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Disorders of Memory Amnesia & Animal Models Disorders of Memory Amnesia & Animal Models

Disorders of Memory Amnesia & Animal Models - PowerPoint Presentation

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Disorders of Memory Amnesia & Animal Models - PPT Presentation

Lecture Outline Disorders of Memory HM Anterograde Amnesia Retrograde Amnesia Korsakoff s Syndrome Animal Models of Memory Anatomy of Memory Prefrontal lobes important for shortterm ID: 908688

amnesia memory cortex term memory amnesia term cortex short temporal confabulation anterograde retrograde hippocampus learning memories intact brain patient

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Slide1

Disorders of MemoryAmnesia & Animal Models

Slide2

Lecture OutlineDisorders of Memory

H.M.Anterograde AmnesiaRetrograde Amnesia

Korsakoff

s SyndromeAnimal Models of Memory

Slide3

Anatomy of Memory

Prefrontal lobes

important for short-term

memory.

processing of short-term to long-term

memory.

Diencephalon

thalamus, hypothalamus, mammillary

bodies.

Temporal lobes

hippocampus and

amygdala.

processing of short-term to long-term memory.

Slide4

Disorders of Memory

Retrograde – loss of memory for events prior to injury.Anterograde – inability to form new

memories.

Post-traumatic Amnesia (PTA) – period of time after brain injury during which new memories can not be formed (patient is also usually disoriented in time and space

).

Slide5

Who is H.M.?

Patient H.M. suffered from epilepsy thought to be caused by a head injury at age 9.H.M.’

s

epilepsy could not be controlled through drug interventions.H.M. underwent bilateral temporal lobotomies

in

1958.

coronal MR slices

H.M. Healthy control

Slide6

The medial temporal lobes (MTL)

Slide7

Surgery successfully treated epileptic seizures, but left severe memory impairments.His memory for the remote past was intact (could remember his childhood), but he had some

retrograde amnesia and severe anterograde amnesia.

If you left H.M. for only a few minutes, upon returning he would most likely forget who you were or that you had already met!

Loss of episodic memory. Semantic memory generally intact.

Semantic – memory for factual based

material.

Episodic – memory for events that can be linked to a time and

place.

Who is H.M.?

Slide8

What is it like to be H.M.?“Right now, I’m wondering, ‘Have I done or said anything amiss?’ You see, at this moment everything looks clear to me, but what happened just before? That’s what worries me. It’s like waking from a

dream.”-- H.M., 1965

“Every day is alone in itself, whatever enjoyment I’ve had, and whatever sorrow I’ve had.”

-- H.M., 1968

Slide9

What Is Memory?

Classic cases of amnesiaThe case of N.A

.

A small lesion in the left

dorsomedial nucleus of the thalamus.Similar pattern of deficits to H.M.

Retrograde amnesia for the 2 years preceding the

accident.

Almost complete anterograde amnesia – can remember virtually nothing of events since the accident.

More verbal than visual memory deficits, although both domains affected (e.g., has spatial memory impairments).

Episodic lost but semantic

intact.

Slide10

What Is Memory?

Classic cases of amnesiaWhat types of functions may be left intact in cases of severe amnesia, such as H.M., Clive and N.A.?

immediate memory – can recite back several words immediately (but within five minutes no recollection of words

).

intact memory for remote events (e.g., from childhood).factual knowledge (e.g. water boils at 100

°C).

perceptual and motor memory (e.g. riding a bike, brushing teeth

).

language and social

skills.

procedural learning (e.g. mirror drawing

).

Other facets of

functioning:PersonalityIntellectual FunctioningInsight into intact and impaired functions in amnesics enables us to learn much about memory

processing.

Slide11

H.M. – procedural learning.

Task – draw object viewed in the mirror.Practice makes perfect – even in H.M.

Never recalls having done the test

!

Implicit memory.stem-completion also intact – e.g., DEFEND, HELIUM, MODIFYDEF__________

DEFEND, DEFEAT, DEFINE

Slide12

Slide13

H.M.’s Contribution to Memory ResearchThe hippocampus is NOT the location of LTM, and is NOT necessary formation of

LTM.can remember childhood.

The hippocampus is NOT the location of

STM.

can carry on conversations.The hippocampus IS responsible for converting STM into LTM.

understands

new information, but a permanent record is never

made.

involved

in consolidating memories

overtime.

Slide14

Hypothesized Memory Processes

Incoming information

Performance

Retrieval

Working memory

Short-term storage

Encoding

Long-term storage

Consolidation

Sensory buffers

Sight

Sound

Smell

Touch

Attention

Rehearsal

Slide15

Anterograde AmnesiaWhat brain regions are critical in anterograde amnesia?

for H.M. the hippocampus and parahippocampal cortex were removed (as was the amygdala

).

