Amnesia, impairments and preserved abilities in brain. In this

Amnesia,
as an organic clinical disorder caused by brain damages, refers to permanent
disturbance of declarative memory despite preserved cognitive functions
(Markowitsch, 2001; Moscovitch, 2004). Patients with anterograde amnesia (AA)
consistently show different degrees of impairment in forming declarative
memory, with normal implicit and working memory. Studying amnesia provides
insights on cognitive and biological mechanism underling memory, and a
representative model is vital for understanding existing data and making
predictions. Although researches on amnesia have progressed a lot since the
famous case of H.M., a convincing and widely accepted model has yet to be
established. One of the main debates concerning it is whether the major
impairment in amnesia, declarative memory, is relating to the damage of an
associative or dissociative neural system. The presentation of amnesia varies
across patients, and data are inconsistent. Hence, it causes a great challenge of
model’s generalizability. Since both of them are rather inconclusive in
explaining all the existing data, it is difficult to tell whether one is
superior to the other. Apart from the models themselves, external factors have
also posed difficulties in determining whether one of them is better. Although declarative
memory could be subdivided, the interdependent nature of the subcomponents
makes it difficult to test them separately in a clean way. Furthermore,
difficulty in making accurate predictions is also a barricade. To predict
impairments from brain lesions, it is essential to localize the neural
substrates of memory in the corresponding brain regions. However, the
plasticity of brain and adoption of compensatory strategies make it difficult
to map the impairments and preserved abilities in brain. In this essay, the associative
model proposed by Squire and the dissociative model proposed by Aggleton and
Brown (A) would be used to illustrate the difficulties in determining
whether one of them better describes amnesia. It is argued that both of them are
inconclusive in explaining all the of existing data. Moreover, the
interdependent nature of subtypes within declarative memory and plasticity of
brain make both of the models not testable or predictable.

 

To
compare on the same ground, Squire’s model has relative strengths in explaining
single dissociation in human cases, while double dissociation in animal studies
seems to support A&B’s model instead. According to the medial temporal lobe
memory model proposed by Squire, declarative memory is
supported by a unitary system which includes hippocampus, entorhinal,
perirhinal and parahippocampal cortex (Squire & Zola-Morgan, 1991). As a single entity, degrees of
impairment should be proportionated to the extent of lesion in the system,
regardless of location (Squire et al., 2004). Whereas, A advocates a
dissociative model concerning the hippocampal-diencephalic system. As claimed
by this model, recollection and familiarity are two distinct pathways (Aggleton
& Brown, 1999). To recall episodic memory, recollection supported by the
Papez circuit is required. This circuit is connected by fornix and
mammillothalamic tract, and includes hippocampus, mamillary bodies (MB) and
anterior thalamus nuclei (ATN). Whereas, recognition is subserved by
recollection and/or familiarity. As long as recognition does not involve relational
binding between elements, familiarity pathway that supported by cortices
(perirhinal, entorhinal and parahippocampal cortex) and medial dorsal thalamic
nuclei (MDTN) is sufficient (Brown & Aggleton, 2001).

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In order to validate
A’s idea, double dissociation between recognition and recall is required.
The clinical evidence that A&B’s model initially built upon were cases
showing selective impairments in recall, which were suggested to be the results
of sole damages in recollection but not familiarity pathway (Aggleton &
Brown, 1999). Further support was provided by subsequent cases that
consistently presented similar selective impairments. For instance, patient KN
and YR who had selective bilateral lesions in hippocampus performed far below
average in recall tasks, but relatively normal in recognition of both verbal
and visual materials (Aggleton et al., 2005; Kopelman et al., 2007). Similarly,
patient DN had recollection pathway disrupted by fornix compression, also
presented selective impairments in recall (Vann et al., 2008). Nevertheless, as
what endorsed by A in their later review (2006), to date there is no
recorded case showing the opposite selective impairments.  Although receiver operating characteristic
(ROC) analysis has successfully differentiated recollection and familiarity
pathway underlying patients’ preserved memory in recognition (Aggleton et al.,
2005; Cipolotti et al., 2006), such statistical dissociation is still
qualitatively different from clinical dissociation. This single dissociation
does not provide convincing evidence for A&B’s model, but is more likely to
go with Squire’s instead. According to his model, recognition could be
independently preserved since it is cognitively less demanding, and would be
impaired only when pathology is severe enough (Squire et al., 2004). In other
words, it is not the location, but the extent of lesion that is important for
explaining patterns of impairments. If this is the case, then impairments in
recognition and recall should be proportionate to each other since they belong
to one single system. Consistent with this, studies adopted MRI scanning found volume
in medial temporal lobe and hippocampus negatively correlated with impairments
in both recall and recognition (Kopelman et al., 2007; Kramer et al., 2005).
However, the discussed evidence is still inconclusive since anatomical lesion
may not be equivalent to functional lesion (Bachevalier, 1996; Aggleton, 2008).
Animal studies enable more confined focal brain lesion, and they could
complement lesion studies in human to investigate the neuroanatomy underlying
patterns of memory impairment.  In
contrast to human cases, animal studies have clearly presented double
dissociation between recall and recognition. Eacott and Norman (2004) defined
episodic-like memory in animals as the interaction of eventual (what), temporal-spatial
(where) and contextual (which) information. Without either where or which
component, animal’s memory of “what” could be supported by familiarity alone.
The speciality of episodic-like memory is probably subserved by the
relational-binding function of hippocampus, which enables mental construction
of scenes (Maguire et al., 2010). Supporting this idea,