AMNESIA WITH FOCUS ON POST TRAUMATIC

AMNESIA
Introduction:
Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma.
Amnesia can also be caused temporarily using various sedatives and hypnotic drugs. The
memory can be either wholly or partially lost due to the extent of damage that was caused.
Some of the different types of Amnesia are:

Anterograde amnesia is 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, encephalitis, surgery, WernickeKorsakoff syndrome, cerebrovascular events,
anoxia or another trauma.

The two brain regions related with this condition are medial temporal lobe and medial
diencephalon. Anterograde amnesia cannot 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.

Retrograde amnesia is 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, tumour, 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. [14] 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.

Dissociative amnesia 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 is 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 defence 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 and 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.[17] 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.
 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.
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 do not 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 time meeting a 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.
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 relate to 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 amnestic drug to
help a patient forget surgery or medical procedures, particularly those not performed
under full anaesthesia, 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.
Situation-specific amnesia can arise in a variety of circumstances (for example,
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.

Post Traumatic Amnesia:

Introduction:
Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following
a traumatic brain injury in which the injured person is disoriented and unable to remember
events that occur after the injury. The person may be unable to state his or her name, where
he or she is, and what time it is. When continuous memory returns, PTA is considered to
have resolved. While PTA lasts, new events cannot be stored in the memory. About a third
of patients with mild head injury are reported to have "islands of memory", in which the
patient can recall only some events. During PTA, the patient's consciousness is
"clouded". Because PTA involves confusion in addition to the memory loss typical of
amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.

Post-traumatic amnesia may be either short term, or longer lasting (often over a month), but
is hardly ever permanent. When continuous memory returns, the person can usually
function normally. Retrograde amnesia sufferers may partially regain memory later, but
memories are never regained with anterograde amnesia because they were
not encoded properly.

Assessment:

Duration of PTA may be difficult to gauge accurately; it may be overestimated (for

example, if the patient is asleep or under the influence of drugs or alcohol for part of the
time) or underestimated (for example, if some memories come back before continuous
memory is regained).

The following tests are administered to assess the level of PTA:

Galvestone Orientation and Amnesia Test:

The Galveston Orientation and Amnesia Test (GOAT) was developed to evaluate cognition
serially during the subacute stage of recovery from closed head injury. This practical scale
measures orientation to person, place, and time, and memory for events preceding and
following the injury. This was the first measure created to test post-traumatic amnesia, and
is still the most widely used test.

The test was created by Harvey S. Levin and colleagues (1979), and features ten questions
that assess temporal and spatial orientation, biographical recall, and memory. Points are
awarded for responses to each question, with a total of 0-100 points possible. A score
greater than 78 for three consecutive days is considered the threshold for emergence from
post-traumatic amnesia.

Assessment consists of 10 items regarding orientation to person (name, address, and

birthdate), place (city/town and building they are in) and time (current time, date, month,
year & date of hospital admission) as well as memory of events both after and prior to the
injury. Oral questions are posed directly to the patient who may respond either orally or in
writing. Error points are awarded for each incorrect response, summed and deducted from
100 to arrive at the total score.

The duration of post traumatic amnesia (PTA) is defined as the period following coma in
which the GOAT score is <75. PTA is considered to have ended if a score 75 is achieved
on three consecutive administrations. In the initial standardization study of Levin et al.
(1979), using patients with mild head injury as a reference group, it was determined that a
score of 75 represented a level achieved by 92% of the standardization group. No patients
with mild head injury scored less than 65 on the GOAT. Scores between 66 and 75 are
considered borderline-abnormal while scores above 75 fall into the range considered
normal within the reference group.

Advantages. The GOAT provides an objective rating of early cognitive recovery

eliminating the need for sometimes ambiguous terminology used to describe mental status,
such as confused (Levin et al. 1979). Rasch analysis demonstrated that items on the
GOAT represent a wide range of difficulty suggesting that the scale is useful for assessing
patients with a wide range of cognitive impairments (Bode et al. 2000).

Limitations. The standard GOAT response format makes administration difficult with
nonverbal patients. The requirement for oral or written expression may result in penalizing
patients who are experiencing deficits of expression but not in orientation or in the retrieval
or consolidation of memory. An aphasia-specific version of the GOAT has been created,
although it requires further evaluation.

