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JMP Y2S1 > Week 40- Global Brain Dysfunction and Cognition > Flashcards

Week 40- Global Brain Dysfunction and Cognition Flashcards

1
Q

What is the roles of the medulla oblongata?

A

Control centre for most vital functions

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2
Q

What is the roles of the reticular-activating system (RAS)?

A

Network of nuclei and neurons throughout brain stem –> connected to many parts of the brain –> determines degree of arousal

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3
Q

What is the role of the cerebellum?

A

Coordination of movements

Posture and balance

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4
Q

What is the role of the thalamus?

A

Relay station for sensory impulses

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5
Q

What is the role of the hypothalamus?

A

Homeostasis
Autonomic nervous system and lots of the endocrine system
Body temp, fluid, food, sleep cycles, stress,

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6
Q

Where is the Basal ganglia located?

A

Deep in the hemispheres

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7
Q

What does the basal ganglia control?

A

Coordination and control of skeletal muscle

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8
Q

What is the limbic system involved in?

A

Aversion/reward

Emotions and memory

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9
Q

What structure is involved in Parkinson’s disease?

A

Basal ganglia

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10
Q

What area is involved in fear and anxiety?

A

Amygdala

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11
Q

What neurons are important for reward/pleasure?

A

Dopaminergic neurons

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12
Q

Where do dopaminergic neurons act for the reward centre?

A

N Accumbens

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13
Q

Where is the source of Dopaminergic neurons?

A

VTA (ventral tegmental area) –> in the midbrain

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14
Q

What increases increased release of dopaminergic neurons in the N.Acc?

A

5-HT

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15
Q

What releases 5-HT?

A

Raphe neurons in the midbrain

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16
Q

What is aphasia?

A

Inability to comprehend or express language

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17
Q

What is expressive aphasia?

A

Inability to speak or write –> damage to Broca’s area –> motor aphasia

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18
Q

What is Receptive aphasia?

A

Inability to understand written or spoken words –> damage to wernicke’s area –> sensory aphasia

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19
Q

What is Dysarthria?

A

Inability to clearly articulate words –> motor dysfunction affecting muscles used in speech

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20
Q

What are the two branches of memory?

A 
Short term (including working memory)
Long term
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21
Q

What are the two branches of long term memory?

A

Explicit (conscious)

Implicit (unconscious)

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22
Q

What is the two branches of Explicit long term memory

A

Episodic (events that happen to a person)

Semantic (general knowledge of the world)

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23
Q

What are the two branches of Implicit long term memory?

A

Priming (Stimulus A affects stimulus B)

Procedural (motor)

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24
Q

What is the entire bases of memory?

A

Synaptic plasticity

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25
Q

What does synaptic strength determine?

A

The affect on the post synaptic side and the generation of an action potential/affect there

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26
Q

How do synapses increase their synaptic strength?

A

More neurotransmitters released
Larger number of post-synaptic receptors
New formation of synapses

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27
Q

What is the importance of the temporal lobe in memory?

A

Partial retrograde and extreme anterograde amnesia for long term factual “declarative” memories

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28
Q

What is Retrograde amnesia?

A

When there is memory loss before the event/trauma

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29
Q

What is Anterograde amnesia?

A

Memory loss after event/trauma

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30
Q

What is the importance of sleep in memory consolidation?

A

Neuronal replay

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31
Q

What is the hippocampus required for in memory?

A

Forming long term memories –> especially declarative

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32
Q

What is the amygdala required for in memory?

A

Emotionally-coloured memories –> emotional charged memories are better preserved

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33
Q

Where are memories stored after they are formed?

A

Mainly in the association cortex

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34
Q

Why is it unlikely that memories are stored in particular discrete places?

A

Because like for thoughts they may be a result of activity of interactive neuronal networks

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35
Q

How does damage spread during Alzheimer’s disease?

A

Starts in the Temporal and prefrontal cortex –> continues along the base structures as well as the parietal lobes –> eventually spreads to all areas outer from the corpus callosum

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36
Q

What happens to the size and weight as people age?

A

Reduction in size and weight.
Narrower gyri
Wider sulci
Enlarged subarachnoid space

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37
Q

Do the number of neurons change as we age?

A

Yes –> they decrease

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38
Q

How does cerebral blood flow change with ageing?

A

Decreases

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39
Q

What are the anatomical changes of the brain with age linked to?

A

Less efficient neural processing

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40
Q

What is Dementia?

