Traumatic Brain Injury in the Context of Neglect and Abuse: Discussion on Etiology and Prognosis

(The Dilemma of too many Smoking Guns) Charles Emmrys PhD L. Psych1 Paper presented to the Grange Annual Conference Ripley UK. September 2012 Introduction A Few Key Concepts in Neuro-Psychological Development The oft lived scenario of assessing and reporting on an adult with a history of childhood maltreatment is so common that everyone involved, including the magistrate, simply assumes that it is, in a general way, a ubiquitous factor that predisposes to delinquent behavior. The stories of severe neglect, sexual interference and physical assaults by care givers fill up our files to such and extent that we, as informers of the court can become so accustomed to their presence that we simply present it as fact with little commentary. The pervasiveness of the scenario does not, however, make it any the less complex or, for that matter, pertinent to the analysis of behavior. Research, particularly those concerned with brain function, have, over the last thirty years, in fact expanded our knowledge on the impact of physical and psychological maltreatment and provided us with an increasingly powerful explicative set of findings that allow us to draw clearly discernable though complex lines of causation between childhood events and child and adult behavior. In this presentation, we will briefly review this literature to assess how it can inform our and the courts understanding of the relationship between physical abuse causing injury to the brain psychological stress caused by maltreatment and its relationship to child and adult behavior. Critical Periods and Child Development Before bending our attention to the topic of child maltreatment, it is worth reminding ourselves that neuropsychological development in childhood proceeds in a rather predictable step wise manner punctuated by critical periods. In these critical periods, certain events need to happen and certain behaviors need to be practiced for the brain to evolve from its rapid growth stage (explosion of cell numbers accompanied by intense dentrification) to its pruning phase (diminution
1

Dr. Emmrys is currently a clinician in private practice in Moncton New Brunswick Canada. The founding director of his provinces treatment service for delinquent youth, he specializes in clinical applications of attachment theory in the treatment of adjudicated youth and the psychosocial and neuropsychological sequelae of neglect and abuse resulting from different forms of residential care.

of neuronal interconnections as unused connections atrophy) to its stabilization of functional behavior supporting neuro-pathways. To ensure that the environment provides the right experiences and practice opportunities for this development to happen, the child will rather masterfully elicit responses from his care givers by prompting them through a series of highly sophisticated (if at times annoying) behaviors from the smiles and cries of early infancy to the rather impressive manipulations and negotiations of early adolescence. This allows, in short, for the home environment, via parental, sibling, extended family and community responses to provide the security and stimulation required for the nervous system to consolidate its structures and support mature pro-social behaviors. Bowlby (1969 1988) would have referred to this ideal developmental milieu as the secure base. More neuroscience focused researchers such as Glaser (2000) would refer to the right series of eliciting stimuli for the symphony of neurochemical and neuroanatomical developments to move towards their genetically ideal adult state. When Things go Wrong If the conditions necessary for the development of healthy pro-social adult behavior is the maturation of a healthy brain in a healthy environment, if follows that the two kinds of events that can throw this development off is a structurally damaged brain in a psycho-emotionally unhealthy environment. We refer here to traumatic brain injury (TBI) and child abuse & neglect often leading to Post Traumatic Stress Disorder (PTSD). Both types of injury co-occur typically in homes where parental dysfunction and poor socio-cultural conditions lead to psychological abuse and physical assaults that all to often cause insults to the brain. Parents who cant parent will hit, parents who cant love will neglect and abuse. The clinical presentation of TBI and psychological stress have distinct if overlapping symptom profiles and, we will argue as others have, both potentiate each other in terms of the life limiting impact they have on the individual. They are the two sides of family dysfunction, the significance of which we are increasingly becoming aware of. To better understand the symptom cluster present in TBI stress induced PTSD comorbidity cases, let us look first at each condition in turn to then review how both conditions together impact the child and the child grown up. Pediatric Traumatic Brain Injury In the developing world, traumatic brain injury (accidental, inflicted, infectious or tumors) is the most common cause of death and neurological disability in children after the period of infancy with TBIs being the most common source of injury (Forsyth & Kirkham, 2012). This stark statistic is a powerful reminder of the developing brains fragility. This fragility is, in a real sense, the price paid by our species for our rather impressive cognitive abilities. If we outdistance our

