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The
impact of traumatic brain injury (TBI) is enormous.
The effect at the individual level is seen in
the changed life of each person who incurs the
TBI.
In the United States, an overall
rough estimate of TBI incidents in 1990 is about
2 million cases. This includes about 51,600
deaths plus 202,000 (220,000 hospital admissions
minus 18,000 deaths occurring after admission)
hospitalized patients who survive, plus 1.74m
cases that only involved physician consultation
or at least one day of disability. These latter
two figures are extrapolated from 1991 and 1977-1981
national data. (Fife, 1987).
To begin with, TBI technically,
(cranio-cerebral trauma) is defined either:
- as an occurrence of injury to the head
that is documented in a medical record with
one or more of the following conditions
(injuries to the head may arise from blunt
or penetrating trauma or from acceleration-deceleration
forces):
- Observed or self reported decreased
level of consciousness, that is, a transient
alteration of consciousness including
partial or complete loss of consciousness,
obtundation, stupor or coma.
- Amnesia, including the time preceding,
during, and subsequent to the injury.
- Skull fracture.
- Objective neurological or neuropsychological
abnormality.
- Diagnosed intracranial lesion.
- or as an occurrence of death resulting
from trauma, with head injury listed on
the death certificate, autopsy report, or
medical examiners report in the sequence
of conditions that resulted in death.
Virtually all of these above
changes have been noted with moderate to severe
head injury unequivocally, that is, where there
was a serious injury, often life threatening,
with obvious disability and the need for specialized
treatment. However, over a number of years a
new population is increasing namely that of
the minor head injury. These are injuries where
patients spent a brief time (if any) in the
hospital, made quick medical recoveries, and
were discharged directly (and often prematurely)
from the ER to home without any perceived need
for formal neuropsychological assistance. What
followed was, though appearing fine, they attempted
to return to their former responsibilities at
home, work, or school. When they did so, a significant
number experience great difficulty. They complained
of inability to remember, concentrate, organize,
handle a number of tasks at once, or be as efficient
as before. The relationship with family, peers,
and bosses often suffered, and they developed
secondary psychological problems. Their doctors
were unable to find anything wrong with them,
and they were thought to have psychiatric problems
- or worse yet, to be malingering. They became
the outcasts of neurologists, psychologists,
psychiatrists, or vocational counselors all
of whose unusual techniques did not produce
positive results.
In such cases the unique problem
if minor TBI readily became apparent despite
swift and complete physical recoveries, and
despite no obvious neurological basis for their
problems, these persons experienced significant
cognitive, emotional, and behavioral deficits
that seriously interfered with their functional
lives.
The trauma itself may have
involved a fall, a blow to the head, or (most
commonly) the head striking a stationary object
as in a motor vehicle accident. Minor TBI may
also occur after a severe whiplash injury, even
if the head is not struck, especially (it appears)
if the whiplash involves some rotation of the
head in addition to linear movement.
The alteration of consciousness
usually, but not always, involves some brief
loss of consciousness. With moderate to severe
head injury, there is a rough correlation between
length of coma and severity of injury (as measured
by outcome). Within the group of minor TBI,
however, when loss of consciousness lasts less
than an hour, there is no demonstrable relationship
between length or alteration of consciousness
and severity of problems. Severe functional
deficits can occur even with transient loss
of consciousness. Those patients have already
"awaken" by the time they arrive at
the hospital after minor TBI, although they
might not recall the events for some period
of time after the accident, despite being awake
and communicating (post-traumatic amnesia).
It is also possible that significant,
long term deficits can occur in the absence
of any documentable loss of consciousness. In
such cases, the alteration of consciousness
may take the form of the patient feeling dazed,
confused or agitated for some period of time
even though consciousness was never lost. The
neuroanatomical sequelae to minor TBI can be
of diffuse or focal nature. The secondary cognitive
deficits in terms of the former are that of
reduced speed and compacity of information processing,
complex attention, learning and memory, and
integrative abstract thinking. In terms of the
latter such deficits may run the gamut of (but
not limited to) word finding difficulties, perception,
(neglect) sensory functions (especially) ansomia,
motor functions, sensory motor integration,
and arithmetic calculations.
