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Brain Injury as a Risk Factor for Psychopathology

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DEVELOPMENTAL CONSIDERATIONS. Brain injuries sustained by children confer different vulnerabilities than similar injuries sustained by adults. Brain development is ... – PowerPoint PPT presentation

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Title: 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.
  • Gages 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 childrens 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).
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