Journal of Neuroscience Nursing:
Mild Traumatic Brain Injury: An Update for Advanced Practice Nurses
Bay, Esther; McLean, Samuel A.
Questions or comments about this article may be directed to Esther Bay, PhD APRN BC CCRN, at firstname.lastname@example.org. She is an assistant professor at the College of Nursing at Michigan State University, East Lansing, MI.
Samuel A. McLean, MD MPH, is from the Department of Emergency Medicine at the University of Michigan and director of the TRYUMPH Research Program (Trauma recovery: Understanding Mechanisms & Promoting Healing).
Nearly 75% of persons with brain injury experience a mild injury. These people do not often enter the healthcare system by traditional means, nor do they always present with visible signs and symptoms of injury. In fact, people who experienced brain trauma are likely to seek help in primary care settings and from advanced practice nurses (APNs). Because the symptom experience can be complicated by impaired perception or mood, delays in seeking help, and faulty explanations for their symptoms, APNs need to rule out competing diagnoses, offer brief psychoeducational treatment, and refer the person to an appropriate specialist for therapy when needed.
Traumatic brain injury (TBI) affects people of all ages, is expensive, has varying levels of severity, and contributes to disability. The majority of those injured are 18‐25 years of age (National Institute of Health [NIH] Consensus Statement, 1999). Conservative estimates of lifetime costs associated with TBI approach $56 billion (Thurman, 2001).
Mild brain injury (MBI) accounts for 75% of all diagnosed head injuries (Bazarian, McClung, Shah, Cheng, Flesher, & Kraus, 2005; de Kruijk, Leffers, Menheere, Meerhoff, Rutten, & Twinjnstra, 2002) and costs the nation nearly $17 billion each year (Centers for Disease Control and Prevention [CDC], 2003). MBI can be treated in emergency department (ED) settings, yet it is estimated that about 25% of those with MBI fail to seek medical attention (Shah, Bazarian, Mattingly, Davis, & Schneider, 2004). The CDC refers to MBI as a “silent epidemic” because the problems experienced by patients with MBI (e.g., dizziness, headache, and memory disturbance) are often not visible and may result in functional loss, and are more difficult for practitioners to detect. Long‐term physical, mental, social, or occupational consequences may result (McCauley, Boake, Levin, Contant, & Song, 2001; Ruffolo, Friedland, Dawson, Colantonio, & Lindsay, 1999; van der Naalt, van Zomeren, Sluiter, & Minderhoud, 1999).
These patients often do not enter the health system through traditional means (CDC, 2003). Instead, their first help‐seeking visit may be an ambulatory clinic, substance abuse support group, or primary care office. Advanced practice nurses (APNs) are in key positions to assess for MBI, provide brief psychoeducational interventions about the consequences and trajectory of brain trauma, and make appropriate referrals. Screening for the presence of brain injury should be done with reliable screening tools and effective interviewing techniques. To accomplish this goal, the APN must understand the reasons the patient may enter the health system and be prepared to detect undiagnosed MBI. This article describes the CDC MBI Screening Tool (CDC, 2003), discusses the symptom experience of the person with MBI, identifies potential differential diagnoses, and provides an overview of diagnostic tests and evidence‐based treatment for persons with MBI.
Pathogenesis of Mild Brain Injury
MBI can be a result of domestic violence, motor vehicle crash, sport‐related concussion, fall, or bicycling‐related injury (CDC, 1999). The neural mechanisms mediating the development of MBI symptoms remain poorly understood. A complex cascade of ionic, metabolic, and physiological events, including release of excitatory transmitters, mitochondrial dysfunction, diminished glucose metabolism, and axonal injury are related to clinical signs and symptoms (Giza & Hovda, 2001). Regardless of the cause, a dynamic and complex process of events occurs involving injuries to the axon or injuries to neurons and glial cells, or both.
Axonal injury, often termed diffuse axonal injury (DAI), is a common consequence of brain injury and is associated with poor outcomes (Bramlett & Dalton, 2004). There are three grades of DAI (Table 1). Grade I is associated with widespread axonal damage of the white matter of the cerebral hemisphere and is found in persons who do not experience coma or those with milder injuries. Grade II DAI consists of tissue tear hemorrhages and axonal abnormalities in the cerebral hemispheres and corpus callosum. Grade III DAI, the most severe, consists of grade II findings in addition to abnormalities in regions of the brainstem (Gennarelli, Thibault, & Graham, 1998). For patients with milder injuries, the presence of DAI can be unclear (Shaw, 2002).
Neuronal and glial cell injury can be associated with secondary injury or disrupted blood flow. A series of events occurs leading to accumulation of excitatory amino acids that could result in calcium influx and cell death (Giza & Hovda, 2001; Marshall, 2000). Neurochemical processes involved in this complex cascade are under study as are processes of apoptosis or programmed cell death, changes in glucose metabolism, and calcium‐mediated neuronal injury. Following MBI, cerebral function may be impaired for weeks with significant changes in cerebral metabolism (Bramlett & Dalton, 2004; Marshall). This underscores the need for in‐depth clinical assessments in order to uncover neurocognitive correlates of MBI.
