Complicated mild pediatric traumatic brain injury: A review
By Robert Eme
Pediatric traumatic brain injury (PTBI) is a major public health problem in the United States (Anderson & Yeates, 2010; Stanley et al., 2012; Yeates, 2010). It is the leading cause of neurobehavioral morbidity and permanent disability from trauma in children (Stanley et al., 2012). PTBI results in 7400 deaths, 60,000 hospitalizations, 600,000 emergency department visits annually in the United States, and is the most common reason that a child will sustain a significant life-long disability (Stanley et al., 2012). Unfortunately, the education of most mental health professionals (including school psychologists) regarding neurobehavioral sequelae of traumatic brain injury (TBI) is vastly insufficient (Silver, McAllister, & Yudofsky, 2011). Negative effects resulting from this educational deficiency may be especially true for mild PTBI (mPTBI), which accounts for 80%-90% of all cases of PTBI treated annually in hospital settings (Kirkwood & Yeates, 2010a), as it has become increasingly clear that complicated cases of mPTBI can cause persistent neurobehavioral impairment. This possibility has historically been largely ignored, even by specialists in PTBI (Kirkwood & Yeates, 2010a, 2010b; Yeates et al., 2012).
The purpose of this paper is to address the knowledge deficits of school psychologists regarding mPTBI. It will begin with a brief overview of PTBI in general that will provide the essential foundation for a review of the recent developments in the understanding of complicated mPTBI.1
Pediatric traumatic brain injury
PTBI is a traumatically induced structural injury or other alteration in brain function as a result of an external force that is indicated by new onset of at least one of the following clinical signs, immediately following the event (Orman et al., 2011)
Any period of loss or of a decreased level of consciousness
Any loss of memory for events immediately before or after injury
Any alteration in mental state at the time of the injury (confusion, disorientation, slowed thinking, etc.)
Neurological deficits (weakness, loss of balance, change in vision, etc.)
Although no single classification of PTBI exists that encompasses all the clinical and neuropathological features, traditionally PTBI has been classified by mechanisms causing the trauma, clinical severity, and assessment of structure damage (Smith, 2011).
This classification distinguishes between focal PTBI caused by penetrating the substance of the brain (e.g., a bullet) or diffuse PTBI caused by closed head, nonpenetrating trauma such as a fall or a car accident (the two most common causes in children) [Smith, 2011;Yeates, 2010]. The injury mechanisms in pediatric closed head injury are usually diffuse, resulting in global effects (Stanford & Dorflinger, 2009). Children are more likely to be affected by diffuse TBI than adults because the biochemical properties of the immature brain render it more vulnerable to trauma than the mature brain of the adult (Yeates, 2010). The diffuse injuries from closed head trauma can be classified into two broad categories: primary and secondary (Yeates, 2010). Primary injuries, which result directly from the trauma itself, include skull fractures, contusions/hemorrhaging, and diffuse axonal injury (DAI). This latter injury, which results in widespread axonal shearing because of the rapid acceleration and deceleration caused by the accident, is the most important cause of mortality and neurobehavioral impairment (Smith, 2011). Secondary injuries, which arise indirectly from the trauma, include brain swelling/edema, increased intracranical pressure and mass lesions.
Severity of brain injury exists across a broad continuum with the most severe and long-lasting neurobehavioral impairments caused by severe TBI (McAllister, 2011; Yeates, 2010). The classification of injury severity focuses predominantly on three parameters: 1) duration of loss of consciousness (LOC) if any, 2) duration of post-traumatic amnesia (PTA), 3) and scores the Glasgow Coma Scale (GCS) which is a simple measure of best speech and language, motor and oculomotor function within 24 hours of the injury (Yeates, 2010). On this scale, which has historically been considered to be the gold standard in the assessment of initial injury severity (Adelson, 2010), individuals are given a total score ranging from 1 to 15 based on degree of impairment of the three functions, with lower scores indicating more impairment. By convention, scores from 13 to 15 represent mild injuries, scores from 9 to 12 represent moderate injuries, and scores of 8 and less represent severe injuries (Yeates, 2010).
