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APPLICATIONS of BIOFEEDBACK in the TREATMENT OF
MILD TRAUMATIC BRAIN INJURY and POST-CONCUSSION SYNDROME
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Edward A. Maitz, Ph.D.
John E. Gordon, Ph.D.
Davis J. Massari, Ph.D.
Introduction to Traumatic Brain Injury
Advances in basic and applied science and medicine over the last 15 years
have vastly altered our understanding of the etiology, neuropathology and
treatment of persons with traumatic brain injury. Thanks to improved imaging
techniques including computerized axial tomography, magnetic resonance
imaging, positron emission tomography, and computerized brain mapping it is
often possible to actually visualize brain structure and function. The
actual visual image of a brain lesion often provides direct evidence to
support clinical inferences about the integrity of the brain based upon
neurological or neuropsychological assessment. Researchers have also
developed elaborate animal models to demonstrate the actual pathophysiology
of traumatic brain injury. As a result, we now know a great deal more about
the mechanisms of, and recovery from, traumatic brain injury. However, the
pathogenesis and treatment of milder injuries, including those injuries
commonly referred to as a mild head injury, mild traumatic brain injury (TBI),
or post-concussion syndrome (PCS) continue to be unclear.
Epidemiological studies indicate that many more people sustain a mild brain
injury than a moderate or severe brain injury, however the actual incidence
of mild traumatic brain injury has never been definitively established.
Kraus and Nourjah (1989) studied patients admitted to a San Diego County
hospital in 1981. They found that the proportion of mild brain injury among
all patients hospitalized for a head injury was 82%. The incidence of mild
brain injury in San Diego County for the same year was 131 per 100,000
people. The extrapolated rate for the entire United States (assuming a
population of 250,000,000 was 325,000 cases of mild brain injury per year at
an annual estimated cost of $900,000,000. Zasler (1993) argues that many
patients are admitted to hospitals with occult TBI that is not listed as a
primary diagnosis, thus the incidence of hospitalized patients with mild TBI
as a secondary or tertiary diagnosis may be even higher. Furthermore,
Frankowski, Annegers & Whitman (1986) estimate that 20%-40% of patients with
mild TBI do not even seek medical treatment. Given this data, it is critical
that health care providers recognize the symptoms of mild traumatic brain
injury and post-concussion syndrome, develop effective intervention programs
to treat the cognitive and psychosocial deficits, and support patients
during the recovery process. This often involves a multidisciplinary
approach that addresses both the cognitive and psychosocial sequelae of the
injury. While traditional biofeedback appears to represent a valuable
adjunctive treatment modality, it is a vastly under-utilized approach for
the treatment of these disorders.
Because patients with mild TBI have little or no loss of consciousness, hard
neurological signs, or positive radiologic findings they are often treated
in the emergency room and discharged to home with little or no follow-up. If
these patients do come to the attention of a health care professional, they
are often incorrectly diagnosed with post-traumatic stress disorder,
somatoform disorder, adjustment disorder, or even malingering. The problem
is compounded by the limitations in our current nosological systems. The
DSM-III-R did not include Post-Concussion Syndrome, although it has been
included in the ICD-9 for several years. The DSM-IV does include
Postconcussional Disorder and Mild Neurocognitive Disorder within the
"Criteria Sets and Axes Provided for Further Study." Even when a correct
diagnosis is made, many physicians still consider a concussion to be a
fairly benign event that does not require treatment or intervention.
Patients are often told that they have a concussion, but that the symptoms
should remit spontaneously and without treatment within three to six months.
While many, if not most patients do recover within three months (Levin,
Eisenberg, & Benton, 1989) many patients continue to be symptomatic for
several years post-injury. Furthermore the marked cognitive and psychosocial
sequelae that often follow from a mild TBI can have dire consequences during
the three to 24 month recovery period. While the person is waiting to
recover, they often experience failure in school or work, and a marked
disruption in marital and other interpersonal relationships. This may lead
to anxiety, depression; and a loss of self-confidence and self-esteem. In
the words of Rutherford (1989), "minor head injuries may give rise to
morbidity which sometimes lasts for many years if not for life."
Models of Post-Concussion Syndrome and Mild TBI; Organic vs. Functional
Explanations
The term post-concussion syndrome has stirred considerable controversy,
discussion and debate. Binder defines it as "a term reserved for patients
who have persisting subjective symptomatology resulting from cerebral
concussion" (1986 p.323). The symptom cluster may include headaches,
fatigue, sleep disturbance, problems with concentration and memory,
dizziness, anxiety, irritability, depression, apathy, withdrawal, social
isolation, nausea and vomiting, decreased tolerance for noise, blurred
vision, decreased language fluency, reduced speed and capacity for
information processing, and impaired executive functions (Alexander, 1992;
Bennett, 1989; Binder, 1986; Boll & Barth, 1983; Cytowich, Stump & Larned,
1988; Gronwall, 1991; Gade & Young, 1984; Kay, 1992; Long & Novack, 1986;
Rimel, Giordani, Barth, Boll & Jane, 1981; and Symonds, 1962). It is rare
for a patient to report all of these symptoms. Moreover, many concussed
patients are initially "in a fog" and have limited awareness of their
cognitive deficits, or they may initially be more preoccupied with their
pain. However, we have found it useful to assess these symptoms in any
patient with a recent whiplash injury or blow to the head. In addition to
providing a clinical interview, many psychologists administer one of the
structured self-administered questionnaires such as the Philadelphia Head
Injury Questionnaire (Curry, Ivins & Gowen, 1991) or the Adult
Neuropsychological Questionnaire (Melendez, 1978) that are designed to
identify neuropsychological symptoms secondary to head injury.
