Brain Mechanisms of Memory Flashcards

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1
Q

How can your memory be better than a computer’s?

A

Much more flexible aand works in special ways which help you remember useful information.

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2
Q

Why is memory important? (6)

A
  • Learning from experience shapes thought and behaviour in an adaptive way
  • Attention is driven by memory
  • Memory underpins conscious and unconscious decisions
  • Culture and society
  • Central to personal identity
  • Language
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3
Q

Who is Clive Wearing?

A
  • Conductor and musicologist who developed dense amnesia

- Using his STM, he can retain about 20 seconds

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4
Q

What parts of Clive Wearing’s memory were in tact?

A
  • He can still read and learn to play new pieces of music
  • He can still remember his wife as he met her before the brain injury
  • Not all LTM is damaged
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5
Q

What happened to Henry Molaison (HM)?

A
  • Performed bilateral medial temporal lobectomy to remove both his hippocampi
  • Epilepsy cured but unexpected consequences for memory
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6
Q

Where is the hippocampus?

A

Embedded deep inside the temporal lobes

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7
Q

What parts of HM’s brain were removed?

A

Virtually all anterior hippocampus and surrounding cortex removed, plus amygdala.
Some posterior hippocampus remains

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8
Q

What is anterograde amnesia?

A

condition in which a person is unable to create new memories after an amnesia-inducing event

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9
Q

What is retrograde amnesia?

A

amnesia where you can’t recall memories that were formed before the event that caused the amnesia

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10
Q

What is temporal gradient?

A

a pattern of retrograde amnesia characterized by greater loss of memory for events from the recent past (i.e., close to the onset of the amnesia) than for events from the remote past.

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11
Q

What memory loss did HM show?

A
  • Unable to learn new things

- Temporal Gradient

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12
Q

What does HM show via the temporal gradient?

A

That the hippocampus is crucial for new learning but not for storing older memories.

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13
Q

What type of amnesia usually shows a temporal gradient?

A

Retrograde amnesia

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14
Q

What other causes are there of amnesia other than surgical lesions?

A
  • Anoxia
  • Head injury
  • Herpes simplex encephalitis
  • Korsakoff’s syndrome
  • Alzheimer’s disease
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15
Q

Why can Anoxia cause amnesia?

A

Hippocampal neurones have a high metabolic rate and so require lots of oxygen.

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16
Q

How does information get from the hippocampus to the cortex?

A

The major outputs from the hippocampus go to the fornix.
The mammillary bodies are a gateway from the fornix to the thalamus.
The thalamus feeds back to the cortex.

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17
Q

What types of memory are conscious and what parts are unconscious?

A

Episodic and Semantic = Conscious memory

Procedural = Unconscious

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18
Q

How does Herpes Simplex Encephalitis cause amnesia?

A

Herpes simplex virus spreads from face along cranial or olfactory nerves to the brain.

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19
Q

How is verbal learning impaired in amnesia?

A
  • Paired-associate learning is tested

Patients with dense amnesia like HM and Ep do not remember studying any words and so cannot attempt this task

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20
Q

How is visual learning impaired in amnesia?

A
  • Rey Figure Copy task
  • If they are asked to recall the picture again after 15 minutes, they don’t have the ability to recall it with any level of detail at all.
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21
Q

How is STM preserved in amnesia?

A
  • Normal ability to hold on to info actively for a few seconds
  • Patients are only impaired when asked to retain the information for later.
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22
Q

How is Semantic Information preserved in amnsesia?

A
  • Normal retention of factual knowledge

- Normal performance on tests such as providing definitions, naming pictures, understanding sentences

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23
Q

Explain preserved implicit memory in terms of classical conditioning.

A

Claparede 1911 shook hands with a patient while he pricked her and the patient later refused to shake his hand despite no recollection with the doctor.

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24
Q

Explain preserved implicit memory in terms of motor learning.

A

Brenda Milner did a mirror drawing task with HM to test his procedural memory.
- HM gets extremely good at the task each time he does it despite having no recollection of having done it before

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25
Q

Explain preserved implicit memory in terms of priming.

