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Abstract
Source amnesia is an explicit memory (declarative) disorder,
particularly episodic, where source or contextual
information concerning facts is severely distorted and/or
unable to be recalled. This paper reviews the literature on
source amnesia, including memory distrust syndrome, and its
accepted correlation with the medial diencephalic system and
the temporal lobes, and the suggested linkage between the
frontal lobes, including special interest with the
prefrontal cortex. Posthypnotic induction was the first
presentation of source amnesia identified in the
literature. The Wisconsin Cart Sorting Test (WCST),
Positron Emission Topography (PET), Phonemic Verbal Fluency
Test, Stroop Color Word Interference Test, and explicit and
implicit memory tests are defined and linked to empirical
research on amnesiacs.
Introduction
One often remembers factual information yet forgets the
contextual information related to the fact (i.e., when,
where, and with whom the fact was learned). In the case of
Jon, recollection of such contextual information was nearly
impossible. At the age of 23, although born premature, Jon
ponders the nature of his apparent ailment.
Neuropathological findings suggest that one of Jon's brain
centers is severely retarded, impairing one route of the
human memory course - namely episodic memory (Baddeley,
Vargha-Khadem et al. 2001). Such an occurrence represents a
loss of source or contextual memory, a phenomenon referred
to as source amnesia (Evans and Thorn 1966; Schacter,
Harbluk et al. 1984). Research conducted in the past two
decades has considerably advanced our comprehension of the
human memory process, and consequently improved our
understanding of the complex mechanisms of source amnesia.
However, until recently, most explanations for amnesia
assumed that the condition was undivided and had a solitary
functional deficit. Using various neurological imaging and
executive function tests only available in the recent past,
researchers now suggest that the frontal region of the
brain, particularly the prefrontal cortex of the frontal
lobes and the medial diencephalic system, is highly
attributable to the storage and retrieval of contextual
details, but plays a minor role in fact recollection.
Therefore, the brain's functional systems for memory for
facts and memory for contexts may be dissociated. In
addition, the deterioration of these neuroanatomical organic
structures due to "normal" aging may contribute to the
degradation of contextual scanning ability, as well as
information encoding and retrieval efficiency. Likewise, in
subject populations where the anatomical structures are not
fully mature (i.e., very young children), amnesic symptoms
should be profound.
The purpose of this paper is to survey and synthesize the
rich research on source amnesia gathered from the 1950s to
the present, with a particular emphasis on the suspected and
identified neurological centers associated with source
memory. Source amnesia genesis and presentation in the
posthypnotic environment is also of interest because the
discovery of source amnesia's symptom of forgetting
context-specific information first occurred in subjects
under hypnosis. Finally, the common assessment tools are
discussed, including neuroimaging techniques, implicit and
explicit memory tests, the Wisconsin Card Sorting Test,
Phonemic Verbal Fluency Test and Stroop Color Word
Interference Test for prefrontal assessment.
Human Memory Process
Cellular and molecular
studies of both implicit and explicit memory suggest that
experience dependent modulation of synaptic strength and
structure is a fundamental mechanism by which implicit and
explicit memories are encoded and stored within the brain.
Before discussing human memory concepts, it is worthwhile
going in brief about memory formation in sensory neurons of
Aplysia (snail) and hippocampal neurons of mouse. The
eleven critical cellular and molecular mechanisms of memory
storage identified are
1.
Neurotransmitter release and short term strengthening of
synaptic connections
2.
Equilibrium between kinase and phosphatase activities at the
synapse
3.
Retrograde transport from the synapse to the nucleus
4.
Activation of nuclear transcription factors
5.
Activity dependent induction of gene expression
6.
Chromatin alteration and epigenetic changes in gene
expression
7.
Synaptic capture of newly synthesized gene products
8.
Local protein synthesis at active synapses
9.
Synaptic growth and the formation of new synapses
10.
Activation of pre existing silent synapses and
11.
Self perpetuating mechanisms and the molecular basis of
memory persistence
The location of the above events
moves from the synapse (1-2) to the nucleus (3-6) and then
back to the synapse (7-11).
