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Memory and Anterograde Amnesia
Francesca Philips
Maths 89S Duke University
6st December 2016
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Memory and Anterograde Amnesia
Patient HM
Perhaps the most notable case study in neuroscience is that of ‘Patient H.M.’. Henry
Gustav Molaison had suffered from epilepsy from the age of ten onwards, and his condition
only continued to worsen with time (Adams,
2013). At the age of 27, he was having up to 11
seizures a week. After determining that the
seizures were beginning in his temporal lobes, a
neurosurgeon named William Scoville decided
to perform what was later seen as essentially
experimental surgery in order to control the
epilepsy (Pearce, 2006). Scoville performed a
bilateral
medial
temporal
lobe
resection,
Figure 1: Henry Molaison (1986)
meaning that he removed most of the temporal lobe on both sides. This can be seen in Figure
2, where HM’s brain can be compared
to a normal brain, and the missing
hippocampi and surrounding tissue is
clear (Pearce, 2006).
After the surgery, the seizures
were milder and could be controlled
by medication. In fact, he suffered no
tonic-clonic or ‘grand-mal’ seizures
for a year after the surgery. However,
Figure 2: Patient HM’s brain vs normal brain
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the surgery had an unanticipated effect; Henry Molaison could no longer retain any new
information for more than a brief time. His old memories remained relatively intact, but this
side effect meant that he could not form any new memories. Molaison’s case is one of the most
‘pure’ cases of anterograde amnesia ever recorded, and allowed for new discoveries in
neuroscience that have completely revolutionised the way that we discuss and understand
memory.
Anterograde Amnesia
Amnesia is a “severe impairment of memory”, and varies in form, cause, and scope.
Anterograde amnesia, which Henry Molaison suffered from, is the inability to form new
memories following an event (Watson and Breedlove, 2012). Often, a patient’s can still make
very short term memories, but will struggle to recall that information moments later. Previously
formed memories usually remain relatively unaffected. For example, Henry was able to
remember much of what happened pre-1953, but could not form new memories or recall details
about his life post-surgery.
For such patients, new information is processed normally, however it is quickly
forgotten and not consolidated in long term memories. Mammillary bodies are located on the
brain’s underside, and are a pair
of small structures. Normally,
when a memory is being formed,
the neurons (nerve cells) in the
mammillary
electrical
bodies
impulses
relay
to
the
thalamus, which is a small
Figure 3: Anatomy of the brain
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structure in the centre of the brain (Milner, 2005). Neurons within the thalamus then send
signals to the brain’s cortex (the outer layer of neural tissue), and it is in the cortex where long
term memories are thought to be ‘stored’. Memories are thought to be passed from a sort of
sensory memory, to short term memory, and then committed to long term memory. However,
many of our memories seem to never be formed as long-term memories; if we remembered
every single aspect of our experiences, just an hour would hold an overwhelming amount of
information. It is thought that the depth of processing of the information, motivation, attention
all play roles in determining what information is formed into long-term memories.
Therefore, anterograde amnesia can be caused by damage to the hypothalamus,
thalamus, and the surrounding cortical structures. If such damage occurs, memory storage can
be inhibited, as the connections between the key systems utilised in the memory circuit are
affected. Anterograde amnesia can also occur as a result of drug abuse, traumatic brain
injuries or surgery, or an event such as a heart attack, epileptic attack or oxygen deprivation
(Ryback, 1970).
One cause of anterograde amnesia that is not often recognised as such is alcohol
intoxication; often times this form of amnesia is referred to as a ‘blackout’. The rapid rise in
blood alcohol concentration over a short period of time can impair or block the brain’s ability
to form long-term memories about events that happen while intoxicated. When alcohol is
rapidly consumed, it is at 0.20% BAC that anterograde amnesia usually occurs, although it
can occur at blood alcohol concentrations as low as 0.14% (Ryback, 1970). The amount of
alcohol consumed correlates positively with the magnitude of the memory loss. However,
this form of anterograde amnesia is temporary, and upon reaching sobriety, the ability to
create long-term memories returns. It is also important to note that short-term memory
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function is often unhindered, and so those affected can still remember what happened
moments before and can function enough to have conversations or participate in social
activities relatively normally. In one of his studies, Ryback writes that the intoxicated
subjects could “carry on conversations during the amnesic state, but could not remember
what they said or did 5 minutes earlier. Their immediate and remote memory were intact”
(Ryback, 1970).