The question arises, now what
are the psychological/behavioral consequences
of minor TBI? There are a number if functional
scenarios that arise following premature discharge
from the ER and limited follow-up medical intervention
at best. First, the patient is assumed to have
completely recovered. However, even in this
"complete recovery" scenario it is
in a modified form. That is, a person may notice
minor problems with memory or problem solving,
but not to the extent they seriously interfere
with functioning or require any conscious adaptation.
It is this population that physicians and attorneys
often describe as completely recovered with
no permanent neuropsychosocial sequelae. However,
this person may experience changes in cognitive
processing abilities, but only rarely and only
at certain times _ such as under extreme stress,
anxiety, fatigue, or after even mild use of
alcohol or drugs. In addition, even after "complete
recovery" the occurrence of cumulative
effect is established. That is, the occurrence
of any subsequent minor head injury (especially,
in sports) eventually produces noticeable deficits,
even though none is any worse than the first
- implying that the initial "complete recovery"
was really a decrement in nervous system integrity
too small to notice behaviorally.
Next is the spontaneous accommodation.
In this case the individual does, as a result
of a minor TBI, experience long term cognitive
impairment but succeeds in adapting successfully
to his cognitive and behavioral changes. His
life and work is disrupted by the impairment.
Finally, the person compensates for the deficits
by making changes in their environment.
On the other hand, there are
a number of dysfunctional scenarios that result
from minor TBI of which the posttraumatic stress
reaction will be the focus. It is precisely
this phenomenon that has caused considerable
controversy in terms of its legitimacy. The
psychological sequelae of minor TBI are typically
conceptualized in terms of organic impairment
with the aforementioned cognitive deficits as
well as emotional functioning. Collectively
these are known as primary psychological reactions
where as Posttraumatic Stress Disorder (PTSD)
is typically a secondary psychological reaction.
However, the minor TBI is a frightening experience,
and the circumstances of the injury may range
from the moderately distressful to the horrific.
While brain injured patients are usually thoroughly
worked up from a medically and neuropsychological
point of view, clinicians have paid rather less
attention to the emotional sequelae of minor
TBI. Thus the importance of recognizing the
potential association of PTSD with minor TBI.
PTSD is a psychological condition
estimated to occur in about 2-20% of civilians
exposed to life-threatening experiences in which
there is no injury to the brain. PTSD is characterized
by 3 "symptom clusters": 1) persistent
and painful re-experiencing of the trauma such
as flashbacks, nightmares, or obsessive thoughts:
2) emotional numbing or societal withdrawal
in attempts to avoid stimuli associated with
the events; 3) increased arousal as manifested
by symptoms such as irritability, poor concentration,
and disturbed sleep. These symptoms require
duration of at least one month to meet the DSM-IV
diagnostic criteria.
With litigation burgeoning,
PTSD have come into prominence. Traditionally,
PTSD has been applied to personal injury claims
based upon the psychological consequences of
automobile, home, industrial accidents and mass
disasters.
A brief history of PTSD reveals
that, in an earlier definition, it was diagnosed
as railway spine in the 19th century. Such injuries
were particularly common with the growth of
railroads. It was thought that concussion of
the spine was a concomitant injury to the sympathetic
nervous system causing the observed traumatic
neurosis (Trimble, 1981). In World Wars I &
II, traumatic stress disorders were called variously
shell shock, battle fatigue, traumatic neurosis
and concentration camp syndrome.
On the surface, logic dictates
that an emotional disturbance caused by a specific
experience must be dependent on the ability
of the person to recall that experience. However,
when an event such as an automobile accident,
fall or assault results in a blunt traumatic
brain injury, the individual typically cannot
remember the traumatic experience, nor the events
that surround its occurrence. This inability
to recall events immediately preceding the event
(retrograde amnesia) and following it (post-traumatic
amnesia) is caused by physical disruption of
brain mechanisms involved in memory function
described earlier. This differs from memory
loss due to emotional (psychogenic/functional)
factors such as a "need to forget"
a life threatening experience. It is at this
juncture the interface between neurological
insult and subsequent cognitive and behavioral
stress-related symptoms in the form of PTSD
is questioned. Because trauma can occur under
a broad range of external conditions, PTSD occurs
with minor TBI in some cases. These instances
make the examination of cognitive status especially
critical. Thus an individual suffering a minor
TBI may incur neurological damage and secondary
cognitive dysfunction; these may produce isolated
performance deficits or a combination of psychological
and behavioral alterations in the form of PTSD.