A

Cognitive impairment that interferes with the ability to function at work or at usual activities

  • -> decreases of prior levels of functioning
  • -> cognitive impairment not explained by delirium or major psychologic disorder
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41
Q

How is dementia diagnosed?

A

Combination of history taking from patient and a knowledgeable informant
Objective cognitive assessment

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42
Q

What is the prevalence of Dementia at >65 years?

A

Approx. 7%

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43
Q

What ranked killer is Alzheimer’s for women in Australia?

A

2nd

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44
Q

What can cause dementia?

A

Many diseases

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45
Q

How is Alzheimer’s disease characterised and what percentage of dementias does it account for?

A

Degenerative cerebral disease –> slow decline of cognition and function

  • -> Driven by protein abnormalities (Plaques and NFT)
  • -> Accounts for 60% of dementias
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46
Q

What is Parkinson’s disease and how many sufferers develop dementia?

A

Chronic neurodegenerative movement disorder

  • -> Characterised by protein abnormalities (alpha- synuclein structures)
  • -> Approx. 30% of patients will develop dementia
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47
Q

What is the second most common form of dementia after Alzheimer’s?

A

Vascular dementia –> problems of brain blood circulation

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48
Q

What does Dementia with Lewy bodies share similarities with?

A

Alzheimer’s and Parkinson’s disease

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49
Q

What are other diseases accounting for less than 5% of dementias?

A

Other degenerative diseases –> e.g. Huntington’s

Prion diseases –> e.g. Creutzfeldt-Jakob disease

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50
Q

What is the usual age onset of Alzheimer’s disease?

A

> 65 (95% of all cases)

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51
Q

What are the areas first affected in Alzheimer’s disease?

A

Entorhinal cortex

Hippocampus

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52
Q

What happens to cause Mild to moderate AD?

A

Cerebral cortex begins to shrink as more neurons stop functioning and die.

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53
Q

What happens in severe AD and what affects does this have on patients?

A

Extreme shrinkage occurs in the brain

Patients will be completely dependant on others for care

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54
Q

What impairments happen during Alzheimer’s disease?

A

Global cognitive impairment –> language, memory, visuospatial skills and personality changes

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55
Q

What do post-mortem tissue slicing immunohistochemistry show for AD?

A 
Neurofibrillary tangles (p-tau)
Senile/neuritic plaques (amyloid-beta)
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56
Q

Is the pattern of Alzheimer’s predictable?

A

Yes

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57
Q

How long does mild to moderate Alzheimer’s usually last?

A

2-10 years

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58
Q

How long can severe Alzheimer’s disease last?

A

1-5 years

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59
Q

What causes vascular dementia?

A

Problems in the blood supply to the brain

–> series of mini strokes leading to cognitive decline

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60
Q

How common is vascular dementia?

A

2nd most common after Alzheimer’s disease

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61
Q

What is commonly said about the progression of vascular dementia?

A

Step-wise –> as affects occur from distinct cerebrovascular events (huge drop and plateau)

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62
Q

What are the two kinds of vascular dementia?

A
  1. Multi-infarct dementia –> cortical strokes damaging regions of language, learning and memory
  2. Binswanger’s disease –> stroke related change to the white matter, hypertension and thickening of arteries
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63
Q

What is Parkinson’s disease clinically characterised by?

A

Motor symptoms –> rigidity, tremor, gait
Non motor symptoms –> mood disturbances, dementia
Difficulty starting voluntary movements –> opposing muscle groups do not relax

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64
Q

What is the potential pathology of Parkinson’s disease?

A

Alpha-synuclein aggregates form Lewy bodies in neuronal bodies and fibrils –> deposited in dopamine producing neurons

Excitatory neurons become more active

Substantia nigra (dopamine neurons that innervate the striatum) damage can give appearance of Parkinson’s disease

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65
Q

What co-occurs commonly with dementia with Lewy bodies?

A

Dementia –> with hallucinations and parkinsonism

Beginning with Parkinson’s disease and progressing to parkinsonian-dementia syndrome

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66
Q

What is Frontotemporal lobular dementia (FTLD)?

A

Progressive atrophy of frontal or temporal lobes of the brain

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67
Q

What are the 2 subtypes of Frontotemporal lobular dementia?

A

Behavioural variant–> (most common), loss of empathy, loss of inhibitions, difficulty reasoning, decline in self care

Progressive non-fluent aphasia –> ability to speak fluently is gradually lost, difficulty reading and spelling

Semantic dementia –> fluent but loss of meaning of words

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68
Q

What are the 3 types of protein inclusions identified in neurons and glial cells in FTLD?