Westmead Post-Traumatic Amnesia Scale (WPTAS):

The Westmead Post-Traumatic Amnesia Scale (WPTAS) is a brief bedside standardised
test that measures length of post-traumatic amnesia (PTA) in patients with traumatic brain
injury. It consists of twelve questions that assess orientation to person, place and time, and
ability to consistently retain new information from one day to another. It is administered
once a day, each and every day, until the patient achieves a perfect score across three
consecutive days, after which the individual is deemed to have emerged from post-traumatic
amnesia.

While other tests of post-traumatic amnesia, such as the Galveston Orientation and
Amnesia Test, tend to focus on the patients memories of the injury, which rely on
potentially biased recall and unverifiable information, the WPTAS is composed of objective
items that examine orientation and the ability to consistently retain simple information from
one day to another.

The WPTAS takes approximately three minutes and is administered according to specific
guidelines. The scale is first administered once a patient is conscious and able to
communicate (either verbally or non-verbally).

On the first administration, the patient is asked seven questions related to orientation (e.g.
what day of the week is it?). Thus, the most a patient can score on the first day of testing
is 7/7. Following the seven questions, the patient is then given the opportunity to learn
information which will form part of five additional memory questions that are asked on
subsequent PTA testing.

This includes the patient being shown three pictures and being specifically asked to
remember the three pictures for tomorrow when they are tested again.

For each subsequent day, the patient is asked the seven orientation questions and the five
memory questions. Thus, from the second day of testing onwards the test is out of 12. The
three pictures that the individual needs to remember remain the same for each daily
administration until the patient achieves a perfect score of 12/12. When the patient achieves
12/12, the patient is then asked to remember three different pictures for the next day.

Testing is ceased once a patient achieves 12/12 on three consecutive days. Duration of PTA
is calculated as being from the time of the accident until the first day of the three consecutive
days in which the individual achieves a score of 12/12. That is, the beginning point in which
the individual demonstrated continuous memory across three consecutive days, or the first
day of a score of 12 for those patients who have been in PTA for greater than four weeks.

The WPTAS is administered in a quiet environment that does not contain obvious cues
around the patient that could assist them with answering the orientation questions (e.g.
clocks or calendars). The scale can be adapted to be used for patients who are unable to
communicate verbally.

Symptoms:

The most obvious symptom is the loss of memory for the present time. The person may
recognise family and friends but be unable to process the fact that they are in hospital or
have had an injury of some kind. Many patients report feeling as though they were being
"held prisoner" and being prevented from carrying on with their daily lives.

Patients also often display behavioural disturbances. Patients may shout, swear and behave
in a disinhibited fashion. Some patients exhibit childlike behaviour. Other patients show
uncharacteristically quiet, friendly and loving behaviour. Although this behaviour may
seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions
repeatedly. Patients may also tend to wander off, which can be a major concern in those
who have suffered additional injuries at the time of trauma, such as injured limbs, as it may
lead to the worsening of these secondary injuries.

Severity:

The severity of post-traumatic amnesia (PTA) is directly related to its duration, although a
longer duration does not necessarily indicate more severe symptoms.

he duration of PTA in brain-injured patients is a useful predictor of the expected long-term

effects of the injury, along with the duration of loss of consciousness(LOC), and scores on
the Glasgow Coma Scale (GCS), which measures degrees of consciousness, with higher
scores indicating higher levels of functioning. A score of 3 indicates complete
unconsciousness, and a score of 15 indicates normal functioning

In patients experiencing PTA for the duration of:

Up to 1 hour The injury is very mild in severity and full recovery is expected. The patient
may experience a few minor post-concussive symptoms (e.g. headaches, dizziness).

1 24 hours The injury is moderate in severity and full recovery is expected. The patient
may experience some minor post-concussive symptoms (e.g. headaches, dizziness).

1 7 days The injury is severe, and recovery may take weeks to months. The patient may
be able to return to work, but may be less capable than before the injury.

1 2 weeks The injury is very severe, and recovery is likely to take many months. The
patient is likely to experience long-lasting cognitive effects such as decreased verbal and
non-verbal intelligence as well as decreased performance on visual tests. Patients should,
however, still can return to work.

2 12 weeks The injury is very severe, and recovery is likely to take a year or more. The
patient is likely to exhibit permanent deficits in memory and cognitive function, and the
patient is unlikely to be able to return to work.