In addition, alterations in neurosensory processing may occur via mechanisms other than direct mechanical neuronal injury and its secondary consequences. For example, stress systems are activated in individuals experiencing a traumatic event to mobilize the optimal response to the event. Numerous animal and human studies have demonstrated that many aspects of cognitive and sensory processing are modulated by stress response system function (Diatchenko, Ackley, Slade, Filling, & Mainer, 2006; Pitman & Delahanty, 2005). The degree to which the dysregulation of these physiologic systems may contribute to disordered neurosensory processing is an active area of investigation.
Classification and Screening for MBI
There is ongoing debate about the best screening and method for classifying patients with MBI. TBI classification is traditionally based on the Glasgow Coma Scale (GCS) score at the scene of the crash or in the ED. Initially, the GCS score was intended to establish coma severity and predict future treatment and outcomes (Teasdale & Jennett, 1974). However, there is now considerable debate about its sensitivity and specificity. A consensus is developing that the motor component subscale alone is sufficiently valid in predicting neurological outcomes (Gill, Windenmuth, Steele, & Green, 2005; Healey et al., 2003; Ross, Leipold, & Terregino, 1998).
Other healthcare experts propose modifications of the GCS with enhanced sensitivity for people with mild injuries, such as the GCS‐Extended (GCS‐E) or the GCS 15 (Batchelor & McGuiness, 2002; Nell, Phil, Yates, & Kruger, 2000). The GCS‐E was proposed to extend the GCS data for patients with milder injuries by adding a scale to define the degree of posttraumatic amnesia (PTA) experienced by the injured person. The amnesia subscale is rated 0‐7 and reflects amnesia from greater than 3 months (scored 0) to no amnesia (scored 7).
Batchelor and McGuiness (2002) proposed that those with a GCS score of 15 have three MBI risk categories based on computed tomography (CT) scan results and symptom clusters. Risk levels are as follows for those with a GCS score of 15 and the following characteristics
* Low risk: no symptoms or previous symptoms of dizziness, headache, or vomiting
* Intermediate risk: reports of loss of consciousness or posttraumatic amnesia
* High risk: severe headache, persistent nausea or more than one vomit.
A management protocol is provided for patients in the high‐risk category that includes performing a head CT scan and 1‐2 days of hospital monitoring followed by home observation (Fabbri et al., 2004).
Despite these proposed models and the understanding that the GCS lacks sensitivity in regards to MBI, clinical practice guidelines continue to support use of the GCS. This suggests that rigorous studies examining the most sensitive measure for detecting MBI are inadequate (National Institute for Clinical Excellence, 2003)
In 2001, a workgroup of MBI experts convened by the CDC reported on appropriate and feasible methods for assessing the incidence and prevalence of MBI in the United States. One outcome of this report was the development of screening criteria that could be used prospectively or retrospectively (CDC, 2003). Using the CDC MBI Screening Tool, determination of MBI could be gathered from chart review, interviews, surveys, or healthcare data sets (Table 2). However, validity and reliability of this tool has yet to be established.
To detect hidden or obvious MBI, screening begins with a direct query about head injury symptoms experienced at the time of the injury or shortly thereafter, a thorough health history, and a comprehensive physical exam. Specific preinjury information known to contribute to postinjury morbidity should be obtained because, it is proposed, those patients with significant preinjury risk factors may benefit from more intensive rehabilitation (Ghaffar, McCullagh, Ouchterlony, & Feinstein, 2006). This includes determining the preinjury presence of psychiatric history, substance abuse, or preinjury social difficulties.
In the following example, Mary, a 35‐year‐old mother of three, was involved in a motor vehicle crash on her way home from taking her children to school. She refused transport to the hospital, stating that she would go home, rest to “settle her nerves,” and then go out to pick up her kids from school. However, the paramedic report indicated she was shaken and dazed at the scene. Over the next month, as she continued her normal routine, her husband became alarmed about the following changes: she was more irritable with the kids and often yelled that they were too noisy, she had difficulty sleeping, her checkbook logging became erratic and erroneous, and she was careless about cooking safely or maintaining home security. She visited her healthcare provider for complaints of headache and irritability. Her physician questioned Mary about the accident and determined that she may have sustained an MBI. Referrals were made to a neurologist who proceeded with appropriate neuropsychological testing, especially because of her prior history of dysthymia. After the diagnosis was supported and baseline data about deficits gathered, outpatient rehabilitation therapies were initiated. This typifies the non‐traditional means of entering the healthcare system and the retrospective data gathering about symptoms of MBI.
The presence of premorbid disorders may be associated with postinjury morbidity, although results from various studies lack full agreement (Dikmen, Bombardier, Machamer, Fann, & Temkin, 2004; Jorge, Robinson, Moser, Tateno, Crespo‐Facorro, & Arndt, 2004; Levin et al., 2001; Moldover, Goldberg, & Prout, 2004). Turner, Kivlahan, Rimmele, and Bombardier (2006) were unable to confirm that patterns of excessive alcohol use contributed to cognitive difficulty after head trauma. Rather, cognitive difficulties were attributed to the severity of the injury. Other experts reported that persons with TBI who are older, have increased preinjury social difficulties, or had a preinjury psychiatric disorder were more likely to have postinjury psychological or physical morbidity (Bay, Kirsch, & Gillespie, 2004; Breed, Flanagan, & Watson, 2004; Fenton, McClelland, Montgomery, MacFlynn, & Rutherford, 1993; Jorge et al., 2004). Thus, obtaining a thorough and specific health history in identifying those at risk for TBI morbidity is critical.
