Types
Refers
to the inability to create new memories due to brain damage, while long-term
memories from before the event remain intact.
The brain damage can be caused by
the effects of long-term alcoholism, severe malnutrition, stroke, head trauma,
surgery, Wernicke-Korsakoff Syndrome, cerebrovascular events, anoxia or other
trauma.
The two brain regions related
with this condition are medial temporal lobe and medial diencephalon.
Anterograde amnesia can't be treated with pharmacological methods due to
neuronal loss.
However, treatment exists in
educating patients to define their daily routines and after several steps they
begin to benefit from their procedural memory.
Likewise, social and emotional
support is critical to improving quality of life for anterograde amnesia
sufferers.
Refers
to inability to recall memories before onset of amnesia. One may be able to
encode new memories after the incident.
Retrograde is usually caused by head
trauma or brain damage to parts of the brain besides the hippocampus.
The
hippocampus is responsible for encoding new memory.
Episodic memory is more
likely to be affected than semantic memory.
The damage is usually caused by
head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or
chronic alcoholism.
People suffering from retrograde amnesia are more likely to
remember general knowledge rather than specifics. Recent memories are less
likely to be recovered, but older memories will be easier to recall due to
strengthening over time.
Retrograde amnesia is usually
temporary and can be treated by exposing them to memories from the loss.
Another type of consolidation
(process by which memories become stable in the brain) occurs over much longer
periods of time/days, weeks, months and years and likely involves transfer of
information from the hippocampus to more permanent storage site in the cortex.
The operation of this longer-term consolidation process is seen in the
retrograde amnesia of patients with hippocampal damage who can recall memories
from childhood relatively normally, but are impaired when recalling experiences
that occurred just a few years prior to the time they became amnesic. (Kirwan
et al.,2008)
is generally due to a head injury (example:
a fall, a knock on the head).
Traumatic amnesia is often transient, but may be
permanent or either anterograde, retrograde, or mixed type.
The extent of the
period covered by the amnesia is related to the degree of injury and may give
an indication of the prognosis for recovery of other functions.
Mild trauma,
such as a car accident that results in no more than mild whiplash, might cause
the occupant of a car to have no memory of the moments just before the accident
due to a brief interruption in the short/long-term memory transfer mechanism.
The sufferer may also lose knowledge of who people are. Having longer periods
of amnesia or consciousness after an injury may be an indication that recovery
from remaining concussion symptoms will take much longer
Results
from a psychological cause as opposed to direct damage to the brain caused by
head injury, physical trauma or disease, which is known as organic amnesia.
Dissociative amnesia can include:
Repressed memory refers
to the inability to recall information, usually about stressful or traumatic
events in persons' lives, such as a violent attack or disaster. The memory is
stored in long-term memory, but access to it is impaired because of
psychological defense mechanisms. Persons retain the capacity to learn new
information and there may be some later partial or complete recovery of memory.
Formerly known as "Psychogenic Amnesia".
Dissociative fugue (formerly psychogenic
fugue) is also known as fugue state. It is caused by psychological trauma and
is usually temporary, unresolved and therefore may return. An individual with
dissociative fugue disorder is unaware or confused about his or her identity
and will travel in journeys away from familiar surroundings to discover or
create new identities.
The Merck Manual defines
it as " one or more episodes of amnesia in which patients cannot recall
some or all of their past and either lose their identity or form a new
identity. The episodes, called fugues, result from trauma or stress.
Dissociative fugue often manifests as sudden, unexpected, purposeful travel
away from home."While popular in fiction, it
is extremely rare.
Posthypnotic amnesia occurs
when events during hypnosis are forgotten, or where past
memories are unable to be recalled. The failure to remember those events is
induced by suggestions made during the hypnosis.[25]
Lacunar amnesia is
the loss of memory about one specific event.
Childhood amnesia (also
known as infantile amnesia) is the common inability to remember events from
one's own childhood. Sigmund Freud notoriously
attributed this to sexual repression,
while modern scientific approaches generally attribute it to aspects of brain development or developmental
psychology, including language development,
which may be why people don't easily remember pre-language events.
Researchers
have found that implicit memories cannot be recalled or described. Remembering
how to play the piano is a common example of implicit memory, as is walking,
speaking and other everyday activities that would be difficult to focus on if
they had to be relearned every time one got up in the morning.
Explicit
memories, on the other hand, can be recalled and described in words.