12+ weeks injury is very severe and accompanied by significant disabilities that will
require long-term rehabilitation and management. The patient is unlikely to be able to
return to work.

TBI Measurement:
PTA has been proposed to be the best measure of head trauma severity, but it may not be a
reliable indicator of outcome. However, PTA duration may be linked to the likelihood that
psychiatric and behavioural problems will occur as consequences of TBI.

Classification systems for determining the severity of TBI may use duration of PTA alone
or with other factors such as Glasgow Coma Scale (GCS) score and duration of loss of
consciousness (LOC) to divide TBI into categories of mild, moderate, and severe.

Mild TBI
Brief loss of consciousness, usually a few seconds or minutes
PTA for less than 1 hour of the TBI
Normal brain imaging results
Moderate TBI
Loss of consciousness for 1 24 hours
 PTA for 1 24 hours of the TBI
Abnormal brain imaging results

Severe TBI
Loss of consciousness or coma for more than 24 hours
PTA for more than 24 hours of the TBI
Abnormal brain imaging results

PTA is considered a hallmark of concussion, and is used as a measure of predicting its

severity, for example in concussion grading scales. It may be more reliable for determining
severity of concussion than GCS because the latter may not be sensitive enough; concussion
sufferers often quickly regain a GCS score of 15.

Longer periods of amnesia or loss of consciousness immediately after the injury may
indicate longer recovery times from residual symptoms from concussion. Increased
duration of PTA is associated with a heightened risk for TBI complications such as post-
traumatic epilepsy.

Pathophysiology:

Currently, the pathophysiological mechanisms which produce post-traumatic amnesia are

not completely known. The most common research strategy to clarify these mechanisms is
the examination of the impaired functional capabilities of people with post-traumatic
amnesia (PTA) after a traumatic brain injury.

Neurological Mechanisms

Research on the effect of emotional trauma on memory retention and amnesic symptoms
has shown that exposure to prolonged levels of extreme stress has a direct effect on
the hippocampus. Elevated stress levels can lead to an increase in the production
of enkephalins and corticosteroids, which can produce abnormal neural activity and
disrupt long-term potentiation (a neural mechanism associated with learning) in the
hippocampus.

Individuals who have been subjected to repeated sexual abuse during childhood or who
have experienced combat show significant impairment and atrophy of the hippocampal
region of the brain. The amygdala, an area of the brain involved in emotional regulation,
may be involved in producing remembrance for some aspects of the trauma. Even though
the trace of a memory for trauma may be lost from the hippocampus, it may remain partially
encoded in the form of an emotional memory in the amygdala where it can be subsequently
recalled in the form of a flashback or partially recovered memory.

Diaschisis
Diaschisis refers to the sudden dysfunction of portions of the brain due to lesions in distant
but connected neurons. Diaschisis is implicated as playing an important role in PTA, more
particularly in the declarative memory impairments observed in patients experiencing an
episode of PTA. The loss of function observed after traumatic brain injuries, as well as the
resulting loss of consciousness, was thought to be mediated by the 'neural shock' associated
with diaschisis.

Diaschisis was originally believed to be a result of disruption to neural tissue, but more
recent evidence implicates increased activity levels of choline acetyltransferase, the
enzyme responsible to produce acetylcholine, as a major cause. Based on these findings,
diaschisis could be helped using drugs that would reduce cholinergic (acetylcholine)
activity, and reduce the levels of acetylcholine in the brain.

This idea is supported by the fact that there is an increase in acetylcholine concentrations
in the brain after head injury. Animal studies have shown that concussive injuries in rats
lead to changes in the central nervous system's cholinergic system. This increase in
acetylcholine levels has also been tied to behavioural suppression and unconsciousness,
both symptoms of PTA. In long-term recovery, acetylcholine levels associated with
diaschisis may continue to play a role in maintaining memory deficits.
Brain-imaging studies
Brain imaging techniques are useful for examining the changes in the brain that occur
because of damage. Metting used CT scans to examine the pathophysiological damage in
patients currently experiencing an episode of PTA, patients with resolved PTA, and
a control group that had not experienced PTA.

Blood flow to the occipital lobe, the caudate nucleus, and the grey matter of the frontal lobe
was significantly reduced in patients who were scanned during the episode of PTA. No
differences were seen between patients with resolved PTA and the control group. This
encouraging finding points to the positive long term prognosis of PTA; most patients return
to normal levels of functioning. The frontal lobes are associated with explicit
memory retrieval, and deficits on explicit memory tasks are often found with patients
experiencing PTA.