A
  • Patients studied a word, then were presented with the begging of the word and asked to finish it.
  • Patients did the same, if not better than the controls
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26
Q

What type of memory seems to be impaired in hippocampal damage?

A
  • Episodic
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27
Q

What evidence is there for preserved implicit memory in amnesia?

A
  • Classical Conditioning
  • Motor learning
  • Priming studies
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28
Q

What does the study of amnesia show us about the hippocampus?

A

Hippocampus is crucial for the conscious retrieval of an experience.

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29
Q

What does a slice through the hippocampus look like?

A

Onion rings

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30
Q

What does hippocampus mean?

A

Seahorse

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31
Q

What structures are within the hippocampus?

A
  • Dentate gyrus
  • Subiculum
  • CA1
  • CA3
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32
Q

What is the role of the dentate gyrus?

A
  • Major input structure of the hippocampus

- Projects to the CA3 field

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33
Q

Where in the hippocampus is the dentate gyrus located?

A

Towards the middle

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34
Q

How are the CA3 and CA1 fields related?

A

They have very dense connections between them

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35
Q

What role are the CA1 and CA3 fields thought to play?

A

The synapses between CA1 and CA3 are supposed to play a critical role in long term memory

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36
Q

Where does CA1 project information to?

A

The subiculum

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37
Q

What is the role of the subiculum?

A

Major output structure of the hippocampus projecting to lots of other parts of the brain

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38
Q

Where is the entorhinal cortex?

A
  • Adjacent to the hippocampus

- Gateway between hippocampus and cortex

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39
Q

Where is the entorhinal cortex?

A
  • Adjacent to the hippocampus

- Gateway between hippocampus and cortex

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40
Q

What types of cortex supply the entorhinal cortex?

A
  • Perirhinal cortex

- Parahippocampal cortex

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41
Q

What is the role of the perirhinal cortex?

A

Important for object recognition

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42
Q

What is the role of the parahippocampal cortex?

A

Spatial layout coding

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43
Q

What are polymodal association areas?

A

Represent information across lots of different modalities of info

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44
Q

What are unimodel association areas?

A

Processing of sensory inputs or motor functions, so they represent only one modality of info

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45
Q

Where does the posterior of the hippocampus receive most of its input?

A

From parahippocampal cortex: spatial memory

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46
Q

Where does the anterior of the hippocampus receive most of its input from?

A
  • Amygdala and perirhinal cortex: emotional memories and familiarity/salience
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47
Q

Why is the hippocampus ideal for associative learning?

A

It contains multiple nested feedback loops

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48
Q

What is long-term potentiation?

A

there are physical changes at the synapse that make it more likely after you formed a memory that all the other parts of the memory will be associated with one part of it

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49
Q

What are cell assemblies?

A

Memories are stored in connections between neurons

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50
Q

What is the idea that ‘cells that fire together, wire together’

A

The idea that when two cells fire at the same time, a stronger connection is formed between them

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51
Q

Is glutamate excitatory or inhibitory?

A

Excitatory

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52
Q

What happens during long-term potentiation?

A
  • Release of some glutamate by pre-synaptic neuron, Na+ channels open briefly
  • Release of lots of glutamate, ion channels in post-synaptic cells open for longer, large influx of Na+ ions
  • This strengthens communication at this particular synapse
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53
Q

What evidence is there for LTP?

A
  • LTP in rabbit hippocampus
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54
Q

What is EPSP?

A

Excitatory postsynaptic potential

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55
Q

What are the two types of glutamate receptors?

A

AMPA

NMDA

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56
Q

When do NMDA receptors open?

A

When the neuron depolarises, then lets calcium in as well as sodium

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57
Q

What is the role of AMPA receptors?

A

Do the legwork in terms of opening channels in response to glutamate.

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58
Q

What happens if you get a big depolarisation event in the postsynaptic neurone during long-term potentiation?

A
  • The NMDA receptors open as well as the AMPA channel
  • This is because on the left-hand side the NMDA receptor is blocked with magnesium but if enough sodium enters the presynaptic neurone, the Mg will get pushed out of the way by electrostatic repulsion.
59
Q

What is synaptic consolidation?