Some experts distinguish complicated from uncomplicated MBI (Borgaro, Prigatano, Kwasnica, & Rexer, 2003; Williams, Levin, & Eisenberg, 1990). Patients classified with complicated MBI meet the criteria for MBI and also have intracranial lesions on MRI or focal neurological deficits such as hemiparesis or aphasia (CDC, 2003; Williams, et al., 1990). Patients classified as having uncomplicated MBI are without demonstrable structure change or deficits. Those with complicated MBI have greater cognitive dysfunction than those with uncomplicated MBI, but do not differ on manifestations of mood disorder (Borgaro et al., 2003).
Symptom Experience After Mild Traumatic Brain Injury
Posttraumatic complaints after MBI are not well understood. This ambiguity centers on issues associated with delays in seeking treatment, healthcare professionals' lack of knowledge about the detection and diagnosis of MBI (CDC, 2003), symptom overlap with other diagnoses or conditions (Borg et al., 2004), heightened endorsement of symptoms in order to benefit from litigation claims (Binder & Rohling, 1996), an underlying mood disorder (Rapoport, McCullagh, Streiner, & Feinstein, 2003), or the lack of sensitive diagnostic tools or biochemical markers that correlate with symptom reports (Borg et al.).
Sensitivity and specificity of symptoms of MBI have been reported and predominately are clustered in the cognitive domain.
Delay in seeking treatment may be important in MBI recovery. These delays are associated with the injured person discounting symptoms, incorrectly interpreting symptoms, guilt over the circumstances involved in the injury, and denial that anything serious occurred (Mooney, Speed, & Sheppard, 2005). Reasons for the delay in seeking treatment have been underinvestigated.
Developmental issues may partially explain delay in seeking treatment after MBI. Persons 18‐25 years old and those over 75 years old are most at risk for TBI (CDC, 1999). Younger people may delay seeking treatment because of their lack of familiarity with illness and the healthcare system, misinterpretation about the significance of symptoms, inadequate medical insurance, or the actual circumstances involving their accident and associated brain injury. In a study of 343 people with head injuries, 16% refused emergency transport. Those refusing transport were younger, male, victims of assault, and less likely to have lost consciousness (Shah et al., 2004). The injury may have been connected to risk‐taking activities such as speeding, drunk driving, or participating in sports. By contrast, those over 75 years may attribute fatigue, dizziness, or change in memory to the aging process or delay treatment because of inadequate medical insurance or fear of reprisal associated with a crash or fall. Collectively, little is known about decisions to seek treatment after TBI (Shah et al.).
The CDC acknowledges an overall lack of understanding about the detection and diagnosis of MBI among healthcare professionals (CDC, 2003). The CDC provides “toolkits” to assist coaches, health professionals, and family members in helping people with brain injury (CDC, 2005). These toolkits contain information about MBI and provide guidelines for prevention, diagnosis, and treatment.
In addition, there are multiple reasons that healthcare professionals experience difficulty in MBI detection. There is overlap of symptoms with other diagnoses or conditions, such as, substance abuse, pain, or depression (Dikmen & Levin, 1993). Malingerers may feign symptoms in order to benefit from litigation claims (Binder & Rohling, 1996; Suhr & Gunstad, 2002). Finally, the lack of biochemical markers or sensitive diagnostic tools for MBI complicates this process (Borg et al., 2004).
Patients who experience MBI display a variety of symptoms. These symptoms usually subside within the first year (Dikmen, Macramé, & Timken, 2001). In a sample of 107 patients admitted to an ED for initial treatment, the most prevalent symptoms reported were forgetfulness, drowsiness, headache, dizziness, trouble concentrating, and lightheadedness. After 6 months, most complaints had diminished with some people still reporting headache, dizziness, and drowsiness. The initial presence of headache, dizziness, and drowsiness in the ED was associated with increased symptoms at the 6‐month evaluation (de Kruijk et al., 2002).
The sensitivity and specificity of symptoms of MBI have been reported and predominately are clustered in the cognitive domain (Gordon, Haddad, Brown, Hibbard, & Sliwinski, 2000). Specific symptoms were also found to predict the likelihood of a complicated MBI. In a systematic review, Borg and associates (2004) noted that when a depressed skull fracture was present along with nausea, vomiting, and headache, the presence of intracranial lesions was likely even in patients with GCS scores of 15. For the APN, questions specifically focused on the cognitive domain are critical, as is determining the presence of headache, nausea, or vomiting.
Between 20% to 80% of people with mild injury will continue to experience symptoms 6 months after the injury (de Kruijk et al., 2002). This phenomenon is termed postconcussion syndrome (PCS). PCS, as defined by the American Psychiatric Association, is associated with quantifiable deficits in memory or attention and the onset or worsening of any three of the following symptoms: tiring easily, disordered sleep, headaches, vertigo/dizziness, irritability, anxiety/depression/affective lability, changes in personality, or apathy (McCauley et al., 2001). Persons at risk for PCS include older females with psychosocial stress, social difficulties, and prolonged posttraumatic amnesia (McCauley et al.). Between 10% to 15% of persons with mild injuries will be symptomatic for a year or longer (Chamelian & Feinstein, 2004; Paniak, Toller‐Lobe, Reynolds, Melnyk, & Nagy, 2000). Sustained postinjury symptoms may result in reduced return‐to‐work potential for those with MBI (Ruffolo et al., 1999). For the APN, correlating memory or attention deficits with presenting and long‐lasting symptoms can be a challenge. Focused interviewing questions and dismissal of competing diagnoses are critical to proper diagnosis and evidence‐based treatment.
