Amnesia an associative model may provide the best explanation

Amnesia is a deficit in, usually episodic, memory
without any other cognitive deficits. It can be an inability to recall new
information (anterograde amnesia) and/or an inability to recall information learned
before the amnestic event (retrograde amnesia). Retrograde amnesia will have a
temporal gradient, i.e. events that occurred relatively recently around the
amnestic event are not remembered. It has been difficult to determine a model
which best describes amnesia due to differing lesions and symptoms between
patients. Furthermore, there is debate surrounding the definition of amnesia,
and which components of memory are affected. Given the difficulties in
describing amnesia, there is no “perfect” explanation. However, an associative
model may provide the best explanation because it attempts to account for most
of these issues, despite its shortcomings. This essay will focus on Squire and
Zola-Morgan’s (1991) associative model, and Aggleton and Brown’s (1999)
dissociative model, and the difficulties they both encounter in describing

Patient HM (Scoville & Milner, 1957) is one of the
most famous memory patients due to his impairment. He had bilateral lesions of
the medial temporal lobe (MTL), including resection of the hippocampus and
amygdala, to reduce seizures. This led to an inability to recollect events and
recognise staff from his hospital stay, however his intellectual abilities and procedural
memory appeared to be unaffected. E.g. HM was able to learn to trace a disc’s
movements, despite an inability to report this experience (Corkin, 1968). This
led to Squire and Zola-Morgan (1991) proposing that the MTL is responsible for
all declarative memory.

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The MTL memory system (MTLMS) comprises of
the entorhinal cortex, perirhinal cortex, and parahippocampal cortex which
forms a reciprocal network with the hippocampus to combine and consolidate
information across the MTLMS before it is stored in the neocortex. Thus, damage
to any part of the system should impair declarative memory. This explains HM’s
deficit because the hippocampus had consolidated memories in his distant past,
but his recent past, and was unable to consolidate memories from after his
surgery. Therefore, the memories of the events could not be stored in the
neocortex due to the damage in the hippocampus. Zola-Morgan and Squire (1984)
attempted to replicate the lesions found in HM in monkeys, and assess their memory
in visual discrimination tasks, tasks in which amnesic patients are impaired,
compared to motor skills acquisition. It was found that the monkeys with MTL
lesions were impaired on visual discrimination tasks, but not on motor skill
learning. This implies that the hippocampus and amygdala, and thus the MTL, are
involved in declarative memory acquisition. Contrary to this, RB (Zola-Morgan,
Squire & Amaral, 1986) suffered severe anterograde amnesia resulting from damage
restricted to the CA1 region of the hippocampus, due to an ischemic episode. It
was, therefore, concluded that damage to the hippocampus alone is sufficient to
produce amnesia. However, there was some damage to the basal ganglia and
somatosensory cortex which may have resulted in cell death without structural
damage. This could have further contributed to the observed memory impairments.
However, human lesions are rarely restricted, and damage to areas outside of
MTL may disrupt connections within the cortex, and produce memory impairments,
highlighting the potential difficulties that MTLMS encounters in explaining

This model proposes that greater damage
causes a larger functional impairment in memory due to the entire MTLMS being involved
in memory. This has been found by Zola-Morgan, Squire and Ramus (1994), who
showed that damage to hippocampus and surrounding cortex (H++) impaired memory
on delayed non-match to sample (DNMTS), and object discrimination tasks more
than hippocampal (H+), and hippocampal and amygdala (H+A) lesions. This
suggests a single memory unit in MTL, so damage to any part impairs declarative
memory. This is further supported by Rempel-Clower, Zola-Morgan, Squire and
Amaral (1996) who showed that more extensive hippocampal damage in humans (GD,
LM, and WH, compared to RB) resulted in more severe amnesia. WH had an
extensive bilateral lesion in the hippocampus, with cell loss in CA1, CA2, CA3,
dentate gyrus, and entorhinal cortex, and suffered severe anterograde and
retrograde amnesia. This further supports the MTLMS, and the proposal that
greater structural damage results in larger functional impairments. However, Baxter
and Murray (2001) found that monkeys were more impaired in the DNMTS task,
which models humans episodic memory, following smaller hippocampal lesions, but
larger rhinal cortex lesions resulted in larger impairments. This implies that
the different components of MTL may have distinct functions within memory, and
cortical regions may play a larger role than was first proposed.