A

a process that enables synapses to retain their strength for a much longer time (days to years), instead of returning to their original value

60
Q

What effects do calcium ions drive?

A
  • Increases in receptor density
  • Increases in neurotransmitter release
  • Enlargement of synapse
  • Division of synapse
  • Formation of new dendritic spines
61
Q

How does the post-synaptic neuron allow a stronger connection with the pre-synaptic neuron during LTP? (Synaptic Consolidation)

A
  • more physical changes start to happen
  • start to get the formation of a cleft
  • allows more surface area for the post-synaptic neuron to receive inputs
  • form new dendrites
62
Q

What anaesthetic used as a recreational drug is an NMDA receptor antagonist?

A

Ketamine

63
Q

How is memory for a single event possible?

A

LTP can be induced by a single high frequency train

64
Q

How are all elements of an experience captured?

A

Associativity

Synapses that are only weakly active at the same time as synapses that are very active, are also strengthened

65
Q

What is the Morris water maze?

A

Put milk powder in water to make it cloudy

There’s a platform under the surface and when the animal finds it, they can stop swimming and then get a food reward

66
Q

What have hippocampal lesions in rats shown us?

A
  • Role of hippocampus in memory tasks
  • Posterior hippocampus is more important for spatial memory
  • Do not show the contribution of specific processes like LTP
67
Q

What have pharmacological studies shown us about the hippocampus?

A

Bathed hippocampus of rats in NMDA receptor antagonist (blocks glutamate binding site)

68
Q

What are transgenic mice?

A

Gene-editing technology where you can splice away particular bits of DNA or replace one bit of DNA with another

69
Q

Where are place cells located?

A

in CA1

70
Q

What is the idea of a cognitive map?

A
  • Hippocampus provides an internal map that codes for spatial relations between objects in the environment
71
Q

What spatial deficits are seen in amnesia?

A
  • In tasks that don’t appear to have a spatial dimension e.g. word lists
  • Yet all episodic memories are encoded and recalled in a spatial location
  • mental time-travel involved reconstructing environment, spatial location is a profound cue to recall
72
Q

What did Eichenbaum & Cohen find about relational memory?

A

Rats with hippocampal lesions can remember individual associations but cannot infer relations

73
Q

What does recollection involve?

A

Relations between items and contexts

74
Q

What are Tulving’s elements of Episodic memory?

A
  • Events
  • Mental time-travel
  • Self-referential
  • Fragile, easily forgotten
  • Affected in amnesia
  • Better when young
75
Q

What are Tulving’s elements of semantic memory?

A
  • Facts
  • Time/place NOT coded
  • NOT self-referential
  • More durable/consolidated
  • Not affected in amnesia
  • Better when old
76
Q

How was episodic and semantic memory affected in Patient KC?

A
  • Inability to remember recent and new events
  • Very pronounced retrograde amnesia
  • Retained some semantic concepts gained as a machinist
77
Q

What is a single dissociation?

A
  • Clear impairment in one type of memory but the other is intact
78
Q

What is a double dissociation?

A

damage to one area of the brain causes a function A to be absent while function B is present, and damage to another area causes function B to be absent while function A is present

79
Q

Why is a single dissociation viewed as insufficient to demonstrate separate systems?

A

Episodic memory might be more vulnerable to damage than semantic memory within a single system

80
Q

What is the key deficit in semantic dementia?

A

Poor understanding of objects and words

81
Q

What is semantic dementia?

A
  • Subtype of frontotemporal dementia (FTD)

- Progressive loss of conceptual knowledge across modalities

82
Q

What double dissociation is there with amnesia and semantic dementia?

A

Amnesia: Episodic impaired, Semantic preserved

Semantic Dementia: Semantic impaired, Episodic preserved

83
Q

Why are the hippocampus and neocortex complimentary?

A

Fast learning in hippocampus

Slower learning in the neocortex

84
Q

Why is learning fast in the hippocampus?

A
  • Quickly bind together the elements of episodes

- Few neurons code for each item, so similar memories can be separated

85
Q

Why is learning slower in the neocortex?

