Traumatic Brain Injury
A brief overview of traumatic injuries and the neurobehavioral
deficits that can occur
Marilyn F. Kraus, M.D.
Associate Professor of Psychiatry and Neurology
Center For Cognitive Medicine
Director, Cognitive Medicine Research Clinic
University of Illinois at Chicago
ph: 312-413-2037
e-mail: mkraus@psych.uic.edu
Contents
What is a neurobehavioral
deficit?
What is the scope of the problem in TBI?
How does TBI cause changes in mental functions?
What are the neurobehavioral deficits that can result?
Common
neurobehavioral disorders of TBI
Postconcussion syndrome
How should someone with these difficulties be evaluated?
What are options for treatment?
Conclusion
References
What is a neurobehavioral deficit?
Neurobehavioral deficits or disorders include impairments of cognition, mood
and/or behavior. Cognition includes intellectual functions of the brain such as
memory, attention, and problem solving.
What is the scope of the problem in TBI?
Traumatic brain injury (TBI) is a widespread and very significant source of
disability, often due to neurobehavioral deficits. But there are no clear
guidelines on how to manage these deficits. There is a critical need for
research in this area.
TBI is an insult to the brain caused by an external physical force that may
produce a diminished or altered state of consciousness. According to the CDC, an
estimated 5.3 million Americans (just over 2% of the population) currently live
with disabilities resulting from TBI. Yearly, 80,000 Americans experience
the onset of long-term disability following TBI. Vehicle crashes are the leading
cause of TBI. Falls are second, and the leading cause of brain injury in the
elderly. Risk of TBI is highest among adolescents, young adults and those older
than 75 years of age. The cost of traumatic brain injury in the US is estimated
to be $48.3 billion annually. The number of TBI patients seeking services has
increased, as survival rates have improved due to improved care.
The purpose of this information is to provide the reader with a basic
knowledge of the mechanics of TBI, and the resulting neurobehavioral deficits.
General information regarding evaluation and treatment will be covered. It is
important to identify problems as early as possible so that appropriate
evaluations and treatment can be established.
How does TBI cause changes in mental functions?
The way in which TBI affects the brain, which is referred to as the
neuropathology of TBI, may be especially pertinent to the risk for
neurobehavioral problems. There are several important components that can
contribute to neurobehavioral (intellect, mood, behavior) outcome:
What was the person’s level of function and medical condition before the
injury?
What is the location and severity of the brain injury?
How diffusely is the brain injured?
Has the person had previous injuries or diseases of the brain?
Has the person used, or still use, certain street drugs or alcohol?
The direct effects of trauma may be skull fractures, contusions (sort of a
brain "bruise"), and/or bleeding into or around the brain. Injury to
the brain can occur at several different levels, and depends upon the nature of
the trauma. Penetrating injuries can be fairly well circumscribed, such as from
a knife or bullet. In injuries such as from motor vehicle accidents or blunt
trauma, common sites of contusions are the front part of the brain (frontal
lobes) and the temporal lobes. This is because these parts of the brain sit next
to bony prominences within the skull (see figure 1).
Figure 1: Picture of the brain with major areas identified. The
frontal and temporal lobes are commonly damaged in trauma such as from motor
vehicle accidents.
The majority of trauma, however, seems to result in diffuse or more
widespread damage, and hence diffuse deficits and symptoms. The more diffuse
injury to the brain is called diffuse axonal injury (DAI). It is
characterized by stretching and shearing of individual axons, which are parts of
the nerve cells. The brain normally floats in fluid within the skull. In
accidents where there is an abrupt change in acceleration or deceleration, such
as in a motor vehicle accident, the brain can be thrust forward and backward
against the inside of the skull. This can cause a contusion to the part of the
brain that directly strikes the skull, but it also results in the more diffuse
injury to other nerve cells in the brain. This diffuse injury may underlie a
broad range of symptomatology, such as deficits in arousal, attention, mood
disturbance, and behavioral changes, even in "mild" head injury.
Severity of TBI:
In assessing severity of the original injury, several
factors are involved. Duration of loss of consciousness (LOC), initial score on
the GCS (Glascow Coma Scale - a 15-point scale that determines depth of coma),
and length of PTA (posttraumatic amnesia) are generally the measures used.