In the following example, a 49‐year‐old female sought medical care for persistent headaches, dizziness, and irritability at work and at home. She had been involved in a motor vehicle crash within the past 3 months, but she did not seek medical treatment at the time because she was very busy at work as a legal assistant. Following the accident, her car required extensive repairs. The APN inquired about the accident by asking if the woman was disoriented at the time of the accident and if anyone had noticed her seizure‐type activities or if she had complained of headache or other neurological symptoms. The injured woman reported that she had kept asking the same questions repeatedly and had experienced a significant headache for the first few days. These headaches recently reoccurred. Since the accident, she reported working longer hours in an effort to keep up with the paperwork. She seemed to read more slowly, disliked interruptions, and became quite irritated when office staff members were loud or boisterous. She reported waves of dizziness when she turned her head too suddenly, but did not experience balance difficulties. This case typifies delays in seeking treatment, compensatory strategies initiated by the injured person in a case of MBI, and symptomatology consistent with PCS.
Two of the prominent symptoms of this individual (i.e., dizziness and headache) are common MBI symptoms. Chamelian and Feinstein (2004) reported that dizziness in those with mild‐to‐moderate TBI was an independent predictor of failure to return to work when assessed in persons who were 6 months from their injury date. They concluded that dizziness was not entirely associated with anxiety or other psychological variables (Chamelian & Feinstein). Headache after MBI is associated with poor outcome (de Kruijk et al., 2002). Other experts claim that headache may be associated with injuries to the musculoskeletal system, inflammation of the sinus tracts, or a combination of biopsychosocial issues (Martelli, Zasler, Bender, & Nicholson, 2004). Headaches after TBI have acute or delayed onset and are associated with more emotional distress, although study of this relationship over time is lacking (Walker, Seel, Curtiss, & Wardent, 2005).
Another competing diagnosis is malingering. In Binder and Rohling's (1996) meta‐analytic review concerning the effects of money on recovery after TBI, there was evidence that—especially in cases of MBI—healthcare professionals should consider the effects of financial incentives, such as disability or litigation claims, on reported symptoms. Suhr, Tranel, Wefel, and Barrash (1997) further reported that memory performance after TBI can result from factors other than the injury. Medication use, psychological distress, malingering, and litigation status were implicated in other explanations for postinjury symptoms (Suhr et al., 1997). Sensitive and specific memory tests have the potential to discriminate malingerers from those with actual MBI. Thus, there are competing diagnoses for common symptoms of brain injury, requiring APNs to perform thorough intake histories about psychological distress, litigation status, and the onset of symptoms in association with aggravating and alleviating factors. Referrals for neuropsychological testing may be warranted to support a definitive diagnosis of MBI.
In addition to cognitive and somatic symptoms associated with MBI, many patients report psychological difficulties. Anxiety, depression, and posttraumatic stress disorder (PTSD) are prevalent after TBI, are not associated with the severity of injury, and yet, are associated with worse outcome (Moldover et al., 2004; Rapoport et al., 2003). Patients with irritability, mood lability, insomnia, or cognitive changes such as forgetfulness or organizational difficulties, should also be assessed for depression, PTSD, or anxiety disorders. In fact, Wang, Chan, and Deng (2006) reported that postconcussive symptoms were similarly present in both an MBI and healthy college sample when depression was used as a covariate. Currently, investigations are being conducted to determine to what degree these psychiatric disorders result from biochemical or neuroanatomical changes (Bryant, 2001; Hibbard, Ashman, Spielman, Chun, Charatz, & Melvin, 2004; Jorge et al., 2004; Levin et al., 2001).
Diagnostic Testing for Mild TBI
After a systematic, yet focused history and physical exam, the treating provider must make decisions about appropriate diagnostic testing for the person with suspected MBI. For a diagnostic test to yield reliable information, it must be relatively free of bias and random error. The test must also be sensitive enough to detect an intracranial lesion, yet safe and cost‐effective. The World Health Organization Collaborating Centre Task Force recently conducted a systematic review concerning the evidence about diagnostic tools available to detect MBI (Borg et al., 2004). A summary of their findings follows.
Twenty‐nine studies provided evidence for the use of CT scans as a diagnostic tool in cases of MBI. Only injured persons who were hospitalized were included in this review, thus not fully representing persons with MBI. The review reported that CT scans can detect unsuspected lesions in patients with MBI. However, pediatric facilities and community and teaching hospitals were noted to have variability in their use of CT testing. Only 8% of those with GCS scores of 15 had abnormal CT results. As the GCS score declined, the likelihood of abnormal CT results increased. For example, 30% of patients with GCS scores of 13 had abnormal CT results. Similar prevalence rates were reported in CT studies with children.
The use of skull X rays was also considered in this review. Fifteen studies reported the use of skull X rays to detect lesions in MBI. X rays were capable of detecting skull fractures known to increase the likelihood of an intracranial lesion. When a depressed skull fracture was present along with vomiting, nausea, and headache, there was increased likelihood of intracranial lesions. No conclusions about the diagnostic value of MRI in detecting abnormalities among those with MBI were delineated in this review.
