#10623 - Visual Memory Deficit Amnesia Lec 5 - Neuropsychology of Memory

Visual Memory Deficit Amnesia

• Greenberg & Rubin (2003) – burger example

• Smell of burgers leads to activation in olfactory cortex

• This via MTL mediation would activate a pattern of firing in visual cortex that represents the memory of a friend once cooking them

• This activity in visual cortex – may stimulate new activity in audiotry cortex - represents the sound of a conversation once had with that friend

• This is the CASCADE of activation

• This activity would also stimulate regions dedicated to language, narrative + emotion - impart the emotional tone to the memory

• The recall of an autobiographical memory occurs over one measurable time period - but not in one brain location => it is located in time – but distributed in space.

• Rubin & Greenwood (1998) When an autobiographical memory is recalled info in widely separated areas of cortex are excited :

• E.g. a familiar sound may lead to activation in auditory cortex – which either directly or via the hippocampal mediation might activate a pattern of firing in visual cortex – stimulating a visual image

• This activity in visual cortex may in turn stimulate new activity in visual, auditory + other cortices - stimulating visual images, sounds, smells - while feed-backing to the original pattern of firing in auditory cortex cascade of activation – produces a patterns of firing similar to that present during the original experience

Most memories have strong visual component:

• Crawley & Eacott (2006)

• Asked to recollect + describe a memory from childhood investigated the extent to which the memory had visual, auditory, spatial etc aspects

• Visual detail is the largest + most regularly reported detail - this is higher than any other sensory component

• Suggestive that memories rely heavily on visual representations

• Rubin (2006)

• Participants are given a cue word - asked to retrieve and episodic memory associated with that word whislt undergoing fMRI

• Asked to hit a button once memory brought to mind

• Large activation of the hippocampus at memory retrieval, PFC activated when making a decision on the memory to think of

• Visual cortex was v. active - retrieval of the memory activated the visual cortex

• Further suggests there is a large amount of visual info in memory representations

What happens to EM if visual association cortex is damaged?

• New experiences will have a degraded visual component and so anterograde memories will be formed with this degraded input. Relative absence of visual component will affect but may not be devastating to memory integrity.

• Pre-existing memories (i.e. retrograde) were formed of events that included an intact visual component. Stored visual component will be degraded/lost.

• For retrograde memories the lack of visual component may also prevent the cascade of associations to other modality components, affecting retrieval of them too. This will effect all retrograde memories equally, so there will be no temporal gradient to retrograde amnesia.

• Hypothesis: the loss of visual association cortex will result in a form of amnesia with the above characteristics. Called Visual Memory Deficit Amnesia (VMDA)

Differences between MTL amnesia

Differences between VMDA + cortical/retinal blindness

1. New exp will not have a visual component + so AA will be formed without it

• Visual association cortex still exists - but will receive no visual input

• Input from other modalities may call up associated visual images from memory to be incorporated

2. Retrograde memories (formed before blindness) were formed of events that included a visual component

• Visual association cortex still exists (although receives no new input)

• Visual memories stored in visual association cortex will still be available

• The visual memories stored in visual association cortex can still cascade to associations to othermodality components - should be no effect of retrograde memories

Detecting a patient with VMDA – Farah’s Model

1. Patient must be able to detect, draw or describe the visual properties of an object

• Demonstrates that the deficit could not have arisen from motor, perceptual or linguistic impairment

2. Patient must not be able to recognise an object on sight alone - indicating its name or function cannot match an intact percept of an object to a stored LTM representation of the object

3. The patient should not be able to draw an object from memory, describe its visual characteristics from memory , or detect its visual image upon introspection cannot access the stored LTM representation of the object

Temporal Gradient – Rubin & Greenwood (1998)

• Predicted that these amnesic patients would have no sparing of childhood memories - which characterises nearly all other forms of amnesia

• The temporal gradient in more common forms of amnesia is thought to arise because consolidation is achieved at various stages of completion leading to a failure in retention of the most recent memories

• In this predicted form of amnesia - the deficit arises NOT from a loss of retention of incompletely consolidated material - but from a loss of visual info itself - even older consolidated memories would be left with big gaps

Rubin & Greenberg (1998)

• 11 cases in the literature met the criteria for a visual memory deficit

• The data available fitted the predictions of VMDA with only 4 exceptions

• VMDA is a new classification of amnesia - unlike other forms of amnesia – is caused by a loss of posterior neocortex rather than damage to the MTL or diencephalon region

• Although it is rare – it is frequent enough to establish that it properties distinguish it from other types of amnesia

Case MH – supportive of VMDA Ogden (1993)

• 24yr old man injured in motorcycle crash

• Damage bilaterally to occipital lobes - no damage reported to frontal or temporal lobes (not MTL or diencephalon – not standard amnesia)

• Originally assessed as blind - 21m later reassessed + responded to some visual stimuli

1. He could copy line drawings in a slow, disjointed fashion - did not recognise what he was drawing

2. Was not good at recognising objects from sight alone – only got 8/30 correct when objects presented to him – cannot match the percept of the object to the stored representation

• Compare this to semantic amnesia (later lec notes)

3. MH could draw more simplistic everyday objects from memory e.g. key + house more complex objects e.g. flower was not recognisable – wouldn’t attempt to draw complex objets such as phone as he expressed his inability to think how they might look

• He was also unable to draw or visualise any specific objects such as the house he grew up in .

• MH conforms to the 3 criteria of VMDA

• Appears that he is unable to visualise (locate in LT store , or bring into awareness) objects + scenes from LTM OR he has lost the visual memory templates themselves

• MH’s memory

• Weschler memory scale immediate recall of passages (normal), associate learning (fine) => moderate impairment in anterograde

• Retrograde memory dense loss of personal memories prior to the accident, Autobiographical memory interview (AMI) : personal semantic schedule + autobiographical incidents schedule -> All info checked with family for childhood period – scores fell in the abnormal range – severed RA with no evidence of a temporal gradient RA>AA

Greenberg et al (2005) Case study of M.S.

• Suffers from long term visual memory loss along with some semantic deficits – also has severe retrograde amnesia + moderate anterograde amnesia

• Suggestion that his visual deficits may be contributing to his autobiographical amnesia

• MRI shows extensive damage to occipital and temporal lobes - including damage to hippocampus in left hemisphere but right hippocampus is intact. (wouldn’t usually predict severe amnesia from this)

• Like M.H. has left hemianopia, is cortically colour blind, prosopagnosic and is an associative agnosic. He has no physical disabilities.

• Patients with long term visual memory loss should suffer from mild anterograde amnesia + should compensate for their deficits by placing greater reliance on non-visual sensory data

• These patients should not show sparing of childhood memories all retrograde memories should be affected since memories from any age would involve visual info

• This pattern of deficits should be the exact opposite to those found in cases of amnesia resulting from MTL damage

1. Copying picture of a rhino was good – used line by line drawing strategy

• Not good at drawing from immediate or delayed memory

• Could not label the animal of the replication he drew

2. MS pretty good at recognising real objects through sight alone – the ones he got wrong were immediately corrected when he touched them - 16/30household objects

• Performance much worse when given pictures of the objects - could not name many of the objects

3. Was bad at drawing objects from memory

• This also highlighted some semantic deficits – on his drawing of a tree labelled the crown as...