There is great interest in how the brain can maintain the
persistent neural activity encoding recent stimuli that is
thought to be the basis of working memory (Fuster, 1988).
Several theoretical mechanisms for the maintenance of
persistent activity have been described (Durstewitz et al.,
2000), including local recurrent feedback and intrinsic
persistent activity on a single-cell basis. Recurrent
excitation at the local circuit level has received the most
attention, from Hopfield models through elaborated
conductance unit networks (Durstewitz et al., 2000; Wang,
2001). Wilson and Cowan suggested that meaningful insight
into the behavior of neural ensembles might be gained by a
mean field approach describing the average rate of firing
over some coherent population (Wilson and Cowan, 1972).
Averaging on a local scale in combination with lateral
connectivity described by a spatial kernel with wider
support leads to a continuum, integrodifferential
description of spatiotemporal neural activity (Wilson and
Cowan, 1973). At the same time, there is now renewed
interest in the concept that individual neurons might have
some inherent ability to sustain persistent activity without
recurrence. The remarkable finding that individual
entorhinal cortical neurons can sustain graded persistent
activity (Egorov et al., 2002) is the perhaps most striking
example to date. At the intersection of these ideas is a
model by Camperi and Wang (C-W) which explores the idea of
bistability in individual neurons within an Amari-type (Amari,
1977) integrodifferential network model (Camperi andWang,
1998).
The biological basis for such bistability remains little
explored. Ca2+ has been shown experimentally (Egorov et al.,
2002) and theoretically (Fransen et al., 2002) to contribute
to persistent firing of neurons, via upregulation of a
nonspecific cation current. Neuromodulators linked to Ca2+
release or Ca2+ sensitive signaling cascades have been shown
to increase synaptic NMDA currents (Seamans et al., 2001)
and the persistent sodium current (Yang and Seamans, 1996),
both of which might increase the efficacy of synaptic input.
There is a fair amount of controversy over the effects of
neuromodulators (Seamans and Yang, 2004).
Numerous theoretical accounts of human memory have
differentiated memory for facts and memory for contexts (Tulving
1972; Schacter 1987). Tulving (1972; 1983) further defined
these two declarative explicit memory concepts (in which
information is consciously registered and recalled) into
semantic memory, where general world knowledge not tied to
specific events is stored, and episodic memory involving the
storage of context specific information about personal
experiences (i.e., time, location, and the surroundings of
personal knowledge). Conversely, implicit memory (non
declarative) may involve unconscious registration (lack of
awareness during encoding), yet definite unconscious
recollection (Schacter 1987). Skills and habits, priming,
and classical conditioning all utilize implicit memory. The
diagram shows an abridged graphical representation of the
human memory process and its general association with source
amnesia (Figure 1).
Figure 1: Source amnesia neuropsychological association
diagram with partial information processing and long term
memory organization chart.
An essential aspect of episodic memory includes date and
time encoding in the subject's past. For such processing,
the details surrounding the memory (i.e., where, when, and
with whom the experience took place) must be preserved and
are necessary for an episodic memory to form, otherwise the
memory would be semantic (Bullock 1998). For example, one
may posses an episodic memory of President John F. Kennedy's
assassination, including watching Walter Cronkite announce
Kennedy’s death on TV. However, if the contextual details of
this event were lost, the remaining would be only a semantic
memory that John F. Kennedy was assassinated. The ability to
recall episodic information concerning a memory is called
source monitoring (Johnson, Hashtroudi et al. 1993), and is
subject to distortion (Johnson, Hashtroudi et al. 1993; Goff
and Roediger 1998) that may be lead to source amnesia.