Definitions can vary, especially in the area of so called "mild"
injury, and can include brain-imaging criteria. In cases of mild injury, the
initial GCS is usually 13-15; moderate 9-15; and for severe, 8 or less. In terms
of LOC, there are also general guidelines. A mild injury usually results in LOC
of less than 30 minutes; moderate injuries up to 24 hours; and severe injuries
may have LOC greater than 24 hours. A mild injury generally results in PTA less
than 1 hour. Within the spectrum of mild injury, attempts have been made to more
accurately classify but there is no real consensus as of yet. Moderate injuries
are associated with PTA of 1 - 24 hours. Moderate-severe injuries have PTA's of
1-7 days, and severe injuries usually result in PTA of over 7 days.
Post traumatic amnesia (PTA): PTA is the period of time after a patient
emerges from coma that he has no continuous memory for day to day events. In
other words, there is impaired memory for new information. Staff has to
continually orient them to time and events. The end of PTA is defined as the
return of continuous memory.
Seizure disorders:
If seizures develop, they may have a role in certain
symptoms. The incidence of seizure disorder or epilepsy developing within five
years of closed head injury (CHI) is about 2 - 5%. The incidence following
penetrating injuries is much higher. Since the type of seizure can often be
complex partial (a type of seizure that may have motor and behavior changes
associated with it), this contributes to the risk of developing mood and/or
behavior symptoms.
Secondary mechanisms of injury:
There are also secondary mechanisms of
injury, besides the direct effects. Secondary mechanisms include delayed damage
to the brain due to the release in the brain of substances that may aggravate
the injury (excitatory neurotransmitters), or derangements in neurotransmitter
function. Neurotransmitters are substances that naturally occur in the brain and
allow cells to communicate and function. Examples include dopamine,
norepinephrine, and serotonin. Although the status of neurotransmitters in more
chronic TBI is not fully understood, disturbances in the function of these
substances may underlie certain problems that follow TBI, such as mood, behavior
or intellect problems. Medications may be used to try and normalize function,
and consequently improve symptoms.
Chronic pain:
Not infrequently, patients will develop acute or chronic
pain after the TBI, such as headaches, which can be quite debilitating and
aggravate mood, thinking, and behavior. Or the pain may be from other injuries
that were sustained. This needs to be fully assessed and adequately treated.
What are the Neurobehavioral Deficits that can result?
TBI can result in variable constellations of cognitive or intellectual
deficits, mood disturbances, personality changes, or behavioral problems (Table
1). The nature and severity of these changes depend upon a number of factors
as mentioned, such as location and size of lesion, duration of coma and
posttraumatic amnesia (PTA). Premorbid level of function, history of any
substance abuse, as well as psychosocial factors also interact with the actual
injury to affect outcome. Other factors also play a role, such as age and
medical health, and history of previous brain injury. Different problems may
arise at different stages of recovery.
Certain types of symptoms or deficits can be explained by the areas that are
commonly damaged in TBI, such as the frontal lobes or temporal lobes. Injury to
these parts of the brain can result in a range of behavioral, mood, and
cognitive problems. But the more diffuse injury that can occur also contributes
to the outcome. In general, there are certain loosely defined syndromes that can
be referred to, such as post-concussion syndrome, or frontal lobe syndrome. But
the qualification and quantification of symptoms that comprise these syndromes
has not been standardized. Certain of these will be reviewed below.
Table 1: COMMON NEUROBEHAVIORAL DISORDERS OF TBI
Post concussion syndrome
Frontal lobe syndromes
Behavioral/personality changes
Cognitive (intellectual) deficits
Mood disorders
Sleep disorders
Post traumatic epilepsy or seizures
Chronic Pain, such as headaches
Postconcussion syndrome (PCS):
The postconcussion syndrome (PCS) has been
poorly defined and controversial for many years. It has come to refer to a
rather broad range of symptoms and signs that can follow a brain injury (table
2). The term PCS is generally used to describe the cluster of symptoms that
often follow mild brain injury and persist for a variable period of time,
although the symptoms themselves can be seen after any severity of injury.
Estimates of how often this syndrome can develop may not be entirely accurate,
as many people do not seek medical attention for milder cases, but reports of
50% or so is not unusual. Although the majority of patients who develop these
symptoms seem to show recovery over time, there appears to be a significant
minority with persistent difficulties. Hence, even milder injuries can result in
disabling symptoms in some cases.