Thus a number of situations can arise on which
physical and psychological components exert
distinct effects on performance or where they
combine to influence diagnostic presentation.
Therefore this raises the question
how is it possible that an individual with minor
TBI can be suffering PTSD, an emotional disturbance
that is dependent on memory for the event that
has caused it? Many clinicians by virtue of
PTSD criteria recheck the notion of the co-occurrence
e.g. Sbordone, 1992. On the other hand studies
by Horton, 1993, Layton and Zonna, 1995 and
Rattok and Ross, 1993 have clearly demonstrated
the possibilities. At the 1993 European meeting
of the International Neuropsychological Society,
Rattok and Ross reported 20% of 40 patients
who suffered TBI with coma of at least one hour
could be diagnosed with PTSD used in modified
criteria for the disorder.
The problem with critics of
this potential co-occurrence of PTSD with minor
TBI is the continual reliance on unitary memory
theory. This position is most represented by
Sbordone's argument that PTSD and retrograde
amnesia seen with legitimate head injury may
not be diagnosed concurrently since memory (or
psychologically repressed memory) for the trauma
is assumed to be a necessary condition for PTSD.
Understanding how there may be coexistence of
minor TBI and PTSD requires a brief introduction
and some information on memory theory.
To begin with it is important
to understand the distinction between explicit
(declarative) vs. implicit (non-declarative)
memory. Explicit memory represents the ability
to recollect consciously earlier experiences:
implicit memory on the other hand, refers to
the retrieval of such information without conscious
attention of the awareness on the part of the
subject. Explicit memory can be assessed using
traditional tests of recall and recognition,
where as implicit memory requires testing under
conditions that obviate the subjects awareness
of the topic or stimulus being investigated.
Recent studies on functional
amnesias also indicate that similar patterns
of memory dysfunction exist in psychologically
distressed patients who have experienced traumatized
events. In these patients, implicit memory abilities
appear to be strikingly preserved despite the
presence of explicit memory deficits (Kaszniak
et. al. 1988).
Such findings suggest a possibility
of a disassociation between these two memory
systems in patients without neurological lesions.
On the basis of this work, some authors (Schacter
and Kihlstrom 1989) have proposed that similar
memory assessment paradigms be used to search
for disassociations between explicit and implicit
memory systems in disorders such as PTSD, in
which recall, processing, and retrieval of certain
types of information are purportedly disrupted.
Thus from the point of view
of minor TBI and PTSD, two features about multiple
memory system theory are essential. First, one
category of implicit memory is sensitization,
defined as increased reactivity to a previously
neutral stimulus as a result of exposure to
an extreme stimulus (the traumatic event and
PTSD). Second, an individual event may have
both explicit and implicit properties and be
stored simultaneously in both systems. This
is the concept of dual storage. For example,
an experience that causes physical trauma may
be registered consciously and later be recalled.
The same trauma also may change the person in
a manner that is independent of conscious memory,
that is, implicit, for example, by altering
responsiveness to events (such as driving through
intersections) which previously had no notable
effect on arousal.
The recent appreciation that
memory is diverse rather than unitary and that
memory systems are autonomous is theoretically
compatible with the position that PTSD may occur
in the absence of recall for the traumatic event.
Hence, sensitizing stimuli in the form of MVAs
and assaults are stored simultaneously in both
implicit and explicit systems and the effect
on behavior of these sensitizing situations
are a result of the combined effects of registration
of both systems. This argument is consistent
with DSM-IV description of the effects of PTSD
in terms of changes in cognition, behavior and
autonomic responsiveness. Thus accidents or
assaults that result in minor TBI, and compromise
functioning of the neural systems that normally
would mediate the ability consciously to recall
the event (that is operation of the explicit
system) is nonetheless stored in the implicit
memory systems with sensitizing aspects of the
event operationally causing the symptoms of
PTSD (Layton and Zonna 1995).
