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PSYC20006 Biological Psychology > Henry Molaison and the Anatomy & Neurobiology of Memory and Memory Disorders > Flashcards

Henry Molaison and the Anatomy & Neurobiology of Memory and Memory Disorders Flashcards

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1
Q

What did Henry Molaison have?

A

Severe temporal lobe epilepsy

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2
Q

What is the word epilepsy from?

A

Epilepsia (Greek) - Taking hold of; being seized > seizures

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3
Q

What do epileptic seizures arise from?

A

Sudden excitation in groups of neurons with a loss of inhibitory potential

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4
Q

What imbalance causes epilepsy?

A

The inhibitory-excitatory balance between GABA and glutamate

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5
Q

What happens at the excitatory synapse?

A

The neurotransmitter glutamate increases the spread of excitation

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6
Q

What is the inhibitory response?

A

The neurotransmitter GABA increases nervous system stability

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7
Q

What happens in seizure?

A

Normal amount of glutamate but reduced GABA, reduced inhibition causes the cell firing to be more vigorous or much more frequent than it usually is

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8
Q

What is the definition of Temporal Lobe Epilepsy (TLE)?

A

Recurrent unprovoked seizures originating from the medial or lateral temporal lobe

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9
Q

What is the difference between simple partial seizures and complex partial seizures?

A

Simple partial seizures are without loss of awareness, complex partial seizures are with loss of awareness

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10
Q

What happens in hippocampal sclerosis (HS)?

A

Neuronal loss and gliosis (excess growth or glial cells after neuronal cell loss occurs in a region), often occurs early in life

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11
Q

What are other aetiologies of pathophysiology of the TLE?

A

Past infections, tumors and vascular malfunctions

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12
Q

What can surgical removal of the lesioned hippocampus do?

A

Can cure or reduce the number of seizures

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13
Q

What surgery did HM undergo?

A

Underwent bilateral resection of an extensive amount of medial temporal tissue, included amygdala, most of hippocampi, part of parahippocampal gyrus

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14
Q

What happened to HN post surgery?

A

Normal attention span, preserved intelligence, retrograde memory essentially recovered over time but suffered from severe anterograde amnesia which only affected his declarative memory

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15
Q

What is retrograde amnesia?

A

Impairment of memories created prior to injury

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16
Q

What is anterograde amnesia?

A

Impairment for memories created after injury, impairment in learning novel information

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17
Q

What is declarative memory?

A

Conscious access to information learned previously

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18
Q

What is procedural memory?

A

Remembering ‘how to’, motor skills

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19
Q

What memory could HM still form post surgery?

A

Procedural memory function continued intact, able to learn new skills, but has no recall of learning them, normal performance on procedural memory tasks

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20
Q

What did HM tell us about memory?

A

Medial temporal lobe structures are essential for memory and more essential for anterograde than retrograde memory, distinction between declarative and procedural memory

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21
Q

What are the Temporal Lobes (TL)?

A

The ‘engine’ of memory

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22
Q

What is the ‘material-specificity’ hypothesis?

A

Patients have ‘material-specific’ memory deficits related to involved medial temporal lobes

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23
Q

What do left MTL lesions result in?

A

Non-verbal/visual memory impairment

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24
Q

What do right MTL lesions result in?

A

Non-verbal/visual memory impairment

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25
Q

What is the hippocampus?

A

Region of the brain first identified to support memory

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26
Q

What is the hippocampus also known as?

A

Cornu ammonis (ammon’s born)

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27
Q

What is the hippocampal formation?

A

Dentate gyrus + CA3 - CA1 + Subiculum

28
Q

What happens after information is integrated in sensory systems?

A

Sent to the hippocampal formation for long term storage

29
Q

How can memories be accessed?

A

By reciprocal connections between the hippocampal formation and temporal neocortex

30
Q

What does the hippocampal formation and surrounding structures do?

A

Essential for learning and consolidating novel information

31
Q

What is the consolidation theory?

A

After a period of consolidation, information can be retrieved independently of hippocampal formation involvement

32
Q

What is the multiple trace theory (MTT)?

A

Retrieval of autobiographical/episodic experiences always involves the hippocampal formation

33
Q

What is the hippocampal formation particularly necessary for?

A

Relational memory tasks

34
Q

What is the paired associate learning test?