In general, the symptoms can occur directly following an injury, or after a
period of time. The role of other variables, such as psychological factors in
delayed PCS is debated. Symptoms fall into several categories including somatic
(physical symptoms), mood, behavior, and cognitive difficulties. They include
headaches, dizziness, sensitivity to noise and light, irritability, anxiety,
depression, fatigue, sleep and appetite disturbances, as well as problems with
information processing, attention, concentration and memory. The symptoms can be
variable and diverse, and very distressing to the patient and family members.
The patient may worry that they sound like a hypochondriac, or that people will
think they are "crazy." But these symptoms can be explained by the
nature of the injury to the brain. Hence, they are truly neurological symptoms,
and not primary psychiatric symptoms.
Loss of consciousness is not necessary for brain injury or for the
development of PCS. In general, a mild injury is usually diagnosed when loss of
consciousness is 30 minutes or less, and the patient does not show evidence of
specific abnormalities on neurologic exam. Brain injury or dysfunction can be
present even if the neurologic exam and tests such as a CT or MRI are normal.
These tests may not be sensitive to the more subtle or diffuse effects of trauma
on the brain (e.g., DAI). Cognitive impairments include deficits in information
processing, attention, and concentration, which can persist in some cases.
Table 2:
POSTCONCUSSION SYNDROME
Drowsiness
Blurred vision
Nausea/vomiting
Headache
Fatigue
Dizziness/light headedness
Memory problems
Concentration/attention problems
Depression
Anxiety/irritability
Insomnia
Sensitivity to noise and light
Somatic complaints
ETOH intolerance
Headaches:
Headaches are fairly common following even mild brain injury.
They can resolve over time, even up to a year out from the injury. In some
cases, they persist, and can be disabling. They can be migrainous, tension type
or mixed in nature. There is very little research on posttraumatic headaches,
and their treatment is often that of other chronic headaches. This approach can
be effective, but not always.
Frontal Lobe Syndromes:
Trauma commonly effects the frontal regions,
either directly or indirectly. Dysfunction of the prefrontal regions can result
in a variety of neurobehavioral symptoms. Generally referred to as "frontal
lobe" syndrome, the profile includes symptoms of behavioral dyscontrol such
as impulsivity and aggression, amotivation, apathy, disorganization, attentional
and memory deficits, and mood dysregulation (e.g., moodiness, irritability,
"mood swings"). Neuropsychological testing (see below) and reports
from family and caretakers who know the patient are essential to the assessment.
Essentially, treatment consists of several components. These include
pharmacologic treatment, behavioral strategies, and education and support of the
family. The frontal lobe patient often losses his ability to control or monitor
his own behavior, but will respond well when consistent external structure is
set up. Treatment can focus on particular aspects, such as dyscontrol,
aggression, or mood disturbances using certain medications.
Mood Disorders:
Mood disturbances following brain injury can present in a
variety of ways. It is not unusual for the mood symptoms to be subtle, but for
behavioral manifestations to predominate, such as irritability,
uncooperativeness, apathy, poor progression or effort in rehabilitation. The
mood disturbances may not necessarily meet traditional psychiatric criteria, but
may present more as a mood lability or dyscontrol. Often, it is more accurate to
refer to a dysregulation of mood, as brain injured patients can show features of
several mood disorders, rather than fit neatly into any one diagnostic category
currently used. The traumatic brain injured population is at increased risk for
developing depressive disorders, with estimates of major depression occurring at
about 25% or higher.
In general, a depressive disorder should be suspected when the patient's
degree of disability is greater than would be expected given the severity of
injury, or when the patient fails to meet rehabilitation goals, or cooperate
with treatment. It is not unusual for some mood disturbed patients to deny a
depressed mood upon questioning. Since mood disturbances can often be missed in
this population, and can have deleterious effects on outcome, it is wise to have
a high level of suspicion.
For depression, the treatment is often similar to that of non-neurologically
impaired depressed patients. Choice of treatment often depends on the patient’s
individual response and side effect profiles of these drugs. Another disturbance
of mood, mania or hypomania, can result, but is not as common. Mania refers to
the presence of pressured speech, inability to stay on topic or on track,
hyperactivity, a feeling of racing thoughts, and sometimes unusual ideas. The
person may seem "wired" and edgy. It is important not to equate
symptoms with diagnosis in this population. A patient who shows features of
mania does not necessarily have a true bipolar disorder, and this may be
over-diagnosed. Damage to the frontal lobes can produce a similar picture, and
may respond to certain treatments.
