|
|
Diagnosis and Treatment of Head Injury
Daniel A. Hoffman, M.D. and Steven Stockdale, Ph.D.
Definitions
There are a number of definitions for mild traumatic brain injury most of
which include some interval of consciousness and/or some period of post
traumatic amnesia. A commonly used definition is unconsciousness for less
than twenty minutes, or no loss of consciousness with a Glasgow Coma Scale
of 13 or above without deterioration and post traumatic amnesia less than 48
hours. The criteria of loss of consciousness and amnesia is controversial
and many clinicians believe them to be of little value for many populations
suffering neurocognitive symptoms (Hoffman, 1994).
Although traditionally mild traumatic brain injury has been associated with
motor vehicle accidents and work related injuries like slip and falls,
similar neurocognitive symptoms occur in subtle brain dysfunction resulting
from a number of other sources including silicone toxicity, environmental
toxins, autoimmune disorders, multiple sclerosis, and even chemotherapy
(Hoffman, et al., 1995; Ritchlin, et al., 1992).
Symptoms of mild traumatic brain injury are typically classified into three
categories which include physical/somatic problems, cognitive dysfunctions
and emotional/personality difficulties. Specific physical/somatic problems
may include headaches, dizziness, fatigue, sleep disturbance, sensitivity to
light or noise, loss of sexual drive, nausea, blurred vision, vomiting,
tinnitus and seizures. Cognitive problems feature impaired attention and
concentration, slow speed of processing information, impaired complex
thinking, problems organizing, distractibility, short term memory problems,
forgetfulness, trouble finding the right word, word substitutions and word
reversal. Emotional/personality symptoms may consist of low frustration
tolerance, irritability, mood lability, anxiety, depression, impatience,
anger, explosive temper and feeling overloaded by too much stimulation.
Epidemiology
Brain injury appears to occur at a frequency ranging from 132 to 367 per
100,000 population. The variability of these figures lies in the different
criteria for diagnosis used in studies (Silver, et al., 1994). It is
estimated that almost 2 million head injuries of non-fatal brain injuries
occur per year. People 15 to 24 years of age are at highest risk, with a
decline in risk occurring during the middle age years and an increase after
age 60. Men have a 2 - 2.8 times higher frequency than women. Mild brain
injuries, those with a Glasgow Coma Index scale of 13-15 are by far the
greatest proportion. Eighty percent appear to be mild, 10% moderate (Glasgow
Coma Score 9-12), and 10% severe (Glasgow Coma Score 8 or less). Slightly
less than half of brain injuries are concussions without fracture of the
skull. Other causes are hemorrhage, contusion and laceration. In mild brain
injury 35% of reported cases demonstrate no loss of consciousness, although
this percent may be much higher since often patients are not diagnosed with
mild head injury unless they have loss of consciousness or post-traumatic
amnesia.
Current Diagnosis of Mild Traumatic Brain Injury
Mild traumatic brain injury causes a great deal of angst for the diagnostic
clinician as well as for the legal system. Traditional methods of evaluation
consist of history, neurologic exam, CAT Scan, MRI, standard EEG, and
neuropsychological testing. Although patients complain of significant
neurocognitive dysfunctions, not uncommonly most of these standard tests are
normal.
Neuropsychological testing appears to be the current mainstay in recognizing
cognitive functioning, however, there are several problems with relying
heavily on this as a diagnostic tool for mild traumatic brain injury.
Interpretation of neuropsychological tests has considerable variability and
subjectivity. It currently causes the legal system concern since two
opposing expert neuropsychologists often differ in their interpretations. As
many as 50% of subtle injuries are not picked up through neuropsychological
testing (Posthuma, 1988). Many neuropsychologic tests have a low ceiling in
which pre-morbidly high-functioning individuals can still score in the
normal range, thus not being sensitive enough to measure a decrease in
functioning. The low ceiling also may account for inaccuracies or inability
to pick up more mild injuries.
SPECT scan, which records cerebral blood profusion that may be decreased in
damaged areas, is demonstrating usefulness in with the head injured
population and in the future may prove a valuable diagnostic tool (Gray, et
al., 1992; Ichise, et al., 1994).
