Neuropsychology week 2

Question 1

4 types of LTM

Answer 1

Episodic memory (autobiographical experience)
Semantic memory (facts) (penguins cant fly)
Procedural/ implicit (typing, playing fifa, riding a bike)
Prospective memory (Planning future events, remember to feed the dog)

Question 2

Why is it key to distinguish between different memory deficits

Answer 2

The different types of memory are dissociable. some people could be good at a certain type of memory.

Question 3

How memory is encoded (sensory memory)

Answer 3

Visual memory
Olfactory memory (smell) (vivid, related to emotional experience)
Gustatory Memory (taste)
Kinaesthetic (touch)

Question 4

Differentiating LTM based on time.

Answer 4

Delayed memory ( some time between encoding and recalling, memory usually decays by then
Recent memory (past few days/weeks)
Remote memory (several months/years)
Prospective (future memory)

Question 5

Explicit vs implicit

Answer 5

Conscious vs unconscious memory (man in the bus)

Question 6

Tulving 1989 types of memory impairments

Answer 6

Episodic impairments
Semantic impairments
Procedural impairments

Question 7

Arrows and boxes

Answer 7

Boxes show that the impairments are disassociated. Arrows show processing direction

Question 8

Procedural memory

Answer 8

impaired by damage to Basal Ganglia (motor region)
Automatic motoric process performed every day

Question 9

Attkinson and Shiffren (1968) modal model

Answer 9

Differentiates between short and long term memory.
Information need to be in STM before being consolidated (transformed to LTM)

Question 10

Types of psychogenic (psychiatric amnesia)

Answer 10

Selective ( inability to remember an episodic experience linked to a traumatic event) (e.g. war)
Fugue (Inability to remember identity due to trauma, usually recover)
Multiple personalities (very rare, identity becomes fractionated,

Question 11

Organic (permanent/transient amnesia)

Answer 11

Permanent is degenerative (progressive worsening) or stable (sever but no deterioration).
Material specific- Certain modality or type of content lost
Global- Total loss of episodic content

Question 12

Types of amnesic presentations

Answer 12

Retrograde- past events (after degeneration begins)
Anterograde- Future events

Question 13

Ribots law

Answer 13

Closer you get to period when trauma started the more information is lost

More severe trauma more memory lost

Question 14

Features of amnesic syndrome (episodic information impairments)

Answer 14

Normal short term memory performance
Normal IQ
Normal procedural memory
Dense anterograde amnesia
Variable retrograde amnesia
Near normal implicit memory
impaired explicit memory

Question 15

testing memory

Answer 15

Delayed word recall. Look for recency and primacy effects.
Anterograde amnesia can usually tell u last 3 words (recency) as theyre still in STM.

Question 16

Contextual processing Hupert and Piercey 1978

Answer 16

Amnesiacs relied on familiarity in absence of context. Amnesiacs have source amnesia- Bad at recalling when information was acquired. Tend to confuse recency with familiarity.

Question 17

Relational memory hypothesis

Answer 17

Episodic memory is the glue which binds together what, where, when. Key in bringing together information into one holistic chunk.

Question 18

Which part of brain is used in consolidation of memory?

Answer 18

Hippocampus medial surface of temporal lobe.

Question 19

HM

Answer 19

Brain injury as child. Hippocampus removed in surgery. Severe reterograde (3-10 years) and severe anterograde amnesia amnesia. Normal STM, implicit and procedural memory

Hippocampus is important for episodic explicit memory. This is noted as HM developed Anterograde amnesia meaning he lost the ability to form new memories. HM has his procedural and STM intact. Implicit memory also seemed undamaged as shown when Milner made him draw a star over and over and he improved whilst thinking the task was novel.

Question 20

What other structures play a key role in episodic memory processing?

Answer 20

Baddeley et al 2001. Perirhinal and Entorhinal cortex.
Neuroplasticity. (brain compensates for early damage by substituting the task of hippocampus to something else) (childhood brain has highest plasticity.
mamiliray bodies in the thalamus which is in the Midline diencepahlon

Question 21

Patient N.A

Answer 21

Fencing damaged left dorsomedial thalamus. Na experienced severe anterograde amnesia and some retrograde amnesia. (mamillary bodies in thalamus in Midline diencephalon implicated in amnesia)

Question 22

Retrograde Amnesia temporal gradient

Answer 22

Variation in ability to remember information depending on when it occurred. Preserved earlier memories. Progressive loss of later memories

Question 23

Consolidation theory

Answer 23

Squire 1992, Relationship between hippocampus and time. Memories initially processed in hippocampus, rehearsed then consolidated to surrounding areas of neocortex. Explains why hippocampal legions can still remember remote memories.