Memory Distrust Syndrome
As source amnesia prohibits the recollection of context
specific information surrounding facts in experienced
events, there is also the inclusive case of confusion
concerning the content or context of events, a highly
attributable factor to confabulation in brain disease. Such
confusion has been loosely termed memory distrust syndrome (Gudjonsson
and MacKeith 1982). A person who suffers from memory
distrust syndrome distrusts their memory and may be
motivated to rely on external (non-self) sources. One known
cause is people who are suffering from Obsessive Compulsive
Disorder (OCD), where repeated relevant checking rituals is
known to cause reductions in memory confidence, vividness
and detail, resulting in memory distrust (Van den Hout and
Kindt, 2003, 2004).
The propensity to accept information from external sources
(i.e., an interrogator) based on the influence of
susceptibility has led to well documented false confessions
(Gudjonsson and MacKeith 1982; 1990; Gudjonsson 1992; 1996;
McCann 1998; Gudjonsson, Kopelman et al. 1999; see
Gudjonsson 2003 for a review). Moreover, the credibility of
a witness that suffers from memory distrust syndrome is
questionable. In a parallel situation, amnesic individuals
may be more susceptible to having their memory manipulated,
perhaps performing non-advantageous acts at the "direction"
of external sources, and experience difficulty
differentiating between imaginary and real experiences.
Given that source amnesia pathology is an identified and
natural occurrence in the criminal law system, psychiatrists
should perform assessment and identification measures to
isolate this disorder in accused individuals and
eyewitnesses.
Assessment and Identification Methods
Tests involving various
interactions and responses are employed on subjects to
determine the type of memory processes that are utilized,
affected, or regulated. Intuitively, accessing such facets
of human memory requires circumlocutory procedures since
implicit memory is understood to be unconsciously registered
and categorically involuntarily recalled. Explicit memory
tests are rather straightforward, although variation exists
within this subcategory. In assessing neurological function
(and dysfunction), standard measure neuropsychological tests
are utilized.
Explicit and Implicit Memory Tests
Different techniques are utilized to reveal and examine
explicit and implicit memory. For explicit memory, there are
four prominent methods for direct examination: free recall,
cued recall, yes-no recognition, and forced-choice
recognition (Leahey and Harris 2001). Free recall is devoid
of any indicators or hints (i.e., the experimenter would ask
questions like "Tell me about [a general topic]…"), whereas
cued recall contains clues (i.e., a fill-in-the-blanks
assessment). A side effect of free recall is the recall of
less accurate information; however, a potential for bias is
nonexistent but present in cued recall.
In the two recognition pathways, one must produce a response
and recognize its validity. With yes-no recognition,
information is presented to the subject and they must
indicate whether it is valid with a "yes" or "no" response.
Finally, the forced-choice recognition measure consists of a
required choice among several options where only one is
correct (i.e., multiple choice exams). Recent reports
indicate that since recognition memory tests depend on
familiarity, amnesiacs perform normally on yes-no
recognition and forced-choice recognition (Hirst and et al.
1986; Aggleton and Shaw 1996) tests in equal proportions (Khoe,
Kroll et al. 2000).
Recent studies of explicit memory have employed delayed
non-matching to sample performance tasks to assess
recognition memory for objects (Gaffan, Gaffan et al. 1984;
Diamond, Zola-Morgan et al. 1989; Gow 1995). The task has
three parts: a familiarization, delay, and test phase.
During the familiarization process, the subject is presented
with a sample object. After a period of delay, the
experimenter presents a new object either to the left or
right of the sample object. The subject's goal is to choose
the novel object (i.e., the object that is not the sample),
and they receive a reward if they are successful. Research
has demonstrated that children enjoy novelty over
consistency (Fantz 1964; Fagan 1970; Cohen and Gelber 1975),
thus they find it easier to understand and proceed with
delayed non-matching than matching to sample tasks (Brush,
Mishkin et al. 1961; Gaffan, Gaffan et al. 1984). The more
objects a subject correctly discriminates, the greater their
recognition memory skill.
Implicit memory evaluations test memory more indirectly by
examining performance on tasks that may obliquely reveal
properties of remembrance. With word-fragment completion,
implicit memory is measured by presenting a fragmented word
(i.e., P_Y_H_L_G_) and asking the subject to identify the
complete word. It should be noted that priming greatly
affects task performance (i.e., presenting the phrase
"mental-health" prior to the aforesaid fragmented word,
"Psychology") (Leahey and Harris 2001).
