TBI Flashcards
Most common causes of TBI
Transportation, falls, and blunt trauma
Infants through falls
School ages through falls or blunt force
Adolescence through MVC (higher in children with low SES)
Neuropathology behind TBI
Overt damage to brain tissue and disruptions in brain function at a cellular level
Excessive production of free radicals, excessive release of excitatory neurotransmitters, alterations in glucose metabolism
What are some secondary neuropathology
Brain swelling, cerebral edema, elevated ICP, hypoxia-ischemia, and mass lesions (e.g., epidural hematoma)
What are some late / delayed issues that might arise from injury
Cerebral atrophy, post traumatic hydrocephalus, and post traumatic epilepsy (seen in 10-20% of those with severe TBI - more common in children with penetrating or inflicted injuries or depressed skull fracture)
How does axonal injury result?
From cascade of biochemical and metabolic reactions that occur after the trauma - overproduction of free radicals and excitatory neurotransmitters that disrupt normal calcium homeostasis and change glucose metabolism
Initial TBI symptoms
Moderate or severe experience acute fluctuations in arousal disorientation, confusion, and memory loss after the injury
25% of children with severe TBI show deficits in stereognosis, finger localization, and graphesthesia and fine motor skills
Deficits that can be seen with TBI
Both verbal and nonverbal deficits
Spontaneous mutism and expressive language deficits
Overt aphasia disorders rarely persist
Language usually improves over time
Pragmatic aspects of language can persist
Deficits with constructional tasks, perceptual or spatial skills that do not involve motor output, attention problems, slower reaction time, sustained, selective, shifting, and divided attention, memory deficits (explicit - implicit memory is less likely)
Executive function deficits can persist for years after injury
Declines in school classroom performance - more likely in children injured at younger age (standardized testing is not always a strong predictor of academic outcomes after TBI)
Social functioning deficits
Word reading and vocabulary are more resistant to injury
Percentage of patients with mild TBI
80-90%
Psychiatric factors after TBI
Increased risk of ODD, ADHD, and personality changes. Also can see obsessive compulsive symptoms, generalized anxiety, separation anxiety, and depression
Risk in adulthood after TBI
Less educational attainment, reduced employment and occupational status, poorer socialization, increased psychiatric disorder and reduction in functional independence
Factors that predict individual differences following TBI
More severe injuries that result in poorer outcomes
Level of consciousness
Duration of impaired consciousness
Length of post traumatic amnesia
Brain stem abnormalities (pupillary reactivity) and elevated ICP
Predictors used for severity
Best predictors are duration of impaired consciousness and length of post traumatic amnesia (better than GCS)
Glasgow coma scale is most frequent metric of injury severity
Days of injury until a child is able to follow command consistently
Lesions do not predict specific functional outcome
Lack of consistency in the characterization of injury severity
Neuroimaging used for TBI
CT is preferred acutely for bleeds but MRI is superior for most pathology associated with TBI
Non injury factors that are important for outcome
SES, family demographics, and family environment (can buffer or exacerbate)
Children with TBI who frequently display more preexisting behavioral, developmental, and learning problems are more likely to come from dysfunctional families
Developmental consideration for TBI
Age at time of injury, amount of time that has passed since the injury, and age at the time of outcome assessment are important for outcomes
Infancy or early childhood are associated with more persistent deficits - younger children demonstrate a slower rate of change over time and more significant residual deficits than older children, particularly after more severe TBI