fellow simians so dramatically, it is because our brains, in addition to being large, take so dreadfully long to develop. In short, it remains plastic and malleable longer than any of those of our cousins allowing us to develop more elaborate neuropathways through experience and practice. But if neuroplasticity can work for us, it can also work against us when injuries create dysfunctional pathways which, if consolidated through repeated use, become hardwired and ultimately disabling (Davidson, 1994; Perry et al., 1995). Understanding the wiring in the brain, therefore, becomes quite important when working with TBI. More particularly, understanding which wires (axons) are more likely to be damaged as a result of a TBI event is rather critical. Bigler & Maxwell (2012) describe how axonal length and their directionality in the brain are perhaps the best predictors of neuro-vulnerability in TBI events. Long axons with oblique path through the brain are susceptible to shearing forces when concussions deform the brain in a coup contrecoup event. Particularly at risk are neurological structures in the reticular activating system (alertness and attention), the hippocampus (encoding of memory), the cingulated gyrus (error detection, mood modulation), most limbic system components (regulation of mood and impulsivity), areas of the frontal lobe (executive functions, impulse inhibition, advanced social reasoning, mood regulation) and the temporal lobes (expressive language, mood stability, the fight flight response) (Bigler & Maxwell, 2012); . Functionally, therefore, TBI injuries affect memory, executive functions, mood stability, impulsivity, verbal and performance based cognitive abilities (IQ), inhibition of aggression and irritability (Ewig-Cobbs, 1997; Barlow et al., 2005; Anderson et al., 2001, 2005). These functional impairment, as you will surely have noted, intersect powerfully with a number of psychiatric conditions but with the important criminogenic factors so often discussed in the delinqueny literature. But every bump to the head, even big ones, will not necessarily lead to all of these symptoms being manifested post TBI. Some functional impairments will be more common where as others will be less frequent. Sometimes few symptoms will appear and resolve rather quickly and completely post injury while at other times, symptom numbers will be high and will persist (Babikian & Asarnow, 2009). The variables that seem most important in determining how many, how seriously and for how long lasting functional limitations will be are (1) severity of the injury, (2) age of injury and (3) psychosocial factors. Let us look now at each of these in turn.

Severity - When assessing TBI severity, a number of tools have been developed based primarily on symptoms present immediately post incident. The Glasgow Coma Scale (Appendix A) provides broadly used definitions on level of consciousness that help divide TIB into mild, moderate and severe categories with duration of unconsciousness and length of post traumatic amnesia being the

other key defining symptoms (table 1). The large majority of TBIs fall in the mild category (85%) (Bigler & Maxwell 2012).
Table 1: Levels of Severity in TBI Mild Loss of Consciousness Less than 30 Minutes Post Trauma Amnesia Glasgow Coma Scale Scores Less than 24 hours 13 to 15

Moderate 30 Minutes to 24 hours 24 hours to 7 days 9 to 12

Severe Over 24 hours Over 7 days 8 or less

Mild TBI victims will, for the most part, experience a small number of mild symptoms post injury with usually no long term functional limitations (Fay, 2009). It remains that 2 to 3 % of children and up to 30% of adults will have some longer lasting sequelae from their injury (Iverson, 2012). And, as noted earlier, neuroimaging shows us that the most important damage is axonal injury and not direct injury to the neurons cell body. With insults to the axolemma (thin membrane of the axonal trunk) comes electrolyte imbalance which in turn causes cell stress and, eventually neuronal death (Bigler, 2012). This can in turn lead to noted brain atrophy in some patients, the tell tale physical manifestation of cell loss (Govind et al., 2002). Mild TBI, in other words, is not necessarily so mild, particularly if MRI results show evidence of intracranial bleeding or swelling (Williams et al., 1990; Smith et al., 2008).
Behavioral symptoms of mild TBI can include weakness in verbal functions, problem solving, memory issues and processing speed. Mild TBI victims also show greater susceptibility to depression and other psychiatric illnesses (Iverson, 2012). Once again, we need to keep in mind that the large majority of mild TBI victims recover completely (Williams et al., 2010). It is those miserable few, however, whose prognosis can be less positive and whose suffering can be considerable. To complicate the picture, mild TBI is often less reported than moderate to severe TBI. This may be particularly true in less well functioning families whose distrust of authority can make acting on a bump to the head less likely. It is often only after very careful history taking that the possible role of mild TBI in the clinical picture becomes clear.