The position can be further
buttressed by the work of Parker 1990, and Deitz
1992 regarding autonomic arousal as defined
in DSM-IV. In addition to the immediate, direct
effects of the minor TBI to brain tissue, a
host of complex acute and delayed biochemical
effects are activated in terms of attendant
stress effects according to Parker. The head
injury is accompanied by a tremendous catecholamine
surge which precipitates electrocardiographic
changes, depression of thyroid function and
hypoxia. In addition there is an outpouring
of other neurotransmitters, neuropeptides, and
hormones. The person's ongoing stress is accompanied
by heightened catecholamine endorphin secretion
with eventual depletion. The behavioral consequences
include anxiety, irritability, explosive outbursts,
insomnia, hyperalertness, and emotional ability.
Thus, some multiple afferent signals through
sensory and emotional pathways induce the secretion
of corticotrophin releasing hormone (CRH) from
the hypothalamus which stimulates the pituitary
gland to produce adrenocorticotrophic hormone
(ACTH). This, in turn, stimulates the secretion
of glucocorticoid hormones such as cortisol
(the classic stress hormone) from the adrenal
cortex.
High levels of this cortisol
appears to depress brain cell function. The
hippocampus, which plays an important role in
memory, contributes to feedback to the adrenal
cortex to modulate the stress response, together
with input from the pituitary, amygdala, septum,
and reticular formation. The hippocampus possesses
receptor sites for vasopressin and glucocorticoids
(example, cortisol), and circulating glucocorticoids
exert feedback effects via the hippocampus.
Therefore, hippocampal damage
or depletion of hippocampal glucocorticoid receptors
after chronic stress leads to an increase in
adrenal secretion via hypersecretion of ACTH.
This is followed by eventual glucocorticoid
depletion. Parker (1990) goes on to sight experimental
evidence showing that impaired adrenocorticial
secretion leads to loss of granule cells in
the dentate gyrus of the hippocampus, which
could account for deficits in cognition. Additionally,
severely disturbing or emotionally arousing
events can result in the release of endogenous
benzodiazepines, which alters hippocampal functioning.
Thus, Parker's (1990) stress
theory of head injury can easily explain the
seemly obverse clinical phenomenon of post-traumatic
stress reaction: intrusive thoughts or memories.
After a biologically important event (physical
or emotional), recently active neuronal circuits
may be "primed" by neurotransmitters
or neurohormonal substances. This produces sensitization
to dangerous stimuli, or generalized stimuli
that resemble them, repeating the trauma and
creating new synaptic connections fixating it.
Next, Deitz's 1992 theory of
brain functions in the post head injury stress
response interim, places location of the sight
of the disorder in the temproalamygdaloid area
consistent with neuroanatomical and neurophysiological
data. This suggests that sensory stimuli and
their subsequent cortical projections follow
two main routes: 1) a broad pathway between
information transmitted to Broca's and Wernicke's
areas concerned with language, and 2) another
pathway where different aspects of the same
information is transmitted to the temporal lobe,
arriving at the amygdalar nuclei.
According to this model, both
Wernicke's area (receptive language) and the
amygdala are connected to the hypothalamus at
the core of the brain where hormonal control
and visceral/emotional reactions are regulated,
but via very different routes. Wernicke's area
is connected to language association cortices
and to the speech center in the motor cortex
(Broca's). From language association cortices,
information penetrates into the hippocampal
formation concerned with the registration of
memory, which is connected to the hypothalamus
by way of the fornix.
The amygdala, which consists
of several densely populated and clearly differentiated
nuclei deep in the temporal lobe, is directly
connected to the hypothalamus. Information processed
through amygdalar pathways can reach the hypothalamus
without higher cortical processing (conscious
awareness). The amygdala splits the sensory
formation it receives into positive and negative
emotional values, relaying this information
to different locations in the hypothalamus (Fonberg
1986). Thus, the hypothalamus receives the amygdalar
output, a distillation of the positive or negative
affective tone associated with the sensory data,
independent of higher thinking processing concerned
with abstract meaning or rational analysis.
For survival purposes, it is
critical that the amygdalar process positive/negative
discrimination be made as fast possible to allow
for appropriate fight/fight or approach/avoid
responses. In order to link the affective turn
to higher processing - the feelings and meanings
connected to language and complicated thought
processes - the second, phylogenetically newer
pathway is need. It is also likely that both
pathways influence each other, the amygdalar
affective tone facilitating the receptivity
of the hypothalamic system reached by neuronal
projections originating in neocortical pathways.