While the symptoms associated with post-concussion syndrome have long been
recognized, there has been considerable disagreement regarding the
pathogenesis of the disorder. In essence, the issue has been whether these
symptoms are the result of damage to the brain secondary to the head injury,
an emotional disorder (i.e. a neurotic reaction to the injury), a
personality structure that predisposes the individual to respond
symptomatically to a non-specific stressor event, or conscious malingering
for financial or other secondary gain.
The functional model
Lidvall, Linderoth, and Norlin (1974) were early proponents of the theory
that PCS is functionally based. They argued that post-concussive complaints
are largely a neurotic response based upon a pre-existing personality
structure which predisposes the person to psychosomatic illnesses. The head
injury represents nothing more than a precipitating event in individuals who
are pre-disposed to emotional problems. While individuals with a personality
disorder have no inherent immunity to head injury, there is no body of
empirical evidence to suggest that these symptoms are merely a manifestation
of a pre-existing emotional condition. In their review of the literature,
Long and Novack (1986) found that neuroticism predating physical injury has
been "difficult to establish among those having problems in recovery" (p.
729).
The malingering theory found early support in the work of Henry Miller. In
an early article (1961), he argued that the symptoms associated with a
post-concussion syndrome were mostly related to litigation and compensation
claims. He suggested that the symptoms are motivated by financial gain, and
that they remit following completion of litigation. After a thorough review
of the literature, Binder (1986) states, "Litigation and compensation claims
are an additional stressor and may contribute to the symptomatology of some
patients, but there is no empirical evidence that the PCS is caused by the
claims process" (p. 331). On the contrary, there is empirical evidence of
persistent post-concussion symptomatology in the absence of litigation
and/or compensation claims.
The organic model
The results of a seminal article by Rimel et al. (1981) argued against the
malingering hypothesis, and added support for the position that
post-concussion symptoms reflect actual changes in brain functioning. The
authors studied 424 patients who had sustained a mild traumatic brain injury
as defined by a history of unconsciousness of less than 20 minutes, a
Glascow Coma score of 13-15, and hospitalization not exceeding 48 hours.
They found that, despite the mild nature of the patients' injuries, only one
sixth of the patients were complaint free at three month follow-up, and that
34% of the patients who had been employed prior to the accident were not
working. A neuropsychological evaluation completed on a representative
subset of 69 patients revealed "mild neuropsychological impairment was
evident on the vast majority of the Halstead-Reitan Neuropsychological
procedures." (p. 226). These findings are especially significant in that
only six of the 424 patients studied were involved in litigation. Subsequent
studies have also reported neuropsychological deficits following mild
traumatic brain injury in the absence of on-going litigation (Merskey and
Wooodford, 1972; Barth, Macciocchi, Giordani, Rimel, Jane and Boll, 1983).
Independent corroboration for these findings was reported in a study by
Gordon and Sadwin (1985). The authors reported neuropsychological test data
collected on 108 patients with traumatic head injury evaluated over a six
year period. Unlike subjects in the Rimel et al. study, almost all of the
subjects in the Gordon and Sadwin study were involved in litigation.
Nevertheless, their findings are "entirely consistent" with the results of
Rimel et al. as patients demonstrated mild impairment on neuropsychological
testing. The marked similarity in the test results argues against the
malingering hypothesis and "supports...an organic substrate underlying the
post-concussion syndrome...." p. 1).
Pathogenesis of post-concussion syndrome and mild TBI
Historically, the model of concussion as an organic (brain based) disorder
has been difficult to demonstrate in that patients with mild TBI or
concussion often demonstrate significant neuropsychological deficits in the
absence of positive findings on traditional measures such as X-rays, CAT
Scan, or even MRI. However, recent animal studies, improved imaging
techniques and histological staining techniques have provided some clues to
the actual pathophysiology of mild TBI.
The actual mechanisms responsible for altered brain functioning, while still
under investigation, are becoming increasingly clear. The nature of this
chapter allows for only a very cursory treatment of what has become a large
body of literature on this subject. For a more detailed discussion, the
reader is referred to Dixon, Taft, and Hayes (1993) and Povlishock & Coburn
(1989). It is clear that a mild traumatic brain injury can produce a myriad
of changes in neurological structure and function. Using animal models,
Gennarelli, Thibault, Adams, Graham, Tompson & Marcincin (1982) and
Povlishock et al. (1989) have demonstrated microscopic diffuse axonal injury
following mild traumatic brain injury with deafferentation from somal and
dendritic targets. In addition, cytoskeletal injury may affect the ability
of the nerve to send messages and contribute to "functional deficits." Dixon
et al. also report membrane depolarization resulting in an abnormal release
of various neurotransmitters, and changes in receptor binding for specific
receptor populations which affects the uptake of various neurotransmitters.
They suggest that biochemical changes in the brain secondary to mild brain
injury specifically impact the cholinergic system, which has been shown to
affect memory and other cognitive functions.