A

Tau
TDP-43
Fused in sarcoma protein (FUS)

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69
Q

What are Tauopathies?

A

A group (over 20) of neurodegenerative diseases marked by a common feature of p-tau aggregates –> associated with synapse and neuronal loss

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70
Q

What causes Creutzfeldt Jakob Disease?

A

Prion disease

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71
Q

What are some symptoms of CJD?

A

Memory loss
Personality change
Hallucinations
Speech impairment

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72
Q

What is the average life expectancy of CJD?

A

1 year

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73
Q

What are the types of CJD?

A

Sporadic –> spontaneous misfolding (85% of all cases)
Familial –> 15% of all cases
Acquired –> 1% of cases from contaminated food

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74
Q

What changes happen in the brain from CJD?

A

Spongiform changes, neuronal loss, amyloid plaque in grey matter
Accumulation of PrP

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75
Q

What are tau?

A

Tau are proteins that help stabilise axonal microtubules

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76
Q

What causes tau protein related issues in Alzheimer’s disease?

A

Tau is regulated via phosphorylation
Hyperphosphorylation –> causes self assembly of tangles (neurofibrillary tangles)
These tangles have been found in affected areas in Alzheimer’s disease

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77
Q

What is Amyloid beta (A-beta)?

A

36-43 amino acid peptide –> derived from amyloid precursor protein (AAP)

78
Q

Where can misfolded aggregates of amyloid beta be found?

A

Frontal, temporal lobes, hippocampus, limbic system

79
Q

What are misfolded aggregates of amyloid beta a main component in?

A

Senile/neuritic plaques

80
Q

The presence of what is required for neuropathologic diagnosis of Alzheimer’s disease?

A

High density of neurofibrillary tangles (NFTs) and senile plaques

81
Q

What are the main component in Lewy bodies?

A

Alpha-synuclein

82
Q

What is TDP-43?

A

Transcriptional repressor –> regulates pre-mRNA splicing and translation

83
Q

What happens to TDP-43 in FTLD?

A

Becomes hyperphosphorylated, cleaved and ubiquinated into a pathologic form and forms aggregates

84
Q

Where are FUS aggregates found?

A

In cytoplasmic inclusions in brains of a subset of FTLD patients

85
Q

What is mixed dementia?

A

More than one type of dementia happening simultaneously

86
Q

What are some common presentations of mixed dementias?

A

Plaques and NFT associated with Alzheimer’s present alongside vessel changes associated with vascular dementia
Plaques and NFT co-exist with Lewy bodies
Plaques, NFT, Lewy bodies and Vascular changes all at once

87
Q

How common are mixed dementia?

A

Pretty common especially in the elderly over 80

88
Q

What are some mechanisms for neurodegeneration?

A

Protein aggregation
Synapse loss
Mitochondrial dysfunction
Excitotoxicity

89
Q

What proteins have been identified to aggregate and cause neurodegeneration?

A 
Amyloid
Tau
alpha-synuclein 
TPD-43
Prion
90
Q

How does the toxic oligomer hypothesis work?

A

Single domain antibody –> recognises common epitope displayed by disease associated proteins
Oligomeric and pre-aggregated forms of these proteins are toxic in vitro

91
Q

How does prion disease cause damage?

A

Can directly damage tissue architecture

92
Q

What happens when there is a accumulation of misfolded protein?

A

Lead to endoplasmic reticulum stress –> prolonged stress activates cell death mechanisms

93
Q

What type of synapses have the strongest correlation for cognitive impairments in AD?

A

Excitatory synapses

94
Q

What do synaptic deficits in Huntington’s disease associate with?

A

Progressive deterioration of psychiatric, motor and cognitive abilities

95
Q

In prion diseases what does synapse loss account for?

A

Development of behavioural symptoms

96
Q

What is one of the main targets of alpha-synuclein accumulation?

A

Mitochondria –> impairs their function –> results in oxidative stress

97
Q

What are one of the early events in AD?

A

Mitochondrial abnormalities

98
Q

What is excitotoxicity?

A

Pathalogical process where nerve cells are damaged or killed by excessive stimulation by glutamate and other molecules

99
Q

What receptors does glutamate activate?

A

Exitatory receptors –> such as NMDA and AMPA

100
Q

What does Excitatory receptor activation do?