The damage associated with TBI may include the following (Smith, 2011): scalp lacerations, skull fractures, contusions (bruising of the surface of the brain), intracranial hemorrhages (bleeding), ischemia (reduced blood flow) and infarction (cell death). Traditionally this damage has been detected by neuroimaging techniques, such as computed tomography (CT) and magnetic resonance imaging (MRI) techniques (Ashwal et al., 2011; McAllister, 2011). However it is now recognized that these conventional techniques may lack adequate sensitivity in detecting brain injury (Ashwal et al., 2011; Rivara, 2012). A number of more sensitive techniques have been developed with diffusion tensor imaging (DTI) being particularly useful for assessing for diffuse axonal injury (DAI), which as previously mentioned is primarily responsible the neuropsychological impairments caused by PTBI (Ashwal et al., 2011). For example, MacDonald and colleagues (2011) recently found that in a study of 63 soldiers who had been diagnosed with a mTBI, 29 percent showed DTI abnormalities, no abnormalities on a MRI scan.
There is overwhelming evidence that juveniles who have sustained a severe PTBI are at increased risk for a multitude of acute neurobehavioral impairments in various domains such as: persisting neurological symptoms, motor dysfunction, communication difficulties, poor attention, reduced memory, slow processing speed, executive dysfunction (e.g., impaired behavioral and emotional regulation), and social and emotional disorders (Anderson & Yeates, 2010;Yeates, 2010). Furthermore, since many of the foregoing impairments are characteristic of Attention-Deficit/Hyperactivity Disorder (ADHD) [Barkley, 2010; Willcutt & Bidwell, 2011], it is not surprising that approximately 30 percent of cases of severe PTBI also develop ADHD, termed secondary ADHD (SADHD) to distinguish it from primary or developmental ADHD (Eme, 2012). Furthermore, a not insignificant number of juveniles with less severe forms of PTBI (e.g., 8 out of 63) can also develop SADHD (Sinopoli, Schachar, & Dennis, 2011).
With regard to long term neurobehavioral outcome, most longitudinal studies have followed children for relatively brief periods (Yeates, 2010). Children with severe TBI generally show significant improvement in their neuropsychological functioning during the first year postinjury; yet recovery begins to plateau after the first year, with negligible change occurring during the following 2 years post injury (Fay et al., 2009). The findings of a 3-5 year follow-up of 37 children with severe PTBI who ranged in age from 6 to 12 years at the time of the injury (Fay et al., 2009) are representative of these studies. Approximately 40 percent of the children had two or more deficits in neuropsychological, behavioral, adaptive or academic functioning. The pattern of functional deficits is influenced by a variety of factors such as severity of injury, premorbid functioning and environmental factors such as socioeconomic status. There is also a growing body of evidence that the adverse neurobehavioral outcomes of severe PTBI extend into young adulthood. Although reports of gross neurobehavioral impairment are rare, where cognitive problems are detected, they tend to be in attention, memory and processing speed with effects being most dramatic for measures assessing quality of life in domains such as work and leisure, relationships, and living skills (Anderson et al., 2011).