A
  • Similar features shared by multiple experiences are encoded strongly
  • Useful for semantic category learning
  • Prevents catastrophic interference (loss of old memories when new material is learned)
86
Q

How do Tulving and Squire’s ideas differ?

A

Tulving: Episodic vs Semantic
Squire: Episodic THEN Semantic

87
Q

What did Kim and Fanselow 1992 find about damage to the hippocampus?

A

When the hippocampus si damaged AFTER learning has occurred, memories are especially vulnerable if they were only recently acquired. Older memories are more preserved.

88
Q

What is reverse temporal gradient in Semantic Dementia?

A

SD patients are almost normal at recalling recent events but impaired at early memories - they show reversal temporal gradients

89
Q

What brain structures are older memories reliant on?

A

More reliant on the neocortex and less dependent on the hippocampus over time, following consolidation

90
Q

How does impaired encoding affect amnesiacs?

A

Poor learning of new events

91
Q

How does impaired retrieval before consolidation affect amnesia patients?

A

Poor retrieval of events just prior to brain injury

92
Q

How is retrieval after consolidation affected in amnesiacs?

A

Not impaired - normal retrieval of events from childhood

93
Q

Why is it necessary to have dense connectivity between the neocortex and the hippocampus?

A

Because the hippocampus allows you to reinstate those cortical representations that your memory depends on.

94
Q

How do connections between the neocortex and hippocampus develop over time?

A

You start to form direct connections within the cortex so the need for these direct connections with the hippocampus begins to diminish.

95
Q

What type of sleep is important for declarative memory consolidation?

A

Slow-wave sleep (SWS)

96
Q

What stage of sleep is SWS?

A

3 and 4

97
Q

How do place cells reactivate during SWS?

A

They recover the same sequence of hippocampal activity. Rats were regenrating the sequence of places that is recently visited while it was asleep

98
Q

What did Diekelmann et al 2011 show about reactivation in humans?

A

Odours represented during sleep or wake. There was better memory with odour cue, and increased hippocampal engagement

99
Q

What is the role of sleep in memory?

A
  • SWS plays active role in stabilising memories
  • During SWS, there may be reactivation of hippocampal-dependent memories
  • This may promote their consolidation - integration with similar memories
100
Q

What is Multiple Trace Theory?

A
  • Hippocampus re-encodes during retrieval to create multiple traces and remains important for any ‘recollection’ experiences (even though most information is transferred to cortex)
101
Q

What areas of the brain are involved in the Default Mode Network?

A
  • Angular gyrus
  • Median PFC
  • Posterior Cingulate
  • Hippocampus
102
Q

What is the Default Mode Network (DMN) implicated in?

A
  • Spontaneous thought
  • Episodic Recollection
    (Relatively automatic memory retrieval)
103
Q

What type of semantic retrieval is the DMN involved in?

A

More automatic semantic retrieval

104
Q

When is the ventrolateral PFC recruited for memory retrieval?

A

During both semantic and episodic memory retrieval when task-relevant information is weak

105
Q

What are other words for the ventrolateral PFC?

A
  • Left inferior frontal gyrus (LIFG)

- Broca’s Area

106
Q

Where does brain activity at encoding predict subsequent memory success?

A

VPFC and hippocampus

107
Q

How do we distinguish between competing memories?

A
  • We have similar memories that inferfere with each other
  • To find the right memory you have to control competition between memories
  • This engages VLPFC
108
Q

What are the different types of interference?

A
  • Proactive interference

- Retroactive interference

109
Q

What is proactive interference?

A

Old learning interferes with new memory

110
Q

What is retroactive interference?

A

New learning interferes with old memory

111
Q

What conditions maximise interference between memories?

A
  • Competing memory was presented recently
  • Competing memory is very similar to target
  • There are many competitors
112
Q

What part of the brain is responsible for retrieving the link between objects and their specific context when there are competing contexts?

A

VLPFC

113
Q

What can interference do to memories?

A

Blocking access

Creating false memories

114
Q

What is negative recency?

A

tendency to recall fewer of the final items of the list than the middle and early items

115
Q

What is poor source memory?