A

Ca2+ influx

101
Q

What does Ca2+ influx do in a neuron to cause death?

A

Excites it –> but activates a number of enzymes and can trigger cascades that lead to cell death

102
Q

What molecule accumulates in Parkinson’s disease?

A

Alpha-synuclein

103
Q

What does accumulation of alpha synuclein lead to?

A

Loss of dopamine neuronal cells

104
Q

What are the mechanisms by which alpha synuclein can cause neuronal death?

A

Impaired mitochondrial activity
Excitotoxic events
Active inflammatory processes –> secretion of potentially toxic cytokines

105
Q

In Parkinson’s disease where are dopamine neurons lost?

A

Substantia nigra

106
Q

What are alpha synuclein aggregates also known as?

A

Lewy bodies

107
Q

What is the inheritance pattern of Dementia?

A

Familial –> 15-25% of cases
Autosomal dominant –> <5% of cases
Sporadic –> 75% of cases

108
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal dominant

109
Q

What is the inheritance pattern of Parkinson’s disease?

A

Autosomal dominant

Autosomal recessive

110
Q

What are the four major dementia subtypes?

A

Alzheimer’s disease (34-54%)
Vascular dementia (18-32%)
Frontotemporal lobar degeneration (10-20%)
Lewy body dementia (4-7%)

111
Q

How common is family history of dementia and how much does it increase lifetime risk of dementia?

A

25% of people over 55 have a family history of dementia

Boosts risk from 10% to approx. 20%

112
Q

What does it mean if a disease in mendelian?

A

Mutation in one gene is necessary and sufficient to cause disease

113
Q

What does it mean if a disease in complex?

A

Normal variation in several genes have to interact to increase disease risk

114
Q

What are some mendelian genes that have been shown to cause AD?

A

APP –> missense, duplications, deletions
PSEN1 –> missense, deletions, insertions
PSEN2 –> missense

115
Q

What kind of inheritance pattern is a PSEN1 mutation?

A

Autosomal dominant

116
Q

What clinical presentation can be expected with someone with PSEN1 mutation?

A

Early onset Cognitive impairment and neurological symptoms at around 30 years of age.
All subjects died 6-8 years after disease onset

117
Q

What do PSEN1 mutations result in within the subsequent protein?

A

Disrupts the tertiary structure of the third transmembrane domain (TM3)

118
Q

How have risk genes been identified for late onset AD?

A

Genome wide association studies (GWAS)

119
Q

What are the categories in the risk spectrum for AD?

A

Mendelian
Genetic risk factors
Non-genetic risk factors –> eg education and trauma events

120
Q

What kind of disorder is Huntington’s disease?

A

It is a tandem repeat disorder

121
Q

What are tandem repeats?

A

Pattern of on or more nucleotides which are repeated directly next to eachother

122
Q

What is the repeat in Huntington’s disease?

A

CAG repeat in the coding region of the HTT gene

123
Q

What does the mutant protein in Huntington’s disease do?

A

Causes the formation of polyglutamine tracts within the protein

Alters:
Neurotransmitter release
Mitochondrial function
Transcriptional activity

124
Q

How do proteins with polyglutamine tracts interact?

A

They aggregate and accumulate in cells and interfere with normal cellular function

125
Q

What does it mean that HTT mutation is autosomal dominant for Huntington’s disease?

A

Only one copy of the abnormal number of CAG repeats is required for disease phenotype

126
Q

How does an increase in CAG repeats in HTT gene affect the disease progression?

A

More severe –> also has earlier onset

127
Q

What is the normal repeat number of CAG in HTT?

A

28 or less

128
Q

What is classified as pre-mutation for HTT?

A

29-34 –> normal but next generation at risk

35-39 –> some will develop HD some wont –> next generation at risk

129
Q

What is characteristic of a pre-mutation allele?

A

It is unstable –> can undergo expansion during gametogenesis –> can develop into full mutation 40+ copy number
–> people with pre-mutation can pass full mutation onto offspring

130
Q

Why does repeat expansion happen?

A

Due to slippage during DNA replication

DNA polymerase can accidentally copy the repeat region more than once –> increasing repeat number

131
Q

How does onset of Huntington’s change across generations?

A

Tend to be earlier

132
Q

What is the earlier onset of Huntington’s across generations due to?

A

Anticipation –> from expansion

133
Q

When is expansion more likely and who is subsequently more at risk?