Moderate to Severe TBI present as more involved cases displaying a greater number of symptoms. In this group, we tend to see important longer term problems in the areas of overall cognitive function with measureable reductions in verbal IQ and to a lesser extent, the performance IQ. Executive functions may be impaired as can various memory functions managed by the hypocampus. Impulse control can be affected as can higher social reasoning abilities (Fay et

al., 2000). Attention and concentration can be affected as well along with processing speed (Max et al., 2001). In this population, we see a dose dependent effect with severity scores reliably predicting the importance of cognitive disabilities. Unlike the mild group, sufferers of this more serious injury can often expect their difficulties to persist with the more serious injuries causing the most important loss of function (Babikian & Asarnow 2009). Neurological imaging will more reliably show the site and extent of the lesions or bleeding events with functional impairments related to the damaged areas.

Age of Injury - As we noted briefly above, age of injury constitutes the second important predictive factor when looking at the impact that various TBI injuries. Individuals affected at an older age tend to have more difficulty recovering function where as younger children seem to do better, especially in the mild TBI subgroup (Babikian & Asarnow, 2009). That being said, there are a number of studies which show that individuals with pediatric injuries, particularly those prior to the age of 7, can show rather important long term delays in development. This seemingly contradictory finding is confirmed by other studies (Donders & Warschausky, 2007; Anderson et al., 2004) and seems to refer to individuals whose developmental is affected more pervasively by their injury. Perry (1994) would argue that this is particularly the case when the child victim experiences continuous stress at home but, for the present, many questions on this finding remain unanswered in my view.
But here again, we must continue to be cognisant of the effects of severity of injury. In children, we note that the more important the injury, the more important the discrepancy between sufferers and normal controls and the wider the gap grows over time. In effect, the child, deprived of the tools of development, fails to keep up with his/her better equipped peers. My own sexual abuse clients often refer to themselves as broken goods. Moderate TBI children do not fully catch up but do not fall behind dramatically, keeping pace but at a few rungs down on the ladder. Mild TBI children generally catch up and become indistinguishable from their cohorts by three years. Severe TBI children tend to see the gap widen (see Appendix B)

Psychosocial Factors In this very organic injury cluster, we find strong psychological variables affecting both vulnerability to injury and the course of rehabilitation. For example, we find that individuals with positive outlooks on life, good problem solving skills and solid social connections will show better outcomes post concussion (Federer & Charney, 2009; Hogue et al., 2007). Success breeds success with TBI recovery.
Family factors also seem to play a role with sports injury sufferers benefiting from good family support, for example, and show more robust and complete recovery than those with less support (Belanger et al., 2005). Good kids from

good families heal faster. Conversely, sufferers from more stressed lower socioeconomic conditions were consistently associated with poorer outcomes in all domains (Fae et al., 2009). Looking more closely on family issues, Taylor et al. (2001, 2002) noted the bidirectionality of influences with severity of injury affecting the stress levels of the parents whish in turn affected the ability of the parents to offer support thus influencing outcome. The findings seem to point to the fact that a secure base not only affects the orderly progression of normal development, it also affects the orderly progression of the rehabilitation process post TBI. We can anticipate, here, that children from stressed homes may have failed to develop the robust neuropathways that would be more immune to injury. Poorly developed pathways would be more damageable.