Mechanism of Injury of Mild Traumatic Brain Injury
Most mild traumatic brain injuries are caused by some form of mechanical
forces such as slip and fall, or motor vehicle accidents. Typically there is
a rapid acceleration/deceleration effect on the brain as well as rotational
and twisting forces around the brain stem. A classical injury would
demonstrate contusions of the brain on the boney structures of the skull
which occur in the frontal and frontal-temporal lobes. These include the
orbital plate of the frontal bone, the sphenoidal ridge, the petrous portion
of the temporal bone, and the sharp edges of the falces. The forces also
account for a shearing effect, known as diffuse axonal injury, in which the
myelin, or insulation of the nerves in the white matter, begins to unravel,
making the fidelity of the electrical signal less than optimal. Secondary
complications also develop as a result of metabolic changes. In the absence
of diffuse axonal injury one might also expect to see focal abnormalities or
a coup-contra-coup effect in which both the injured site and 180 degrees
opposite the injured site are both effected when the forces cause the brain
to bounce against the skull along the trajectory of the point of impact.
Advances in Diagnosis of Mild Traumatic Brain Injury
In March, 1979, Robert Thatcher, Ph.D. began work on a normative or
reference EEG database. Seven hundred and twenty three subjects were tested
from 1979 to 1985. Of these, 511 met the criteria for normalcy and were
included in the database. The criteria included an uneventful prenatal,
perinatal, or postnatal period, no disorders of consciousness, no head
injury with cerebral symptoms, no history of central nervous disease, no
seizures, and no abnormal deviations with regard to mental and physical
development. Additional criteria for entry were a full scale I.Q. greater
than 70, a WRAT-R school achievement score greater than 89 on at least 2
subjects, and a grade point average of C or better in major academic
classes. Both offline and online artifact rejection was utilized. The age
distribution consisted of a developmental period from 2 months through
adulthood. More subjects were skewed towards the younger ages since
development is most rapid in children. Demographically there is a mixture of
males and females, different ethnic backgrounds and socioeconomic status
representative of the North American population. The normative database
provides a statistical analysis in which a patient's EEG can be expressed as
a deviation from the normative group in Z score units, i.e., standard
deviations from the mean. The EEG norms are replicated in several places (Matousek
and Petersen, 1973; Thatcher, 1980; Epstein, 1980; Hudspeth, 1985; and
Hudspeth and Pribram, 1990:1991). The advent of such databases allows a
patient's EEG, when digitalized (quantitative EEG, QEEG or computer enhanced
EEG), to be compared with a reference population.
If a statistically significant number of Z scores greater than 2 appears
when comparing the patient's EEG with the reference database, and the
pattern forms around an anatomical location, pathology can be assumed when
correlated with clinical history and presentation. This technique, for the
first time, aids in the examination of subtle and even microscopic changes
which previously went undetected by standard methods of evaluation. In 1989,
Thatcher and his colleagues developed a discriminant analysis for mechanical
head injury and diffuse axonal injury for the mild head trauma population
which identifies a particular pattern of pathology. EEG power spectral
analysis was obtained on 608 mild head trauma patients and 108 age matched
normal subjects. Three classes of neurophysiologic variables were attributed
to mechanical head injury. These consisted of increased coherence and
decreased phase in the frontal and frontal-temporal regions, decreased power
differences between anterior and posterior cortical regions, and reduced
alpha power in posterior cortical regions (Thatcher, et al., 1989).
Coherence measures commonality between two different anatomical locations,
that is, how they share activity or energy in the brain. It demonstrates how
synchronously the brain is interacting with itself. Since the human brain is
multifaceted and able to multi-task, coherence has a normative value. Mild
head injury frequently causes increased coherence, resulting in the brain
digressing to a more primitive level by acting more uniformly. This makes
multi-tasking difficult and slows mental processing. Much like the fuzziness
on a television screen when the cable insulation is damaged, the fidelity of
the brain's electrical circuitry presents the patient with a foggy, unclear
pattern. Some lesions actually cause neuronal uncoupling, in which case
coherence would decrease.