A

More likely in spermatogenesis –> children of affected males more at risk

134
Q

How can risk of diseases such as Huntington’s be predicted?

A

Genetic testing

135
Q

What is Parkinson’s disease characterised by?

A

Deficiency of dopamine

136
Q

What kind of disease genetically is Parkinson’s?

A

Complex, heterogenous disease

137
Q

What are the two main genetic forms of Parkinson’s?

A

Monogenic –> caused by mutations in single genes

Multifactorial –> interaction of multiple genes and/or environmental factors

138
Q

What are some of the considerations when doing genetic population screening?

A

Consent –> should parents be allowed to decline child testing?

Informed consent –> amount of information needed

Harm vs benefit of the test

Anxiety of parents in
response to results at vulnerable stage

Fear of information misuse for insurance etc

Is targeted screening racial or ethnic profiling?

139
Q

What is population screening?

A

Tests apparently healthy populations to identify unrecognised disease

140
Q

What groups do population screens include?

A

Newborn screening

Targeted group screening

141
Q

What does carrier testing achieve?

A

Identifies people who are not affected by the disease but risk having children with the disease eg. Cystic fibrosis, sickle-cell anaemia etc

142
Q

What are the issues of carrier testing?

A
  • Few options for people identified as carriers in terms of childbearing:
    Donor egg or sperm
    Preimplantation testing
  • Obligation to offer education and counselling
143
Q

What are the two types of predictive testing?

A

Presymptomatic testing

Susceptibility testing

144
Q

What does Presymptomatic testing look for?

A

Genetic mutations that have high penetrance –> usually autosomal dominant
Identify the individuals who are likely to have devastating disease in the future
Eg Huntington’s and Early onset AD

145
Q

What does Susceptibility testing look for?

A

Genetic mutations that increase risk for a disease
Usually multifactorial disease
E.g. BRCA1 and BRCA2 mutations

146
Q

What are the ethical considerations of identifying disease risk?

A

Results provide false hope or false belief
Should children be tested?
Interpretation can be difficult especially in susceptibility testing –> does it give useful information?
Need for education, counselling and support on results basis

147
Q

What does prenatal testing involve?

A

Testing a foetus prior to birth

148
Q

What are two methods of prenatal testing?

A

Amniocentesis –> foetal cells gathered from amniotic fluid

Chorionic Villi sampling –> suction tube used to remove foetal cells prom chorion (where placenta will develop)

149
Q

What are some considerations when it comes to prenatal testing?

A

Respect for couples beliefs and values
Potential harm and risk of miscarriage
Potential for pressure on couples not having children that deviate from ‘normal’
Possible termination from ambiguous information

150
Q

What does pre-implantation diagnosis involve?

A

Detect genetic abnormalities in embryos created using assisted reproductive techniques such as IVF before being implanted into the uterus

151
Q

What are the pre-implantation testing considerations?

A

Are embryos by IVF ‘life’?
What is the extent of selection (gender etc)
No guarantee that embryos will develop normally (is it false hope?)

152
Q

What type of analysis is involved in Forensic testing?

A

VNTR/STR analysis –> enables a ‘fingerprint’ over enough loci –> highly accurate

153
Q

What are the considerations of forensic testing?

A

Storage and use of samples
Need for consent
Confidentiality
Support needed in light of results

154
Q

What is some other ‘bonus’ ethical considerations of genetic testing?

A

Lack of population knowledge/education understanding of genetic testing
only 26% of people know what DNA is
Physicians lack adequate knowledge

155
Q

How does the clinical presentation differ in dementia compared to delirium?

A

Dementia –> anatomical changes in brain –> slower onset –> irreversible
Delirium –> acute illness or drug toxicity –> acute onset –> reversible

156
Q

What is Dementia?

A

Encompasses many disease pathologies –> decline in memory, language, problem-solving

157
Q

What is Alzheimer’s disease caused by?

A

Tau protein aggregates (NFTs)

Alpha-synuclein aggregates

158
Q

What is vascular dementia caused by?

A

Vascular causes –> stepwise progression –> mini-strokes –> plateaus of brain damage

159
Q

What is Frontotemporal Dementia caused by?

A

Protein aggregates:
Tau
TDP-43
Fused in sarcoma protein (FUS)

160
Q

What is Dementia with Lewy bodies caused by?

A

Alpha-synuclein aggregates (Lewy bodies)

161
Q

How is Dementia investigated?