In summary, traumatic learning
experiences be they minor TBI or PTSD are believed
to be the origins in most anxiety disorders.
During traumatic experiences, learning occurs
through these two separate memory systems. The
individual forms conscious, explicit/declarative
memories through the temporal lobe memory system
involving the hippocampus and related cortical
areas, but also forms implicit/nondeclarative
emotional memories through our memory system
centered around the amygdala that most likely
operates unconsciously. The neural pathways
through which the amygdala participates in the
acquisition and expression of implicit traumatic
learning demonstrates that malfunctions in the
prefrontal cortex can make implicit emotional
memories especially resistant to extinction.
Stressful experiences can interfere with hippocampal
and facilitate amygdala memory functions, thereby
forming especially potent and difficult to eliminate
implicit emotional memories, sometimes in the
absence of a well formed explicit memory of
the experience as seen with retrograde amnesia
in the minor TBI case.
This finally brings us to an
elegant model presented by McLaurin and Titchener
(1982). These researchers observed that the
traditional disputes in the professional community
regarding whether the syndrome arises "principally
from mental and emotional reactions to head
trauma or from disordered neurophysiological
mechanisms and brain damage" go on to point
out that such conflicts can be avoided by recognizing
that complex casual change are involved in minor
TBI, including neurophysiological, psychological,
and probably unknown factors. This conceptual
framework, in turn, leads McLaurin and Titchener
to discuss the syndrome in terms of "organic
and psychic" causes.
Their model of the post-traumatic
event be it the concussion, post-traumatic reaction
or ongoing symptom complaint persistent beyond
3 months after the injury (post-concussion syndrome)
started with a "massively threatening situation"
represented by injury to the head. Incidentally
this specific type of severe anxiety was noted
many years earlier by Schilder (1934). This
model begins with the trauma, resulting alteration
of consciousness, gradual recovery during a
period of confusion, possible amnesia for the
injury and signs of PTSD. At this time the patient's
intellectual functions are disorganized. From
a biological point of view, the person is essentially
helpless.
McLaurin and Titchener postulate
that the problem moves from this biological
stage of helplessness to its psychological counterpart
as a result of "actual flooding of the
psychic apparatus with the terror of the moment."
The individual attempts to recover from this
condition by "mastering the traumatic event";
the victim relives the accident in dreams as
well as in the waking state and maintains an
intense vigilance to protect himself against
any further stimuli which might overwhelm his
adaptive apparatus. The next step in this process
is found in those persons in which the disorder
becomes severe and chronic and results in sematization
of the traumatic anxiety. The post-traumatic
reactions then become more generalized and integrated
with any pre-existing anxiety tendencies that
the individual may have had. For example, depression
will blend with elements of the post-traumatic
reaction and become intensified.
All these factors lead to increased
feelings of defensiveness, limitation of interest,
and change of relations with the outside world,
collectively identified in the post-traumatic
reaction. Thus, McLaurin and Titchener identified
these changes as representing personality constriction
in which the individual is principally interested
in protecting himself against a restorative
change, resisting novel experiences and narrowing
his range of experience. At this stage the person
begins to view all aspects of his life in terms
of his injury. He may relate every personal
inadequacy to the head injury or traumatic event.
Any personal professional difficulty may automatically
attributed to the accident.
There appears to be a distinct
interaction, however, between the customary
neurological and psychological effects of head
injury and this situation almost certainly would
represent the basis for expecting discrepancies
among individual experts with respect to assessment
of ideology, especially among patients with
minor TBI. This is clearly represented by the
different positions of Sbordone vs. Layton &
Zonna already discussed on co-occurrence of
minor TBI and post-traumatic reaction. However,
there are other factors that can be identified
that contribute to such discrepancies. First,
investigators often compare their samples of
patients from various populations. Some samples
may include disproportionate numbers of persons
who were anxious and emotionally disturbed before
the injury. Much, for instance, has been written
in the literature to the effect that these subjects
tend to exaggerate their symptoms and are even
malingering. However, these claims are grossly
exaggerated. Second, as with recovery from any
injury considerable variability would be expected
among patients, either in terms of residual
deficits or the time scale for recovery. Thirdly,
premorbid emotional status of the patient is
important. Head injury and PTSD victims have
a great range of personalities and often include
persons with deviant or even unstable characteristics.
