Disorders of memory Flashcards
What are the strengths of studying patients with memory deficits to inform theory
- patients who present with different characteristic memory impairments arising from different lesion locations provide insight into the fractionation within the domain of memory and candidate neural correlates
- the systematic errors patients make provide insights into the mechanisms that underpin these processes
- particularly important for studying declarative forms of memory (episodic and semantic) that are challenging to study using animal models
- the foundation for our understanding of memory
what are the limitations to patient studies informing theories of memory
- underpowered: small sample sizes with an overreliance on case studies
- naturally occurring lesions do not respect functional boundaries
- historically, inaccurate reports of lesion location have drive research and theory to focus on the wrong areas or overemphasise idiosyncratic deficits (overfitting) e.g HM and Ribot’s law
- leads to a modular view of brain function when current insight from newer imaging and computational approaches support distributed network account of brain function
- lesions in one area can affect function in distal regions particularly if white matter tracts are damaged (diaschesis)
-mechanisms have to be inferred e.g difficult to acertain whether anterograde amnesia is a deficit in encoding or retrieval (reliant on behavioural output)
-need to combine with convergent evidence from in tact memory systems in healthy people (e.g neuroimaging, TMS) and neurpsysiological studies possible in animal models
Does anterograde amnesia reflect a deficit in encoding or retrieval?
Norman et al., 2019
implanted electrodes in the hippocampus and cortex of epileptic patients to examine encoding and retrieval signals during an episodic memory task
participants were presentation of different visual images of famous faces and places then given a 1 minute interference task before they were tested on free recall for the previously viewed images
identified rapid bursts in the hippocampus: sharp wave ripples
hippocampal SWRs at encoding predicted which pictures were subsequently recalled
a transient increase in SWR that anticipated onset of recall
neurons in higher-order ventral visual stream were preferentially activated by faces or places
this category specific activation was recapitulated during recall
such that the amplitude of activity in these areas was significantly higher when participants recalled the preferred stimuli and this activation was time-locked to HPC SWR
how has patient HM informed the study of memory?
Scoville & Milner, 1957
following bilateral MTL resection to relieve intractable epilepsy HM developed profound anterograde and severe but graded (11 years) retrograde amnesia
could not learn new episodic or semantic information regardless of sensory modality for verbal and nonverbal material
could not recall previously acquired memory close to the onset of the amnesia
the ability to learn new motor skills (mirror drawing, procedural memory), classical conditioning and repetition priming were intact
short term memory was intact
Augustinack et al., 2014
post mortem examination revealed that HM’s lesions of the MTL encompassed all of the entorhinal cortex, most of the perirhinal cortex, amygdala and dentate gyrus
the tail and medial hippocampus were intact
more accurate account is a deafferented HPC
the remaining HPC tissue may explain the gradient in retrograde amnesia
what evidence is there from patient studies of the acquisition of semantic information despite episodic memory impairments
Warrington & McCarthy (1988)
RFR, patient with severe selective encephalitic amnesia
retrograde amnesia for personal and public events encompassed his entire adult life
However he retained knowledge of words introduced into the vocabulary during the retrograde period: AIDs, telecom, Thatcherism, Shuttle and provisionals
note HM was not able to do this e.g was not able to define words such as jacuzzi which had been introduced into the lexicon following his surger (Milner)
Vargha-Khadem (1997)
patients with developmental amnesia due to early HPC damage were able to attend mainstream school and could learn new information including language literacy and factual knowledge within the low to average range
suggests that semantics information can be encoded independently of the hippocampus and are separate from epsiodic memory
what is ribot’s law and how has it influenced theories of memory formation
There is a temporal gradient in retrograde amnesia such that earliest memories survive the best
lead to consolidation hypothesis: oldest memories are more robust than newer ones because declarative memories are not dependent on the MTL forever
consolidation is the process of increasing resilience to memory loss by assimilation with existing knowledge and memories
Squire’s standard consolidation model (1992)
hippocampal-cortical interactions are required for consolidation
but memories are eventually transferred to the neocortex until the hippocampus is no longer required for retrieval
what is the evidence against Squire’s (1992) Standard Consolidation Model
Cannot explain flat gradient of retrograde amnesia observed when the entire hippocampus is lesioned
Barry & Maguire (2019)
rodent hippocampal lesions result in retrograde amnesia for contextual memory extended of 100 days pre-surgery
Nadel & Moscovitch 1997
patients with large hippocampal lesions display no gradient for the most recent three decades with little to no autobiographical memory
it seems implausible that there would be an adaptive mechanism for memory consolidation that extends beyond the average lifespan of humans throughout history
change in neural representation of the memroy without a corresponding change in the psychology
what theories of consolidation are able to account for flat gradient retrograde amnesia
Mutliple trace theory (Nadel & Moscovitch, 1997)
Memories are encoded as traces in the hippocampus linked to cortical networks
reactivation leads to multiple traces
retrieval of contextual rich episodes depends on the hippocampus which provides the spatial and temporal context for a memory
retreival of remote semantic memories is still possible in the absence of the hippocampus
the hippocampus is still important for remote memory
able to account for the dissociation in episodic and semantic memory in both anterograde and retrograde amnesia
trace transformation theory (wincour et al., 2010)
information about events are encoded and retained in multiple forms in parallel
the relative dominance in expression changes with time and experience such that they interact dynamically
Each psychological mnemonic trace depends on distinct functional and neural substrates such that there is neural-psychological representation correspondence. This means that remote episodic memories that retain their details also retain hippocampal dependent neurobiological characteristics, irrespective of memory age. It is proposed that episodic representations depend on the posterior hippocampus, gist traces depends on anterior hippocampus, schematic traces are supported by the ventromedial prefrontal cortex and posterior cortical interactions while semantic traces depend on the anterior temporal lobe and posterior cortex (Gilboa & Moscovitch, 2021).
BUT very short lifespan of HPC neurons
scene construction theory (Hassabis & Maguire, 2007)
memory traces do not persist in the hippocampus over time but are recruited during recall
the hippocampus reconstructs remote memories in the absence of the original trace by assembling consolidated neocortical elements into spatially coherent scenes via vmPFC input
process oriented approach able to account for evidence that the HPC is recruited for mental representations beyond the domain of memory