Working memory deficits are a common symptom in patients with PTA. The duration of
an episode of PTA was correlated with reduced blood flow to the right hemisphere, a
finding which was consistent with functional MRI studies that link working memory with
right frontal activity. The prefrontal cortex, which plays an important role in explicit
memory retrieval, was also found to have decreased neural activation in patients scanned
during the episode of PTA. Researchers noted that the damage was related
to vascularization and neural functionality, but not to structural injury, suggesting that the
resolution of PTA is dependent on functional changes.

Memory and new learning involve the cerebral cortex, the subcortical projections,
the hippocampus, the diencephalon and the thalamus, areas that often suffer damage
because of TBI.

Frontal lobe lesions may also play a role in PTA, as damage to these areas is associated
with changes in behaviour, including irritability, aggressiveness, disinhibition, and a loss
of judgment. Damage to this area may account for the uncharacteristic behaviour often
exhibited in PTA patients.
Accelerated forgetting
Researchers have also found that individuals experiencing PTA show accelerated
forgetting. This contrasts with the normal forgetting observed by patients with normal
amnesia related to brain damage. The temporal lobes are often the most vulnerable to the
diffuse (widely distributed) and focal (more specifically localized) effects of TBI and it is
possible that temporal lobe lesions may account for the accelerated forgetting observed in
patients with PTA.

These predictions were supported by the finding that most of the patients who showed rapid
forgetting also had lesions to the temporal lobe. Bilateral damage to the temporal lobes also
causes severe anterograde amnesia, making it likely that lesions to this area would be
involved in PTA. Patients exhibit a temporal gradient with memory loss, meaning that older
memories are preserved at the expense of newer memories. Temporal lobe damage has been
linked to a temporal gradient of this sort, because older memories are less dependent on the
hippocampus and thus are less influenced by its damage.

There is a significant link between individuals currently suffering from PTA and their
performance on the Wechsler Adult Intelligence Scale (WAIS). The scores of those
currently experiencing an episode of PTA were compared to individuals who had
previously suffered a traumatic brain injury resulting in PTA. Those still suffering from
PTA performed significantly worse on both the performance and the verbal subscales of
the WAIS. Also, people in early stages of PTA have substantial impairment to anterograde
memory function. For example, in the case report of a patient referred to as "JL", Demery
noted that his memory impairments were so severe following his injury that he had
forgotten that he had attended a Major League Baseball game less than 30 minutes after
returning to the centre where he was being treated.

Most neuropsychological studies available have suggested that the medial temporal lobes
are the most important system in the pathophysiology of PTA. However, there is little
research done on this topic, and as new research is done, more information should come
forth concerning functionality in these areas in PTA patients.

One MRI study showed that a long duration of PTA was correlated with damage in the
hemispheric and central areas, regardless of whether the duration of the coma was relatively
short. In patients who had a longer coma duration, deeper lesions in the central area were
observed without extensive damage to the hemispheric area.

Rehabilitation:
Rehabilitation is effective using an interdisciplinary approach, and close liaison with the
patient, family and carers. The focus is on issues such as retraining in activities of daily
living, pain management, cognitive and behavioural therapies, and pharmacological
management.

The social burden of TBI is significant, and therefore family education and counselling, and
support of patient and carers, is important.

As with all rehabilitation, the goal is to help the person achieve the maximum degree of
return to their previous level of functioning. TBI rehabilitation is best managed by a
specialised interdisciplinary team of health professionals. Some of them include:

Patient and patient's family

General practitioner
Rehabilitation medicine physician
Rehabilitation nurse
Allied health professionals: physiotherapist, occupational therapist, speech
pathologist, social worker
Neuropsychologist, clinical psychologist
Vocational rehabilitation services and counsellors
Other medical specialties: neurosurgery, orthopaedic surgery

Inpatient management is required for those with more severe and acute physical, cognitive
and/or behavioural deficits. The focus is on issues such as PTA monitoring, retraining in
activities of daily living, pain management, cognitive and behavioural therapies,
pharmacological management, assistive technology (e.g., prescription wheelchairs and gait
aids), environmental manipulation (e.g., installation of lifts, ramps and rails, and bathroom
alterations), as well as family education and counselling.