Alcohol, if consumed rapidly and in large quantities, can disrupt activity in the
hippocampus (a region which is centrally involved in the formation of new autobiographical
memories) (White, 2004). This theory is based on observations that such alcohol
consumption creates a similar amnesiac effect to that produced by damage to the
hippocampus. Both impact the brain’s ability to store long-term explicit memories, while
leaving short-term memory storage and previously formed long-term memory relatively
intact (Milner, 2005). The alcohol has selective effects on neurotransmitter systems which
allow for communication between nerve cells. It has been shown that alcohol affects the
activity of proteins that bind neurotransmitters, meaning that connections cannot be made
between core sections of the memory circuit.
It is often only ‘explicit memory’ which is affected by anterograde amnesia. There are
two types of long-term memories: explicit memories and implicit memories. Explicit memories
are those that we consciously recall and use to explain; they are the kinds of memories we
utilise in answering ‘what’ questions (Watson and Breedlove, 2012). Implicit, or procedural
memory, is typically not as affected. These types of memories are shown by performance, and
do not require conscious recollection. For example, remembering how to ride a bike is an
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example of an implicit memory, while remembering who the 34th president of the United States
is would be an explicit memory (Watson and Breedlove, 2012).
Figure 4: Mirror tracing task
But why is it that explicit memory is affected, while implicit is not? In the case of HM,
a select few tests show this difference in impact. One of these tests was a mirror tracing test.
As seen in Figure 4, Henry had to trace a picture of a star, but he could only see this star in a
mirror. Henry could never recognise that he had previously performed the task, but his errors
per day gradually decreased and demonstrated a long-term implicit memory. Implicit memory
does not rely on the hippocampus and surrounding tissues in the same way that explicit memory
does, and so often times the memory circuit for implicit memory is left relatively intact. While
still in the process of determining exactly what this circuit is, neuroscientists theorise that there
is a different memory system being utilised. This is what allowed Henry to learn the new skill
of mirror drawing, even though he had forgotten ever having performing the task before. The
last time that he performed the test, Henry declared, “Well, this is strange. I thought that that
would be difficult. But it seems as though I’ve done it quite well.” (Watson and Breedlove,
2012)
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Treating Anterograde Amnesia
The approaches that are used when treating anterograde amnesia primarily treat the
symptoms of the condition rather than the cause itself. Techniques such as diaries and extensive
note taking are suggested as ways to cope with the condition, but do not offer long-term
solutions. There is no cure for anterograde amnesia, and this is mainly due to the current lack
of deep understanding about the way that the mind works and the way that memories are stored.
Of course, anterograde amnesia exists on a spectrum, with some patients able to remember
some select memories made after an event and have improvements in their long-term memory,
while others like Henry Molaison remember nothing. The brain’s ‘neuroplasticity’ offers some
explanation for why some patients’ conditions can improve over time. Neuroplasticity refers
to the brain’s ability to ‘re-map’ neural pathways and adapt to new situations. It is this
characteristic that allows the brain an opportunity to achieve nearly normal memory function
after damage to key areas of the memory circuit. However, if the damage is too extensive, this
ability is still not sufficient to allow the return of normal memory function (Watson and
Breedlove, 2012).
Conclusion
From our understanding of memory and amnesia, a distinction can be made between
learning and memory. Learning is the process of acquiring new information, while memory is
the ability to store and retrieve that information. Further research and studies about memory
and amnesia may hold clues to ways in which we can better remember, and comprehend the
world around us. However, neuroscientists’ current knowledge of human memory remains
limited and the knowledge is not sufficient to allow us to ‘map’ the human brain and determine
which parts are responsible for different functions. This information may allow us to treat
anterograde amnesia and other forms of brain damage more easily.
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Bibliography
Adams, T. (2013, May 4). Henry Molaison. Retrieved December 1, 2016, from The
Guardian: https://www.theguardian.com/science/2013/may/05/henry-molaisonamnesiac-corkin-book-feature
Milner, B. (2005). The Medial Temporal-Lobe Amnesic Syndrome. Psychiatric Clinics of
North America.
Pearce, J. M. (2006). Amnesia. European Neurology.
Ryback, R. S. (1970). Alcohol amnesia. Observations in seven drinking inpatient alcoholics.
Q J Stud Alcohol.
Teuber, H. L., Milner, B., & Vaughn, H. G. (1968). Persistent Anterograde Amnesia After
Stab Wound of Basal Brain. Neuropsychologia, 6, 267-282.
Watson, N. V., & Breedlove, S. M. (2012). The Mind's Machine. Simon and Schuster.
White, A. M. (2004, July). What Happened? Alcohol, Memory Blackouts, and the Brain.
Retrieved December 2, 2016, from National Institute on Alcohol Abuse and
Alcoholism: http://pubs.niaaa.nih.gov/publications/arh27-2/186-196.htm
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