Two Symptom Clusters Associated with TBI Having reviewed the rather long list of psychosocial and cognitive sequelae of TBI and the factors affecting their impact on functionality it remains important to note that the research findings has identified two symptom clusters that seem to vary independently to some degree. The first cluster is those symptoms that are more properly described as cognitive and that would include intellectual functions measured on IQ tests, executive function, memory, attention and problem solving. This cluster of symptoms vary primarily according to the severity of the neuronal injury as we have seen. The second cluster of symptoms include disturbances that are described as more behavioural and would include mood and anger problems, impulse control, irritability, depression and relationship instability. This second cluster is most affected both by premorbid personal and family function and by the quality of the support offered afterwards (Kinsella et al., 1999; Taylor et al., 2001, 20002; Rivera et al., 1994). This finding should not be interpreted, in my view and the view of others, to mean that behavioural symptoms are not affected by TBI severity but it does mean that it is not as powerfully defined by it as are the more cognitive functions (Janusz, 2002).
Childhood Abuse, Neglect & PSD Child abuse and neglect can be defined as a pattern of harmful and stress inducing interactions between a developing child and the significant persons in their environment which to a greater or lesser extent, comes to define the relationship (Cicchetti & Barnett, 1991). The definition implies that these interactions have both frequency over time and are perceived by the child as severe. Also implied is a subjective experience of horror and a powerlessness to correct or change the source of the maltreatment. The stress induced by this treatment typically leads to a series of behavioural consequences such as disregulation of behaviour, hypervigilance, withdrawal, inattentiveness and academic underachievement (Erikson & Egeland, 1996).

To return to our developmental template introduced earlier, we should conceptualized development as a bidirectional interaction defined by elicitations and consequent responses by both the child and his/her care givers. The younger the child, the more this environment is defined by the primary caregivers. The healthy dance is characterised by frequent comforting behaviours, the sharing of affection, the setting of appropriate limits and the frequent mutual experiencing of the joy of being together. Where there is strong emotion, there is strong brain activity. As the child engages the mother positively, their brain stem releases dopamine which in turn stimulates the production of pleasure inducing endorphins (Shore 1996). Dysfunctional families are often led by parents who are poorly equipped to participate in this dance. Avoidance and aggression replaces engagement and participation. Pleasure becomes pain. The resulting impact on the developing brain is, of course, considerable. In these next sections we will begin by looking at the effects of stress on the growing nervous system after which we shall look at the core neurological functions of arousal and ontogenesis. This will be followed by a discussion on the effects of abuse and neglect on attention, memory, IQ, executive functions and verbal abilities. We shall also look at the persons management of arousal, mood regulation, impulse control, social problem solving and the ability to secure and properly manage significant attachment relationships.

Some Neurochemical Features of Stress During Childhood The bodys stress response is managed primarily by the hypothalamus pituitary adrenal axis (HPA). Via a complex process of activation in which the amigdala plays a key role, the body is prepared to deal with whatever is perceived as threat by modifying heart rate, vigilance, anger-fear responses and cognition as well as immune system activity and blood sugar levels. As part of this complex response system, serum cortisol becomes elevated (Kim & Jung, 2006). For some children, the threshold of external threat needed to start up the system is considerable where as for others, the response is very easily elicited. Temperment seems to play a key role in determining who will be the rapid responders and which will not (Boyce et al., 1992). What also seems temperament dependent is how easily a person can dampen the stress response after the perceived emergency is over and how easily it can be reactivated. Generally, the body deals well with the occasional stress resonse. It does not do to well if stress is a way of life. Core Neuropsychological Functions of Arousal Reassurance and Ontogenesis The stress response is but one form of nervous system arousal. Intensely pleasurable ones also cause a cascade of neuronal activity that have their own systems of elicitation and dampening. One of the first acquisitions in a healthy

maturational exchange between a significant care giver and a child is the regulation of arousal. In early childhood, the management of all forms of arousal is a central developmental goal. In his animal studies, Hofer (1994) showed how good maternal care after a stressful event led to both a physiological and behavioural modulation of arousal in pups in the first days of life. As we noted earlier, the emotional experience related to this modulation of arousal is connection and security (Shore 1996). Clearly, though temperament determines to some extent the ease with which arousal takes place, the management of arousal is also a learned ability that emerges, as does so much else in child development, from interactions with significant caregivers. If the opportunity to learn arousal management is not present due to abuse or neglect, the skill is simply not learned, regardless of how well disposed one was in terms of temperment (van der Kolk & Fisher, 1994). In the case of negative arousal states induced by maltreatment, particularly fear, the excitatory messages coming from the amigdala are managed by the inhibitory influences of the prefrontal cortext and the moderating influence of the hyppocampus. The relative health of these TBI vulnerable regions of the brain are crucial, therefore, to the management of negative arousal states. For individuals who master the art of managing arousal and successfully consolidate those neuropathways, one of the most important acquisitions is a sense of self. Ontogenesis refers to the development of a sense of who we are and how we function. This, sense of self emerges as successive experiences of parent assisted regulation of arousal and eventually self regulation experiences come to define our self in the world and establishes a trust that our self can cope with what the world brings us (Cicchitti & Tucker, 1994). With a sense of self comes self esteem (faith that one can regulate ones arousal). And self esteem is, as we have seen, a key resilience factor in recovering from TBI.