Phase is the time delay between two points of the brain. With loss of myelin
integrity there is more "noise" to the signal. According to Thatcher,
clinically this may be seen in such symptoms as difficulty focusing or
holding a thought. This finding can be responsible for some patients'
complaints of forgetfulness and short term memory problems since the amount
of time one can track a thought helps determine if it gets imprinted and
thus is retrievable later as a memory.
In summary, QEEG, through the use of a digitalized signal, allows the
opportunity to compare the patient's brain with a reference database, and
then further submit it to the multi-variant regression analysis which
discriminates for mechanical head injury and, in part, diffuse axonal
injury. Utilizing QEEG in the assessment of mild traumatic brain injury is
beginning to appear in professional literature as an additional testing
standard (Taylor and Price, 1994; Rumpl, 1993; McAllister, 1994; Packard and
Ham, 1994; Duffy, 1994).
Treatment of Mild Traumatic Brain Injury
Traditionally, treatment for mild closed head injuries has included early
intervention, education, family and professional support, group therapy,
individual psychotherapy, marital and family therapy, stress reduction,
coping skills training, multidisciplinary pain management,
neuropsychological rehabilitation, vocational counseling, work skills
training and multidisciplinary psychological rehabilitation (Howard, 1993).
Treatment has focused on medical management, individual counseling and
psychotherapy, coping skills, pain management, vocational rehabilitation and
cognitive rehabilitation. These treatments have been provided by a
collection of professionals including physicians, psychologists, social
workers, speech therapists, occupational therapists, physical therapists,
chiropractors, massage therapists and biofeedback therapists, to mention a
few.
Approximately two-thirds of mildly injured patients will regain 80% of their
functioning within the first six months of recovery and continue to improve
over the next one and one-half years. Treatment, therefore, should be
relegated to those patients who are not improving, whose improvement has
reached a plateau, or who after six months still have significant
dysfunction. The literature is controversial in terms of the role cognitive
rehabilitation plays in mild traumatic brain injury (Rattok and Ross, 1994).
Clearly, many patients develop compensatory strategies for their neuro-functioning.
Cognitive rehabilitation is often divided into two general levels;
functional and generic. The functional level trains abilities necessary for
practical functioning, such as activities of daily living. The second level
trains generic cognitive skills such as attention, memory, and problem
solving. While it is clear that moderate or severe injuries respond to this
type of intervention, the literature is mixed on its effect in the mildly
injured patient. In research performed by Niemann, et al., (1990) results of
cognitive rehabilitation were equivocal. One reason may be that the
neuropsychological batteries used were not sensitive enough to detect small
changes in specific cognitive functions. Other treatments were also ongoing
at the time, as it is almost impossible to provide cognitive rehabilitation
in isolation of other forms of treatment. In general, traumatic brain
injured patients can receive up to two to three hundred hours of treatment,
which varies with the severity of the injury.
An emerging and promising treatment approach is the use of quantitative EEG
technology and EEG neurofeedback training (neurotraining) for the treatment
of mild traumatic brain injury. Since the end of the 1960's Barry Sterman
demonstrated the ability to control brain wave rhythms through operant
conditioning and biofeedback techniques in the epileptic population through
suppression of SMR (12-14 Hz) (Sterman and Wyrwicka, 1967; Sterman, Wyrwicka
and Roth, 1969; Wyrwicka and Sterman, 1968; Sterman and Friar, 1971; Sterman,
Macdonald, and Stone, 1974; Sterman and Macdonald, 1978; Sterman and Shouse,
1980). Joel Lubar and Sterman then continued this work, discovering that
patients demonstrated increased attentiveness, focus and concentration
during feedback. Lubar went on to find that improvements in distractibility
and attentional gains in academic settings resulted in increased school
performance and grades (Lubar and Shouse, 1976a,b; Lubar and Lubar, 1984).
Since the early 80's there have been reports of clinicians treating the
symptoms of mild traumatic brain injury with EEG neurofeedback. Many
approaches have been utilized. Bruner (1989) described using alpha training
in three cases, demonstrating a return to pre-morbid functioning. It should
be noted that his definition of alpha was 10-14 hertz which spread between
what normally would be considered high alpha and SMR. Tansey (1983, 1991)
and others have used SMR, or more precisely 14 hertz reinforcement in their
treatments. Both referential and bi-polar placements have been reported.