Mild pediatric traumatic brain injury
The discussion of mild TBI (mTBI) in the scientific literature has employed an array of designations with the terms concussion and mild TBI being the most common (DeMatteo et al., 2010). Despite some inconsistency among researchers in defining mPTBI (Kirkwood & Yeates, 2010b), individuals with LOC that is less than 30 minutes, with duration of posttraumatic amnesia2 that is less than 24 hours, and with GCS scores of 13-15 are usually considered to have had a mTBI (McAllister, 2011). However, classification based upon GCSs is less accurate for children than it is for adults for several reasons. First, in general, the GCS is considered to be a crude tool for assessing “…one of the most complex heterogeneous disorders in the most complex organ in the body and dumbing it down to mild, moderate, and severe” (Miller, 2010, p. 297). Indeed several studies have shown the development of traumatic intracranial brain hematomas in 15-20 percent of individuals with a perfect GCS score of 15 (Hessen, 2010). For example Kirkwood and Yeates (2010a) presented a case history of a 15-year-old male with a mTBI who despite a perfect GCS score of 15 had a small right frontal hematoma, and at six weeks postinjury experienced impaired functioning on a neuropsychological evaluation, and severe academic problems. Second, the GCS has never been fully validated for use with children (Adelson, 2010; Stanford & Dorflinger, 2009). As a consequence of these limitations, many cases of PTBI classified as mild are in reality more severe and hence more likely to result in negative neurobehavioral outcomes.
Despite some inconsistency among researchers in defining mPTBI, an adequate understanding of its natural history does exist (Kirkwood et al., 2008). In the first days and weeks after a mild PTBI there is a constellation of neurobehavioral sequelae referred to as postconcussive symptoms (PCS) that can be reliably clustered into two dimensions for juveniles: cognitive (e.g. trouble sustaining attention, confusion, forgetfulness) and somatic (e.g. headache, dizziness, nausea) (Ayr et al., 2009).
The duration of PCS is a topic of considerable scientific controversy since it depends upon how the symptoms are assessed. Experimental work suggests that the pathophysiological effects of mTBI most often result in temporary rather than permanent brain damage (Kirkwood & Yeates, 2010a). Hence well-controlled studies using standardized neuropsychological and academic achievement tests indicate that cognitive or achievement deficits are generally not evident two to three months post injury for most children (Kirkwood et al., 2008). However, in a sizable minority, PCS based upon child and parent self report last months or even years longer despite a resolution of whatever cognitive or achievement deficits were initially seen, and are associated with significant functional deficits (Yeates & Taylor, 2005; Yeates et al., 2009, 2012). Although noninjury factors undoubtedly account for some of these findings, it now accepted that injury related or neurogenic variables are also involved. These cases represent a PTBI that is termed complicated mPTBI (Hessen, 2010; Kirkwood & Yeates, 2010a,b; McAllister, 2011).
Complicated mild PTBI
There has been increasing recognition that mPTBI, like all instances of PTBI, exists on a continuum with even cases in the mild range being at risk of persistent adverse neurobehavioral outcomes (Hessen, 2010; Kirkwood & Yeates, 2010a,b). The term complicated was coined in 1990 to designate these cases at the severe end of mPTBI when it was discovered that the presence of abnormal CT findings in mild cases of adult TBI revealed complications of brain physiology and predicted more persistent problems (Williams, Levin, & Eisenburg, 1990). Since then research has been accumulating that supports this initial finding not only for adults (McAllister, 2011) but also for juveniles (Hessen, 2010; Levin et al., 20078; Kirkwood & Yeates, 2010a,b).
Criteria for indentifying complicated mild pediatric traumatic brain injury
Although distinguishing between complicated and uncomplicated mTBI has received far less attention in pediatric than adult cases (Kirkwood & Yeates, 2010a), several well-designed prospective studies have recently been conducted that provide valuable information for this differential diagnosis (Kirkwood & Yeates, 2010a).
Levin and colleagues (2007) examined the one year postinjury outcomes of 80 mTBI cases who were 5-15 years of age at the time of injury. Of these cases, 32 were considered to have complicated mTBI because postinjury CT scans revealed complications of brain physiology such as contusions, hemorrhages or swelling. At one year, the findings paralleled the results in adult cases in that the juveniles with complicated mTBI performed worse in multiple cognitive (e.g,, measures of working memory, episodic memory, and processing speed) and academic domains (i.e., Calculation and Letter-Word Identification tests from the Woodcock Johnson III Tests of Achievement when compared with those with uncomplicated mTBI.