A

Reversible causes ruled out –> e.g. delirium
MMSE –> mini-mental state examination
Cognitive testing
Blood tests –> infection, anaemia etc
Brain scans (CT MRI)–> show atrophy or other causes e.g. tumour, stroke areas, hydrocephalus etc

162
Q

How common is dementia in Australia and who is affected?

A

Second leading cause of death of Australians
2/3 of dementia in women
Mainly affects people over 65

163
Q

What are the impacts of dementia diagnosis?

A

Incurable
Degenerative
Loss of independence
Family genetic implications

164
Q

What are the common causes of delirium?

A 
Medications/drugs
Alcohol
Withdrawal
Metabolic changes --> low sodium, low calcium, low glucose
Severe chronic illness
Fever/acute infection (particularly in children)
UTI, pneumonia and flu 
Dehydration
Pain
Anaesthesia
165
Q

Where is the primary motor cortex located?

A

Pre-central Gyrus (posterior to the central sulcus)

166
Q

How does the brain generate movement when conscious?

A

Primary motor cortex –> motor map (homunculus map) –> signals cross the midline to innervate muscles on the opposite side

167
Q

How does the brain inhibit movement when asleep?

A

Brain stem signals –> relax muscles essential for posture and limb movement –> inhibits movement while asleep

168
Q

What is the role of basal ganglia in movement?

A

Initiation and execution of movements

Facilitate desired movement while inhibiting unwanted/competing movement

169
Q

What is declarative memory?

A

Type of long term memory –> involves recall of facts and events

170
Q

What is skill memory?

A

Procedural memory –> how to ride a bike etc

171
Q

What is working memory?

A

Part of short-term memory –> immediate conscious perceptual and linguistic processing

172
Q

What is short term memory?

A

Information held in an active readily available state for a short period of time

173
Q

What is immediate long-term memory?

A

Type of memory of recalled recently presented information like a street address –> may be forgotten immediately after use

174
Q

What is long term memory?

A

Memory type for extended storage

175
Q

What score is the Glasgow coma score out of?

A

15

176
Q

What are the three sections of the coma score?

A

Eye-opening
Best motor response
Verbal response

177
Q

What are the aspects of consciousness?

A

Vigilance –> readiness to respond
Selective Attention –> choosing the response target
Conscious access –> the ‘user privileges’ of the brain

178
Q

What does vigilance vary with?

A

Wakefulness

179
Q

What is the main system involved in Vigilance?

A

Reticular activating system –> in the brain stem –> processes to the cortex to ‘wake it up’.

180
Q

What does selective attention generally refer to?

A

Emotional valence –> contrast, amplitude, salience, novelty
Usually determined unconsciously
–> determines what attracts your attention

181
Q

What brain structure is important for selective attention?

A

Amygdala –> filter incoming messages

182
Q

Is selective attention always unconsciously attended?

A

No it can be consciously done in tasks such as finding keys etc –> amplifying relevant information and inhibits the remainder

183
Q

What does conscious access generally refer to?

A

Parts of the brain a person has access –> eg controlling eye movements –> not things like heart rate

184
Q

What are some classifications of disorders of consciousness?

A

Brainstem injury –> brainstem stroke, Trauma
Widespread injury to sub-cortical white matter –> trauma, demyelination, infection
Widespread cortical injury –> encephalitis, hypertensive encephalopathy, hypoxic encephalopathy, trauma

185
Q

What are some outcomes of coma?

A
  1. Recovery
  2. Locked-in syndrome –> conscious access but no communication ability (can sometimes use eye blinks)
  3. Brain death
  4. Vegetative state:
    - Branch 1 –> persistent –> death
    - Branch 2 –> minimally conscious state –> confusional state –> increased independence
186
Q

What is episodic memory?

A

What where we doing and when were we doing it?

187
Q

What is semantic memory?

A

The factual stuff in the world

188
Q

What is procedural memory?

A

Riding a bike, laces,

189
Q

What is prospective memory?

A

Memory that is most liable to disruption –> remembering to do something in the future

190
Q

What is needed to consolidate long-term memory?

A

Sleep! –> neuronal replay in hippocampus

191
Q

What is the Mini-mental state examination?

A

A score out of 30 –> similar to Glasgow coma score –> can be used for determining chance of dementia.

192
Q

What is the 2 purposes that Glasgow coma score used for?

A
  1. Rapid assessment of head injury severity

Monitoring of head injury patient by non-expert observers

JMP Y2S1 (24 decks)

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