One of the criticisms of the organic model is that, in and of itself, it can
not account for the finding that patient outcome does not always correlate
with the severity of the injury. However, severity is often determined by
post-traumatic amnesia (PTA), which refers to the length of time post injury
for which the patient is unable to recall day-to-day events. It is a very
subjective measure that is often difficult to establish. Moreover, the
degree of relationship between PTA and subsequent psychiatric and
intellectual status is rather modest even in cases of severe traumatic brain
injury (Benton, 1979), and may be even less valuable in cases of mild brain
injury (Rutherford, Merrett, & McDonald, 1977). Another criticism of the
organic hypothesis is that patients often report an increase in symptoms
over time. One would normally expect symptom reduction as a result of
spontaneous recovery. The finding that patients often report increased
cognitive complaints over time is more difficult to explain. However,
patients with mild TBI often have pain and other physical injuries. They may
become aware of their cognitive deficits only after their pain remits.
Moreover, the cognitive deficits themselves affect the patient's
self-perception. They may not be fully cognizant of their cognitive deficits
until "the fog begins to lift."
It appears as if neither the organic or psychosocial model is able to fully
reconcile all of the empirical and clinical data. Many clinicians agree with
Gronwall and Wrightson (1974) who maintain that postconcussive
symptomatology often reflects the interaction of emotional and cognitive
sequelae. They suggest that the emotional problems following a mild
traumatic brain injury are a secondary response to an organically based
injury, and that organic damage to the brain produces cognitive deficits
that result in a loss of self-confidence and neurosis. Thus, in order to
fully understand and treat the symptoms associated with a post-concussion
syndrome, both organic and secondary emotional factors must be considered.
An integrated model of post-concussion syndrome and mild TBI
Given that a traumatic brain injury is an event that affects people, and
that people bring to the event a personality based upon a lifetime of
personal experiences, any model that attempts to account for the effects of
TBI must consider many variables including the organic brain injury, the
status of litigation, and the individual's unique personality structure and
psychological makeup. The most comprehensive integrated model of functional
outcome following mild TBI was published by Kay, Newman, Cavallo, Ezrachi,
and Resnick (1992). Their model attempts to account for the interaction of
neurological factors, cognitive symptoms, physical factors, and
psychological factors. They argue that all of these factors are
inter-related and combine to affect the person's "functional outcome."
Although the theoretical foundation for the model is beyond the scope of
this chapter, the following diagram, taken from their article, illustrates
the basic concepts.
FIGURE 1
Kay and his colleagues offer an example in which "underlying neuropathology
(a neurological factor) may lead to attention lapses (an objective cognitive
factor), which may lead to the experience of not being able to keep focused
(a subjective cognitive factor). This inability to focus may in itself
increase the person's anxiety in performance situations, which in turn may
further interfere with the ability to focus (a subjective cognitive factor
influencing a psychological factor). In addition performance breaks down due
to poor concentration (itself influenced by anxiety) may also lead to
increased anxiety (a functional outcome affecting psychological factors."
(pp 331). Although the model may appear complex and somewhat cumbersome, it
helps to account for the interaction of organic, personality, and
psychological factors, and their contribution to functional outcome. It also
demonstrates the value of an integrated treatment program for patients with
mild TBI and Post-Concussion Syndrome.
Anxiety in post-concussion syndrome and mild TBI; An alternative model
It should be evident, given the preceding discussion, that anxiety is not
typically the primary cause of cognitive dysfunction following mild TBI;
however, it may be a very natural response to the person's inability to
function cognitively at a level that is consistent with his\her pre-injury
ability. Moreover, as indicated in the model proposed by Kay et al. it may
be a "factor" that contributes to prolonged symptomatology and interferes
with functional outcome. There is little doubt that anxiety is a common
symptom following traumatic brain injury. Cytowick et al. (1988) reported
depression/neurasthenia in 28% of his sample of patients treated as
out-patients following a traumatic head injury. Tom-Harold (1987) reported
anxiety, depression and insomnia three to five years following mild
traumatic brain injury. Barth et al. (1983) reported that "mild dysphoria
and general psychological discomfort" (p 531) were associated with cognitive
dysfunction. Binder (1986) reported findings by Lidvall et al. (1984) and
Adler (1945) indicating anxiety reactions in patients with post-concussion
syndrome. Cicerone (1991) argued that anxiety may be even higher in a
symptomatic clinical population, since concern about one's cognitive
deficits is often the primary factor that motivates people to seek
treatment.
As indicated earlier, some clinicians and researchers have attributed
anxiety to a pre-existing psychological condition or to a neurotic reaction
to the accident. These explanations certainly apply to some patients, and
should be considered when interviewing a patient who presents with
post-concussive symptoms. In our experience, there is a relatively small
subset of patients who appear to have a mild traumatic brain injury
superimposed upon a pre-existing personality disorder or neurosis. Other
patients do indeed develop anxiety neurosis secondary to their accident,
and/or the physical and cognitive sequelae. However, these explanations also
appear to be incomplete. They do not account for the significant number of
patients who sustain a mild traumatic brain injury who appear to be
generally well adjusted with no history of a pre-existing personality
disorder or neurotic anxiety disorder who nevertheless become anxious and
insecure when they are confronted by a challenging cognitive task following
even a mild traumatic brain injury. Very often, these patients demonstrate
subtle (and not so subtle) cognitive deficits including problems with
concentration, memory, problem solving, etc. which interfere with their
ability to function efficiently and effectively. Their inability to perform
at the level they did prior to the injury produces anxiety, which in turn
exacerbates their already impaired cognitive functioning, resulting in
greater stress and anxiety. This results in a destructive self-perpetuating
cycle in which subtle cognitive deficits produce anticipatory anxiety in the
face of a challenging task, which further impairs cognitive skills, leading
to continued feelings of "failure" and frustration as reflected in the
following diagram.