Ayers has probably done the most work with the head injured population by
inhibiting theta (4-7 hertz) and enhancing 15-18 hertz beta. By looking at a
digitally filtered raw wave of theta she may have identified high peaks of
voltage that occur in some forms of brain damage. While these findings are
often seen in the sensory motor strip, she trains wherever the damage is
most prominent and where the neuroanatomy fits the deficits. This work
centers around the concept of normalizing the EEG.
It should be noted that most of these treatment approaches have one thing in
common; the reduction or inhibition of 4-7 hertz theta.
The most common question asked about using EEG neurofeedback for the
treatment of mild traumatic brain injury centers around the training
protocol. The authors' view of the use of this technology for the treatment
of mild traumatic brain injury is that there is no one protocol. We advocate
designing the treatment protocol based on the full diagnostic workup
described above. The purpose of the training is to normalize the EEG. We
find that this training tends to correlate with a resolution of symptoms. As
a result, a number of different training protocols have been used, as
mentioned above, including beta enhancement with theta suppression, SMR
enhancement with theta suppression, alpha enhancement with beta suppression,
alpha enhancement with theta suppression, and ipsilateral as well as
contralateral bandwidth or coherence training.
To know where to begin with the EEG neurofeedback training, a diagnostic
evaluation is needed. The evaluation includes a comprehensive history,
mental status examination, review of past medical records, a medical
evaluation, neuropsychological screening, open and direct communication with
all professionals dealing with the patient, and a computer-enhanced EEG
assessment including discriminate analysis, reference database comparison
and spectral analysis. The purpose of this evaluation is twofold. First is
to establish the statistical likelihood of either diffuse axonal injury and
focal injuries from contusion or coup-contra-coup effects. Additionally,
this evaluation process establishes an appropriate baseline and designs a
treatment protocol for the EEG neurofeedback training.
Our approach to the treatment of mild traumatic injury is multimodal and has
a strong educational orientation. The average number of training sessions
for the head injury rehabilitation work using EEG neurofeedback is 40,
significantly less than other traditional types of cognitive rehabilitation.
As part of the training, a patient's physical/somatic, cognitive, and
emotional/personality symptoms are reevaluated every five training sessions.
The presence of physiologic trending of the data in the desired directions
are also quantified and tracked each session. Patients come in for a one
hour neurofeedback session at least twice weekly. It is not uncommon to see
an improvement in some symptoms in as few as five sessions. Our clinical
experience in using this treatment is that 80 percent of patients learn
neuronal control and attain a minimum of 70 percent improvement in self
reported symptoms. Generally we do not begin treatment until at least six
months post injury. We have also attained good clinical results with
patients several years after injury.
In the field of brain injury diagnostic and rehabilitation work, the use of
EEG based technology for evaluation and treatment demands further attention
and research.
Moderate to Severe Head Injury
As mentioned earlier, it has been Sterman's work which demonstrated that
patients with seizures unresponsive to medication have done well with EEG
neurofeedback and which began the field of self-regulation and control of
EEG. By extrapolating this and Lubar's discoveries with attentional
problems, as well as the work done with mild traumatic head injury through
Ayers' contributions, it appears that with the use of the right equipment
and technology, treatment of moderate to severe head injuries is also
possible. According to Ayers, when combining EEG neurofeedback with
traditional rehabilitation such as physical and occupational therapy,
patients suffering from stroke, cerebral palsy, major trauma, coma, and even
persistent vegetative states improve dramatically. Thatcher (1991) has
written about the ability to predict outcome of head injured patients,
demonstrating a 85% degree of accuracy in predicting the level of a
patient's functioning one year after trauma.
Conclusions
The diagnostic use of QEEG in mild traumatic brain injury is growing in
popularity and usefulness, the advancements of which are acknowledged in
recent professional literature. Treatment for this population, as well as
the more severely injured patients, requires more traditional scientific
studies to continue demonstrating its effectiveness. It may ultimately
promise the shortest, most cost-effective treatment method, offering the
greatest improvement of any cognitive rehabilitation to date.