Impact of Long Term Neglect and Abuse Related Stress on the Nervous System With chronic negative arousal states created by abuse and neglect situations, the brain is exposed to prolonged elevated levels of serum cortisol. Unfortunately, cortisol is not a neutral substance for the nervous system. Long periods of elevated cortisol levels is actually toxic to a number of brain areas, particularly the left hippocampus which is most concerned with verbal memory but that participates richly in many functions related to psychosocial health (Bremner & Narayan, 1998). Also affected is the prefrontal cortext and the cingulated gyrus, regions of the brain which are involved in problem solving, reasoning and managing emotional responses to the environment. The elevated levels of adrenalin and noradrenalin produced during stressful periods suppresses the function of these brain areas leading to problems of attention and impulse control very similar to what one would see in ADHD (McEwen et al., 1992). A supporting if troubling finding also indicates that ongoing stress leads to volume

asymmetry in the prefrontal cortex (Davidson, 1994) as well as that of the hippocampus (Bremner et al., 1995). The rather dramatic impact of stress on the hippocampus in particular may help explain the symptomatology of PTSD where in memories or traumatic events are typically poorly encoded and difficult to talk about, hinting at a poor encoding process that would give access to the memory through narrative. Being able to speak out ones trauma competently would presumably make it less emotionally paralysing. In support of this idea, Stein found a correlation between volume loss in the hippocampus and the severity of early onset PTSD symptoms (from childhood abuse) were positively correlated. Finally, stress does have a predictably complex impact on the neurotransmitter system in the brain. Serotonin, dopaminergic and adrenergic systems are all affected. But of the imbalances, Dopamine Beta Hydroxylase (which helps metabolize Dopamine to norepinephrine) seems to me important to mention in this summary. The levels are typically lower in stress victims because of a down regulation response to high norepinephrin levels. Lower levels are associated with behavioural symptoms, particularly irritability rejection of authority with authority and express oppositionality to social conventions, all of which are part of the antisocial symptom cluster (Galvin et al., 1995).

The Protrotective Effects If stress is clearly hurtful to the brain, there are a number of factors that mitigates against these harmful effects. Probably the most important are, as noted earlier, factors connected to temperament. Individuals who are proactive, who have an internal locus of control and who are committed to their life project tend to show resilience in the face of stress (Zakin et al., 2003). These temperament or personality factors are, as we have seen, a function of both genetics and the quality of early experience. Evidence also indicates that when key people in a sufferers life reach out to offer support and accompaniment, the chances that major stressors will lead to neurological symptoms is reduced. Good genetics and good support is a powerful way to protect against stressful events. The ability of the child to receive support from willing supporters may, however, be contingent on stress and trauma severity. All of us have cases where individuals close themselves to support if the stress is too overwhelming (King et al., 2003). In other words, the stress load can neutralize protective factors.
Looking at the Comorbidity, a Complex Bidirectional Interaction From the above, it is clear that the degree of overlap between the neurological sequelae of stress and the phenomenology of TBI injuries overlaps tremendously. Both affect roughly the same brain areas and subsequently the same behavioural functions. A differential diagnosis presents, therefore, a