Behavioral / Personality Changes:
Depending on the location and severity
of the injury, different types of behavioral disturbances can occur. These
include irritability, lability, impulsivity, disinhibition, aggression, poor
motivation, poor self-regulation of behavior, poor judgement and insight, risk
taking, or sexual disturbances. Certain of these symptoms are separated out for
purposes of discussing assessment and treatment, but clinically, they often
occur together, as in a more generalized frontal lobe syndrome. Aggression
can occur following brain injury, particularly in the more acute stages, and
cause significant disruption of rehabilitation efforts. It can range from mild
verbal abusiveness to physical assaultiveness. It is important to characterize
the aggressive behavior. Is the patient labile? Is the patient impulsive and
unable to self regulate? Is there a mood change associated with the behavior?
What are the triggers? Is the aggression against self, others, or objects? A
thorough evaluation of the behavior is needed. Only then can an appropriate
behavioral strategy and possibly pharmacologic intervention be instituted.
Behavioral strategies are beyond the scope of this review, but can be very
helpful.
Aggression is a symptom that can have a variety of underlying causes. For
example, if it is part of a frontal lobe syndrome, then the treatment may be
different than for aggression resulting from psychosis, mood disturbance, or
seizure disorder. This is often not obvious, and treatment may be trial and
error. Polypharmacy (the use of more than one medication) may be unavoidable in
the complex patient, and it is best to obtain a consultation.
Personality Changes
can be viewed as existing on a spectrum with other
behavioral problems. The patient may not seem like his or her "old
self." On the milder end, you can see an exaggeration of the patient's
premorbid negative personality traits. For example, an impulsive, irritable
person may become more so. In more serious cases, it is common for families to
complain that the patient has become a "different person." Children
can appear hyperactive or develop symptoms consistent with attention deficit
disorder, or conduct disorder.
Personality and behavioral changes can be seen as a result of two factors.
First, damage to structures directly responsible for behavior and emotion.
Second, cognitive (intellectual) deficits can alter and impair the patient’s
interpretation of the environment or a situation, which in turn effects the
patient's response.
It is important to educate the families concerning these possible changes, as
they will tend to interpret the patient as purposefully aggravating them or
being mean or difficult. Pharmacologic treatment is usually aimed at a syndrome,
such as PCS or frontal dysfunction, or could target predominant symptoms such as
depression or irritability.
Cognitive Deficits:
These can be a significant cause of disability and
distress for the patient and family. In general, the common nonspecific symptoms
are disturbances in arousal, attention and concentration. Memory impairments can
occur, either due to direct effects on memory function, or secondary to poor
attention and concentration. Disturbances of higher level or executive functions
(frontal lobe functions) are fairly common, due to the high percentage with
frontal lobe involvement. These include poor planning, sequencing, and judgment.
The patient may make errors due to impulsivity, and have trouble shifting
between tasks. Specific deficits in cognition will depend upon location and
severity of injury, as well as some of the factors already mentioned, such as
level of education. These deficits may not be apparent while the patient is
recovering at home, if no real intellectual challenges are present. Not
uncommonly, the patient will realize these problems when they try and return to
work, and they find they can’t do the quality or amount of work they used to
do.
Pharmacotherapy
has expanded and has great potential in the area of
cognition. Cognitive Rehabilitation is gaining increased acceptance as an
important component in the rehabilitation of brain injured patients. It may be
particularly critical in the acute stage of recovery (up to 6 months
post-injury), and could complement pharmacotherapy. It often involves techniques
to retrain the patient in specific domains such as memory and attention.
Different theoretical frameworks have been proposed to guide remediation
strategies, and recent assessments support their effectiveness.
Sleep disturbance:
This can be a significant problem following brain
injury. It can be overlooked, but can significantly impede the patient's
rehabilitation. Lack of sleep can worsen cognition, behavior and mood, and
undermine treatment attempts. Disturbed sleep is very common in the first few
months following traumatic brain injury, and may or may not resolve. Daytime
sleepiness can also be a problem. There is often a reversal of the sleep-wake
cycle, which seems to be part of a general dysregulation that can also be seen
in other functions such as appetite. Treatment consists of medication and
behavioral management. Behaviorally, standard sleep hygiene should be used. The
patient should keep regular hours, avoid caffeine, alcohol and tobacco, and
activities that are too stimulating before bedtime. If a sleep disorder is
persistent and treatment refractory, a sleep study is warranted. In our clinic
there have been at cases of sleep apnea identified after an injury, although
there is no clear data on the incidence of this disorder following trauma.
How should someone with these difficulties be evaluated?