The review also considered whether cognitive assessments were sensitive in the detection of MBI. Reviewers concluded that although there is limited evidence supporting the benefit of specific cognitive assessments in the detection of MBI, there is beginning evidence that specific cognitive tests may detect sport‐related concussive injuries (Lovell & Collins, 2002).
Reviewers also concluded that for persons with MBI, there was good evidence predicting those at risk for complications. Surgical intervention was more likely within 2 hours of admission for those with MBI who were 65 years of age or older, vomiting twice or more, with evidence of basal skull fracture, suspected open or depressed skull fracture, dangerous injury mechanism, or anterograde amnesia of more than 30 minutes (Borg et al., 2004). Consequently, careful clinical assessment coupled with diagnostic tests can predict those patients likely to have MBI complications.
There are studies correlating more sensitive diagnostic tests, such as MRI, single photon emission computed tomography (SPECT), and quantitative magnetic resonance (QMR) imaging with brain abnormalities in those with milder injuries (Kesler, Adams, & Bigler, 2000; Umile, Plotkin, & Sandel, 1998; Wallesch, Curio, Kutz, Jost, Bartels, & Synowitz, 2001). However, findings are unclear about their sensitivity and relevance because of limited ability to recruit persons with similar injuries and length of time since the injury. Gowda and associates (2006) suggested that SPECT was able to detect significant hypoperfusion in the frontal lobes of adults who had evidence of PTA, loss of consciousness, or PCS (Gowda et al., 2006). In addition, it is likely that persons with milder injuries and persistent symptoms have increased likelihood of temporal lobe injury as evidenced with animals and human studies of MBI (Umile, Sandel, Alavi, Terry, & Plotkin, 2002). Further research is being conducted about these relationships.
Biochemical Markers for Persons with Mild TBI
Because diagnostic and cognitive tests have limited ability to predict long‐term outcomes for persons with MBI, investigators are focused on searching for biochemical markers that may be useful in diagnosis and prognosis. One area of research involves S100 proteins. These are present intracellularly and involved in calcium homeostasis, one of the biological mechanisms involved in brain trauma (Nygren‐deBoussard, Fredman, Lundin, Andersson, Edman, & Borg, 2004). In a well‐designed study of persons with MBI compared with a normal control group and a non‐TBI trauma comparison group who were followed for 14 days, the investigators concluded that these biomarker proteins were not useful in detecting acute injuries but the S100AIB protein might be appropriate in identifying patients likely to experience long‐term symptom progression (Townend, Guy, Pani, Martin, & Yates, 2002). Recently, scientists suggested that further study of the S100B protein in the management of MBI and sport‐related concussion injury is required in order to predict who requires further diagnostic testing and management (Stalnacke, Tegner, & Sojka, 2004). Identification of biochemical markers sensitive in the detection and prognosis of MBI remains under investigation.
In summary, APNs are in regular contact with persons who may have experienced MBI. Expert interviewing and assessment is required to ascertain that the diagnosis is appropriate and that differentials are eliminated to the extent possible. Referrals to specialists may be required for further diagnostic testing or neuropsychological evaluation. Once there is a definitive diagnosis, a management plan can be developed and evaluated. Management of MBI is based on evidence‐based practices.
Evidence‐Based Treatment for MBI
After the screening, assessment, and diagnosis for MBI are completed, decisions are made about treatment. Treatment for patients with mild‐TBI focuses on symptom management, teaching compensatory strategies and environmental modifications, support during gradual resumption of work and social responsibilities, and psychoeducation with the patient and family. Recently, Cicerone, Dahlberg, Malec, Langenbahn, Felicetti & Kneipp (2005) published an evidence‐based review article focused on cognitive rehabilitation after stroke and TBI. They found evidence to support training in the use of external aids, such as a memory diary or voice organizer, and in assisting persons known to have moderate to severe memory impairment after TBI, even for patients who are many years postinjury. Compensatory strategies included using a portable pager to address specific problems of everyday function or a voice organizer to remediate for memory impairments (Hart, Hawkey, & Whyte, 2002; Wilson, Emslie, Quirk, & Evans, 1999; Wilson, Emslie, Quirk, & Evans, 2001; Wright et al., 2001). Typically, speech or occupational therapists focus on teaching people with MBI compensatory strategies for their cognitive dysfunction. The APN may be equipped to offer initial strategies to compensate for cognitive dysfunction and make appropriate referrals.
Comprehensive neuropsychological rehabilitation therapies involving combination therapies for persons with cognitive, emotional, interpersonal, and motivational deficits associated with TBI are focused on those with moderate to severe brain trauma. In Cicerone and associates' review (2005) of four studies focused on combination therapies, it was noted that although there is evidence that rehabilitation is beneficial for improving community integration and return to work for persons with moderate‐to‐severe injuries, this evidence is not available for those with milder injuries. Research concerning optimal treatment for those with MBI suggests that less expensive approaches may be effective and that the more comprehensive, multidisciplinary treatment should be targeted toward those with preinjury psychiatric problems (Ghaffar et al., 2006).
Cost‐effective interventions (e.g., giving the patient an information booklet about symptoms and coping strategies, a telephone follow‐up, or “as‐needed services”) were effective in alleviating chronic symptom development (Ponsford, 2005; Paniak et al., 2000; Mittenberg, Tremont, Zielinski, Fichera, & Rayls, 1996). Still, other healthcare professionals suggest that cognitive rehabilitation and emotional support are likely to improve the outcomes for persons with MBI (Tiersky et al., 2005; Paniak et al.). Clearly, additional intervention research is needed for those with MBI (Ponsford).