Remembering the first day that you met your piano teacher is an example of
explicit memories.
Transient global
amnesia is a well-described medical and clinical phenomenon.
This form of amnesia is distinct in that abnormalities in the hippocampus can
sometimes be visualized using a special form of magnetic
resonance imaging of the brain known as diffusion-weighted
imaging (DWI).
Symptoms typically last for less than a day and
there is often no clear precipitating factor or any other neurological
deficits. The cause of this syndrome is not clear. The hypothesis of the
syndrome includes transient reduced blood flow, possible seizure or an atypical
type of migraine. Patients are typically amnestic of events more than a few
minutes in the past, though immediate recall is usually preserved.
Source amnesia is
the inability to remember where, when or how previously learned information has
been acquired, while retaining the factual knowledge.
Source amnesia is both part of
ordinary forgetting and can
be a memory disorder caused by different factors.
People suffering from source amnesia
can also get confused about the content of what is remembered.
This confusion
has been loosely termed memory distrust
syndrome. Individuals who suffer from this syndrome distrust their
memory and may be motivated to rely on external (non-self) sources.
Korsakoff's syndrome can
result from long-term alcoholism or malnutrition.
It is caused by brain damage
due to a vitamin B1 deficiency and will be progressive if
alcohol intake and nutrition pattern are not modified.
Other neurological
problems are likely to be present in combination with this type of Amnesia.
Korsakoff's syndrome is also known to be connected with confabulation. It
should be noted that the person's short-term memory may appear to be normal,
but the person may have a difficult time attempting to recall a past story, or
with unrelated words, as well as complicated patterns.
Drug-induced amnesia is
intentionally caused by injection of an amnesiac drug to help a patient forget
surgery or medical procedures, particularly those not performed under
full anesthesia,
or likely to be particularly traumatic.
Such drugs are also referred to as
"premedicants." Most commonly a 2'-halogenated benzodiazepine such
as midazolam or flunitrazepam is
the drug of choice, although other strongly amnestic drugs such as propofol or scopolamine may
also be used for this application.
Memories of the short time-frame in which
the procedure was performed are permanently lost or at least substantially
reduced, but once the drug wears off, memory is no longer affected.
Prosopamnesia is
the inability to recognize or remember faces, even in the presence of intact
facial recognition capabilities. Both acquired and inborn cases have been
documented.
Situation-Specific
amnesia can arise in a variety of circumstances (e.g.,
committing an offence, child sexual abuse)
resulting in PTSD. It has been claimed
that it involves a narrowing of consciousness with attention focused on central
perceptual details and/or that the emotional or traumatic events are processed
differently from ordinary memories.
Transient
epileptic amnesia is a rare and unrecognized form of temporal
lobe epilepsy, which is typically an episodic isolated memory loss. It has been
recognized as a treatment-responsive syndrome congenial to anti-epileptic
drugs.
Acquisition Of New Memories
Patients with amnesia can
learn new information, particularly non-declarative knowledge. However, some
patients with dense anterograde amnesia do not remember the episodes during
which they learned or observed the information previously.
Acquisition of new declarative
information
Some patients with anterograde
amnesia can still acquire some semantic information, even though it might be
more difficult and might remain rather unrelated to more general knowledge.
H.M. could accurately draw a floor plan of the home in which he lived after
surgery, even though he had not lived there in years.
The reason patients
couldn't form new episodic memories is likely because the CA1 region of the
hippocampus was lesioned, and thus the hippocampus couldn't make connections to
the cortex.
After an ischemic episode following surgery, an MRI of patient R.B.
showed his hippocampus to be intact except for a specific lesion restricted to
the CA1 pyramidal cells.
Acquisition of new
non-declarative information
Some retrograde and
anterograde amnesics are capable of non-declarative memory, including implicit
learning and procedural learning. For example, some patients show improvement
on the pseudorandom sequences experiment as healthy people do.
Therefore,
procedural learning can proceed independently of the brain system required for
declarative memory.
According to fMRI studies, the acquisition of procedural
memories activates the basal ganglia, the premotor cortex and the supplementary
motor area, regions which are not normally associated with the formation of
declarative memories.
This type of dissociation between declarative and
procedural memory can also be found in patients with diencephalic amnesia such
as Korsakoff’s syndrome.
Another example demonstrated by some patients, such as
K.C. and H.M, who have medial temporal damage and anterograde amnesia, still
have perceptual priming.
Those patients did well in the word fragment
completion test.
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