In examining amnesiacs, the priming effect is quite
noticeable in patients undergoing surgical procedures
requiring general anesthesia. The patients were more likely
to produce words of a given category if they had heard them
while under anesthesia (Millar 1987; Charlton, Wang et al.
1993), even though there was no explicit conscious memory
for the information heard under anesthesia.
Positron Emission Topography (PET)
Neurological imaging techniques have been used extensively
in amnesiac studies to locate the neurological areas
attributable to memory and cognitive functions. Positron
Emission Tomography (PET) scans provide biochemical
resolution of a patient's body without the use of invasive
measures. While other imaging scans such as CT and MRI
isolate organic anatomical changes in the body, PET scanners
are capable of molecular biology detail (even prior to
anatomical change) via the use of radioisotopes highly
metabolized in cancerous tissues. Regarding source amnesia
neuropsychological research, the changing of regional blood
flows in various anatomical structures (as a measure of the
injected glucose emitter) can be visualized and relatively
quantified with a PET scan (Cabeza, Kapur et al. 1997).
The three common tests used to
assess executive function are
1.
Wisconsin
Card Sorting Test (WCST)
2.
Phonemic Verbal Fluency Test
3.
Stroop Color Word Interference Test
Wisconsin Card Sorting Test (WCST)
The Wisconsin Card Sorting Test (WCST), developed by Berg
(1948), is the most common assessment tool for executive
function (Bullock 1998). It assesses
1.
Cognitive flexibility
2.
Problem solving and
3.
Response maintenance
The subject is presented with four model cards that differ
in color, number, and shape. The subject is instructed to
place the response cards (consisting of all possible
combinations of shape, color, and number traits) directly
below the model cards that they believe match. Feedback is
given to the subject about whether they correctly associated
the cards. If the subject fails to correctly match the cards
according to the unstated guidelines, they must be able to
alter their sorting strategy (Bullock 1998). The WCST model
without the number attribute has been adopted for testing on
very young children, thereby providing an extensive range
for a potential population based on age.
Throughout the WCST procedure, the subject is not informed
of the reasoning behind the experimenter's "right" or
"wrong" feedback. Thus, a great level of ambiguity exists
for novice and skilled subjects performing the task. The
main calculating factor of the WCST is the number of
preservative errors committed (when the subject can not
alter the sorting criterion despite being given feedback
that their selection is erroneous). The next important
significant variable as an index of executive function is
the total number of categories attained by the subject. A
credited category occurs when the subject has correctly
sorted a given number of successive cards (usually ten).
Although the WCST is an valuable indicator of prefrontal
function (Nelson 1976), its sole use to discern a group of
front damage patients from a control set is unreliable
(Anderson, Damasio et al. 1991; Mountain and Snow 1993). It
is because in addition to the activation of dorsolateral
prefrontal cortex, it is found that activation of
ventromedial and orbitofrontal prefrontal cortex, inferior
parietal cortex, basal ganglia, tempero parietal association
cortex, occipito temporal, temporal pole and occipital
cortices also occur during performance of WCST. It is also
unclear whether left or right prefrontal cortex is
stimulated by WCST. But it is accepted that bilaterally
intact prefrontal cortex, especially dorsolateral is
necessary for normal WCST performance.
For the above reasons, WCST is a sensitive, but not a
specific test to assess prefrontal function.
Phonemic Verbal Fluency Test
The Phonemic Verbal Fluency Test is another test used to
assess executive function, especially of the frontal cortex.
In this, the participants are instructed to say or write as
many words as possible beginning with a specific letter.
People with frontal lesions (especially left) perform poorly
(Troyer et al., 1998). Like WCST, this test is very
sensitive but not very specific for assessing functioning of
Prefrontal lobes.