Rivera and colleagues (2011) examined postinjury outcomes in health-related quality of life, adaptive skills, and participation in social and community activities at 12 and 24 months after TBI in a sample of 729 juveniles 18 and younger and a comparison group of 197 juveniles with an arm injury. At 3 months children with complicated mTBI had lower quality of life scores than the comparison group. Although this difference was not evident at 12 months, the authors concluded that the adverse consequences of complicated mPTBI warrants further investigation.
In the most sophisticated study to date, a team of researchers (Fay et al., 2010; Taylor et al., 2010, Yeates et al., 2009, 2012) studied outcomes of parent reported PCS and physical and psychological functioning in 186 juveniles aged 8-15 with mTBI in comparison to 99 juveniles with mild orthopedic injuries within 3 weeks of injury, and at 1, 3 and 12 months post injury. At the initial assessment (within three weeks of injury), parents also provided retrospective ratings of preinjury child behavioral adjustment and family functioning. Hence, this study was able to control for and rule out two common confounds in other studies of PTBI, namely the failure to rule out the effects of trauma in general, or preexisting symptoms rather than brain insult as causes of adverse neurobehavioral outcome (Taylor et al., 2010). At 12 months postinjury, children with more severe cases of mPTBI characterized by abnormalities on MRI and a greater duration of loss of consciousness (median = 1 minute, range = 1-15 minutes) were significantly more likely than those with orthopedic injuries to exhibit cognitive PCS such as “trouble sustaining attention, forgetfulness, easily confused” (Ayr et al., 2009) and declines in health-related quality of life as assessed by parent ratings of their children’s physical and psychosocial functioning on a 50 item questionnaire (Yeates et al., 2012).
In the longest followup of a prospective study to date, Hessen (2010) studied neuropsychological outcomes 23 years postinjury of 119 Norwegian juveniles with mTBI who were 15 years or younger at the time of injury. They were assessed on an extensive battery of 24 tests which were combined to yield an overall measure of neuropsychological deficit. When compared to the test battery normative group, all scores for the 24 neuropsychological tests were in the normal range. However, after controlling for a variety of pre and post-injury risk factors, juveniles with complicated mPTBI, as indexed by posttraumatic amnesia beyond 30 minutes and a pathological EEG within the first 24 hours, were at greater risk for neuropsychological deficits such as impairments in attention and processing speed than those with uncomplicated mPTBI.
Lastly, although the literature does contain conflicting results, the cumulative findings from animal and human studies suggests that risk for a mPTBI being complicated is increased by the number of prior occurrences of mPTBI (Wilde et al., 2012). This may be especially true when a juvenile sustains a second mTBI (termed “second-impact syndrome”) before fully recovering from the prior mTBI (Wilde et al., 2012). Additional evidence comes from the recent recognition that multiple concussive or subconcussive head impacts associated with sports as well as other activities such as physical abuse and head banging can result in neurodegenerative disease termed chronic traumatic encephalopathy (CTE) (Gavett, Stern, & McKee, 2011; McKee et al., 2009). The onset of CTE is typically in midlife (Gavett, Stern, & McKee, 2011), though it can occur much earlier as evidenced by the autopsy results of an 18 year old who sustained multiple concussions playing high school football (Miller, 2007). Although it is not known what severity or recurrence of concussion is required to initiate CTE, there is no doubt that prior occurrences increase risk for complicated mPTBI (Kirkwood & Yeates, 2010a).
