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APPLICATIONS of BIOFEEDBACK in the TREATMENT OF MILD TRAUMATIC BRAIN INJURY and POST-CONCUSSION SYNDROME

A chapter from the Textbook of Neurofeedback, EEG Biofeedback and Brain Self Regulation
edited by Rob Kall and Joe Kamiya

APPLICATIONS of BIOFEEDBACK in the TREATMENT OF MILD TRAUMATIC BRAIN INJURY and POST-CONCUSSION SYNDROME



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<