Learning and Memory 1: Hippocampus

Question 1

What did HM have done? Effect?

Answer 1

Bilateral medial temporal lobectomy. Anterograde amnesia (couldn’t form new memories) due to loss of hippocampuses.

Question 2

What’s the difference between declarative and non-declarative memory?

Answer 2

Declarative - something that can be put into words

Non-declarative - behavioral change in response to stimulus

Question 3

What is episodic memory?

Answer 3

“Autobiographical” memories - of scenes, context, etc. Emphasis on being from personal experience. (E.g. remembering watching Barack Obama’s election)

Question 4

What is semantic memory?

Answer 4

Factual knowledge. Remembering that Obama’s the president, scissors are for cutting, the symptoms of Walenberg syndrome, etc.

Question 5

What is familiarity?

Answer 5

The sense that you’ve seen something or someone before. Loss of familiarity may lead people to think family members have been replaced by imposters.

Question 6

What is recollection?

Answer 6

Related to familiarity and episodic memory, it’s when the “flood of context” associated with, for example, a person and why they are familiar to you comes into conscious thought. (“Oh! He was in that movie with Kevin Bacon…”)

Question 7

What are the 3 stages of processing of episodic memory?

Answer 7

Encoding, storage/consolidation, retrieval.

Question 8

What are the 3 parts of the hippocampal formation?

Answer 8

Subfields, dentate, subiculum.

Question 9

What are 3 extrahippocampal medial temporal structures?

Answer 9

Entorhinal cortex, parahippocampus, and perirhinal cortex.

Question 10

Do the medial temporal lobes receive input from multiple sensory modalities?

Answer 10

Yes.

Question 11

What process allows you remember your night out just from hearing the name of the bar? What structure seems to be particularly important for this?

Answer 11

Binding. The hippocampus - takes input from multiple sensory modalities and forms associations.

Question 12

What extrahippocampal medial temporal structure is involved with the “what?” (ventral visual pathway) for object memory?

Answer 12

The perirhinal cortex.

Question 13

What extrahippocampal medial temporal structure is involved with the “where?” (dorsal visual pathway) for spatial/contextual memory?

Answer 13

The parahippocampus.

Question 14

A lesion to what structure might cause you to specifically lose familiarity?

Answer 14

Lesion to the perirhinal cortex.

Question 15

A lesion to what structure might give you problems with recollection? (linking the familiarity with the context)

Answer 15

The hippocampus.

Question 16

What is Capgras delusion/syndrome? What is it often associated with?

Answer 16

Distortion of familiarity -> thinking family member has been replaced by an imposter. Occurs in Alzheimer’s.

Question 17

What’s Fregoli syndrome?

Answer 17

Another disorder of familiarity, but here you think everybody is familiar (or even that a stranger is embodying a friend/family member)

Question 18

What pathological process can cause Deja Vu?

Answer 18

Medial temporal lobe seizures.

Question 19

Review: What structures are in the Papez circuit? What happens if you lesion a part of it?

Answer 19

Fornix, mamillary bodies, anterior thalamic nucleus, posterior cingulate/retrosplenial cortex.
Lesions result in amnesia similar to hippocampal lesion.

Question 20

What’s one notable lesions to the Papez circuit? Specific structure affected? Effects on memory? Underlying cause of disease?

Answer 20

Wernicke-Korsakoff Syndrome. Lesion to mamillary bodies. Both anterograde and retrograde amnesia. Thiamine deficiency (most often associated with alcoholism).

Question 21

What is Ribot’s Law? When does it apply?

Answer 21

recent memories are more likely to be lost than the more remote memories in retrograde amnesia *updated

Creates a temporal gradient of amnesia in hippocampal / temporal-limbic amnesia. (doesn’t apply when there’s more extensive medial temporal lobe / neocortex involvement)

Question 22

Do lesions that affect episodic memory affect semantic memory?

Answer 22

Yes. (and if they’re hippocampal, the retrograde memory loss follows Ribot’s Law, i.e. has a temporal gradient)

Question 23

If a patient performs much better memorizing a list when asked to visualize the items vs. “unconstrained free recall”, where might the lesion localize?

Answer 23

Frontal lobes - which appear to be important for spontaneous encoding / retrieval of memories.

Question 24

Lesions to what area might increase false memories or memory distortions?

Answer 24

Frontal lobes

Question 25

Major differences between amnesia from medial temporal lobe vs. frontal lobe lesion? (2-3 things)

Answer 25

Frontal lobe amnesia is improved with cues and environmental (contextual) information. Frontal lobe lesions have a high tendency for false memory.

Question 26

How can testing memory of word lists discriminated between storage and retrieval deficits?

Answer 26

If patients can get it with multiple choice, it’s primarily retrieval. If they can’t, it’s primarily storage.

Question 27

Might the lateral parietal lobes be involved with memory?

Answer 27

Yeah… they might be….

Question 28

What is the concept of “reactivation” apply to recalling memories of objects?

Answer 28

Sensory areas of the modalities in which the object was initially introduced are more strongly reactivated upon recall. (E.g. if you saw a picture of a hammer, your visual areas will light when asked to think about a hammer; if someone plays a sound of hammering, your auditory centers might light up when later asked to think about a hammer)

Question 29

What are the two main pathological features of Alzheimer’s Disease (AD)? Which one is more proximal in the disease process?

Answer 29

Amyloid plaques - more proximal

Neurofibrillary Tangles - more indicative of severe disease

Question 30

What are amyloid plaques?

Answer 30

extracellular A-beta fragment of Amyloid Precursor Protein.

Question 31

What are neurofibrillary tangles?

Answer 31

Intracellualr, paired helical structures made of hyperphosphorylated Tau.

Question 32

What percentage of AD cases are considered sporadic? (genetically speaking)

Answer 32

95% ish

Question 33

What do all the genes associated with autosomal dominant AD inheritance have in common?

Answer 33

All associated with processing of amyloid precursor protein.

Question 34

How does AD memory loss contrast with the normal memory loss of aging?

Answer 34

Memory using environmental context should be spared in memory loss of aging, but is not in AD.

Question 35

How does AD cause amnesia? How can it be seen with imaging?

Answer 35

Damage to the hippocampus and extrahippocampal structures. Progressive atrophy can be seen on MRI.

Question 36

Why shouldn’t people with AD take scopolamine for sea-sickness?

Answer 36

Scopolamine is anti-cholinergic. ACh signaling appears to be necessary for memory formation, and people with AD are particularly susceptible to anti-cholinergic treatment.

Question 37

What drugs can be used to improve memory in AD? (2 types)

Answer 37

Cholinesterase inhibitors (-stigmines, Aricept, others)
NMDA antagonists (memantine)