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Jackie Thill
Physiological Psychology
May 1, 2012
Final Paper
Amnesia
The human brain encodes, stores, and retrieves information; this process is what
is referred to as one’s memory. Research has shown that memories are created, stored,
and created in parts of the limbic system, especially the hippocampus (Carlson, 2010).
There are three main types of memories sensory memory, short-term memory and
long-term memory. Sensory memory is memory that takes less than a half of a second
for one to be able to describe the item (Carlson, 2010). Short-term memory is the
memory of the incident or the stimulus that last usually a few seconds and no more
than a minute. Long-term memory is the storage of short-term memory and sensory
memory that lasts for a greater length of time but not forever. Memories are one of
the most important aspects of a person.
Memories are how one remembers our
childhoods, the faces of the one’s you love, and the moments that have changed your
life making you the person you are today. What if you lost these precious memories or
could not create new memories? “Amnesia refers to a deficit in memory that can be at
the same time dense and yet circumscribed (Duff et. al, 2008).”
In other words,
amnesia is a condition in which a part of an individual’s memory is lost. There are
many different types of amnesia and many different ways in which an individual can
lose their memory.
In this paper, there will be a focus on four types of amnesia,
anterograde amnesia, retrograde amnesia, post-traumatic amnesia, and Korsakoff's
syndrome and the research along with them. I personally chose this topic because my
memories are the one thing I cannot imagine living without because my memories are
the priceless.
Anterograde Amnesia
The first type of amnesia to look at is anterograde amnesia.
Anterograde
amnesia refers to the inability to learn new information after amnesia takes effect.
Anterograde amnesia is one of the most studied and fascinating phenomena caused by
brain damage usually a traumatic brain injury though there are other causes such as
drugs, shock, or even illness (Carlson, 2010). Anterograde amnesia is the inability to
create new long-term memories after the event of some sort of brain disturbance
(Carlson, 2010). The likeliness of ‘pure’ retrograde amnesia is rare (Carlson, 2010).
Normally patients with anterograde amnesia can create some new memories such as
muscle memory. There has been a lot of research on anterograde especially because it
is one of the hardest types of amnesia to cope with because the individual cannot learn
anything new.
Like many forms of amnesia, anterograde amnesia is not known to be caused by
a specific location in the limbic system. Though, John Aggleton found that anterograde
amnesia is regularly associated to the medial temporal lobe and the medial
diencephalon (Aggleton, 2008). Looking through different studies, there is a different
focus on each of the causes.
Aggleton looked at a group of individuals with
anterograde amnesia that was caused by fornix lesions and hippocampal lesions
(Aggleton, 2008). Akira Midorikawa and Mitsuru Kawamura looked at a case study of a
man who had his meningiomas, or tumors in the meninges, removed; after which he
began to have seizures which then lead into anterograde amnesia (Midorikawa and
Kawamura, 2007). Melissa Duff and others looked at a case study of an elderly woman
who suffered from a closed head injury which then caused severe anterograde amnesia
(Duff et. al, 2008).
All studies show some of the different causes of anterograde
amnesia.
The article by Akira Midorikawa and Mitsuru Kawamura and the article by Melissa
Duff both looked at how individual case studies dealt with their anterograde amnesia.
Midorikawa and Kawamura looked at the effects of an antiepileptic drug (AED) on
anterograde amnesia (Midorikawa and Kawamura, 2007).
Antiepileptic drugs have
been used to help prevent epileptic seizures and accelerated forgetting, but no studies
have extensively shown the affects it has on anterograde amnesia (Midorikawa and
Kawamura, 2007). Anterograde amnesia is such an extreme and powerful phenomenon
that finding some kind of treatment is imperative. Midorikawa and Kawamura found
that the AED had no effect on anterograde amnesia and that more than likely this type
of amnesia is irreversible (Midorikawa and Kawamura, 2007). Duff, on the other hand,
went a different way in her approach with treatment. In her case study, the older
woman with anterograde amnesia was every bit as severe as the famous H.M. case
(Duff et. al, 2008).
impairments.
Duff looked at ways to help individuals to cope with their memory
It worked remarkably well, the patient developed real-world abilities
(Duff et. al, 2008). This included breaking down tasks into smaller more practicable
tasks and using lists/reminders to help her with responsibilities such as in the shower
(Duff et. al, 2008). Though this also did not reverse the anterograde amnesia it made
life more manageable and the patient was able to have a ‘successful’ life (Duff et. al,
2008).
Retrograde Amnesia
The second type of amnesia to look at is retrograde amnesia.
retrograde amnesia to refer to the opposite of anterograde amnesia.