considerable challenge. What is brain injury and what is the result of stress. What is hard wired and what is transitory. Let us begin this part of the discussion by noting that there is good evidence that TBI predisposes one to PTSD. The evidence, primarily from adult studies of war veterans, shows that those individuals exposed to life threatening events have an increased chance of developing PTSD and depression if the event caused a TBI. Further more, the sufferers ability to process the trauma in therapy was negatively affected if a TBI was also part of the clinical picture (Verfaellie, 2012, Conway et al., 2000). One could see how decreased cognitive abilities would have interfered in the establishment of a clinical relationship. The evidence that stress in the family affects the symptomatic impact of TBI is also present. The evidence already alluded to re the impact of family support post TBI address this question as does the date re personality characterisitics that predict TBI symptomatology. Both conditions affect verbal memory, attention and executive functions as well as mood regulation, social competence and control over arousal, symptom clusters that are eerily similar to both pathologies (Geracioti et al., 2006). Key brain areas affected in both conditions such as the prefrontal cortext, the limbic system and more particularly the hippocampus are also remarkably consistent in both conditions (see Apendix C). To the court reporter, the challenge is helping the court understand the bidirectionality of effects between these conditions, that their cooccurence affects not only their severity but also the duration of associated symptoms and that their co-occurrence affects the sufferers ability to participate in therapy. The thorny issue of which symptoms seem most affected by one of the other condition is more difficult. On the one hand, one can rely on the data that predicts symptom intensity and duration in TBI which is difficult from the more chronic symptoms associated with child maltreatment. One can also, in a general way, see TBI as affecting cognitive abilities such as IQ, executive functions and memory where as stress would affect the more psychosocial symptoms, a distinction that can only be offered, in my view, with carefully articulated qualifiers given the above. Yet, the evidence for the difference in the level of impact that each condition has on these two broad symptom clusters is defendable. In conclusion, as court reporters, it is important, in my view, that we bring to the court room an intelligent and compelling explanation of the relationship between behaviour and brain function. This imperative serves to help shift our discussion

from a blame to an understanding perspective. To achieve this is to serve the court well and to serve the public well.

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Appendix A
Glasgow Coma Scale
The Glasgow Coma Scale provides a score in the range 3-15; patients with scores of 3-8 are usually said to be in a coma. The total score is the sum of the scores in three categories. For adults the scores are as follows: Spontaneous--open with blinking at baseline Eye Opening Response Opens to verbal command, speech, or shout Opens to pain, not applied to face None Oriented Verbal Response Inappropriate responses, words discernible Incomprehensible speech None Obeys commands for movement Purposeful movement to painful stimulus Motor Response Withdraws from pain Abnormal (spastic) flexion, decorticate posture Extensor (rigid) response, decerebrate posture None For children under 5, the verbal response criteria are adjusted as follow SCORE 5 4 3 2 1 2 to 5 YRS Inappropriate words Grunts No response 0 TO 23 Mos. Cries and consolable Grunts or is agitated or restless No response 4 points 3 points 2 points 1 point 5 points 3 points 2 points 1 point 6 points 5 points 4 points 3 points 2 points 1 point

Confused conversation, but able to answer questions 4 points

Appropriate words or phrases Smiles or coos appropriately Persistent cries and/or screams Persistent inappropriate crying &/or screaming

Appendix B
Pediatric TBI and their expected rehabilitation pathways
Control Mild Moderate Severe

Recovery

Time of Injury

Time

From Babikian et al., 2009

Appendix C

Hypothalamic Pituitary Adrenal Axis (HPA) Activates the bodys stress responses and elevates serum cortisol Cingulate Gyrus (CG) Error Detection System & Control of Anxiety Hypocampus Memory Encoding, Executive Functioning, Problem Solving Left for Verbal Right for Visual

Abuse and Neglect Persistent activation makes the system hyper-responsive to stress. Persistent activation does not necessarily lead to long term hypersensitivity to arousal. Positive Maternal Attachment is a powerful damper on the response and promotes long term Good PFC control over the arousal mechanism Particularly sensitive to high serum cortisol levels

TBI Particularly vulnerable to concussion injury.

Vulnerable to impact injury.

Amigdala Manages the fight flight response of the autonomic nervous system Prefrontal Cortex (PFC) Seat of the Executive Functions Inhibits excessive amigdaloid HPA arousal Dopamine Beta Hydroxylase System

Elevated serum cortisol interferes with memory setting activities and is associated with cell death in the hypocampus (more on the left) leading to decreased volume but not necessarily to long term loss of memory functions. High Cortisol levels also makes the hypocampal cells more vulnerable to TBI and adult onset PTSD injury effects. Could be related to often noted V-P split in the IQ of children with conduct disorders. Particularly sensitive to high serum cortisol levels but not adversely affected

Vulnerable because of axonal length and direction.

Particularly sensitive to high serum cortisol levels

Vulnerable because of axonal length and direction

Seemingly chronic down regulation of this Noradrenaline related system related to symptoms of conduct disorder.