dementia

A

alpha-synnuclein

brainstem lewy bodies

75
Q

list the pathophysiology of LBD

A

alpha synuclein

limbic/cortical lewby bodies

76
Q

list the pathophysiology of vascular dementia

A

chronic small vessel disease (insidious)

77
Q

which dementia is associated with the following pathology:

tauopathy

A

FTD

78
Q

which dementia is associated with the following pathology:

APOE4

A

alzheimers

79
Q

which dementia is associated with the following pathology:

alpha synuclein

A

FTD and PDD

80
Q

which dementia is associated with the following pathology:

brainstem lewy bodies

A

NCD due to parkinsons

81
Q

which dementia is associated with the following pathology:

chronic small vessel disease

A

vascular

82
Q

which dementia is associated with the following pathology:

post synaptic serotonin deficit

A

FTD

83
Q

which dementia is associated with the following pathology:

reactive glia

A

alzheimers

84
Q

which dementia is associated with the following pathology:

loss of cholinergic neurons in the forebrain

A

alzheimers

85
Q

which dementia is associated with the following pathology:

SPARED cholinergic neurons

A

FTD

86
Q

which dementia is associated with the following pathology:

limbic/cortical lewy bodies

A

LBD

87
Q

which dementia is associated with the following pathology:

causative gene on chromosome 17

A

FTD

88
Q

which dementia is associated with the following pathology:

neurofibrillary tangles

A

alzheimers

89
Q

which dementia is associated with the following pathology:

amyloid angiopathy

A

alzheimers

90
Q

what do you see on SPECT for alzheimers

A

bilateral tempoparietal hypometabolism

91
Q

what do you see on SPECT for FTD

A

more frontal

92
Q

what do you see on SPECT for PDD

A

loss of dopamine uptake

93
Q

what do you see on SPECT for LBD

A

functional impairment of primary visual cortex

loss of dopamine uptake

94
Q

what do you see on CT for alzheimers

A

atrophy

95
Q

in FTD, what part of the brain is most affected if the deficit is:

executive function

A

dorsolateral

96
Q

in FTD, what part of the brain is most affected if the deficit is:

social deficit

A

orbitofrontal

97
Q

in FTD, what part of the brain is most affected if the deficit is:

apathy

A

medial frontal

98
Q

in FTD, what part of the brain is most affected if the deficit is:

nonfluent/agrammatic aphasia

A

left post frontotemporal

99
Q

in FTD, what part of the brain is most affected if the deficit is:

semantic aphasia

A

anterior temporal

100
Q

treatment for alzheimers disease

A

cholinesterase inhibitor

memantine (if severe)

101
Q

how might you treat irritability in FTD

A

trazodone

102
Q

how do you treat PDD

A

cholinesterase inhibitor

memantine sometimes

quetiapine or clozapine

103
Q

how do you treat LBD

A

cholinesterase inhibitor sometimes used, memantine sometimes used

RIVASTIGMINE CAN DECREASE HALLUCINATIONS

AVOID APs

104
Q

how do you treat vascular dementia

A

cholinesterase inhibitor

105
Q

what are the two types of working memory

A

verbal/phonologic

spatial

106
Q

where is semantic memory stored in the brain

A

inferolateral temporal lobes

107
Q

list the core features of the classical amnestic syndromes

A

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
Q

what is prosopagnosia

A

“face selective” visual amnesia

109
Q

what is the only prominent clinical deficit in Korsakoffs syndrome

A

memory impairment

persists after WKS resolves

severe impairment of recent memory vs remote memory

110
Q

what is the most common features Wernicke Korsakoff syndrome

A

confusion and/or stupor

*severe impairment of attention, concentration, orientation, memory

*apathy and/or drowsiness

*distractability, perseveration

111
Q

what % of people with Korsakoff syndrome NEVER (or only minimally) improve

A

50%

(25% improve but still have deficits over months to years, 25% recover completely)

112
Q

when does transient global amnesia typically first appear

A

late in life–> after age 40, but usually around 60

113
Q

when might provoke an episode of transient global amnesia

A

extreme physical stress (i.e cold shock, hot shower, orgasm) or psychological stress

angiography

driving or riding in a motor vehicle

114
Q

what is typically IMPAIRED in transient global amnesia

A

anterograde and retrograde memory (but anterograde memory is worse)

115
Q

what is generally PRESERVED in transient global amnesia

A

preserved insight–> great concern over their disorientation

preserved attention and “immediate” memory

116
Q

how long does it usually take for transient global amnesia to recover

A

about 24 hours, with an island of memory loss for the ictus

117
Q

list risk factors for transient global amnesia

A

migraine

temporal love epilepsy

CV risk factors

valsalva maneuver

118
Q

do you ever see severe retrograde amnesia in the absence of anterograde amnesia in an “organic” amnesia