A

Task where patient is required to remember an association between arbitrary pieces of information (e.g. word and object)

35
Q

What are the three regions of the extra-temporal brain that are particularly involved in memory?

A

Papez’s circuit, frontal lobes and diencephalon

36
Q

What did James Papez propose in 1937?

A

That a specific brain circuit was devoted to emotional experiences and expression, which was the limbic system

37
Q

What is in the limbic system?

A

Papez circuit and amygdala

38
Q

What does the amygdala do in memory?

A

Plays a key role in supporting memory for emotionally arousing experiences, classical fear conditioning, facilitates rich representations of emotional experiences

39
Q

What do lesions in the amygdala result in?

A

Loos of conditioned fear and impairment of new fear learning, reduced memory for emotionally laden events

40
Q

What does Papez’s circuit comprise of?

A

Mamillary bodies, fornix, anterior thalamic nuclei (ATN), cingulate gyrus and the hippocampus

41
Q

What do lesions to Papez’s circuit result in?

A

Declarative memory impairment, poor relational memory/encoding

42
Q

Where is declarative memory impairment most common?

A

The hippocampus or ATN

43
Q

What are the frontal lobes involved in?

A

Motor programming, motor and premotor cortices. Cognitive control processes, prefrontal cortex

44
Q

How are the frontal lobes involved in memory?

A

Involved in developing and implementing strategies for appropriate memory encoding and retrieval

45
Q

What do lesions to the frontal lobes result in?

A

Lesions to the frontal lobes cause impairment in remembering contextual details

46
Q

What is confabulation?

A

Production of statements involving bizarre distortions of memory

47
Q

What is the diencephalon?

A

‘interbrain’

48
Q

What does the diencephalon comprise of?

A

Thalamus and hypothalamus

49
Q

What does anterior and medial lesions to the thalamus do?

A

Likely to cause memory deficits than posterior or lateral lesions

50
Q

What is dense amnesic syndrome associated with?

A

Associated with damage to the mammillo-thalamic tract, MTT connect the anterior thalamus and the hippocampus

51
Q

What do cases with medio dorsal nucleus (MDN) and/or internal medullary lamina (IML) damage but spared MTT show?

A

Specific retrieval difficulties but preserved recognition

52
Q

What parts of the thalamus are involved in memory?

A

The dorsal medial, midline and intralaminar nuclei

53
Q

What does damage to the dorsal medial part of the thalamus do?

A

Deficits in selecting the appropriate information to be retrieved, ‘active retrieval’

54
Q

What does damage to the intralaminar/midline of the thalamus do?

A

Deficits seen in semantic memory, memory retrieval

55
Q

What does learning involve?

A

Synaptic plasticity

56
Q

What is synaptic plasticity?

A

The biochemistry of synapses changing to alter the effect on the post-synaptic neuron

57
Q

What is long-term potentiation?

A

A long term increase in the excitability of a neuron to a particular synaptic input caused by repeated high frequency activity of that input

58
Q

What is Hebb’s rule?

A

When an axon of cell A, excites cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficency as one of the cell’s firing B is increased

59
Q

What was the baseline EPSP measured for?

A

A single electrical stimulus

60
Q

What did increased EPSP for subsequent single electrical stimulus cause?

A

Caused LTP, cell has initial baseline EPSP, after rapid firing, cell now has hyper response

61
Q

What does LTP cause?

A

Causes new receptors to be inserted in post-synaptic membrane

62
Q

What changes does LTP cause at the synapse that allows LTP to continue beyond a few hours with glutamate?

A

Increased sensitivity of receptors to glutamate, increased amount of glutamate released by the pre-synaptic terminal button, protein synthesis in post-synaptic dendrites

63
Q

Where does LTP occur?

A

Hippocampus, entorhinal cortex, prefrontal cortex, motor cortex, thalamus, amygdala, visual cortex

64
Q

What is long-term depression?

A

Low frequency stimulation at the synapse can decrease synaptic strength

65
Q

What is habituation?

A

Repeated stimulation reduces strength of synaptic response (reduced neurotransmitter release)

66
Q

What is sensitisation?

A

A single noxious stimulus causes exaggerated synaptic response to repeat presentation of noxious stimulus

PSYC20006 Biological Psychology (16 decks)

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