Two studies focused on symptom management for those with mild injury. Symptom management, although a focus of nursing intervention, has not been systematically studied.
Mittenberg, Tremont, Zielinski, Fichera, & Rayls (1996) provided a 10‐page printed manual and a 1‐hour treatment session about symptom management to a small group of patients with MBI and compared this group to a usual treatment control group. Both groups were recontacted 6 months later. The treatment group reported fewer and less severe symptoms. This study of 48 persons suggests that a brief, psychoeducational intervention may be effective in preventing prolonged symptoms after MBI. Cicerone and associates (1996) incorporated cognitive rehabilitation and symptom management strategies in a consecutive series of therapies for a group of persons referred because of MBI (Cicerone et al., 1996). They reported positive outcomes in cognitive function and symptom control for those identified as exhibiting “good clinical outcomes” compared to those with “poor clinical outcomes.” Unfortunately, there was no control comparison group and the sample only included 20 persons with MBI. However, this study suggests that symptom management and helping persons develop skills in managing dizziness and visual or linguistic abilities can be beneficial. Clearly, more systematic study of symptom management after MBI is needed.
APNs are in key positions to uncover presenting signs and symptoms of mild TBI. Screening tools developed by the CDC can guide this process and identify retrospectively whether neurological impairment occurred at the time of the accident. However, the APN must also consider other potential differential diagnoses (e.g., mood disorder, headache associated with muscular skeletal impairment, or balance problems associated with eighth cranial nerve dysfunction) that can complicate the symptom experience for the injured person. Generally, diagnostic testing is not sensitive to mild TBI, but research is underway to identify screening tests that can be used to diagnose and predict the treatment outcomes. Currently, there are suggestions that cognitive rehabilitation therapies are useful in improving the outcomes and quality of life for persons with mild injury, although there is a need for larger clinical trials showing these relationships.
Batchelor, J., & McGuiness, A. (2002). A meta-analysis of GCS 15 head-injured patients with loss of consciousness or post-traumatic amnesia. Emergency Medicine Journal, 19
Bay, E., Kirsch, N., & Gillespie, B. (2004). Chronic stress conditions do explain post-TBI depression. Research and Theory for Nursing Practice, 18
Bazarian, J., McClung, J., Shah, M., Cheng, Y., Flesher, W., & Kraus, J. (2005). Mild traumatic brain injury in the United States, 1998-2000. Brain Injury, 19
Binder, L., & Rohling, M. (1996). Money matters: A meta-analytic review of the effects of financial incentives on recovery after closed-head injury. American Journal of Psychiatry, 153
Borg, J., Holm, L., Cassidy, D., Peloso, P., Carroll, L., Holst, H., et al. (2004). Diagnostic procedures in mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on mild traumatic brain injury. Journal of Rehabilitation Medicine, 43
Borgaro, S., Prigatano, G., Kwasnica, C., & Rexer, J. (2003). Cognitive and affective sequelae in complicated and uncomplicated mild traumatic brain injury. Brain Injury, 17
Bramlett, H., & Dalton, D. W. (2004). Pathophysiology of cerebral ischemia and brain trauma: Similarities and differences. Journal of Cerebral Blood Flow & Metabolism, 24
Breed, S., Flanagan, S., & Watson, K. (2004). The relationship between age and the self-report of health symptoms in persons with traumatic brain injury. Archives of Physical Medicine Rehabilitation, 85
Bryant, R. (2001). Posttraumatic stress disorder and mild brain injury: Controversies, causes and consequences. Journal of Clinical and Experimental Neuropsychology, 23
Centers for Disease Control and Prevention (CDC). (1999). Traumatic brain injury in the United States: A report to Congress.
Atlanta, GA: U.S. Department of Health & Human Services.
Centers for Disease Control and Prevention. (2003). Report to Congress on mild traumatic brain injury in the United States: Steps to prevent a serious public health problem.
Atlanta, GA: U.S. Department of Health & Human Services.