Figure 2
It should be emphasized that the person need not be significantly impaired
in order for this cycle to develop. Even borderline or mild deficits may be
sufficient to produce anxiety, especially in patients who were previously
above average intellectually, have high personal aspirations, or work in
very demanding or competitive jobs. These patients are not malingering or
exaggerating their complaints; they do not have a flawed personality
structure; nor can they be said to have anxiety neurosis as defined by the
DSM-IV. There is no apparent unconscious conflict, or obsessive rumination
regarding their injuries. In our opinion, the anxiety is a learned response
to the person's inability to function at the level he/she did prior to the
injury. The anxiety may persist, and continue to affect the individual's
cognitive potential because it has become a learned or conditioned emotional
response to the presentation of a cognitive task.
In our opinion, this phenomenon can be best explained by the classical
conditioning paradigm first described by Pavlov in the early 1900's. Pavlov
discovered that a neutral stimulus (such as a bell) that regularly precedes
the presentation of food eventually elicits salivation in dogs. A
conditioned response is a learned response that occurs when a neutral
stimulus (bell) is repeatedly paired with an unconditioned stimulus (food)
such that the conditioned stimulus is eventually able to elicit the
conditioned response (salivation). In the case of mild brain injury, a
cognitive task represents a neutral stimulus which is repeatedly paired with
an unconditioned stimulus (embarrassment, fear of failure, anxiety, etc.)
such that the cognitive task eventually elicits the conditioned response
(anxiety). Thus a self-perpetuating cycle develops in which the individual
experiences anticipatory anxiety as he/she approaches a cognitive task. The
anticipatory anxiety further interferes with cognitive functioning thus
reinforcing a self-perpetuating cycle. The anxiety persists unless the
cognitive task can be repeatedly paired with a more adaptive conditioned
stimulus. This occurs when the cognitive task is no longer paired with
anxiety, either because 1) the person's cognitive skills improve as a result
of cognitive rehabilitation and/or spontaneous recovery or 2) a different
emotional response is learned and substituted for anxiety.
Treatment of Post-Concussion Syndrome and Mild TBI
Cognitive Rehabilitation
Persons with traumatic brain injury are typically provided with cognitive
rehabilitation. The practice of cognitive rehabilitation began primarily in
the United States and Germany during World War I. There was very little
interest or professional activity until World War II once again produced
many patients with traumatic brain injury. Although there were some advances
in stroke rehabilitation following World War II, treatment for individuals
with traumatic brain injury again languished until the early 1970s. As a
result, cognitive rehabilitation for patients with traumatic brain injury is
still a relatively new field. A review of the theory and practice of
cognitive rehabilitation is well beyond the scope of this chapter. For a
more comprehensive review of the literature, the reader is referred to Maitz,
Gordon, and Massari (1996); Kreutzer & Wehman (1991); Meier, Benton, and
Diller (1987); Sohlberg & Mateer (1989); Wood and Fussey (1990); and
Harrell, Parente, Bellingrath, and Lisicia (1992).
Cognitive rehabilitation therapy typically takes one of three forms. One
approach is to attempt to modify the patient's environment in order to
maximize their existing skills. The therapist may for example suggest that a
student sit in the front of the class or seek tutoring to help him\her
through school. If the patient has problems with visual scanning, the
therapist may help the patient organize his\her work area. A second approach
is to develop compensatory strategies to minimize the functional impact of
the person's cognitive deficits. This may include a system of cues or
prompts to remind the patient to take their medication; or using an
effective diary, log or appointment book to assist with memory. It should be
obvious that these techniques are not designed to actually improve upon an
area of cognitive deficit, but to help the person better cope with his\her
deficits. The third approach is to employ techniques to actually improve
cognitive skills that have been effected by the injury. (The reader is
referred to Maitz, Gordon, and Massari [1996] for a more thorough discussion
of the application of various cognitive rehabilitation techniques.) To date,
there are very few well controlled empirical studies to demonstrate the
efficacy of cognitive rehabilitation. However, there is both clinical and
research data to support the use of these techniques. In a thorough review
of the literature, Haffey & Lewis (1989) found that cognitive rehabilitation
appears to improve the "every day lives" of persons with TBI. In a separate
review, Bleiberg, Cope, and Spector (1989) concluded, "Clearly, it is now
possible to respond to the question of whether or not neuropsychological
rehabilitation works by citing numerous well-designed studies to the effect
that it does." (p.112). Moreover, patients report less anxiety and
depression as their cognitive skills improve and they are once again able to
function intellectually at the level they did prior to their injury.
Despite the obvious relationship between anxiety and intellectual
performance, there have been no attempts to actively and systematically
reduce the anxiety associated with a mild traumatic brain injury in order to
facilitate cognitive functioning. Many authors and clinicians have
emphasized the importance of encouragement, support, education and
information; while others have suggested individual or group psychotherapy.