Some believe
Retrograde
amnesia refers to the inability to recall old information after amnesia takes effect. Like
anterograde amnesia, retrograde amnesia is caused by brain damage usually a
traumatic brain injury or emotional trauma though there are other causes such as drugs
or even illness (Carlson, 2010). Retrograde amnesia is a failure to access memories of
events that happened, or information that was encoded, before the event of some sort
of brain disturbance (Carlson, 2010).
temporary.
Retrograde amnesia is usually found to be
Along with this, more new memories that are closer to the ‘brain
disturbance’ are more likely to be elapsed than the memories farther away from the
incident (Carlson, 2010).
Narinder Kapur writes an analysis of the differences between the two types of
retrograde amnesia, episodic amnesia and semantic amnesia (Kapur, 1999). Bernhard
Sehm writes his findings on focal retrograde amnesia (FRA) (Sehm et. al, 2011).
Episodic retrograde amnesia is described as forgetting personally experienced events or
autobiographical information (Kapur, 1999).
With episodic amnesia, the individual
forgets things like their eleventh birthday or first day of school. Semantic retrograde
amnesia is described as forgetting connections of knowledge or factual information
(Kapur, 1999).
With semantic amnesia, the individual forgets things such as
geography or historical dates.
FRA, also known as functional amnesia “is a rare
neurocognitive disorder presenting with an isolated loss of retrograde memory (Sehm
et. al, 2011).” Kapur found that “Extensive episodic and semantic retrograde amnesia
generally entails lesions to a wide range of neocortical structures, particularly those in
the temporal lobe (Kapur, 1999).”
Along with that, Kapur also found that lesions to the frontal lobe and the
thalamus can result in either of the two retrograde amnesias (semantic or episodic
amnesia) though there is not a direct causation (Kapur, 1999). Sehm found that FRA
was in the outcome of epileptic seizure (Sehm et. al, 2011). Andrei Miu looked at how
high emotions can produce emotion-induced retrograde amnesia (ERA) (Miu et. al,
2005).
Emotions play a huge role as a developmental factor and symptom of retrograde
amnesia. Miu looked intently into how emotional arousal can enhance or severely harm
one’s amnesia (Miu et. al, 2005). Miu showed this by giving participants emotionally
arousing words which in turn produced either a positive or negative memory response
(Miu et. al, 2005). Kapur found similar results saying that the emotional significant of
the incident correlates with the severity of the retrograde amnesia (Kapur, 1999).
Sehm found that patients with retrograde amnesia caused symptoms of emotional
issues (Sehm et. al, 2011).
Some symptoms included insecurity is social settings,
because of fear of meeting people they should already know, anxiety of learning new
things, and depression (Sehm et. al, 2011).
Post-Traumatic Amnesia
The third type of amnesia to look at is post-traumatic amnesia. Post-traumatic
amnesia refers to a mixture of anterograde and retrograde amnesia that is caused by a
traumatic brain injury (TBI); in addition individuals suffering from post-traumatic
amnesia might not be able to remember specific people and the events around that
person as well (Langhorn, et. al, 2010). Post-traumatic amnesia is caused by any TBI
but usually from some sort of blow to the head. Statistics show that around seventy
percent of TBIs patients will experience post-traumatic amnesia (Langhorn, et. al,
2010). Depending on the severity of the trauma correlates with the severity of the
amnesia (De Monte, et. al, 2006).
Veronica Eileen de Monte looked at the different effects of post-traumatic
amnesia from a mild TBI on information processing (De Monte, et. al, 2006). It is
important to look at the effects of mild traumatic brain injuries because that is most
common brain injuries. De Monte “showed that patients with [mild traumatic brain
injuries] in [post-traumatic amnesia] recalled fewer words after two presentations and
after a delay and completed fewer symbols in 90 seconds on Digit Symbol than patients
with [mild traumatic brain injuries] not in [post-traumatic amnesia] (De Monte, et. al,
2006).”
With these results, De Monte concluded the patients with post- traumatic
amnesia caused by mild traumatic brain injury have slower verbal memory and
information processing (De Monte, et. al, 2006).
Leanne Langhorn and E. Noé both looked at the rehabilitation of post-traumatic
amnesia.
Langhorn looked to understand if the fast medical personal started
rehabilitation on individuals with post-traumatic amnesia the better affect the
rehabilitation will have (Langhorn, et. al, 2010). Noé looked at how the apolipoprotein
E genotype affects verbal memory recovery (Noé, et. al, 2010). Taking in the fact that
the less severe the TBI is the easier the recovery it is; it is essential to look at the
recovery especially of more extreme cases.