Most patients also require rehabilitation for associated trauma (e.g., fractures). People with
catastrophic injury may need prescription of major equipment (e.g., hoists to facilitate
patient transfer, modifications to cars such as special seating) and modifications to their
home environment (e.g., bathroom modifications, grab rails, non-skid flooring).

Patients may also require retraining in daily living activities for home and community living
(e.g., household tasks such as doing the laundry, and community living skills such as
crossing roads, banking, etc.). This can be done through outpatient programs or through a
transitional living unit, where patients are largely self-managing under health professional
supervision.

Community rehabilitation follows discharge from an inpatient rehabilitation service.

Helping a person with TBI return to maximum independence and participation in the
community is an extremely difficult task. Family support, education and counselling are
vital and likely to be needed for a prolonged period.

Rehabilitation of Children with PTA

Traditionally, children have been reported to have better outcomes than adults after TBI.
However, while fewer focal deficits may be apparent, children appear to develop blunting
across all areas of higher cognitive functioning. These deficits may not become apparent
until later in the child's development.

Children with TBI face difficulties because of impaired new learning, inability to take on
social cues, and behavioural, educational and schooling problems. These problems pose
difficulties for parents, teachers and healthcare workers.

There may be a poor fit between the needs of children with TBI, and typical school
educational programs. Parents are faced with many challenges, including coping with
changed academic aspirations for their child.
The North Star Project
THE NORTH STAR Project is an initiative taken by members of the Traumatic Brain
Injury (TBI) Program, a multidisciplinary team of front-line rehabilitation specialists who
deliver professional care to an average of 350 patients with TBI each year.

The North Star Project was developed by researchers at McGill University. Researchers
developed a "reality orientation", which involved discussing general facts (e.g. date, time,
names of family members, etc.) with amnesic patients twice a day to lessen their confusion
during the early stages of their recovery. Younger patients often had shorter amnesic
episodes than older patients, especially those in the North Star group.

Although more improvements were noted in the North Star group than in the control group,
researchers did not find a statistically significant effect of their intervention. The North Star
project also allows the family to become more actively involved in the treatment of their
loved one. Further study is required to evaluate this intervention strategy to improve
orientation for the patient with TBI.

Findings
A comprehensive analysis of literature based on the effects of early rehabilitation of
traumatic brain injury concluded that there is no strong evidence linking any one practice
of post-injury care to a reduced severity in symptoms. However, even in the absence of a
concrete correlation between a specific rehabilitation program and improved outcomes, the
evidence and research available can provide many good suggestions for how to proceed
with treatment. All rehabilitation strategies reviewed had positive effects on recovery, but
none more so than the others.

The most accurate measure of determining the length of amnesia is still a behavioural
measure, the duration of the episode of post-traumatic amnesia, rather than a neuroimaging
technique or an electrophysiological or biochemical technique. The length of amnesia is
also one of the most accurate predictors for determining later cognitive problems, even
more so than the duration of either the coma or the period of loss of consciousness. The
duration of amnesia after TBI, therefore, can be very useful in the planning the length and
intensity of rehabilitation programs for persons afflicted with PTA.

Treatment:
Usage Vasopressin on Animals
Early research pointed to vasopressin as a potential treatment for improving the memory of
patients living with post-traumatic amnesia
(PTA). Lysine vasopressin, a modified form of the
vasopressin molecule, had positive effects on memory
when administered by injection to patients with amnesia
resulting from traumatic brain injury.

Subsequent animal studies with rats found similar

results, particularly in aversion and avoidance learning
tasks. Rats lacking adequate vasopressin, either due to genetic defect or hypophysectomy
(surgical removal of the pituitary gland), exhibited significant improvements in memory
and learning functions when exogenous vasopressin was administered. Particularly
encouraging was the finding that a short treatment period produced long-lasting
improvements, in both humans and rats.

However, the animal models of PTA are highly limited, as the dimension of self-awareness
and orientation is almost impossible to model adequately. PTA in animals, especially rats,
is often observed post-trauma (commonly post-surgery), but it is often only measured in
terms of impaired learning or unusual behaviour

Usage of Vasopressin on Humans

One subsequent human study found no effects of vasopressin on memory. The
nonsignificant results were attributed to the study's many potential flaws, particularly its
small sample size, the inability of vasopressin to penetrate the blood brain barrier when
administered as a nasal spray, inadequate dosing and differences in severity of head injury
between the samples. However, Eames et al. (1999) found statistically significant
improvements on several tests of memory with the use of a vasopressin nasal spray, with
no reported ill effects. Although the degree of improvement was mild, and it could be
attributed to numerous other factors of the rehabilitative program, the lack of any ill effects
suggests that vasopressin is, at the least, a possible enhancement for a treatment regimen.