Although these techniques no doubt serve to help the person learn to better
cope with their problems, they may not directly address the anticipatory
anxiety associated with cognitive activity. Nor do they necessarily
interrupt the self-perpetuating cycle described earlier. Given the model
being proposed, the most effective intervention strategy would be one that
includes cognitive rehabilitation to minimize the person's cognitive
deficits, and stress management to reduce anticipatory anxiety associated
with the introduction of a cognitive task, thereby intervening at two points
in the cycle.
Incorporating Biofeedback Training in Cognitive Rehabilitation
Any patient who experiences persistent cognitive deficits secondary to a
concussion or traumatic brain injury should be provided with a neurological
workup; appropriate clinical studies; and a comprehensive neuropsychological
evaluation to assess the nature, severity, and etiology of their cognitive
deficits. If appropriate the patient should also be provided with cognitive
rehabilitation therapy individually designed to address his/her areas of
cognitive impairment. If the patient has developed anxiety secondary to
his/her cognitive deficits, a stress management program should also be
incorporated into the patient's treatment program. In our opinion,
traditional biofeedback training alone will not enhance cognitive
functioning in a patient with post-concussion syndrome or traumatic brain
injury. However, biofeedback training can potentiate the effectiveness of
the cognitive rehabilitation program by reducing the individual's
concomitant anxiety and stress. We prefer to begin the cognitive
rehabilitation exercises first, then introduce biofeedback training. The
biofeedback training program includes a psychophysiological assessment
followed by an individually designed intervention program.
During the biofeedback assessment session we measure the person's
electromyographic activity, peripheral skin temperature, and electrodermal
activity during baseline, stress, and recovery conditions. Baseline measures
are taken with eyes open and eyes closed for a total of six minutes at the
beginning of the session during which the client is asked to just sit
quietly. The patient is then exposed to a three minute stress condition
during which they are instructed to complete a cognitive task. During the
recovery period, the task is discontinued and the client is asked to once
again sit quietly with eyes open and eyes closed for a total of six minutes.
We always ask the patient to describe what they were thinking and feeling
during each of the six conditions.
The data are analyzed in two ways. The person's readings are compared to a
comparison group in order to determine whether they are within the average
range. Secondly, the person's performance across conditions is assessed.
Psychophysiological dysregulation is typically expressed in one of three
ways. Some patients demonstrate psychophysiological stress during the
baseline condition. These clients often exhibit generalized anxiety as a
result of increased psychophysiological arousal in a variety of situations.
They are constantly anxious and stressed. This may represent a longstanding
personality trait or psychological disorder; or it may reflect an adjustment
reaction or post-traumatic stress reaction secondary to the accident. The
clinician must use his/her clinical skills to further evaluate the nature
and etiology of the problem. A second subgroup demonstrates a greater than
expected increase in anxiety with the introduction of the stressor event
(i.e. mentally counting backwards by sevens). This can be a demanding task
for an individual with a traumatic brain injury; and it is not uncommon for
clients with a traumatic brain injury to become extraordinarily anxious with
the presentation of the task. They appear to experience anxiety in
anticipation that they will not perform well or become anxious during
performance of the task. Given the previous discussion, it is not surprising
that persons with a traumatic brain injury often demonstrate greater anxiety
and psychophysiogical arousal with the introduction of a cognitive task in
comparison to the general population. The third pattern, and one that was
not anticipated when we began working with these patients, is that many of
our clients with mild TBI fail to show a normal return to baseline during
the recovery condition. In fact, their level of psychophysiological stress
may actually increase during recovery. These clients typically continue to
think about how poorly they performed on the cognitive task during the
recovery period. In our opinion, this is an important and somewhat
unexpected finding which adds support to the belief that people who sustain
a brain injury devalue their performance and become self-critical, which
reinforces their anxiety and interferes with their performance.
The second phase of treatment involves stress management training and
acquisition of the relaxation response. We typically provide patients with
several relaxation strategies in order to determine which techniques are
most effective for them. In most cases this includes some form of
biofeedback training in conjunction with muscle relaxation, imagery,
autogenic training, and/or cognitive/behavioral interventions. After the
individual gains some facility with these techniques, he/she is provided
with tapes with which to practice at home. These tapes are made specifically
for the individual client, and may be changed from time to time in order to
minimize habituation. Clients are trained to criterion on measures of
electromyographic activity, skin temperature, and electrodermal activity.
After the individual has demonstrated the ability to achieve and maintain
criterion on all three measures, we begin to introduce cognitive tasks
during the biofeedback session. Since these clients have also been involved
in traditional cognitive rehabilitation sessions, they are accustomed to
working on cognitive exercises. The goal is for the client to maintain
his/her level of relaxation while working on a challenging task. The
difficulty of the exercises is increased as the individual demonstrates the
ability to meet the cognitive demands of the task and remain relaxed. The
final phase of treatment involves providing the individual with brief
relaxation strategies that he/she can incorporate into their daily routine
at home, school, or work.