Bibliography
Ayers, M., (1981). "A report on the study of the utilization of
electroencephalography (neuroanalyzer) for the treatment of cerebral
vascular lesion syndromes." In: Electromyometric Biofeedback Therapy,
Taylor, Ayers, Tom, (Eds.) Chapter VII. Biofeedback and Advanced Therapy
Institute.
Ayers, M., (1983). "Electroencephalographic feedback and head trauma." Head
and Neck Trauma: The Latest Information and Perspectives on Patients with a
Less Than Optimal Recovery. U.C.L.A. Neuropsychiatric Institute.
Ayers, M., (1993). "A controlled study of EEG neurofeedback training and
clinical psychotherapy for right hemispheric closed head injury."
Biofeedback and Self Regulation. 18(3):Sept.
Bruner, R., (1989). "Treatment of post concussion syndrome with alpha EEG
biofeedback training: three case studies." Presented at The Pennsylvania
Society of Behavioral Medicine and Biofeedback.
Duffy, F., Hughes, J., Miranda, F., Bernad, P., Cook, P., (1994). "Status of
quantitative EEG (QEEG) in clinical practice." Clinical
Electroencephalography. 25(4):VI-XXII.
Epstein, H., (1980). "EEG developmental stages." Developmental
Psychobiology. 13:629-631.
Gray, B., Ichise, M., Chung, D., Kirsh, J., Franks, W., (1992).
"Technetium-99-HMPAO SPECT in the evaluation of patients with a remote
history of traumatic brain injury: a comparison with X-ray computed
tomography." Journal of Nuclear Medicine. 33(1):52-58.
Hoffman, D. (1994). "Subtypes of postconcussional disorder." Journal of
Neuropsychiatry and Clinical Neurosciences. 6(3):332-333.
Hoffman, D., Stockdale, S., Hicks, L., Schwaninger, J., (1995). "Neurocognitive
symptoms and quantitative EEG results in women presenting with silicone
induced autoimmune disorder." International Journal of Occupational Medicine
and Toxicology. Accepted for publication.
Howard, M.E., (submitted 1993). "Mild brain injury: causes, damages,
diagnosis, and treatment." In: Damages in Tort Actions. Matthew Bender and
Sons.
Hudspeth, W., (1985). "Developmental neuropsychology: functional
implications of quantitative EEG maturation (abstract)." Journal of Clinical
and Experimental Neuropsychology. 7:606.
Hudspeth, W., Pribram, K., (1990). "Stages of brain and cognitive
maturation." Journal of Educational Psychology. 82:881-884.
Hudspeth, W., Pribram, K., (1991). "Physiological indices of cerebral
maturation." International Journal of Psychophysiology. 12:19-29.
Ichise, M., Chung, D., Wang, P., Wortzman, G., Gray, B., Franks, W., (1994).
"Technetium-99-HMPAO SPECT, CT and MRI in the evaluation of patients with
chronic traumatic brain injury: a correlation with neuropsychological
performance." Journal of Nuclear Medicine. 35(2):217-225.
Johnstone, J., Thatcher, R., (1991). "Quantitative EEG analysis and
rehabilitation issues in mild traumatic brain injury." Journal of Insurance
Medicine. 23(4):228-232.
Lubar, J.F., Shouse, M.N., (1976a). "EEG and behavioral changes in a
hyperkinetic child concurrent with training of the sensorimotor rhythm (SMR):
a preliminary report." Biofeedback and Self-Regulation. 3:293-306.
Lubar, J.F., Shouse, M.N., (1976b). "Use of biofeedback in the treatment of
seizure disorders and hyperactivity." Advances in Clinical Child Psychology.
1:203-265.
Lubar, J.O., Lubar, J.F., (1984). "Electroencephalographic biofeedback of
SMR and beta for treatment of attention deficit disorder." Biofeedback and
Self-Regulation. 9(1):1-23.
Matousek, M., Petersen, L., (1973). "Frequency analysis of the EEG
background activity by means of age dependent EEG quotients." In: Automation
of Clinical Electroencephalography, Kellaway and Petersen (Eds.). Raven
Press, New York.
McAllister, T., (1994). "Mild traumatic brain injury and the post concussive
syndrome." In: The Neuropsychiatry of Traumatic Brain Injury, Silver, J.,
Yudofsky, S., Hales, R., (Eds), American Psychiatric Press, Washington D.C.,
357-392.