Norepinephrine Antagonists
Diaschisis, as mentioned earlier, has been linked to the mechanism of PTA. The
noradrenergic systems may play a role in diaschisis. Norepinephrine, also known as
noradrenalin, is a catecholamine neurotransmitter. Administering a norepinephrine
receptor agonist (a substance that initiates a cell response when it binds with a receptor) to
patients promoted the recovery of memory and many other cognitive functions after a
traumatic brain injury.

Conversely, the administration of norepinephrine antagonists slowed recovery, and could

lead to the reinstatement of deficits when administered after recovery. Noradrenergic
antagonists were not prescribed for the purposes of slowing the recovery of memory.
Rather, these findings are based on the effects of other commonly prescribed drugs that
happen to block noradrenergic receptors.

The alpha-1 adrenergic receptor is specifically implicated. Although it has not yet been
thoroughly investigated, there is potential for stimulants, which promote catecholamine
release, to be an effective treatment in the early stages of recovery from brain trauma, and
these positive effects could reduce the symptoms of PTA.

History of PTA:
It was the British physician C. P. Symonds who first discussed the specific amnesiac
symptoms that often follow a cerebral contusion, which is a specific kind of traumatic brain
injury. Symonds observed that the patient remains "stuperose, restless and irritable" after
recovering consciousness. He also identified a recovery period of days to weeks for this
post-concussive state.

Presumably, shorter durations of PTA, which are now included in the definition, were not
thought to be serious enough for documentation. Most importantly, he identified the
amnesia that the patient experiences during this period of recovery, and recommended the
use of "formal tests for memory and retention" to assess recovery.

In WWI soldiers

Although there was a general lack of knowledge about its mechanisms, a review of patients
seen during WWI combat reveals the symptoms of post-traumatic amnesia (PTA) in many
soldiers. The term shell shock was used to refer to the acute psychological state that
accompanied exposure to exploding shells, and more generally, exposure to combat
conditions. There are a number of documented cases of shell shock victims. These soldiers
commonly displayed dizziness, varying degrees of consciousness, a loss of non-traumatic
personal information, and a lack of normal self-awareness lasting anywhere from hours to
days. Many of the symptoms of shell shock are highly like those of PTA.

Researchers found that physicians had documented reports of combatants where "both
central and peripheral details of the traumatic experience were lost." Patients displayed gaps
in memory recollection for the period following the trauma, sometimes up to the time of
hospitalization, which could be weeks later.

An initial assessment supported the role of concussions in causing these symptoms.

Concussions could account for the anterograde amnesia and retrograde amnesia observed
in patients, as well as the periods of fluctuating consciousness or delirium that sometimes
followed. However, many soldiers who showed these amnesiac effects did not suffer
injuries that would have led to concussions.

Thus, there was controversy over the possible causes of PTA in these non-concussed
soldiers, with a separation between proponents of Freudian repression and those supporting
a dissociative view of the condition. This dissociative view was ultimately supported, and
accounted for the fugue state seen in soldiers who were thought to have dissociated from
normal consciousness.
Case Study:
Patient Outline
JM is an 80-year-old woman who was involved in a pedestrian vs. car accident on the 15th
December 2011. She sustained a loss of consciousness and her Glasgow Coma Scale was
initially 14/15 at the scene reducing to 12/15. She was admitted to Royal Melbourne
Hospital where CT brain scan indicated subarachnoid haemorrhage, a small left subdural
haemorrhage and multiple intra-cerebral haemorrhages in her right parafalcine area. She
also sustained a left intra-cerebral haemorrhage. Further injuries included fracture to the
right parietal bone extending to the temporal bone. Fracture to right zygoma, several broken
teeth and a lip laceration. She had a scalp laceration, which was sutured.