We have not yet completed controlled studies to demonstrate the efficacy of
this approach. However, our clinical impression and the subjective report of
clients and family members is that for many patients the relaxation training
greatly potentiates the effectiveness of the cognitive rehabilitation
program. The combination of cognitive rehabilitation and stress management
allows the therapist to intervene at two points in the process, thereby
breaking the self-perpetuating cycle described earlier. It should be
reiterated that traditional biofeedback training will not in and of itself
remediate cognitive deficits. It is critical that the patient be provided
with an appropriate cognitive rehabilitation program as well as stress
management training. The anxiety and stress are the result of perceived
deficits in cognitive functioning. If the person's cognitive deficits are
not addressed, he/she will continue to experience "failure", and frustration
with their cognitive skills and abilities. The learned relaxation response
will eventually be extinguished and the anxiety will return, thereby
reactivating the same self-perpetuating cycle. However, our experience with
patients has repeatedly demonstrated that biofeedback training used in
conjunction with cognitive rehabilitation can help to restore cognitive
skills and abilities in patients with persistent cognitive deficits
secondary to a concussion or mild TBI. A sample protocol for integrating
cognitive rehabilitation and biofeedback is provided in Appendix A.
Post-traumatic vertigo and the application of biofeedback training
Introduction to post-traumatic vertigo
Post-traumatic vertigo or dizziness is not an uncommon phenomenon following
mild TBI. Rutherford, Merrett and McDonald (1977) followed 145 patients
admitted to a Belfast Hospital with a diagnosis of concussion. Six weeks
after discharge, 14.5% of the patients continued to complain of dizziness.
These results are fairly consistent with the results of a study by
Coonley-Hoganson, Sachs, Desei and Whitman (1984) who found that 11% of
patients seen in the emergency room of a Chicago hospital and discharged
with a minor head injury were still reporting dizziness one week
post-injury.
There are many types of post-traumatic vertigo, each with its own etiology
and course. However, a blow to the head or whiplash injury is the most
common cause of dizziness. Damage to brain stem structures can result in
dizziness, disequilibrium, and problems with balance. Trauma to the head can
also produce dizziness due to peripheral injuries as opposed to central
nervous system (brain) dysfunction. A perilymph fistula, most often caused
by a blow to the head, is a tear in one of the thin membranes between the
middle and inner ears. Endolymphatic hydrops is a condition in which the
fluid in the inner ear fluctuates with the body's overall fluid/blood
system. This may cause tinnitus, hearing loss, dizziness, and imbalance.
Although endolymphatic hydrops has several causes, it often results from a
blow to the head. Probably the most common vestibular disorder is benign
paroxysmal positional vertigo (BPPV). In fact, Drachman and Hart (1972)
studied 155 patients who sought treatment at a "dizziness clinic", and found
that positional vertigo occurred twice as frequently as any other vestibular
disorder. It typically produces brief periods of dizziness secondary to
conflicting input from the visual system and the inner ear. Although the
pathophysiology of BPPV is unclear, the most common cause is a blow to the
head.
Dizziness and vertigo are often treated with medications such as Antivert or
Meclizine which often provide symptomatic relief. However, some physicians
are reluctant to prescribe these medications since, while they may suppress
the patient's symptoms, they interfere with the person's ability to
habituate to the conflicting input. Labyrinthine exercises and gaze fixation
(McCabe, 1970; Tangeman and Wheeler, 1986; Oates, J, 1992) have been used to
help patients learn to habituate and ultimately accommodate, thereby
reducing dizziness and disequilibrium. These exercises are most often
prescribed by a physician or physical therapist.
There have been some attempts to treat dizziness, vertigo, and motion
sickness with biofeedback training. Bagshaw, Med and Stott (1985) described
a behavioral program that included biofeedback training to treat air
sickness in 37 student pilots in the Royal Air Force. During the first phase
of treatment, students were provided with general relaxation training and
progressive relaxation training. During the symptom management phase,
students were required to develop "self-initiated counter measures" to
combat vestibular dysfunction. Upon completion of the training, 35 of the 37
students were able to complete flight training with no recurrence of air
sickness; the other two students dropped out of the program for reasons
unrelated to motion sickness. According to the authors, the student's
relaxed state facilitated early identification of their sickness symptoms
while diaphragmatic breathing and cue evoked relaxation provided the student
with a "personal tool" with which to confront the symptoms. Diaphragmatic
breathing was encouraged as it prevents "air swallowing" and
hyperventilation. Cowings and Toscano (1982) were able to demonstrate
increased autonomic nervous system activity including increased heart rate,
peripheral vasoconstriction, and increased skin conductance in people who
were susceptible to air sickness. However, after six hours of relaxation
training, subjects showed a greater resistance to motion sickness than the
no treatment group or a group that was provided with information but no
relaxation training. (The reader is referred to Jones, Levy and Gardner
[1985]; Giles and Lockridge [1985]; and Levy, Jones and Carlson [1981] for
additional studies in the use of biofeedback training and stress management
in the treatment of motion sickness).
Although biofeedback training, in combination with other behavioral
techniques, appears to be effective in the treatment of motion sickness in
otherwise healthy adults, there have been very few attempts to apply
biofeedback to the treatment of post-traumatic vertigo. Shutty, Dawdy,
McMahon and Buckelew (1991) did publish the results of a single case study
of a 26 year old woman who was diagnosed with post-traumatic paroxysmal
positional vertigo following a closed head injury. She was treated with a
combination of education, self training and monitoring, biofeedback assisted
relaxation training, stress management and psychological counseling, gaze
fixation training, and desensitization and generalization training. Prior to
treatment, she reported 48 episodes of dizzy spells a week. After a nine
week treatment program, she reported a 90% reduction in the frequency of her
dizzy spells, and reported their overall severity as a 2 on a scale of 1 to
10.
