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Mild traumatic brain injury in persons with multiple trauma: the problem of delayed diagnosis.

With all that is currently known about symptoms that indicate mild traumatic brain injury (MTBI), it is unfortunate that many individuals go undiagnosed for long periods of time after sustaining such an injury. As noted by Zasler (1993), MTBI is poorly understood and often under diagnosed or misdiagnosed by health care professionals. The stereotypical constellation of symptoms produced by MTBI includes memory difficulties, problems with attention and concentration, lethargy, sleep disturbance, irritability, depression, headaches (Alves, Macciocchi, & Barth, 1993; Bigler, 1990; Cullum, Kuck, & Ruff, 1990; Gennarelli, 1986; Kwentus, Hart, Peck, & Kornstein, 1985), speed of processing information (Kay, Newman, Cavallo, Ezrachi, & Resnick, 1992), and sometimes seizures (Brown, Fann, & Grant, 1994; Verduyn, 1992). Each of these could be attributed to other causes, and in the face of multiple traumatic injuries, may be overlooked as symptoms which, when combined, are indicative of MTBI.

Memory, attention deficits, and speed of processing information have been identified as some of the longer lasting and more pervasive neuropsychological symptoms seen in head injured adults (Kay et al., 1994; Telzrow, 1990), though psychomotor slowing and seizures present further functional problems such as danger of additional injuries and the inability to drive (Brown et al., 1994; Cullum et al., 1990; Verduyn, 1992). The presence of emotional, behavioral, and personality change after head injury has been recognized since at least 1942. Although there is some question as to whether these symptoms are based in physiology or are a product of psychological reaction to the injury, they are often much more seriously handicapping than residual cognitive and physical disabilities (Cullum et al., 1990; Lezak & O'Brien, 1990). Yet even in individuals who show many or all of these symptoms, a diagnosis may not be made until several months, or even several years after the initial injury.

When MTBI is suspected, "(a)ll too often, global indices such as intelligence test scores are used to presumably (yet inadequately) gauge the severity of [an individual's] deficits..." (Cullum et al., 1990, p. 134). Although seventeen studies of intellectual recovery consistently found a decrease in overall intellectual test performance in the early stages of recovery, most individuals showed improvement after two to three years, with many returning to near premorbid levels on global IQ. If intelligence is found to be at or near the premorbid level, uninformed professionals might rule out MTBI. Deficits can also be masked if the person was intellectually high functioning premorbidly (Cullum et al., 1990). Deficits in higher cognitive functions can occur in the face of relatively normal performance on other more basic tasks (Cullum et al., 1990), explaining the improvement in intelligence tests scores without a comparable improvement in function. Wood (1987) showed that attention, which is often impaired by MTBI, is more important than intelligence (measured by IQ) during the learning of a simple discrimination task, and suggests that attention permeates all aspects of behavior. This helps to clarify why functional deficits continue in the face of intellectual recovery. Deficits in attention are particularly serious because there is little evidence for success of attention training procedures (Bigler, 1990).

The purpose in studying the following three cases was to describe the process of arriving at the diagnosis of MTBI in persons with multiple traumatic injuries, and the constellation of symptoms present in each case. The difficulty of and delay in establishing the presence of MTBI in persons with multiple traumatic injuries is apparent from these cases.

Method

Subjects

All three individuals involved in this study were married white males. One was in his early thirties and the other two in their mid-forties. One was injured in an industrial accident, and the other two in motor vehicle accidents. One was diagnosed with MTBI six months post injury, one was diagnosed 1 year 8 months post injury, and the individual injured in the industrial accident was not diagnosed for almost four years. All were involved in litigation, and none had been gainfully employed since injury.

Instrumentation

A standard interview form was loosely followed in a clinical interview with each man and his wife, and follow up questioning was guided by the responses received. Exhaustive medical and psychological records were reviewed for each, and physicians were consulted by telephone, mail, or both.

Procedure

Medical and psychological records were reviewed for each person studied, and each was interviewed at least twice, at least one time with his wife present. Information was compiled over a six month to two year period in each case, and then retrieved from existing records for this study.

Results

Case 1

This 47 year old male subject, was injured in a motor vehicle accident in which he sustained multiple orthopedic injuries. Two months later he underwent treatment for previously undetected internal injuries. He did not undergo assessment for traumatic brain injury until six months post injury. This assessment was precipitated by symptoms including headaches, depression, forgetfulness, confusion, and emotional lability, and may have been delayed due to his other medical treatments. The assessment resulted in a diagnosis of MTBI, and cognitive retraining was begun. As noted by Telzrow (1990) little change in attention or concentration has been noted though this man was 2 years 9 months post injury at the time of this study.

Though decorated in the military and a model employee prior to injury, shortly after injury this man attempted to pay bills that were not due and make payments with canceled checks. He became angry when others attempted to correct him to such a degree that the canceled check was accepted by a utility company and his wife was notified. Depression and concentration continue to be his most serious areas of deficit, and as predicted by Cullum et al. (1990), neither has resolved entirely. His IQ score did return to the normal range, which is assumed to be comparable to his premorbid level, but function did not follow.