While there is some evidence supporting a
singular MTLMS, there are some issues with this model. Firstly, there is debate
surrounding the definition of amnesia. This model assumes that all declarative
memory is affected by amnesia. However, evidence from developmental amnesia
patients implies a dissociation between episodic and semantic memory.
Vargha-Khadem et al. (1997) investigated which abilities are spared in three
cases of developmental amnesia – amnesia resulting from trauma early in life.
These cases all had bilateral damage to the hippocampus, and were impaired in
episodic memory tasks, but not on semantic memory tasks, when tested aged 12-19
years. This suggests that amnesia is a deficit in episodic memory only, and
that the hippocampus is involved in consolidation of episodic memories.
However, caution must be taken when interpreting the findings of developmental
amnesia due to the development of strategy use to recall information, as well
as neural plasticity, i.e. neurons change in form and function in response to
changes in their environment, such as damage to a structure. Therefore, it may
be that the hippocampus is also involved in semantic memory and this preserved
semantic knowledge is due to other cortical structures adapting the function of
the impaired hippocampus. Squire, Wixted and Clark (2007), therefore, suggests
that episodic memory recall is more sensitive to impairment, as recall is more
difficult than recognition/semantic knowledge, thus episodic memory traces must
be stronger to resist impairment.

Furthermore, the conflicting evidence
regarding a single entity suggests that this associative model of amnesia is a
simplistic view. E.g., BJ (Dusoir, Kapur, Byrnes, McKinstry & Hoare, 1990)
suffered from damage to the basal regions of the brain, including the mamillary
bodies, due to a snooker cue entering his nose. He suffered severe anterograde
and retrograde amnesia. While his anterograde amnesia improved, verbal memory remained
as impaired as other amnesic patients, and retrograde amnesia covering a period
of 6 months, persisted. This suggests that the hippocampus is not the only
structure involved in amnesia, and thus causes further difficulty in using an
associative model to describe amnesia.

Moreover, there are a wide range of
aetiologies which causes damage in the human brain, and due to this, damage is
rarely limited to one region. Annese et al. (2014) reviewed HM’s lesion,
finding that damage was not complete in MTL, with CA4 region of the hippocampus
being spared, and damage extending beyond MTL, including into the left frontal
lobe being damaged. Likewise, Corkin (2002) suggests that the use of
anti-epileptic drugs, such as that used by HM, can cause cortical
disintegration. This could account for HM’s extensive retrograde amnesia. Therefore,
the memory loss observed in all patients may not be a direct result of damage
to MTL structures, and further highlighting the difficulties that arise in
attempting to formulate a model to describe amnesia.

While this model provides an account of
retrograde amnesia, there is difficulty in explaining this deficit due to
differing temporal gradients between patients, and limited evidence on the
temporal nature of consolidation in the hippocampus. E.g. HM’s temporal
gradient was 11years, while BJ’s was 6months. This model attempts to explain retrograde
amnesia in terms of severity of hippocampal damage (Squire, 1994). However,
animal literature shows that consolidation can be in the order of minutes, e.g.
long-term potentiation. Dudai, Karni and Born (2015) propose that consolidation
and underlying mechanisms differ depending on the task, and how new information
relates to previously learned information. This may account for the
inconsistencies, though further research is needed to confirm this. Overall,
conflicting ideas on consolidation, and the differing temporal gradients further
emphasise the difficulties which arise in explaining amnesia.

In sum, there does seem to be a wealth of
support for an associative model of amnesia wherein consolidation of declarative
memory is dependent on hippocampal function. However, there is evidence of
amnesia occurring without damage to the hippocampus which highlights the
difficulties in using this model to describe all cases of amnesia.

Aggleton and Brown (1999) propose a dissociation
between semantic and episodic memory. This extends the associative model,
proposing that the MTL and the extended hippocampal system, including the
thalamus, are involved in declarative memory. They suggest that the medial
dorsal thalamus and perirhinal and parahippocampal cortex are involved in
familiarity (analogous to semantic memory), while the anterior thalamus and
hippocampus are involved in recollection (akin to episodic memory). This is
supported by single dissociations in animal and human lesion data. Patients KN
and YR (Aggleton et al., 2005) have shrinkage of the hippocampus, and spared
surrounding cortex. They have consistently poor recall ability, but intact
recognition. This suggests that there is a dual system underlying episodic
memory that could account for differing symptoms evident in different patients.
Furthermore, patient NA (Squire, Amaral, Zola-Morgan, Kritchevsky, & Press,
1989) had damage localised to the thalamus, and suffered severe anterograde
amnesia, especially in recall of verbal material. According to an associative
model, this patient should not suffer anterograde amnesia, as the hippocampus
was reportedly intact, so consolidation of memories should not be affected.
However, this was not found, further emphasising the importance of the
diencephalic system in memory and amnesia. However, pure diencephalic amnesia
is rare and further investigation of NA’s pathology showed cortical damage
around the hippocampus in the MTL, so further research into the role of the
thalamus in memory is needed.