Encouraged by these earlier studies, we have been treating patients with
post-traumatic vertigo with a combination of education, psychological
counseling, biofeedback training and stress management, and vestibular
exercises prescribed by a physical therapist. The protocol is similar to the
one described earlier. The patient is asked to maintain a record of the
frequency and severity of their symptoms, as well as a record of when and
under what circumstances the dizziness occurs. They are then provided with a
biofeedback/stress management program in which they are trained in several
relaxation techniques. They are instructed to practice both the relaxation
techniques and the vestibular exercises daily. After the patient reaches
criterion on measures of muscle tension, peripheral skin temperature, and
skin conductance the vestibular exercises are introduced during the
biofeedback training sessions. The patient is instructed to use the
relaxation techniques in order to maintain low levels of psychophysiological
arousal while engaging in the vestibular exercises that are designed to
induce vertigo and dizziness. This desensitization process typically results
in a marked decrease in symptoms of vertigo. Although most patients are not
completely asymptomatic at termination, they do typically report a
significant reduction in the frequency and severity of their symptoms.
Moreover, most patients are able to resume working without the use of
medication. However, our experience is limited in that we have only been
able to treat approximately six patients with true post-traumatic vertigo.
Case Study
Ms. B. was a 39 year old married woman who sustained damage to the left
fronto-temporal and right temporal regions secondary to toxic encephalopathy
on February 2, 1989. At the time of her injury, she was employed as a police
dispatcher, when the emergency batteries in the police station exploded,
emitting toxic fumes. Although she continued to complain of cognitive
problems (including difficulty with concentration and memory) and vertigo,
these problems had been largely ignored. She was finally referred to Dr. G.
for a neuropsychological evaluation on December 4, 1989. Dr. G. identified
problems with expressive language, memory, and psychomotor proficiency. He
referred her to a neuro-otologist for treatment of her vertigo, and to the
primary author for cognitive rehabilitation.
Ms. B.'s medical history prior to her injury was unremarkable with the
exception of a pulmonary embolism and hysterectomy. Her developmental and
psychiatric histories were also unremarkable. She was a high school graduate
with one year of nursing school. She
lived with her husband, to whom she has been married for 17 years. They have
two daughters, ages 17 and 12, both of whom where living at home. At the
time of the intake interview (2/7/90), Ms. B. had not yet returned to work
due to the ongoing physical, cognitive, and emotional problems secondary to
her accident.
During the clinical interview, Ms. B. reported residual physical symptoms
including fatigue, blurred vision, headaches, and dizziness with
disequilibrium and balance problems. A neuro-otologic evaluation revealed
vestibular dysfunction secondary to anoxic encephalopathy. The
neuro-otologist prescribed Antivert and Valium. She also complained of
cognitive deficits including problems with attention, concentration, recall,
reading comprehension, inability to return to task when interrupted,
hypersensitivity to noise, and problems with simultaneous processing. She
acknowledged feeling anxious and stressed especially when confronted with a
difficult problem or decision. Her emotional mood was labile and irritable.
Ms. B.'s cognitive rehabilitation program initially focused on developing
effective compensatory strategies to help her manage and organize her time.
She began to use an appointment book, scheduler, to-do lists, etc. This
allowed her to better organize and plan her time, be more efficient, and
allow for more rest and leisure activities. She then began to work on visual
and auditory attention and concentration skills, with and without background
distraction. As she progressed, Ms. B. began working on exercises designed
to improve her ability to shift her attention and concentration. She then
completed exercises designed to improve multiple level processing and
simultaneous processing. Finally, she worked on improving her memory and
recall for both visual and auditory-verbal information.
Concurrent with the cognitive remediation, Ms. B. was seen for a
psychophysiological assessment. The psychophysiological evaluation revealed
elevated muscle tension in the frontalis muscles across baseline, stress,
and recovery conditions. However, her peripheral skin temperature
(adrenergic sympathetic nervous system) and peripheral skin conductance
(cholinergic sympathetic nervous system) were essentially within the average
range across all conditions. It was the therapist's opinion that Ms. B.
experienced stress in the form of muscle tension, and that her stress
contributed to her headaches and exacerbated her cognitive deficits. In the
therapist's opinion, her continued cognitive deficits produced anticipatory
anxiety when she was confronted by a cognitive task, and this anxiety
further exacerbated her cognitive problems. She was provided with
traditional biofeedback training including muscle relaxation and abdominal
breathing, which resulted in decreased muscle tension and increased
peripheral skin temperature. After Ms. B. mastered the relaxation
strategies, she began working on a challenging cognitive task while being
monitored on the biofeedback equipment. This helped to reduce her
anticipatory anxiety and allowed her to maximize her cognitive skills and
abilities.
As the biofeedback training continued, Ms. B. became aware that relaxation
helped to reduce her vertigo. She was referred to a physical therapist, Dr.
N., who specializes in the treatment of vertigo in patients with traumatic
brain injury. Dr. N. recommended that Ms. B. begin a series of vestibular
habituation exercises as an alternative to medication. Ms. B. practiced
these exercises at home, and in the office when she was being monitored on
the biofeedback equipment. She learned to reduce the anxiety associated with
vertigo, and reduce vestibular and visual "overload." Ms. B. soon reported
marked improvement in the frequency, duration, and severity of the vertigo.