Niemann, H., Ruff, R., Baser, C., (1990). "Computer-assisted attention
retraining in head-injured individuals: a control efficacy study of an
outpatient program." Journal of Consulting Clinical Psychology. 58:811-817.
Packard, R., Ham, L., (1994). "Promising techniques in the assessment of
mild head injury." Seminars in Neurology. 14(1):74-83.
Posthuma, A., Wild, U., (1988). "Use of neuropsychological testing in mild
traumatic head injuries." Cognitive Rehabilitation. March/April:22-24.
Rattok, J., Ross, B., (1994). "Cognitive Rehabilitation." In: The
Neuropsychiatry of Traumatic Brain Injury, Silver, J., Yudofsky, S., Hales,
R., (Eds), American Psychiatric Press, Washington D.C., 703-729.
Ritchlin, C., Charabot, R., Alper K., Buyon, M., Belmont, H.M., Roubey, R.,
Abramson, S., (1992). "Quantitative encephalography: a new approach to
diagnosis of cerebral dysfunction and systemic lupus erythematosus."
Arthritis and Rheumatism. 35(11):1330-1342.
Rumpl, E., (1993). "Craniocerebral trauma." In: Electroencephalography,
Niedermeyer, F., Da Silva, L., (Eds), Williams & Wilkins, Baltimore,
383-403.
Sterman, M.B., Wyrwicka, W., (1967). "EEG correlates of sleep: evidence for
separate forebrain substrates." Brain Research. 6:143-163.
Sterman, M.B., Macdonald, L.R., Stone, R.K., (1974). "Biofeedback training
of the sensorimotor electroencephalogram rhythm in man: effects on
epilepsy." Epilepsia. 15:395-416.
Sterman, M.B., Macdonald, L.R., (1978). "Effects of central EEG feedback
training on incidence of poorly controlled seizures." Epilepsia. 19:207-222.
Sterman, M.B., Wyrwicka, W., Roth, S.R., (1969). "Electrophysiological
correlates and neural substrates of alimentary behavior in the cat." Annals
of New York Academy of Science. 157:723-739.
Sterman, M.B., Friar, L. (1972). "Suppression of seizures in an epileptic
following sensorimotor training." Electroencephalography and Clinical
Neurophysiology. 33:89-95.
Sterman, M.B., Shouse, M.N., (1980). "Quantitative analysis of training,
sleep EEG and clinical response to EEG operant conditioning in epileptics."
Electroencephalography and Clinical Neurophysiology. 49:558-576.
Tansey, M., Bruner, R., (1983). "EMG and EEG biofeedback in the treatment of
a 10-year old hyperactive boy with a developmental reading disorder."
Biofeedback and Self Regulation. 8:25-37.
Tansey, M., (1991). "Wechsler (WISC-R) changes following treatment of
learning disabilities via EEG biofeedback training in a private practice
setting. Australian Journal of Psychology. 43(3):147-153.
Taylor, C., Price, T., (1994). "Neuropsychiatric Assessment." In: The
Neuropsychiatry of Traumatic Brain Injury, Silver, J., Yudofsky, S., Hales,
R., (Eds), American Psychiatric Press, Washington D.C., 81-160.
Thatcher, R., (1980). "Neurolinguistics: theoretical and evolutionary
perspectives." Brain and Language. 11:235-260.
Thatcher, R., (1987). "Normative EEG database." Personal Communication
Copyright.
Thatcher, R., Walker, R., Gerson, I., Geisler, F., (1989). "EEG:
discriminant analysis of mild head trauma." Electroencephalography and
Clinical Neurophysiology. 73:94-106.
Thatcher, R., Cantor, D., McCalaster, R., Geisler, F., Krause, P., (1991).
"Comprehensive predictions of outcome in closed head injured patients: the
development of prognostic equations." Annals of New York Academy of
Sciences. 620:82-101.
Wyrwicka, W., Sterman, M.B., (1968). "Instrumental conditioning of
sensorimotor cortex EEG spindles in the waking cat." Physiology and
Behavior. 3:903-907. |
|
|
3