Parahippocampal

cortex: A region of limbic cortex adjacent to the hippocampal formation that, along with the perirhinal cortex, relays information

between the entorhinal

cortex and other regions of

the brain

.

amygdala is probably only important for the emotional content of memories – flashbulb

memories.

amnesic

patients can perform memory tasks, but they cannot learn anything they learned from it.

Slide16

Double Dissociation Proof the hippocampus mediates consolidation?

Patient S.M. - bilateral amygdala

damage.

could not establish conditioned emotional responses.Patient W.C. - bilateral

hippocampal

damage.

could

not remember testing

procedure.

episodic

(declarative) memory impaired.

Patient R.H. - bilateral damage to both.

both kinds of learning impaired.

Slide17

Korsakoff’s amnesia

severe anterograde amnesia.destruction of parts of diencephalon (

mammilo

-thalamic tract

).temporally graded retrograde amnesia.lose declarative memories but not procedural ones.

confabulation is

common.

caused by thiamine deficiency due to alcoholism and poor

diet.

Slide18

Retrograde amnesia and the temporal gradient

Korsakoff’s patients show a steep temporal gradient in their remote memories

1990

1980

1970

1960

1950

1940

Korsakoff’s

patients

MTL

amnesics

% correct

Slide19

temporal gradient to retrograde amnesia.for closed head injury or even ECT (shock therapy) – memory loss is greatest for most recent events and rarely extends beyond a few

years.retrograde amnesia is quite severe in Wernicke-Korsakoff’s

syndrome but still maintains a temporal gradient – suggests hippocampus is not the only structure necessary for

memory.

Retrograde amnesia and consolidation

Slide20

Confabulation

more than just “filling-in-the-blanks”.patients with Wernicke-

Korsakoff’s

will make up information to hide a memory

deficit.indicative of a lack of awareness of the memory impairment (frontal lobe involvements).

Slide21

The story so far…Memory involves multiple brain regions

medial temporal lobeshippocampusentorhinal cortex

parahippocampal

cortex

amygdalasubcortical structuresmammilo-thalamic tractneocortexposterior superior temporal gyrus

dorsolateral prefrontal cortex

Slide22

Animal Models of Memory Research

We have learned a lot about memory from case studies, but individual cases are not as statistically powerful as group studies.

We know that different brain structures have different roles in learning and

memory.

Human memory research provides research direction, but animal

research is needed for

in depth

analysis

.

Slide23

Animal models of memory

Delayed match to sample

Delayed non-match to sample

Slide24

Spatial memory – animal models

hippocampal lesions disrupt learning in a radial arm maze or Morris water maze.

Now have Virtual Reality Morris water mazes for humans

Slide25

Prefrontal cortex

output from BG – thalamus, from there to prefrontal and SMApremotor, SMA involved in planning & execution

important for learning sequences of movements

Slide26

Triple Dissociation

MacDonald & White used the radial arm maze (RAM) to examine declarative, procedural and emotional memory.Evidence for different memory systems mediated by different brain

structures.

Lesions to the hippocampus produced deficits in declarative

memory.Lesions to the basal ganglia produced deficits in procedural

memory.

Lesions to the amygdala produced deficits in emotional

memory.

Slide27

1) People with anterograde amnesiaA) are unable to recall childhood experiences.B) show impairments in motor memory.C) show normal complex relational learning.D) are unable to learn new information.

E) show facilitated stimulus-response learning.2) The most profound symptom of Korsakoff's syndrome isA) anterograde amnesia.B) total amnesia.

C) combative behavior

D) delirium tremens.

E) auditory and visual hallucinations.3 ) Which of the following is true of confabulation?A) Confabulation is seen in persons who simply mix up their memories.B) Confabulation is intentional.C) Patient H.M. shows severe confabulation.D) Korsakoff's patients fail to show confabulation.E) Confabulation is the report of a fictitious event by a person with amnesia.

Review Questions

Slide28

4) One striking aspect of H.M.'s memory deficit is that heA) can learn some new tasks, but is unaware of having learned them.B) only remembers recent facts.C) reverses word order in repeated sentences.

D) indicates he remembers things he has never seen.E) show signs of confabulation.5) Which of the following is true of short-term memory?A) Immediate memory precedes short-term memory.B) Short-term memory has a limited capacity.

C) Short-term memory is impaired by repetition of verbal material.

D) Short-term memory has an unlimited capacity.

E) Immediate memory is distinct from short-term memory.6) When tested in an 8-arm maze, a rat with hippocampal damage willA) repeatedly visit arms from which they have already eaten a food pellet.B) be unable to visit all of the arms.C) be more efficient at getting food than is an intact rat.D) only visit arms that have never held food in the past.E) perform more efficiently than will a rat with damage to the fornix or entorhinal cortex.

Review Questions