During the course of treatment, Ms. B. was encouraged to apply for a
volunteer position. She experience some success, however, her anxiety and
vertigo continued to interfere with her work performance. Ms. B. continued
to practice the vestibular exercises and biofeedback training. With
continued treatment her symptoms subsided, and Ms. B. was eventually able to
obtain a full time position as an executive secretary to the vice-president
of a major manufacturing firm. She is still employed in this position three
years after terminating treatment.
In our opinion, biofeedback training has historically been a vastly
under-utilized modality in the treatment of patients with mild traumatic
brain injury and post-concussion syndrome. However, we have found it to be
very effective in post-concussive symptoms. We have also used biofeedback to
treat symptoms of dyscontrol syndrome in a patient who had approximately 30%
of his frontal lobes surgically removed following a severe frontal lobe
injury.
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Appendix A
BIOFEEDBACK PROTOCOL FOR INCORPORATION IN COGNITIVE REHABILITATION
I. INTERVIEW AND PSYCHOPHYSIOLOGICAL ASSESSMENT
A. Interview
1. Identify situations that elicit anxiety
2. Identify precipitating events and environmental variables
3. Establish stress rating system 0-10 (0=absolutely no stress;
10=unmanageable stress)
4. Review and discuss relevant medical evaluations
B. Assessment - Obtain electromyographic, electrothermal, and electrodermal
measures under the following conditions:
1. Baseline Eyes Open (sitting quietly for 3 minutes)
2. Baseline Eyes Closed (sitting quietly for 3 minutes)
3. Stress (introduction of a cognitive task)
4. Recovery Eyes Open (sitting quietly for 3 minutes)
5. Recovery Eyes Closed (sitting quietly for 3 minutes)
C. Query
1.Ask client to recall thoughts and feelings during each stage of assessment
2. Ask client when he/she felt most relaxed and most stressed
II. TREATMENT
A. Provide information regarding cognition and the effects of stress
B.Anxiety reduction and introduction of relaxation strategies (eyes closed)
1. Determine client's response to relaxation techniques
a. Muscle relaxation
b.Abdominal breathing
c. Mind calm
d.Music
e.Imagery
2. Discuss cognitive/behavioral interventions
3. Provide relaxation tapes to use at home
4. Ask client to rate his/her stress for the week; and prior to, and at
completion of training session (0-10)
5. Ask client to estimate readings (EMG, TEMP & EDG)
6. Review session data with client
C. Generalization training (eyes open)
1. Continue above but with environmental modifications (seated in upright
position, lights on, eyes open)
2. Provide brief exercises that can be incorporated into his/her daily
routine
3. Modify relaxation techniques as necessary
4. Emphasize generalization of previously mastered techniques
D. Introduction of cognitive rehabilitation exercises
1. Emphasis on maintaining relaxation response while engaged in a
challenging cognitive task
2. Encourage practicing cognitive rehabilitation exercises at home while
maintaining relaxation
3. Desensitization training (if necessary)
E. Review and Termination
1. Focus on review and integration of treatment
2. Ensure generalization
3. Follow-up if necessary
Appendix B
BIOFEEDBACK PROTOCOL FOR TREATMENT OF VERTIGO
I.INTERVIEW AND PSYCHOPHYSIOLOGICAL ASSESSMENT
A. INTERVIEW
1. Identify frequency, duration, and severity of vertigo
2. Identify precipitating events and environmental variables
3. Establish stress rating system 0-10 (0 = absolutely no stress; 10 =
unmanageable stress)
4. Establish a dizziness rating system 0-10 (0 = no dizziness, 10 =
uncontrolled dizziness requiring that the patient lie down)
B. ASSESSMENT - Obtain electromyographic, electrothermal, and electrodermal
measures under the following conditions:
1. Baseline Eyes Open (sitting quietly for 3 minutes)
2. Baseline Eyes Closed (sitting quietly for 3 minutes)
3. Stress (introduction of a cognitive task)
4. Recovery Eyes Open (sitting quietly for 3 minutes)
5. Recovery Eyes Closed (sitting quietly for 3 minutes)
C. QUERY
1. Ask client to recall thoughts and feelings during each stage of
assessment.
2. Ask client when he/she felt most relaxed and most stressed
II. TREATMENT
A. Provide information regarding vertigo and the effects of stress
B. Anxiety reduction and introduction of relaxation strategies (eyes closed)
1. Determine client's response to relaxation techniques
a. Muscle relaxation
b. Abdominal breathing
c. Mind calm
d. Music
e. Imagery
2. Assess client's response to analogue vs. digital feedback
3. Discuss cognitive/behavioral interventions
4. Provide relaxation tapes to use at home
5. Ask client to rate his/her stress for the week; and prior to, and at
completion of training session (0-10)
6. Ask client to estimate readings (EMG, TEMP & EDG)
7. Review session data with client
C. Generalization training (eyes open)
1. Continue above with environmental modifications (seated in upright
position, lights on, eyes open)
2. Provide brief exercises that can be incorporated into his/her daily
routine
3. Modify relaxation techniques as necessary
4. Emphasis generalization of previously mastered techniques
D. Introduction of Exercises
1. Emphasis on maintaining relaxation response while engaged in exercises
designed to elicit vertigo.
2. Encourage practicing exercises at home while maintaining relaxation
3. Desensitization training (if necessary)
E. Review and Termination
1. Focus on review and integration of treatment
2. Ensure generalization
3. Follow-up if necessary |
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