A

Problems discriminating between similar memories?

116
Q

How is confabulation affected following damage to PFC?

A
  • Failure to inhibit irrelevant thoughts/memories

- Failure to detect implausible responses

117
Q

What is Korsakoff’s Syndrome?

A
  • Amnesia associated with long-term alcholism
  • Caused by thiamine deficiency
  • Widespread damage to brain: mammiliary bodies and PFC severely affected
118
Q

What memory problems are present in Korsakoff’s Syndrome?

A
  • Problem with retrieval as well as formation of memory - retrieval can be cued
  • Behavioural changes e.g. apathy
119
Q

How is competition controlled?

A

By supressing one memory in favour of another

120
Q

Why do patients with semantic dementia fail the same tests as those with semantic aphasia?

A

Patients with semantic dementia and aphasia have difficulties with both verbal and non-verbal semantic tests.
Dementia: might be losing the conceptual knowledge which is stored in the anterior lobes
Aphasia: might be having difficulty retrieving relevant parts of knowledge but they might still retain their conceptual information just not be able to get it out in a useful way

121
Q

How are patients with semantic aphasia and lesions of VLPFC’s episodic memory affected?

A
  • Have false episodic memories when semantic distractors are presented
  • Have false semantic associations when items are linked episodically
122
Q

What is the difference between default mode network and controlled memory retrieval network?

A

DMN: Retrieval from strong cues
CMRN: Resolving competition, retrieving weak targets

123
Q

Why can selective remembering be bad?

A

Selective remembering one aspect of memory or one association can worsen memory for other aspects

124
Q

What is Retrieval-Induced Forgetting (RIF)

A

phenomenon that suggests that forgetting of some items is in part a consequence of remembering other items

125
Q

Explain the neural basis of retrieval-induced forgetting.

A

Repeated retrieval leads to reduced activation of VLPFC (because task is easier)

126
Q

What does the Go/No-Go Task measure?

A
  • Measures inhibitory control over action

- Press a button when letter appears, but don’t press button if letter = X

127
Q

What is behavioural control?

A

The ability to control actions based on goals

128
Q

What is cognitive control?

A
  • The ability to flexibly control thoughts in accordance with goals?
  • Stop unwanted thoughts from entering consciousness.
129
Q

What task can you use to measure cognitive control?

A

Think/No-Think Task

130
Q

What does the Think/No-Think task measure?

A

Measures inhibitoru control over memory

131
Q

What is supressing retrieval related to?

A

Increased activity in control regions:
- PFC and Anterior Cingulate Cortex
- Also involved in motor inhibition
Decreased activity in the episodic memory area:
- The hippocampus
- Suggests that people can intentionally regulate hippocampal activity to disengage recollection

132
Q

How can trauma affect memory?

A

Can lead to vivid and intrusive memories

- PTSD

133
Q

What is PTSD?

A

Trauma results in persistent anxiety, often accompanied by flashbacks

134
Q

How common is PTSD?

A
  • 15-40% of people exposed to a traumatic event, such as war
135
Q

How could PTSD develop?

A

Linked to difficulty in using PFC to suppress emotive memories

136
Q

What affects to PTSD-resistant people show?

A

Poorer memory for the inforamtion in the no-think condition.

137
Q

What does prefrontal damage lead to?

A

Problems with retrieval and personality

138
Q

What does anterior temporal damage lead to?

A

Problems with semantic memory and language

139
Q

Where does Herpes Simplex Encephalitis focus?

A

Focussed in anterior areas (e.g. hippocampus)

Also damage to anterior temporal and inferior medial frontal cortex

140
Q

How do you get Hypoxic Brain Injury?

A

Brain cells start to die after 4-6 mins of oxygen deprivation.

141
Q

What are the effects of hypoxia?

A

Severe into the hippocampus

Can cause amnesia

142
Q

What can cause hypoxic brain injury?

A

Heart attack, respiratory failure, carbon monoxide poisoning, and disruption in blood flow to brain e.g. from a haemmorhage

143
Q

What are early-stage symptoms of Alzheimer’s?

A

Problems with memory, language, decision making and planning/reasoning