A

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
Q

what does the Trails Making test (Trails B) test assess

A

visuospatial and motor tracking

conceptualization

set shift

120
Q

what does the Wisconsin Card Sorting test look at

A

attention

working memory

visual processing

abstract thinking

set shifting

L>R hemisphere

121
Q

list some of the diseases that can affect the frontal lobes

A

TBI

frontal lobe seizures

vascular disease

tumours

MS

degenerative diseases (i.e Picks disease, Huntingtons)

Infectious disease

psychiatric illness

122
Q

which areas of the brain are more vulnerable in the closed head injury (and resultant stretching/shearing of fibers and resultant diffuse axonal injury)

A

orbitofrontal and temporal lobes

123
Q

what usually causes frontal lobe seizures

A

usually secondary to trauma

124
Q

what area of the brain is damaged in an ACA infarction

A

medial frontal area

125
Q

what area of the brain is damaged in MCA territory infarction

A

dorsolateral frontal lobe

126
Q

what might you see clinically if a patient has had an Anterior Communicating artery aneurysm rupture

A

personality change

emotional disturbance

confabulation–> combination of damage to forebrain and frontal damage

127
Q

what types of brain tumour might result in profound personality changes and dementia

A

subfrontal and olfactory groove meningiomas

128
Q

where in the brain has the second highest number of plaques int he brain of someone with MS

A

frontal lobes

can result in mood lability, memory problems, cognitive and behavioural affects

129
Q

what infectious diseases may result in frontal symptomrs

A

neurosyphillis

HSV encephalitis (frontal and temporal)

130
Q

what is the main excitatory neurotransmitter in the frontal lobe

A

glutamate

131
Q

what is the main inhibitory neurotransmitter in the frontal lobe

A

GABA

132
Q

what is the main neurotransmitter in the basal ganglia

A

serotonin–5HT1

133
Q

what do you use for decreasing the elevated sex drive that can be seen in frontal lobe syndromes

A

SSRI (HIGH DOSE)

134
Q

list some medications that can be used in management of frontal lobe syndromes

A

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
Q

why might you use antipsychotics in treating frontal lobe syndromes

A

behavioural control

136
Q

why might you use SSRIs in treating frontal lobe syndromes

A

agitation

high dose for decreasing sex drive

137
Q

what are the core features of LBD

A

fluctuating cognition, varying attention/alertness

recurrent visual hallucinations, well formed, detailed

spontaneous features of parkinsonism

**2 for probably, 1 for possible

138
Q

list 3 LBD indicative biomarkers

A
  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
Q

which areas of the brain are relatively preserved on MRI/CT in LBD

A

temporal lobes

140
Q

which cholinesterase inhibitor has the best evidence in PDD/LBD

A

rivastigmine

141
Q

what is the preferred parkinsons disease med to maintain mobility in patients with PDD/LBD

A

L-dopa

*avoid dopamine agonists, amantadine, selegiline

142
Q

which antipsychotic has the best results for PDD/LBD psychotic symptoms

A

clozapine

but QUETIAPINE is a “reasonable first choice”

abilify is uncertain

143
Q

what antipsychotics should be AVOIDED in PDD/LBD

A

risperidone
olanzapine
typical antipsychotics

144
Q

what is an antidepressant that can be used an as alternative for sleep/nonspecific agitation in PDD/LBD

A

trazodone

145
Q

what is the underlying pathology of Multiple System Atrophy

A

synucleinopathy like PDD/LBD

146
Q

what is the course of evolution of symptoms of Multiple System Atrophy

A

rapid–4-7 years

147
Q

what are the features of Multiple System Atrophy

A

autonomic failure with POSTURAL HYPOTENSION

ataxis and parkinsonian subtypes

cognitive impairment is MILDER

FRONTAL-CORTICAL

148
Q

what is the underlying pathology of progressive supranucleur palsy (PSP)

A

tauopathy

149
Q

what type of aphasia is associated with progressive supranucleur palsy

A

progressive NONfluent aphasia

150
Q

what is the pattern of cognitive changes seen in progressive supranucleur palsy

A

frontal subcortical

151
Q

what physical symptoms are characteristic of progressive supranucleur palsy

A

impaired vertical gaze doe voluntary saccades

swallowing difficulties

falls

axial rigidity

NO tremor

152
Q

what medication might be considered in progressive supranucleur palsy

A

small % respond to L-dopa

153
Q

what is the underlying pathophysiology of Corticobasal Degeneration

A

tauopathy

154
Q

what is the type of aphasia associated with Corticobasal Degeneration

A

progressive NONfluent aphasia

155
Q

what physical symptoms are associated with Corticobasal Degeneration

A

UNILATERAL rigidity

myoclonus

apraxia

“ALIEN LIMB”

speech apraxia

swallowing problems

156
Q

list some of the “parkinsons like dementias”

A

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

2. Geriatric Psychiatry + Neuroanatomy (14 decks)

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