Question 24

Temporal gradient of retrograde amnesia of Korsakoff syndrome vs Alzheimer’s

Answer 24

Alzheimer’s lower baseline. Korsakoff steeper decline.

Question 25

Korsakoff syndrome

Answer 25

Severe alcohol consumption and not eating. Thiamine deficiency. Present with sever anterograde and retrograde amnesia. Present with confabulations as frontal lobes very impaired.
Midline diencephalon implicated.

Question 26

Role of the frontal lobes in memory

Answer 26

Acts as a filtering system that enables differentiation between plausible and non plausible memories.

Question 27

Memory as a reconstructive process

Answer 27

Predictive hypothesis of what occurred at a particular time. Korsakoff patients tend to struggle with the hypothesis testing.

Question 28

Confabulations

Answer 28

Construction of memories that didn’t occur.
Confabulators make lots of false positive errors.
Confabulations can be provoked, as patients produce incorrect information, they produce more incorrect information to remain consistent.
How do you deal with confabulations? ethics, philosophical.
Damage to medial prefrontal cortex. leads to damage in making distinctions between what is real and not real

Question 29

Persistent de Ja vu- recollective confabulations

Answer 29

Everything linked to a sense of familiarity. familiarity system malfunctioning so everything seems familiar. try to justify our sense of familiarity. try to make sense of world. TV MAN has been here before.

Question 30

Which test do you use for Verbal memory

Answer 30

California verbal learning test. has a version for children

Question 31

Which test do you use for visual memory

Answer 31

REY complex figure
Ask patient to draw a complex figure (copying)
test them again in 5 and then again in 30.
Test visual, spatial apraxia. Test planning and LTM.

Question 32

Weschler memory test 3

Answer 32

very long test, tests multiple domains and produces a total cognitive score.

Question 33

Testing executive function

Answer 33

Wisconsin memory test

Question 34

River mead behavioural memory test (Wilson 1991)

Answer 34

Measures level of practical memory problems patients often experience.
validated in numerous age groups.
Better predicts patients everyday problems than standard clinical assessment. (ecological validity)
expensive and difficult to train
Good at identifying unique strengths and weaknesses of client.

Question 35

How to test for prospective memory?

Answer 35

Take clients watch, hide it, ask them to take it back at a certain time, test if they remember what the timer is for

Question 36

Why assess memory impairments?

Answer 36

Profile kind of problems patient has.
See if you can use information to facilitate forms of treatment

Question 37

What makes a good assessment?

Answer 37

• Highly sensitive to memory impairments (E.G. WMS) (eliminate other neurological deficits)
• Predict everyday problems. (E.G. RBMT)
• Analyse the nature of deficits in theoretical terms. (to facilitate treatment)
• Identify unique strengths and weaknesses of patient. E.g. if they have a retrieval problem can focus on working out cues for patients.

Question 38

White coat effect

Answer 38

People tend to be more anxious/ behave differently when sat in clinic in front of doctor. Maybe be better to administer assessment at home or in a recognised safe environment for them. This can give you more realistic profile.

Question 39

3 Approaches for memory therapy

Answer 39

Retraining of impaired function (ideal) assumes training can reorganise brain structures (plasticity). regain use of an otherwise impaired function. Utilise brain plasticity. Not always possible as patient may be severely impaired. also neurodegenerative diseases no point as taught skill will just get worse
functional adaptation (substitution) (Alternative functions can be employed to achieve desired outcome) (tactile kinaesthetic therapy for reading issue) use another form of cognitive reserve to get job done.
compensation. Increasing efficiency of impaired function. e.g use an external memory aid. e.g. diary.

Question 40

What is empowerment

Answer 40

client plays an active role in their treatment. Individualised treatment. Use a multifactorial approach which uses more than one of the treatment rehabilitation techniques

Question 41

Internal methods of managing memory problems.

Answer 41

Making associations, mnemonics, method of loci, mental retracing, errorless learning, PQRST. Consider clients strengths and weaknesses. Visual scaffolding (mind maps) if good at visual memory. many of these learning techniques are employed by people who don’t have brain injury.

Question 42

External methods of managing memory problems

Answer 42

Memory aids, diaries, calendars, wall planner, note book, lists, memo pad.
Environmental modifications: sign posts, labels on items, coloured doors