It is important to see someone with expertise in the assessment of TBI, as it
is a specialized area. This is a multidisciplinary area, so there are
neurologists, rehabilitation doctors, neuropsychiatrists, neuropsychologists,
and other specialists who can provide components of the assessment.
Physician Exam:
Part of the evaluation often consists of an examination
by a physician with expertise in TBI. This may include obtaining a thorough
history, as well as a neurological examination.
Neuropsychological testing:
Another important part of the assessment is a
battery of tests referred to as the neuropsychological assessment. This will
give a clear picture of the quantity and type of intellectual deficits, as well
as assess emotional and behavior problems. This evaluation may take several
hours or longer, depending on the length of the battery. The results provide an
excellent "map" of the actual brain functions that can serve as a
guide to direct treatment.
Brain Imaging:
With the advances in neuroimaging, or brain scanning
techniques, it is rapidly becoming an excellent tool to help assess brain
injury. Usually it is most helpful in conjunction with the other parts of the
evaluation. In resting imaging, such as with CT or MRI, we can
take a snapshot of the brain to look for structural changes. Brain injury,
particularly the more diffuse kind, is not always visible on routine brain
imaging, such as CT or routine MRI. There are now more specialized ways to image
this type of injury, such as advanced techniques with MRI.
Functional imaging such as with MRI (magnetic resonance imaging), PET
(positron emission tomography) or SPECT (single photon emission computed
tomography) may be more likely to show areas of injury or dysfunction in the
brain, but are not usually routine in a clinical setting. In functional imaging,
the patient is asked to perform certain tasks such as finger tapping,
remembering a list of words, or choosing a response while in the scanner. This
allows us a window to look at how the brain actually works during a task.
Details of types of brain imaging will be covered in another review. Brain
imaging also has allowed us to advance the type of research we can do. It
provides a way to assess how certain drugs or other interventions may work in
TBI.
What are Options for Treatment?
Neuropharmacology:
This is a complicated and evolving area that shows considerable promise for
improving outcome and quality of life for brain injured patients. Treatment is
driven by several considerations: alleviation of specific syndromes/symptoms
(such as depression or apathy), the underlying neuropathology (nature of the
injury) , improving cognition, and potential effects on recovery. Choice of a
medication that can cover more than one area is always preferable. Specific
medications will be covered in separate reviews.
General guidelines to pharmacologic treatment can be followed:
-
Use neuropharmacology based on underlying disturbances related to TBI-
such as knowledge about which neurotransmitters or brain chemicals are
affected.
-
In addition, certain target symptoms, such as insomnia, fatigue,
depression or attentional problems can be addressed
-
Associated problems such as chronic pain or seizures must be addressed and
adequately treated.
-
All efforts to be made to avid drugs for any condition that could worsen
mental status or possibly interfere with recovery
Conclusion:
As technology improves, more people who suffer brain injury can survive. And
even the less life threatening forms of TBI can result in significant problems
that may persist, or even arise down the road from the injury. These individuals
are often young, and otherwise healthy. Persistent cognitive, behavioral, or
mood disturbances significantly affect short and long term outcomes. They are
commonly referred to as the "walking wounded." They may appear
physically recovered, but problems reintegrating into family, work, or school
can quickly become apparent. They become labeled as difficult, lazy, somatic, or
histrionic. They may be diagnosed and treated incorrectly, resulting in a
worsening of the situation.
Education and appropriate referrals /interventions must be initiated as early
as possible. Too often, these patients receive excellent acute care and initial
rehabilitation, then are lost to follow-up. The loop of care must be closed. A
significant number of these patients can achieve good function, but will require
continuous and possibly life long access to various components of an
interdisciplinary team. This ensures maximized quality of life, and is the most
efficient, cost-effective route in the long term. This process should start at
the initial contact with the patient and family. It should involve close
collaboration between the family, patient, neurosurgeons, neuropsychiatrists,
rehabilitation medicine, neurologists, other therapists, rehabilitation
facilities, the workplace if applicable, and community groups.
Our emphasis on the neurologic basis for the outcome of TBI in no way negates
the important role of other factors and non-medication treatments. TBI patients
suffer significant losses, and these should be addressed. In general, supportive
therapy and education of the patient as well as family are important components
of treatment. Also, behavioral strategies are an essential component in the
management of these patients. Cognitive rehabilitation is a promising and
expanding area, that may either by itself or in conjunction with medication
result in improved outcomes and function. Medication alone is rarely adequate.
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