JM was transferred to the Acquired Brain Injury Unit at Epworth Rehabilitation

Camberwell 13 days following her injury (28th of December 2011). On admission, she was
noted to have a severe receptive and expressive dysphasia with significant neologisms and
anomia. She was unable to perform repetition, nor read or write. She required assistance
with personal care and ambulation and she was on a modified diet. As a further
complication, she had a urinary tract infection, which was treated with success. Other
relevant information, JM was born in Japan and had lived in Australia for 40 years. She
spoke English with her family. Prior to her injury, JM was living independently and enjoyed
activities including playing golf, photography, writing a daily blog and staying in touch
with family and friends (worldwide via electronic methods) in English.

Method
Once JM was observed to comprehend the questions and understand the need to choose a
response, the modified multiple-choice WPTAS assessment was completed daily with the
Speech Pathologist. Clinical observations included monitoring of her behaviour, attention,
engagement, sleep-wake cycle and mood. This information was collected by the multi-
disciplinary team across the day and night and overseen by the Neuropsychologist.

Result
The modified multi-choice WPTAS was shown to be a more sensitive data collection
method for JMs orientation and memory skills and assisted determine the resolution of her
amnesia. After receiving a score of 12/12 on the 24th January 2011, in conjunction with
behavioural observations, JM was deemed out of PTA by the Neuropsychologist in
consultation with the multi-disciplinary team. Tate et al., (2006) have suggested that
patients who are in PTA for greater than 4 weeks have likely emerged from PTA when they
first score 12/12 on the WPTAS, and this
criterion can replace the traditional criterion
of three consecutive days. Concurrent to her
scoring 12/12 on the modified WPTAS, JM
was noted to have an appropriate level of
engagement in tasks, improved attention,
appeared more settled (indicating
improved behaviour) and was more bright
and reactive in mood. She maintained a normal sleep-wake cycle and was further
independent with all self-care. Total length of PTA was estimated to be approximately 41
days.
Talk about the day of the accident. What do you remember about the day of the accident
before the accident?

I had been up at 4:30 and gone to the gym. I intended to stop at the grocery store on the
way to work to pick up a couple of things. I left the gym and went to the store across the
street from my office and purchased broccoli and apples, and, thats all I know.

Do you remember checking out?

I believe I remember getting out of the checkout stand, but I dont know whether thats a
legitimate memory or thats just because Ive been to the grocery store so many times that
that seems like the most logical way that youd actually leave.

How long would it take you to get from what you were doing to the last thing you remember
until where the accident happened?

Probably 10-15 minutes.

Whats the next thing you remember?

I remember on July 4rth my sister called me and asked me if I was coming to her BBQ
party.

You dont remember being in the accident?

No

You remember being in the hospital?

No
You have any recollection, at all of anybody visiting you in the hospital or being there at
all?

No. Ive been told stories about it.

So, the first thing you remember is about 2 weeks alter youre invited to do what?

Well I was at home, and my sister called me. She asked me where are you? I said Im at
home. She said well are you coming? I said coming where? She said to the house, for the
BBQ party. I said I didnt know there was a bbq. She said were having a BBQ I told you
about it yesterday. At that moment, I realised that I didnt remember the conversation that
I had yesterday, but that I didnt remember anything. Like, I didnt remember any of the
details what had happened, and I didnt even know how long that had been at that point.

After that episode, did you have accurate memories going forward, or is it unreliable?

It was unreliable, it still is unreliable even today.

Did you go back to work, shortly after?

Yes.

What happened when you went back to work?

When I went, they didnt give me back all my loans all at the same time. They gave me
back a couple of loans, and overtime they started re-entering me back into the pipeline. But,
I remember, that as I was working on loans, I wouldnt know what I was doing on them.
Somebody came into my cubicle and asked me a question, I didnt know what I had done,
so I would have to start again. I couldnt understand why, because I knew how to do this.
Even today, on an indivisual loan, I can tell you what needs to be done in that file, because
I had done it for so long. But, when I went back to work, the difficulty in deciding that you
have these many things that need to be done and you dont know what youve dont, so you
need to assess what youve done and then do things on this, like order and appraisal, for
example. For whatever was needed to be done, I used to have a system on how to get it
done, but I knew on every file what was there and what was missing, and I just knew that
in my head. When I went back to work, that part was missing, but I didnt know why. I
wasnt given a lot of information about my dream actually, but anytime anyone interrupted
me while I was at work, im working on something, I would lose all the information I was
working on as soon as they interrupted me. I would become so overwhelmed and I would
cry. So I cried a lot in my cubicle, by myself.