Langhorn found that through literary
analysis that there is not complete evidence to prove that either way the effect of early
rehabilitation for individuals with post-traumatic amnesia (Langhorn, et. al, 2010). Noé
found “APOE genotype seems to be associated with the trajectory of cognitive recovery
after TBI, but does not play a determinant role in the efficacy of memory rehabilitation
in this population (Noé, et. al, 2010).”
Korsakoff's Syndrome
The last type of amnesia that this paper will look at is Korsakoff’s syndrome.
Korsakoff’s syndrome is defined as a more extreme case of anterograde amnesia
referring to the inability to form any new memories but can recall all the old memories
(Carlson, 2010).
Patients can normally function, remember, and converse normally
even though they have the inability to retain new information or events. Like the other
amnesias, Korsakoff’s syndrome is caused by brain damage, in this case, from due to a
vitamin B1 deficiency usually due to chronic alcohol abuse or malnutrition (Carlson,
2010).
Roos Van Oort and Roy P. C. Kessels stressed the importance of executive
deficits in individual’s with Korsakoff’s syndrome will greatly affect their daily living (Van
Oort, R., Kessels, R. C. (2009). Van Oort and Kessels believed that a DSM-IV criterion
does not fully encompass the how much Korsakoff’s syndrome affects the individual. In
the end Van Oort and Kessels conclude that “Next to amnesia, executive deficits are a
prominent characteristic of cognitive impairment in Korsakoff patients. It is argued that
the new DSM criteria should consider incorporating executive dysfunction as an
important feature of alcohol-induced persistent cognitive disorder (Van Oort, R.,
Kessels, R. C. (2009).”
Maria de Fatima Alves Monteiro and Roy P. C. Kessels both looked at the how
Korsakoff’s syndrome affect the individual and what steps can be taken toward helping
the individuals.
Kessels looked at how Korsakoff’s syndrome can produce fake
memories (Kessels, et. al, 2008). Alves Monterio looked at how there are different
rehabilitation.
Kessels concluded after his studies, “There were deficits in source
memory, in which patients incorrectly assigned previously learned words to an incorrect
word list. Also, Korsakoff patients had extensive executive deficits, but no relationship
between the severity of these deficits and the severity of confabulation or intrusions on
a memory task was found (Kessels, et. al, 2008).” Alves Monterio found that individuals
with Korsakoff’s syndrome respond positively were teaching individuals to be aware of
their illness, find routine in life, and therapy for depression (Alves Monteiro, et. al,
2011).
There are many other types of amnesia such as dissociative amnesia, Lacunar
amnesia, and transient global amnesia. This paper talked about the four major types of
amnesia and the research along with it. There is much research that still needs to be
looked at so more options of rehabilitation and understanding of the different kinds of
amnesia.
Works Cited
Aggleton, J. P. (2008). Understanding anterograde amnesia: Disconnections and hidden
lesions. The Quarterly Journal Of Experimental Psychology, 61(10), 1441-1471.
doi:10.1080/17470210802215335
Alves Monteiro, M., Prado Bolognani, S., Rivero, T., & Amodeo Bueno, O. (2011).
Neuropsychological intervention in a case of Korsakoff's amnesia. Brain
Impairment, 12(3), 231-238. doi:10.1375/brim.12.3.231
Carlson, N. R. (2010). Physiology of behavior. (10 ed., pp. 465-482). Boston: Allyn &
Bacon.
De Monte, V., Geffen, G., & Massavelli, B. (2006). The effects of post-traumatic
amnesia on information processing following mild traumatic brain injury. Brain
Injury, 20(13-14), 1345-1354. doi:10.1080/02699050601082073
Duff, M. C., Wszalek, T., Tranel, D., & Cohen, N. J. (2008). Successful life outcome and
management of real-world memory demands despite profound anterograde
amnesia. Journal Of Clinical And Experimental Neuropsychology, 30(8), 931-945.
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Kapur, N. (1999). Syndromes of retrograde amnesia: A conceptual and empirical
synthesis. Psychological Bulletin, 125(6), 800-825. doi:10.1037/00332909.125.6.800
Kessels, R. C., Kortrijk, H. E., Wester, A. J., & Nys, G. S. (2008). Confabulation behavior
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Langhorn, L., Sorensen, J. C., & Pedersen, P. U. (2010). A critical review of the
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Midorikawa, A., & Kawamura, M. (2007). Recovery of long-term anterograde amnesia,
but not retrograde amnesia, after initiation of an anti-epileptic drug in a case of
transient epileptic amnesia. Neurocase, 13(5-6), 385-389.
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Time to revise the DSM criteria for alcohol-induced persisting amnestic disorder?.
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