Case 2

This 47 year old man was injured in a motor vehicle accident at the age of 43. He sustained lung, rib, knee, shoulder, and facial injuries. Even though facial injuries were evident, no TBI assessment was performed until almost 2 years post injury. Fatigue, forgetfulness, frustration, debilitating headaches, angry outbursts, depression, and seizures were present from the time of injury, but no diagnosis was made until 1 year 9 months post injury. Again, multiple surgeries, including nasal and dental procedures, and effects of medication, could have overshadowed the concern about TBI symptoms.

Seizures are associated with TBI (Brown et al., 1994; Verduynl 1992), but are not as common as forgetfulness, emotional lability, headaches, and confusion, and have multiple possible etiologies. One noteworthy functional deficit peculiar to seizure activity is that the patient can not drive until the seizures are controlled. In the case of this man and others, the seizures were not controlled, and physicians have suggested that they may not be. Verduyn (1992) noted that although some benefit is typically derived from anticonvulsant medication, premorbid levels of social and vocational function were rarely observed.

Prior to injury this individual was a very successful businessman possessing one graduate degree, and was pursuing a doctoral degree. He obviously had a high level of intellectual functioning, but even with a significant drop, he was not diagnosed for quite a long time.

Case 3

This 33 year old man was injured in an industrial accident when he fell from a height of approximately 25 feet onto a paved roadway, landing on both feet. He sustained multiple orthopedic injuries including ankle, heel, and back injuries, for which he continued to undergo physical rehabilitation for at least four years post injury. There was no loss of consciousness, and no investigation of possible MTBI at the time of injury. Three years, eight months post injury, during an interview, it was noted that he had memory deficits, noticeable mood swings, including uncharacteristic tearfulness and angry outbursts, and severe headaches almost daily. When referred to a neuropsychologist for evaluation of possible MTBI, it was conclusively established that he had sustained MTBI, having such severe deficits that it was recommended that he discontinue driving a motor vehicle.

This individual, though being treated by multiple physicians, having his case managed by a psychiatrist, and receiving worker's compensation benefits with all of the accompanying analyses, had an undetected brain injury for almost four years. Treatment had focused on surgical repair of orthopedic injuries, and management of pain. His treating psychiatrist, who monitored all of his medications, was primarily focusing on pain, post traumatic stress disorder (PISD), and depression to the exclusion of other related symptoms of MTBI including headaches, angry outbursts, and extreme forgetfulness to the point that he would repeatedly ask the same question throughout a day. When combined with the symptoms of lethargy and tearfulness which were presumed to be due to depression, one has the primary constellation of symptoms found in MTBI. Because this man did not strike his head during his fall, brain injury was not investigated, but a fall from a height of 25-30 feet would be the equivalent of coming to an abrupt stop while traveling approximately 22 miles per hour. It is known that nonimpact brain injury can result from acceleration and deceleration forces, and can result in more severe damage than a direct blow to the head (Bigler, 1987; Sweeney, 1992).

In reviewing case materials, it was noted that this individual's intellectual functioning was well below average prior to injury, and this may have served to mask symptoms, such as the typical loss of intellectual functioning (Cullum et al., 1990). It is difficult to say if the course of recovery after the MTBI followed that predicted by previous studies due to a lack of repeat testing, but he still had substantial deficits after a 3 year 8 month recovery period.

Discussion

All of these men showed classical symptoms of MTBI, yet none was diagnosed before six months post injury. Two were diagnosed much later. One explanation for this is that orthopedic and tissue injuries are more visible, more easily diagnosed, and more easily treated. This encourages an emphasis on these types of injuries, resulting in less emphasis on cognitive and behavioral changes. None of these three individuals lost consciousness when they were injured. Had they, screening for TBI would most likely have been performed.

Another related explanation is that most physicians only come in contact with a traumatically injured person at or after the time of injury, and do not have knowledge of premorbid characteristics, which is essential in the diagnosis of MTBI. This author found that asking family members about changes in the person is a better preliminary screen for MTBI than questions asked of the patient. Examples would be to ask a spouse "Does your spouse cry more often than before the injury?" "Is your spouse more forgetful than before the injury?" or "Have your spouse's moods changed since the injury?" Typically if the spouse's response to these and similar questions is emphatic, the neuropsychological assessment will confirm the presence of MTBI. Follow up with a complete neuropsychological assessment is imperative to verify the presence of MTBI.

The primary concern resulting from the findings of this study is that initial diagnosis of MTBI seems to lag behind diagnoses in other areas in persons with multiple traumatic injuries. Although there are limits to MTBI treatment, just an understanding of the origin of new deficits, and a physical rather than purely psychological explanation, can be comforting. Kay et al. (1992) found that some individuals develop psychological problems after MTBI in response to the frustration and failure they experience because of functional deficits caused by the undiagnosed brain injury. The functional limitations are exacerbated by psychological reaction and result in a more debilitating syndrome than might have otherwise occurred. Earlier diagnosis also enables the person to begin treatment such as cognitive retraining (generally provided by specialized rehabilitation professionals) earlier to regain as much function as possible (Prigatano, 1990; Prigatano & Klonoff, 1990).