It is now clear, contrary to historical assumptions, that some cases of mPTBI, termed complicated mPTBI can result in persistent cognitive impairments, with impairments of attention, memory, and processing speed being the most common in mild as well as moderate and severe TBI in children and adults (Mathias & Wheaton, 2007; McAllister, 2008; Wilde et al., 2012; Yeates, 2010). The reason for this change in thinking is the recognition that mPTBI resides along a spectrum of severity with some of those at the severe end continuing to suffer from neuronal damage and thus continuing to have neurobehavioral impairments. Cases of mPTBI that are more likely to be complicated are characterized by pathological findings on brain scans, greater than five minutes of loss of consciousness and posttraumatic amnesia (Kirkwood & Yeates, 2010a), less than perfect scores on the GCS (i.e., 13-14), and occurrence(s) of prior mPTBIs. Moreover, since two of the most common methods of assessing severity of PTBI, the GCS scale and CT scan, are frequently insensitive measures of brain neuropathology, many cases assessed as mild are in reality more severe.
Guidelines for school management
The following guidelines are based on the recommended protocol provided by Kirk, Slomine, & Dise-Lewis (2012) for the school based management of mPTBI.
Step 1: Communication
As Kirk, Slomine, & Dise-Lewis (2012, p. 327) observed, “One of the most common pitfalls in implementing appropriate educational services for the child with TBI is the lack of communication among medical professionals, parents, and educational professionals.” If the mTBI occurred in the school setting, then school would presumably be aware of the event and hence the first step would be accomplished. However, if the mTBI occurred outside of school, since even the experts have not historically appreciated the potential seriousness of mPTBI, parents may not have informed the school. They may not have taken their child to a medical provider, or if they did, the injury may not have been formally diagnosed as a TBI (Kirkwood & Yeates, 2010a; Orman et al., 2011). Indeed, parents are very likely to wrongly think that “My child doesn’t have a brain injury, he only has a concussion” (DeMatteo et al., 2010, p. 327). Hence, under the assumption that a child who has sustained mTBI will probably miss school for a least a day because of physical symptoms such as headache, nausea, dizziness, etc., it is incumbent upon school personnel to always inquire about the possibility of a mTBI as a reason for missing school if the parents have not provided one. Once it has been established that a child has sustained a mTBI, the second step should be implemented.
Step 2: Identifying a school case manager and monitoring the student
The school should appoint a case manager who is well educated on PTBI and who will take the lead among the child’s educational team. The manager should receive the initial information regarding the child’s mTBI as well as any recommendations that may have been given by a medical provider for the child’s treatment. Second, this information should be evaluated using the previously discussed criteria that have been found to be predictive of a complicated mTBI. Third, if it seems likely that this is the case, various informal temporary accommodations and modifications should initially be established upon the child’s return to school as the child with a complicated mTBI should not be expected to immediately function at the same pre TBI level. For example, a transition plan to school can be developed which might include provision such as a gradual return-to-school-day, reduced class and homework assignments, having the juvenile meet with the case manager at the end of each day to assess school functioning, etc. Fourth, the child’s progress should be carefully monitored. If after two to three months postinjury (by which time most children with a mTBI will have experienced complete recovery), the child is continuing to experience significant problems in academic functioning, continues to miss a significant amount of school, or evidences any of the classic cognitive impairments in attention, memory, and processing speed (the likelihood of which is higher in children with a complicated mTBI), a referral to a health care specialist with expertise in PTBI to assist with providing a formal supportive safety net.
Step 3: Providing a formal supportive safety net
When temporary, informal accommodations and modifications prove inadequate, a referral for a neuropsychological evaluation is warranted. Furthermore, since it is a truism that “almost certainly” (Kirkwood & Yeates, 2010a, p.15) any symptoms subsequent to PTBI reflect a complex constellation of both injury and non-injury related factors, this evaluation should also include an assessment for premorbid psychiatric features or situational stresses that may be complicating recovery. Such a comprehensive evaluation will provide the necessary information for a Section 504 Plan or an IEP (Kirk, Slomine, & Dise-Lewis, 2012) that will replace the informal safety net that was initially implemented.
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Robert Eme, PhD, ABPP
Illinois School of Professional Psychology at Argosy University Schaumburg Campus