Although post-traumatic stress reaction may
occur in someone who previously had not the
slightest psychiatric difficulty, it usually
strikes the emotionally predisposed. That is,
the man or woman whose pre-trauma personality
was characterized by hyperconscientiousness,
obsessive perfectionism, militant self-reliance,
overachievement, denial and displacement onto
others of emotional conflicts and disappointment,
and great emphasis on physical appearance, activity
and stamina, coupled with an intolerance of
weakness or impairment. Thus a psychologically
fragile person can develop a post-traumatic
stress disorder after minimal stress while a
psychologically strong, healthy person has little
predisposition to this diagnosis and will develop
one only if confronted with enormous stress
- and is more likely to make a rapid and complete
recovery. Hence, the severity of the underlying
emotional predisposition inversely determines
that of the precipitating stress (or proximate
cause).
Finally, the customary clinical
methods for evaluating residual effects of head
injury are rather gross and insensitive. Many
persons do not demonstrate any abnormalities
on neurological examination, EEG, or CT of the
brain. In these cases, there may be a natural
tendency to conclude that no neurological deficits
were sustained as a result of the injury and
the person's complaints are therefore concluded
to be PTSD and minimized at that.
Obviously, the presence of
emotional difficulties in the form of the PTSD
have important clinical ramifications. In most
cases a complete neuropsychosocial examination
(NPE) can differentiate between psychological
and neuropsychosocial deficits in the minor
TBI. The NPE can offer the opportunity to investigate
conditions under which the cognitive deficits
are effected by extreme emotional experience
if it is PTSD, and the way in which these changes
mediate subsequent behavioral response.
Thus the NPE can be used to
evaluate (a) how basic mental processes (example,
problem-solving, attention, memory) are effected,
in PTSD, and (b) whether changes in these functions
play a part in the etiology or maintenance of
symptoms found in this disorder. Whether the
diagnosis is minor TBI or PTSD, the NPE can
determine baseline functioning after psychological
or physical trauma, or their combination; (c)
NPE can determine functioning under conditions
of changes in symptompatology (example, heightened
arousal); (d) NPE can assess cognitive capacities
for certain PTSD treatment (example, imaginal
or exposure-based approaches); (e) NPE can validate
the patient's subjective complaints regardless
if minor TBI or PTSD. For instance, often patients
with PTSD claim cognitive deficits in the form
of decreased concentration, and memory deficits.
These deficits are also noted with minor TBI.
The examination can make overt if these deficits
have any basis in terms of head injury vs. the
post-traumatic reaction.
This information in conjunction
with other findings not only aids in better
understanding the condition of the patient whether
its a minor TBI or PTSD, but functionally expresses
how the patient is going about adapting to their
world. For all practical intents and purposes
whether the adjustment problem is because of
minor TBI or PTSD, it is important to understand
the format for problematic areas that undermine
the person's efficient daily adaptive functioning.
The patient's interpretations of their conditions
during self-report to the clinician are entitled
to be represented with inaccuracies. On the
other hand, the clinician through proper history
taking and observation on neuropsychological
examination can not only qualify and validate
the patient's symptom reports, but also establish
a treatment plan on how to handle the behavioral
and cognitive impairments be they from the minor
TBI, post-traumatic stress reaction or a combination
of both.
Therefore, neuropsychologists'
input into the analysis of the medical, neuropsychological
and behavioral data in instances where traumatic
exposure has occurred with central nervous system
damage or in the psychological arena in the
form of PTSD, we can help to distinguish symptoms
that are more emotionally based from those that
represent sequelae of known brain damage. Assessment
of both quantitative and qualitative changes
in cognitive performance can aid in the determination
of multiple diagnoses and define the need for
a variety of rehabilitation services. This ultimately
benefits the unfortunate patient whose case
brings to mind the legal phrase, "absence
of evidence is not evidence of absence"
when evaluating the relationship between minor
TBI and PTSD.
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©1996 by
The American Academy of Experts in Traumatic
Stress, Inc.
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