Stroop Color Word Interference Test
The Stroop Color Word Interference Test is another measure
to assess frontal cortex function, especially selective
attention (Blenner, 1993; Carter et al., 1995; Goodglass and
Kaplan, 1979; Lezak, 1995; Macleod, 1991; Stuss et al.,
2001). In this test, participants are exposed to three sets
of stimuli namely
1.
Color words printed in black ink
2.
Color patches or colored Xs or
3.
Color words printed in incongruous colored ink (eg. The word
red printed in blue ink)
Participants are requested to read
the color words of the first sheet, colors on the second
sheet and color of the INK on the third sheet. In the third
task, the normal tendency to read the words, rather than the
color of the ink in which the words are printed, elicits a
significant slowing in reaction time (RT) call the "Stroop
Effect" or the interference effect.
Persons with left frontal lobe
lesions (especially of lateral and superior medial and not
orbitofrontal) display significantly longer interference
trial RTs than those with non frontal lobe lesion.
Etiology
Since source amnesia involves the lack of source memory
recollection - although the fact itself is remembered - one
would expect the prominent occurrence of source amnesia with
pre-mature, deteriorated, or damaged neurological centers
responsible for episodic memory. Such dysfunction may be due
to encoding, retrieval, or storage processing errors,
including inefficient source monitoring.
The prefrontal
cortex has been associated with the processing of executive
functions, including the organization of information; goal
intended behavior, and planning and inhibition. Thus,
performance on such functions has become an accepted
indicator of prefrontal function (i.e., the WCST). In
addition, recent investigations have attributed episodic
memory to be another function of the prefrontal cortex even
though the role of the prefrontal cortex is still disputed (Swick
and Knight 1999; Heckers, Curran et al. 2000; Mayes and
Montaldi 2001; Rossi, Cappa et al. 2001; Lee, Robbins et al.
2002; Wagner 2002).
Posthypnotic Induction
Posthypnotic source amnesia occurs when some fact is learned
under hypnosis and the information is forwarded to the
conscious or walking state, but the knowledge that it was
learned under hypnosis is forgotten (contextual-specific
information). In contrast, posthypnotic recall amnesia is
used to describe similar hypnotic situations with the loss
of factual information instead of contextual information
(Thorn 1960).
In a typical posthypnotic source amnesia experiment, the
subject is told the answers to previously unknown questions
under hypnosis (i.e., Harare is the capital of Zimbabwe).
The time, place, and experimenter-specific information are
recorded (i.e., number of experimenters and which one
informed the patient of the fact). After the hypnotic
session, the awakened subject is questioned concerning the
learned facts and the contextual specifics. In order to
credit the subject with source amnesia, they must answer the
questions correctly but fail to identify the source of the
information.
Thorn's study (1960) implemented such hypnotic procedures
and, most importantly, amnesia was never suggested to the
subjects; thus, the measure was for spontaneous posthypnotic
source amnesia. Based on his procedural conditions, Thorn
demonstrated that source amnesia was an authentic effect of
hypnosis and not an artifact of the demand characteristics
of the situation (Cooper 1966). Furthermore, Cooper (1966)
suggested source amnesia to patients (i.e., informed the
hypnotized subject to forget the source of information) and
noticed a greater frequency of source amnesia in the
suggested than in the spontaneous subjects, further
validating source amnesia as a genuine hypnotic phenomenon.
Evans and Thorn's (1963) early hypnotic research forged a
path for current scientists to follow regarding the
multifaceted machinery of source amnesia, and permitted
Schater (1984) to systematically demonstrate source amnesia
in amnesic patients.