Although a sample of three is quite small, the consistency among cases and with previous literature points to an area in need of further investigation. An implication for medical practice in the treatment of persons with traumatic injuries could be that screening for symptoms of MTBI be incorporated into post traumatic diagnostic routines. This could be accomplished fairly easily even if treatment for such deficits was not performed in the acute phase after injury. It is important that MTBI not be overlooked as an explanation for ongoing problems experienced by these individuals beyond the acute phase of treatment.

Even if persons with traumatic injuries are not screened for MTBI during the acute stage after sustaining their injury(ies), they will often have contact with rehabilitation professionals before they leave the healthcare system entirely. In the process of post traumatic rehabilitation, rehabilitation professionals could incorporate a brief MTBI screening instrument into the intake process, or include a neuropsychological evaluation into whatever assessment battery is performed. Rehabilitation professionals are in the unique position of being able to catch those cases of MTBI that have filtered through the system without being identified.

References

Alves, W., Macciocchi S. N., & Barth, J. T. (1993). Postconcussive symptoms after uncomplicated mild head injury. Journal of Head Injury Rehabilitation. 8, 48-59.

Bigler, E. D. (1990). Neuropathology of traumatic brain injury. In Traumatic Brain Injury: Mechanisms of Damage. Assessment. Intervention. and Outcome pp. 13-50. Edited by Erin D. Bigler. Austin, TX: Pro-Ed.

Bigler, E. D. (1987). Neuropathy of acquired cerebral trauma. Journal of Learning Disabilities. 20, 458-473.

Brown, S. J., Fann, J. R., & Grant, I. (1994). Postconcussional disorder: Time to acknowledge a common source of neurobehavioral morbidity. The Journal of Neuropsychiatry. and Clinical Neurosciences. 6, 15-22.

Cullum, C. M., Kuck, J., & Ruff, R. M. (1990). Neuropsychological assessment of traumatic brain injury in adults. In Traumatic Brain Injury: Mechanisms of Damage. Assessment. Intervention. and Outcome pp. 129-164. Edited by Erin D. Bigler. Austin, TX: Pro-Ed.

Gennarelli, T. A. (1986). Mechanisms and pathophysiology of cerebral concussion. Journal of Head Trauma Rehabilitation. 1, 23-30.

Kay, T., Newman, B., Cavallo, M., Ezrachi, D., & Resnick, M. (1992). Toward a neuropsychological model of functional disability after mild traumatic brain injury. NeuroPsychology. 6, 371-384.

Kwentus, J. A., Hart, R. P., Peck, E. T., & Komstein, S. (1985). Psychiatric complications of closed head trauma. Psychosomatics, 26, 8-17.

Lezak, M. D., & O'Brien, K. P. (1990). Chronic emotional, social, and physical changes after traumatic brain injury. Traumatic Brain Injury: Mechanisms of Damage. Assessment, Intervention. and Outcome. Edited by Erin D. Bigler Austin, TX: Pro-Ed.

Prigatano, G. P. (1990). Recovery and cognitive retraining after cognitive brain injury. In Traumatic Brain Injury: Mechanisms of Damage. Assessment. Intervention. and Outcome pp. 273-296. Edited by Erin D. Bigler. Austin, TX: Pro-Ed.

Prigatano, G. P., & Klonoff, P. S. (1990). Psychotherapy and neuropsychological assessment after brain injury. In Traumatic Brain Injury: Mechanisms of Damage. Assessment. Intervention. and Outcome. Edited by Erin D. Bigler. Austin, TX: Pro-Ed.

Sweeney, J. E. (1992). Nonimpact brain injury: Grounds for clinical study of the neuropsychological effects of acceleration forces. Clinical Neuropsychologist. 6, 443-457.

Telzrow, C. F. (1990). Management of academic and educational problems in traumatic brain injury. In Traumatic Brain Injury: Mechanisms of Damage. Assessment. Intervention, and Outcome pp. 251-272. Edited by Erin D. Bigler. Austin, TX: Pro-Ed.

Verduyn, W. H. (1992). Multiple partial seizure-like symptoms following "minor" closed head injury. Brain Injury. 6, 245-260.

Wood, R. L. (1987). Brain injury rehabilitation: A neuropsychological approach. London: Croom Helm.

Zasler, N. D. (1993). Mild traumatic brain injury: Medical assessment and intervention. Journal of Head Trauma Rehabilitation, 8(3), 13-29.

Andrea D. Clements, Human Development and Learning, East Tennessee State University, Johnson City, Tennessee 37614-0548.
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Author:Clements, Andrea D.
Publication:The Journal of Rehabilitation
Date:Jan 1, 1997
Words:2590
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