| 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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