Neuropsychology of Episodic Memory
Neuroanatomical evidence for the correlation of explicit
memory - and hence semantic and episodic memory - to the
temporal lobe dates back to the 1950s (Milner 1964). Since
then it has been recognized that the medial diencephalic
structures, in addition to the temporal lobe, are involved
with episodic memory (Diamond, Towle et al. 1994; Andreasen,
O'Leary et al. 1995; Buckner, Petersen et al. 1995; Nyberg,
Tulving et al. 1995; Cabeza, Kapur et al. 1997; Buckner,
Koutstaal et al. 1998; Buckner, Koutstaal et al. 1998; Reed
and Squire 1999). Through magnetic resonance imaging (MRI)
(Alvarez, Zola-Morgan et al. 1995), two-choice recognition
tasks (Reed and Squire 1999), and delayed non-matching to
sample performance tasks (Diamond, Towle et al. 1994),
source memory has been attributed to medial diencephalic
system activity. The structures of the medial diencephalic
system include the hippocampus, perirhinal cortex,
parahippocampal cortex, entorhinal cortex, and direct
connections to the limbic system (Kaut 2001).
The reliance of source memory on the prefrontal cortex (a
division of the frontal lobes) has been recently suggested (Shimamura
and Squire 1987; Janowsky, Shimamura et al. 1989; Shimamura
and Squire 1991; Knowlton and Squire 1995; Squire and
Knowlton 1995; Bullock 1998; Senkfor and Van Petten 1998;
Wilding 1999; Drummey and Newcombe 2002). Patients with
prefrontal damage have exhibited a higher propensity to
source amnesia than normal controls (Schacter, Harbluk et
al. 1984; Shimamura and Squire 1987; Janowsky, Shimamura et
al. 1989).
Age Associated Source Amnesia: Neurological Maturation
and Deterioration
It has been hypothesized that the frontal lobes fully mature
between the ages of four to seven years old (Luria 1963)
and, remarkably, is the last area of the brain to fully
develop. Neuroimaging (PET) (Chugani 1987),
electroencephalographs (EEG) (Thatcher 1991), and research
on monkeys (Diamond, Zola-Morgan et al. 1989) have
demonstrated that the frontal lobes mature relatively late.
Therefore, on the premise of structure-function parallels in
this area of neuroanatomy, very young children with
pre-mature frontal lobes should display significance in
source recollection errors and thus greater source amnesia
than those with mature frontal lobes.
As predicted, Bullock's study (1998) showed that four-year
old children showed a significant amount of source amnesia
(as an index of the WCST). In addition, she found that
eight-year olds (who have fully mature frontal lobes)
exhibited "dramatically less" source amnesia than four-year
olds. Aside from the associated frontal lobe maturation that
occurs during this four-year interval, the episodic memory
changes in childhood may be attributable to the simultaneous
development of other neuroanatomical structures yet to be
identified.
Although the frontal lobes are the last neuroanatomical
region to fully mature (Bullock 1998) during the normal
aging process, they are considered the first to deteriorate
(Huttenlocher 1979; Haug, Barmwater et al. 1983; Raz, Torres
et al. 1993). As people age, memory for context tends to
deteriorate at a fast rate (Salthouse 1982; Craik 1983),
while memory for facts declines relatively little (Salthouse
1982). Researchers have discovered that frontal lobe
dysfunction correlates to the normal aging course
neuroanatomically (Whelihan and Lesher 1985),
neuropyschologically (Whelihan and Lesher 1985), and
electrophysiologically (Woodruf 1985).
Prefrontal cortex correlation studies of the normal aging
process have varied, but the majority of research has shown
prefrontal association. For example, McIntyre and Craik
(1987) and Craik (1990) showed a parallel correlation, while
Spencer and Raz (Spencer and Raz 1994) found non-significant
associations. However, studies using neuroimaging techniques
(Kapur 1998; Rossi, Cappa et al. 2001) have mapped the
prefrontal cortex to episodic memory processing (see Mayes
and Montaldi 2001 for review). Thus, the variations in the
relationships between the normal aging process and the
prefrontal cortex may be credited to a lack of proper
prefrontal assessment (i.e., the lack of standardization
measures) and the nature of the subjects in the studies
(i.e., variability in health status and cognitive
abilities). However, Bullock (1998) found significant
amounts of source amnesia in very young children, and
identified prefrontal function linkage with source amnesia
incidence on the basis of prefrontal cortex maturation. One
can suggest that episodic memory, particularly memory for
source, may rely on the prefrontal cortex in addition to the
temporal regions and the medial diencephalic structures of
the brain. However, it is possible that deteriorated (as in
the course of the normal aging process) compared to
pre-mature (i.e., very young children) frontal cortexes
perform significantly different in memory tasks.
