Amnesia

by John Lenahan

     In cognitive neuropsychology, amnesia is looked at
to attempt to explain memory disorders in the terms of
impairments compared to the normal processes of memory.
There are three types of memory failure, failure of
retention, a failure of registration, and a failure of
retrieval (Ellis and Young, 1988). 
     Symptoms for a person with an inability to register
new memory traces would include a normal memory for
events occurring before the onset of an illness. If a
person had problems with registration, they would
experience difficulties remembering anything that has
happened since the onset of the illness (Ellis and Young,
1988). This type of problem is called anterograde
amnesia. A person with anterograde amnesia has
difficulties in learning new information. They can
remember events that occurred in the past before any
brain damage took place, yet have no recollection of
information exposed to after the damage. The opposite of
this is retrograde amnesia, a type of organic amnesia
such as a head injury, which is the inability to recall
events occurring before any brain damage happened. This
is seen more often in patients than anterograde amnesia,
which is very rare (Carlson, 1994).
     Dissociative amnesia is usually caused by
psychological stress and appears in five patterns. There
is localized amnesia, were all events that occurred
before a certain period of time are blocked. In selective
amnesia, a person forgets only certain events that
occurred during a specific period of time. In generalized
amnesia, the person forgets their whole past. A person
with continuous amnesia forgets all the events that occur
after a specified period until the present. This includes
events that happened after the onset of amnesia. When
systematized amnesia occurs, the person forgets only
certain segments of information, all other memories
remain intact (Alloy, Acocella, and Bootzin, 1996).
     People with generalized and continuous amnesia lose
their episodic memory, which is memory of personal
experience. Their semantic memory, which is their general
intelligence, is usually intact. Procedural memory, which
is a person's memory for acquired skills, is also usually
intact. Amnesiacs are usually able to read and write, add
and subtract (Alloy, Acocella, and Bootzin, 1996). 
     There is evidence that shows anterograde amnesia
indicative of a registration deficit. Ellis and Young
(1988) reported from a study by Liepmann, a patient who
suffered a brain injury. He was able to remember much of
his life before the injury, yet had no memory for any
events that followed. The patient was able to retain most
of his mathematical and chess playing skills before the
accident, despite his amnesia. 
     There was also an incident reported by Syz (1937) of
a man who fell backwards on a shovel while working. He
suffered a complete, yet temporary memory loss for the
events before the accident. He was able to recall the
events of his life before the incident, and remembered
topics such as geography and astronomy. He was able to
define words and could tell the difference between words
of similar meaning. Any memories for new events appeared
to fade rapidly.
     A more famous case of anterograde amnesia, involves
a patient named HM, who in his mid-20' received a
bilateral resection of the medial portions of the
temporal lobes, and had partial removal of the
hippocampus and amygdala on each side (Scoville and
Milner, 1957).
He remembered very little of what happened to him after
the operation. he would do the same jigsaw puzzle
everyday not knowing it is different. His early memories
were still intact and he can refer to times when he was a
boy (Scoville and Milner, 1957). He also shows retrograde
amnesia for events that happened before his operation.
This goes back several years, yet is not as extreme as
the anterograde amnesia (Ellis and Young, 1988). 
     In the immediate memory span, which is one measure
of the capacity of the short term memory system has shown
consistency to be normal in amnesic patients (Warrington,
1976). A study by Baddelely and Warrington (1970), they
compared the performance of six amnesic subjects and six
control subjects on an adaptation of the Brown-Peterson
short-term memory forgetting task. The control group had
extra-cerebral neurological disease and they were matched
for age and intelligence with the amnesic group.
Intervals of sixty seconds were used and the results
showed no difference between the two groups at any
interval. There have been no qualitative differences
between recall and recognition using short term memory
paradigms in amnesics (Warrington, 1976). It is the
cued-recall and the breakdown of the normal relationship
between recall and recognition that have been stated as
being the two major differences between normal and
amnesic memory.
     Scovile and Milner (1957) examined eight psychotic
patients and found that some of these had anterograde
amnesia. The only time this occurred was when the
hippocampus was removed. They concluded that the
hippocampus was a critical structure in memory. It was
later found that bilateral temporal lobectomy caused
anterograde amnesia. Surgeons then began to perform
unilateral temporal lobectomies and the memory problems
were less severe (Carlson, 1994). It was later found that
the unilateral removal of the medial temporal lobe
produced anterograde amnesia. Postmortem examinations of
the patients brains showed that the hippocampus on the
other side of the brain had also been damaged very early