Further research relies on animals,
allowing for more precise lesions to be completed, and for potential double
dissociations between recollection and familiarity memory. Using the
what-where-when (Tulving, 1983) and what-where-which (Eacott & Norman, 2004)
compounds, animals’ memories can model human episodic memories, wherein human episodic
memory contains contextual information (e.g. time) linked with an event and location.
E.g. scrub-jays can locate worms and peanuts after short (24hr) and long
(124hr) delays, respectively (clayton & Dickinson, 1998). This was interpreted
as showing that animals also possess episodic-like memory as they could recall what they had cached where, and when (i.e. how long ago) they
had cached items. Eacott and Norman (2004), however, showed that the “when”
component of episodic-like memory is difficult for humans and animals as
memories are not date-stamped, so propose that “which occasion” (i.e. context) is
a more accurate term that can aid recall of temporal information. They showed
that rats with fornix lesions explored a novel what-where-which combinations less
than rats with perirhinal and postrhinal lesions, while controls could
simultaneously retain similar but distinct what-where-which information for two
events over periods up to an hour. This highlights the importance of
hippocampal projections in recognition memory. However, recognition tasks can
be solved using recollection or familiarity, so results only indicate a single dissociation
between recollection and recognition. Eacott, Easton, and Zinkivskay (2005)
modified this set-up to allow for dissociation between recollection and
familiarity judgements by using an E-shaped maze. Following familiarisation of
objects’ locations in the backbones of different backgrounds, the objects were
hidden in the arms of one of the contexts. A rat was, therefore, using
recollection if they turned towards the correct arm in test phases, but were
using familiarity when the objects were seen in training. Eacott & Gaffan (2005)
found that rats with hippocampal lesions had unimpaired recognition memory in this
task, as well as performing well on components of the what-where-which combination,
but were severely impaired on recollective components of this task, showing
that hippocampal projections are involved in recognition, and not recollection.
Parker, Eacott and Gaffan (1997) have also found that mediodorsal thalamic
lesions in macaque monkeys are impaired in DNMTS task for large stimulus sets
only, suggesting that the mediodorsal thalamus is involved in recognition
memory. Combining Eacott and Gaffan’s (2005) and Parker et al.’s (1997) studies
gives a double dissociation that supports a dissociative model of amnesia.
However, there is conflicting evidence that presents further difficulties in
describing amnesia. Merkow, Burke and Kahana (2015), for example, used
high-frequency activity measurements and showed that the hippocampus supports
both recollection and familiarity in humans, thus does not support the
dissociative model, and adds further support to the associative model. Furthermore,
Pergola et al. (2012) who found that the deficits in recollection and
recognition memory correlated with the loss in stroke patients’ mediodorsal
thalamus. This does not support the dissociative model, and lends further
support to an associative model of amnesia.

It is difficult to present a double
dissociation study investigating the neural underpinnings of recollection and
familiarity, due to both processes being involved in recognition, and pure
diencephalic amnesia being rare. However, Bowles et al. (2007) investigated NB
using the remember/know paradigm, which allows for measurement of degree of recollection
and familiarity for events. NB had damage to the entorhinal and perirhinal cortices
but spared hippocampus, and it was found that NB’s recollection memory
(“remember”) was unimpaired, while familiarity memory (“know”) was
significantly impaired. While this study does support a dissociative model, it
is only a single case study, but when compared with RB (Zola-Morgan, Squire
& Amaral, 1996), a double dissociation in support of the dissociative model
is found. Additional support is found in developmental amnesic patients,
wherein the shrinkage/damage to mamillary bodies correlates with the deficit in
recollection, despite preserved recognition and semantic memory (Dzieciol et
al., 2017). There are several limitations with studies of developmental
amnesia, as discussed previously, that present further issues in describing
amnesia using a prescribed model. Wixted and Squire (2010) have reviewed
hippocampal involvement in recognition, concluding that evidence is converging
on a less sharp distinction between familiarity and recollection, and between the
functions of the perirhinal cortex and hippocampus, because patients are rarely
only impaired in recollection or familiarity, implying that the MTL cannot be
divided up as crudely as proposed by a dissociative model.

Unlike an associative model, this model does
not attempt to account for retrograde amnesia, and so cannot describe all cases
of amnesia. This presents a further difficulty in describing amnesia using this
model because patients who only suffer anterograde amnesia, such as NA, can be
explained. This implies that an associative model provides a better account of
amnesia as it can account for both anterograde and retrograde amnesia, despite
being simplistic in its account.

Overall, there is a wide body of support for both
associative and dissociative models of amnesia, though no one model adequately
describes all cases of amnesia, due to differing symptoms and pathologies in patients.
An associative model, compared with a dissociative model, seems to best
overcome these difficulties by explaining amnesia in terms of consolidation, accounting
for retrograde and anterograde amnesia, and explaining recollection/familiarity
differences in terms of difficulty.