The prevalence for source amnesia has been well documented
in elderly populations owing to the neurological
deterioration of the frontal region, namely the medial
diencephalic system and the frontal lobes, including special
interest with the prefrontal cortex (see Figure 1 for
diagram). However, most studies have indicated mild source
amnesia in young children undergoing frontal lobe
maturation, but only in direct comparison with newly fully
developed patients (i.e., the eight year olds in Bullock's
(1998) study). Thus, the organic deterioration of the
frontal lobes in the process of normal aging has a greater
influence on episodic memory than pre-mature lobes in young
children. The differentiating mechanisms between the
maturation and deterioration, if any, are unknown at this
time.
Conclusion
The discussion done in this review is just the tip of the
iceberg in the understanding of source amnesia and the day
will definitely come in future whereby different treatment
options for source amnesia become available. Until we
understand the simple and complex neural circuitry, map the
neurological centers responsible for episodic memory and
thus source amnesia, and identify the pathways for neuro-biological
and -psychological maturation, deterioration, and damage,
source amnesia and related conditions will remain largely
unsolved. However, at this stage, we have pieced together a
portion of the puzzle and, remarkably, eradicated the
old-fashion notion that amnesia is a unitary disorder. As an
episodic memory disorder, source amnesia is attributable to
the dysfunction of the normal memory process involving
encoding, storage, and retrieval. Thus, a parallel exists
between advancements in the human memory process and
neuropsychology and our comprehension of source amnesia.
In future, it is fully expected that many more fascinating
details of the molecular mechanisms responsible for memory
formation and stabilization processes will come to light.
Toward that end, the field will continue to benefit from the
rich contribution of the diverse disciplines including
psychology, physiology, pharmacology, cellular and molecular
biology, biochemistry, genetics, biophysics and
bioinformatics that have already shaped the study of memory
during the last four decades. Although the ultimate goal of
this multidisciplinary approach will be to explain, in
molecular detail, how specific memories are encoded and
maintained within the human brain, experiments in the
different animal model systems, will continue to pave the
way. The major question that now also needs to be addressed
relates to the system properties of memory storage, such as
how synaptic changes at different points in an explicit
network, give rise to the storage capacity of the system.
The long-term prospects are extremely exciting (Angel Barco,
Craig H. Bailey and Eric R. Kandel. 2006).
Presently, on the clinical side, it has been found that
amnesiacs in general perform better in verbal recall when
the retroactive interference is diminished by placing them
in a dark quiet room (Nelson Cowan, Nicoletta Beschin and
Sergio Della Sala, 2004). Also it has been understood that
recognition memory deficit in amnesia is attenuated under
conditions that increased the salience of study-induced
fluency possibly because memory for a past experience can be
based on recollection of specific details from the
experience or on a sense of familiarity that accompanies
re-exposure to information from that episode (Margaret M.
Keane, Frances Orlando, Mieke Verfaellie 2006). This is just
a small step in the understanding of amnesia in general and
the day will definitely come in future whereby different
treatment options for source amnesia become available.
There are no specific preventive measures for source amnesia
but the general guidelines outlined below can be followed.
1. Keep
brain cells active by reading, doing puzzles, singing,
exercising, conversing and eating a balanced diet to
stimulate blood flow, improve activity and preserve them
from degeneration
2.
Antioxidants like Vitamin E and Selegiline can be taken when
appropriate
3. Avoid
head injuries. Wear seat belt and helmet at all times during
driving. Children, adolescents and adults should also be
taught sports safety guidelines.
4. Strokes,
which can cause amnesia, should be prevented by treating
predisposing factors like hypertension, obesity, diabetes
mellitus, dyslipidemia, smoking, alcoholism, stress and
hyperhomocystinemia.
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