in life (Penfield and Milner, 1958;Warrington and Duchen,
1992).
     Damage to the hippocampus or any of its regions that
support its inputs and receive outputs causes anterograde
amnesia. The hippocampal formations (HF) most substantial
input is entorhinal cortex. The neurons have axons that
end in the dentate gyrus. The entorhinal cortex receives
its inputs from the cingulate cortex and all the areas of
the association cortex. The outputs of the hippocampal
system come primarily from the subiculum. HF also
receives input form subcortical regions from the fornix.
The ventral tegmental area, locus coeruleus, raphe nuclei
and the medial septum all play a part in the
neurotransmitter release that modulates the hippocampal
formation (Carlson, 1994). The HF sends efferent fibers
to the mammillary bodies, that are located at the end of
the hypothalamus. The mammillary bodies send axons to the
anterior thalamus, which then sends axons to the
cingulate cortex.. The entorhinal cortex also sends
information from the amygdala to the HF (Carlson,1994).
     I have stated evidence that shows the importance of
the hippocampus in memory impairments. For the remainder
of this paper, I would like to discuss lesions in the
brain caused from chronic alcoholism, usually causing a
syndrome called Korsakoff's syndrome, producing 
anterograde amnesia. Postmortem examination of the brains
of patients who had Korsakoff's syndrome, revealed most
every time a severe degeneration of the mammillary bodies
(Carlson, 1994). Victor, Adams, and Collins (1971) showed
from autopsies of Korsakoff's patients, that amnesia was
even more reliably associated with damage to the
dorsomedial thalamus.
     A deficiency of the vitamin thiamine appears to
accompany the prolonged alcohol abuse and causes damage
to several thalamic and hypothalamic structures that
surround the third ventricle of the brain. Some areas
included may be the dorsomedial nucleus of the thalamus
and the mammillary bodies (Butters, 1984). It has also
been claimed that a combination of thiamine deficiency
and the direct neurotoxic action of alcohol is required
to produce a persistent memory loss in Korsakoff's
syndrome (Freund, 1973; Butters and Cermak, 1980).
McEntee (1993) pointed out that alcohol reduces both the
absorption of thiamine and also the activity of the
enzyme which converts it to its active form. 
     Kopelman (1995) has stated there is a genetic factor
postulated to explain why only a certain amount of heavy
drinkers developed the syndrome. He also states that
Transketolase is an enzyme that requires thiamine
pyrophosphate (TPP) to accompany it. It was speculated by
Blass and Gibson (1977) that a hereditary abnormality of
transketolase metabolism may predispose some alcoholics
to the Korsakoff syndrome. Thiamine correction therapy
has been found to reverse some acute symptoms of the
Wernike state  (Butters and Cermak, 1980).
     Kopelman (1995)  combined recent evidence that
showed the circuit involving the mammillary bodies, the
mamillo-thalamic tract and the anterior thalamus are
particularly critical in the formation of memory. This is
different from early suggestions that the medial-dorsal
nucleus of the thalamus was essential in the formation of
memory. He also concluded in his article that structural
and/or neurochemical abnormalities within the
limbic/diencephalic circuits account for anterograde
amnesia. Patients who had acute Wernike's encephalopathy
and did not receive thiamine treatment, may show evidence
of hemorrhagic lesions in the region around the
diencephalon (Butters and Stuss 1989).
     Other factors such as frontal lobe dysfunction, are
considered to be the cause of retrograde memory loss that
is commonly found in Korsakoff's syndrome. There have
been neuro-imaging studies that have confirmed autopsy
findings of more widespread structural and metabolic
abnormalities, which involve the frontal lobes (Kopelman,
1995). Shimamura et al (1988) did a study with seven
alcoholic Korsakoff patients, seven non-Korsakoff
alcoholics, and seven healthy controls. It was reported
that their were significant enlargements of the third
ventricle and widening of the Sylvian fissures and the
left frontal sulcus. Various aspects of the memory
deficits found in Korsakoff patients have been correlated
to frontal dysfunction (Kopelman, 1989, 1991a). 
     Conway and Rubin (1993) stated that frontal lobe
amnesia's appear to be associated directly with
inabilities to construct autobiographical memories, and
also the disruption  of cyclic retrieval. Baddeley and
Wilson (1986) did a study that  showed some of their
patients were unable to make detailed memories even
though they could recall specific events. The patients
were unable to fully incorporate event specific knowledge
into their memories.
     Albert (1984) and Butters (1984) proposed a
two-factor theory saying the temporally graded retrograde
amnesia in Korsakoff syndrome, may be the result of an
essentially uniform retrieval deficit that may be
superimposed upon a long-standing and progressive
registration impairment. Older memories of the Korsakoff
amnesic that are well established and consolidated are
more likely to accessible after the onset of retrieval
impairment than are more recent memories that are weakly
established and poorly consolidated after years of
alcohol abuse.

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Copyright © 1997, Dr. John M. Morgan, All rights reserved - This page last edited March 17, 1997
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