Brain Injury as a Risk Factor for Psychopathology

1. Brain Injury as a Risk Factor for Psychopathology Chapter 10 Katherine Shannon Bowen and Lisa M. Gatzke-Kopp

2. HISTORICAL CONTEXT • In1848, a railroad worker Phineas Gage survived an accident in which an explosion propelled a 3-foot-long iron rod through the frontal portion of his skull and brain. • Gage’s recovery of memory, communication, and most other basic mental functions were not affected. • The accident did create permanent changes to his personality, resulting in self-destructive and socially inappropriate behaviors stemming from poor judgment.

3. TERMINOLOGICAL AND CONCEPTUAL ISSUES • Prevalence • Children between the ages of 0 and 4 years, and adolescents between the ages of 15 and 19 years, are most likely to sustain a brain injury (Faul, Xu, Wald, & Coronado, 2010). • Abuse is a common cause of head injuries among infants and toddlers, representing an estimated 22% of all TBIs among those 0 and 3 years old (Leventhal, Martin, & Asnes, 2010). • Rates of occurrence are higher in males and among individuals of lower socioeconomic status (Bruns & Hauser, 2003; Faul et al., 2010). • Debate continues regarding impulsivity as a risk factor for head injuries, including whether head injuries and externalizing behaviors are multifinal consequences of other environmental risks.

4. ETIOLOGICAL FORMULATION • Mechanisms of Brain Injury • Trauma • Traumatic brain injury (TBI) is defined as a change in brain function that manifests as confusion, altered level of consciousness, coma, seizure, acute sensory or motor neurological deficit, neuropsychological deficit, or behavioral change, resulting from any blunt or penetrating force to the head (Bruns & Hauser, 2003). • TBI occurs when rapid deceleration of the brain against the bony inner surface of the skull produces tissue compression, resulting in neuronal and vascular damage (Finnie & Blumbergs, 2002). • Focal tissue damage occurs most often in injuries resulting from a translational force applied along the linear axis of the brain (Yeates, 2000).

5. ETIOLOGICAL FORMULATION • Hypoxia • Hypoxia refers to a reduction in the supply of oxygen necessary for normal cellular function and can occur through both respiratory and circulatory failures (Nyakas, Buwalda, & Luiten, 1996). • Hypoxia leads to brain damage through both acute and protracted pathways. Acute reduction in oxygen inhibits metabolic processes in cells and results in release of neurotransmitters with excitotoxic effects (Golan & Huleihel, 2006). • This cytotoxic process induces a stress response that propagates chemical signaling of the self-destructive process known as apoptosis. The accumulation of cell loss over these several weeks is often what leads to behavioral deficits (Golan & Huleihel, 2006).

6. ETIOLOGICAL FORMULATION • Advances in Neuroimaging and Pediatric TBI • Computed tomography (CT) • Magnetic resonance imaging (MRI) • Susceptibility-weighed imaging (SWI) • Diffusion tensor imaging (DTI) • Magnetic resonance spectroscopy (MRS) • Advances in statistical analyses have also provided better understanding of the sequelea of damage, but only recently have these methods been used among children.

7. DEVELOPMENTAL CONSIDERATIONS • Brain injuries sustained by children confer different vulnerabilities than similar injuries sustained by adults. • Brain development is substantially incomplete at birth with developmental changes continuing well into the postnatal period through adolescence and early adulthood (Johnson, 1999). • Damage sustained during peak developmental sensitive periods may be most likely to induce long-term deficits (Ewing-Cobbs, Prasad, Landry, Kramer, & DeLeon, 2004). • There are individual differences in biological susceptibility and resilience to injury and individual factors such as cognitive ability and sex appear to moderate outcomes.

8. BRAIN INJURY AND THE FRONTAL LOBE • Dorsolateral Prefrontal Cortex (DLPFC) • Respond to a wide array of cognitive demands requiring problem solving and executive functioning (Duncan & Owen, 2000). • Because executive functions are crucial in allowing children to adapt to changing developmental demands, early damage to this region may establish cascading effects of decrements across multiple domains. • At first, impacts of injury may not be noticeable; however, the interrupted developmental progression in self-control is likely to reveal itself increasingly over time (Eslinger, Biddle, & Grattan, 1997).

9. BRAIN INJURY AND THE FRONTAL LOBE • Orbitofrontal Cortex • Is associated with social/emotional functioning important in interpersonal relationships, including the ability to read social and emotional cues and to use this information in a self-regulatory manner (Bachevalier & Loveland, 2003). • Damage in this region is also associated with an inability to develop and/or use internal cues of potential punishment to guide behavior (Damasio, Tranel, & Damasio, 1990). • Orbitofrontal damage acquired by children often results in more extensive deficits in social behavior than lesions acquired in adulthood (Anderson et al., 1999; Bachevalier & Loveland, 2003).

10. GENETICS AND HERITABLITY • Individual differences in functional and structural deficits incurred in response to brain injury may be influenced by genetic factors. • Allelic variants of genes associated with cognitive function, as well as variants of genes that are known to enhance or impede postinjury cellular recovery, moderate outcomes following neurological insult (Jordan, 2007; McAllister et al., 2008; McAllister, 2010). • Genes appear to be critical in the degree of pathological response to brain injury, establishing the potential for important Gene × Environment interactions applicable to psychological function.

11. CLINICAL CONSIDERATIONS • Brain injury can play a causal role in the pathogenesis of specific psychological disorders by compromising neural systems directly. • Children with a history of mild TBI prior to age 5 are more likely to evidence clinical impairment in adolescence, with a 4.2 fold increase in ADHD, a 6.2 fold increase in conduct and oppositional defiant disorders, a 3.6 fold increase in the development of substance abuse, and a 3.1 fold increase in prevalence of a mood disorders (McKinlay, Grace, Horwood, Fergusson, & MacFarlane, 2009). • Children with mild/moderate TBI are exacerbated for individuals exposed to high levels of authoritarian or permissive parenting indicating that parents are an especially important influence in children’s coping with, and compensating for, functional impairments resulting from more mild brain injuries (Yeates et al., 2010).

12. SYNTHESES AND FUTURE DIRECTIONS • Advances in neuroimaging have allowed for increased detection of microscopic injury that have the potential to cause lasting effects, but these methods have not been readily adopted into clinical practice. • Research on the genetics of brain injury may also assist in identifying individuals at high risk. • The next steps in understanding pediatric brain injury should focus on multidisciplinary, translational research, which capitalizes on recent advances in neuroimaging, behavioral research, and clinical practice (Anderson et al., 2011).