Chamelian, L., & Feinstein, A. (2004). Outcome after mild to moderate traumatic brain injury: The role of dizziness. Archives in Physical Medicine Rehabilitation, 85
Cicerone, K., Smith, L., Ellmo, W., Mangel, H., Nelson, P., Chase, R., et al. (1996). Neuropsychological rehabilitation of mild traumatic brain injury. Brain Injury, 10
Cicerone, K. D., Dahlberg, C., Malec, J., Langenbahn, D., Felicetti, T., Kneipp, S., et al. (2005). Evidence-based cognitive rehabilitation: Updated review of the literature from 1998 through 2002. Archives in Physical Medicine Rehabilitation, 86
de Kruijk, J., Leffers, P., Menheere, P., Meerhoff, S., Rutten, J., & Twijnstra, A. (2002). Prediction of post-traumatic complaints after mild traumatic brain injury: Early symptoms and biochemical markers. Journal of Neurology, Neurosurgery and Psychiatry, 73
Diatchenko, L., Nackley, A. G., Slade, G. D., Fillingim, R. B., & Maixner, W. (2006). Idiopathic pain disorders: Pathways of vulnerability. Pain, 123
Dikmen, S., & Levin, H. (1993). Methodological issues in the study of mild head injury. Journal of Head Trauma Rehabilitation, 8
Dikmen, S., Macramé, J., & Timken, N. (2001). Mild head injury: Facts and artifacts. Journal of Clinical and Experimental Neuropsychology, 23
Dikmen, S. S., Bombardier, C. H., Machamer, J. E., Fann, J. R., & Temkin, N. R., (2004). Natural history of depression in traumatic brain injury. Archives in Physical Medicine Rehabilitation, 85
Fabbri, A., Pervade, F., Marchesini, G., Morselli-Labate, A., Dente, M., Iervese, T., et al. (2004). Prospective validation of a proposal for diagnosis and management of patients attending the emergency department for mild head injury. Journal of Neurology
, Neurosurgery and Psychiatry, 75
Fenton, G., McClelland, R., Montgomery, A., MacFlynn, G., & Rutherford, W. (1993). The postconcussional syndrome: Social antecedents and psychological sequelae. British Journal of Psychiatry, 162
Gennarelli, T., Thibault, L., & Graham, D. (1998). Diffuse axonal injury: An important form of traumatic brain damage. The Neuroscientist, 4
Ghaffar, O., McCullagh, S., Ouchterlony, D., & Feinstein, A. (2006). Randomized treatment trial in mild traumatic brain injury. Journal of Psychosomatic Research, 61
Gill, M., Windemuth, R., Steele, R., & Green, S. (2005). A comparison of the Glasgow Coma Scale score to simplified alternative scores for the prediction of traumatic brain injury outcomes. Annals of Emergency Medicine, 45
Giza, C., & Hovda, D. (2001). The neurometabolic cascade of concussion. Journal of Athletic Training, 36
Gordon, W., Haddad, L., Brown, M., Hibbard, M., & Sliwinski, M. (2000). The sensitivity and specificity of self-reported symptoms in individuals with traumatic brain injury. Brain Injury, 14
Gowda, N. K., Agrawal, D., Bal, C., Chandrashekar, N., Tripati, M., Bandopadhyaya, G.P., et al., (2006). Technetium Tc-99m ethyl cysteinate dimer brain single-photon emission CT in mild traumatic brain injury: A prospective study. American Journal of Neuroradiology, 27
Hart, T., Hawkey, K., & Whyte, J. (2002). Use of a portable voice organizer to remember therapy goals in traumatic brain injury rehabilitation: A within-subjects trial. Journal of Head Trauma Rehabilitation, 17
Healey, C., Osler, T. M., Rogers, F., Healey, M., Glance, L., Kilgo, P., et al. (2003). Improving the Glasgow Coma Scale score: Motor score is a better predictor. Journal of Trauma Injury, Infection and Critical Care, 54
Hibbard, M. R., Ashman, T. A., Spielman, L. A., Chun, D., Charatz, H. J., & Melvin, S. (2004). Relationship between depression and psychosocial functioning after traumatic brain injury. Archives in Physical Medicine Rehabilitation, 85
(Suppl. 2), S43-53.
Jorge, R., Robinson, R., Moser, D., Tateno, A., Crespo-Facorro, B., & Arndt, S. (2004). Major depression following traumatic brain injury. Archives in General Psychiatry, 61
Kesler, S. R., Adams, H. F., & Bigler, E. D. (2000). SPECT, MRI and quantitative MR imaging: Correlates with neuropsychological and psychological outcome in traumatic brain injury. Brain Injury, 14
Levin, H. S., Brown, S. A., Song, J. X., McCauley, S. R., Boake, C., Contant, C. F., et al. (2001). Depression and posttraumatic stress disorder at three months after mild to moderate traumatic brain injury. Journal of Clinical Experimental Neuropsychology, 23
Lovell, M., & Collins, M. (2002). Immediate PostConcussion Assessment and Cognitive Testing (IMPACT)
. Pittsburgh: University of Pittsburgh.
Marshall, L. (2000). Head injury: Recent, past, present, future. Neurosurgery, 47
Martelli, M., Zasler, N., Bender, M., & Nicholson, K. (2004). Psychological, neurophysiological, and medical considerations in assessment and management of pain. Journal of Head Trauma Rehabilitation, 19
McCauley, S. R., Boake, C., Levin, H. S., Contant, C. F., & Song, J. X. (2001). Postconcussional disorder following mild to moderate traumatic brain injury: Anxiety, depression, and social support as risk factors and comorbidities. Journal of Clinical Experimental Neuropsychology, 23
Mittenberg, W., Tremont, G., Zielinski, R., Fichera, & Rayls, K. (1996). Cognitive-behavioral prevention of post-concussion syndrome. Archives of Clinical Neuropsychology 11
Moldover, J. E., Goldberg, K. B., & Prout, M. F. (2004). Depression after traumatic brain injury: A review of evidence for clinical heterogeneity. Neuropsychology Review, 14
Mooney, G., Speed, J., & Sheppard, S. (2005). Factors related to recovery after mild traumatic brain injury. Brain Injury, 19
National Institute for Clinical Excellence. National Collaborating Centre for Acute Care. (2003). Head injury: Triage, assessment, investigation and early management of head injury in infants, children and adults.
London (UK). Retrieved January 6, 2007, from http://www.nice.org.uk/guidance/CG4/guidance.pdf/English.
National Institute of Health (NIH) Consensus Panel. (1999). Rehabilitation of persons with traumatic brain injury: NIH Consensus statement. Journal of the American Medical Association
Nell, V., Phil, D., Yates, D., & Kruger, J. (2000). An extended Glasgow Coma Scale (GCS-E) with enhanced sensitivity to mild brain injury. Archives of Physical Medicine Rehabilitation, 81
Nygren-deBoussard, C., Fredman, P., Lundin, A., Andersson, K., Edman, G., & Borg, J. (2004). S100 in mild traumatic brain injury. Brain Injury, 18
Paniak, C., Toller-Lobe, G., Reynolds, S., Melnyk, A., & Nagy, J. (2000). A randomized trial of two treatments for mild traumatic brain injury: 1-year follow-up. Brain Injury, 14
Pitman, R. K., & Delahanty, D. L. (2005). Conceptually driven pharmacologic approaches to acute trauma. CNS Spectrum, 10
Ponsford, J. (2005). Rehabilitation interventions after mild head injury. Current Opinion in Neurology, 18
Rapoport, M. J., McCullagh, S., Streiner, D., & Feinstein, A. (2003). The clinical significance of major depression following mild traumatic brain injury. Psychosomatics, 44
Ross, S., Leipold, C., & Terregino, C. (1998). Efficacy of the motor component of the Glasgow Coma Scale in trauma triage. Journal of Trauma
Ruffolo, C., Friedland, J., Dawson, D., Colantonio, A., & Lindsay, P. (1999). Mild traumatic brain injury from motor vehicle accidents: Factors associated with return to work. Archives of Physical Medicine and Rehabilitation, 80
Shah, M., Bazarian, J., Mattingly, A, Davis, E., & Schneider, S. (2004). Patient with head injuries refusing emergency medical services transport. Brain Injury, 18
Shaw, N. (2002). The neurophysiology of concussion. Progress in Neurobiology, 67
Stalnacke, B., Tegner, Y., & Sojka, P. (2004). Playing soccer increases serum concentrations of the biochemical markers of brain damage S-100b and neurospecific enolase in elite players: A pilot study. Brain Injury, 18
Suhr, J., & Gunstad, J. (2002). Postconcussive symptom report: The relative influence of head injury and depression. Journal of Clinical and Experimental Neuropsychology, 24
Suhr, J., Tranel, D., Wefel, J., & Barrash, J. (1997). Memory performance after head injury: Contributions of malingering, litigation status, psychological factors, and medication use. Journal of Clinical and Experimental Neuropsychology, 19
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: A practical scale. Lancet, 2
Thurman, D. J. (2001). The epidemiology and economics of head trauma.
New York: John Wiley & Sons.
Tiersky, L.A., Anselmi, V., Johnston, M.V., Kurtyka, J., Roosen, E., & Schwartz, T., et al. (2005). A trial of neuropsychological rehabilitation in mild-spectrum traumatic brain injury. Archives of Physical Medicine and Rehabilitation 86
Townend, W., Guy, M., Pani, M., Martin, B., & Yates, D. (2002). Head injury outcome prediction in the emergency department: A role for protein S-100B. Journal of Neurology, Neurosurgery and Psychiatry, 73
Turner, A., Kivlahan, D. R., Rimmele, C. & Bombardier, C. H. (2006). Does preinjury alcohol use or blood alcohol level influence cognitive functioning after traumatic brain injury? Rehabilitation Psychology, 51
Umile, E., Plotkin, R., & Sandel, M. (1998). Functional assessment of mild traumatic brain injury using SPECT and neuropsychological testing. Brain Injury, 12
Umile, E., Sandel, E., Alavi, A., Terry, C., & Plotkin, R. (2002). Dynamic imaging in mild traumatic brain injury: Support for the theory of medial temporal vulnerability. Archives of Physical Medicine and Rehabilitation, 83
van der Naalt, J., van Zomeren, A. H., Sluiter, W. J., & Minderhoud, J. M. (1999). One-year outcome in mild to moderate head injury: The predictive value of acute injury characteristics related to complaints and return to work. Journal of Neurology, Neurosurgery and Psychiatry, 66
Walker, W., Seel, R., Curtiss, G., & Wardent, D. (2005). Headache after moderate and severe traumatic brain injury: A longitudinal analysis. Archives in Physical Medicine Rehabilitation, 86
Wallesch, C. W., Curio, N., Kutz, S., Jost, S., Bartels, C., & Synowitz, H. (2001). Outcome after mild-to-moderate blunt head injury: Effects of focal lesions and diffuse axonal injury. Brain Injury, 15
Wang, Y. W., Chan, R., & Deng, Y. (2006). Examination of post concussion-like symptoms in healthy university students: Relationships to subjective and objective neuropsychological function performance. Archives of Clinical Neuropsychology
Williams, D. H., Levin, H. S., & Eisenberg, H. M. (1990). Mild head injury classification. Neurosurgery, 27
Wilson, B., Emslie, H., Quirk, K., & Evans, J. J. (1999). George: Learning to live independently with Neuropage. Rehabilitation Psychology, 44
Wilson, B. A., Emslie, H. C., Quirk, K., & Evans, J. (2001). Reducing everyday memory and planning problems by means of a paging system: A randomized control crossover study. Journal of Neurology, Neurosurgery and Psychiatry, 70
Wright, P., Rogers, N., Hall, C., Wilson, B., Evans, J., Emslie, H., et al., (2001). Comparison of pocket-computer memory aids for people with brain injury. Brain Injury, 15
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