Pediatric TBI

Etiology,Pathophysiology,Treatment Mark LiVecchi,DMD,MD Unity Health System

Overview
Epidemiology Pathophysiology Common Cognitive Sequlae Neurostimulant Treatment

Epidemiology
TBI-most common cause of acquired disability in childhood Incidence-200/100K per year in USA Cause varies with age <14yo-injuries,abuse,falls >14yo-MVA,assaults,violence Overall-2X Boys versus Girls

Injury Mechanisms
Pediatrics-larger head to body ratio Predisposes to more head strikes during play and from falls Impact generally occurs in Frontal and Temporal lobes of brain Skull projections-jagged contours in Frontal and Temporal regions leads to contusions and vascular tears;hemorrhages High speed insults-DAI-Diffuse Axonal Injury DAI-shearing of axons in multiple locations-result of acceleration and deceleration forces

RiskFactors
Poverty Parental Instability Lack of safety devices-bike /sports helmets,car seats,seat belts,secured changing tables Alcohol/Drugs-adolescent population

Shaken Baby Syndrome

Large head to body ratio Weak neck musculature Shaking intensifies and transmits shearing forces to brain Repetitive acceleration/deceleration forces lead to DAI Several neuronal connections disrupted Retinal,Subdural,Subarachnoid hemorrhages are common /occult cervical spine injuries

Chemical Mediators
Primary injury-damage that result from forces at time of impact Chemical cascade of events is set into motion subsequent to primary injury Secondary injury-chemically mediated events such as ischemia,cerebral edema,increased intracranial pressure,lead to further damage Free radicals/excitatory amino acids/prostaglandins/calcium -culprits

Secondary Injury
Effects of this are more diffuse based on cellular,circulatory, and metabolic mechanisms-appears to partially account for diaschisis Diaschisis-areas of brain distant from primary injury;even contralateral,can manifest abnormal responses when placed under functional demand-distant damage

Research
Aimed at quelling of secondary injury Blood pressure control post injury Temperature control-cooling Pharmacologic treatment-free radical scavengers/arachadonic acid inhibitiondecrease inflammation Metabolic treatments-ATP production

Anatomy
Frontal lobes-immature in children,incompletely myelinated Function attention,focus,concentration Insult-widespread deficits in cognitive skills such as memory and planning which are predicated on focus and attention

Anatomy
Temporal lobes-home of the hippocampus Responsible for short term memory Utilizes a tremendous amount of glucose and oxygen Highly susceptible to injury during TBI Primary-skull projections/location Secondary-blood flow/metabolic/edema

Neurostimulants
Amantadine-Dopaminergic agonist Older antiviral agent-Influenza A Increases dopaminergic transmission in the frontal lobes-promotes increased attention and arousal Assists with ability to translate movement thoughts into action[ideomotor planning]

Neurostimulants
Amantadine is useful for children with ideomotor apraxia-inability to execute volitional motor functions Dosing:Start low/Go slow Begin at 5mg/kg/day-usual dose is given BID-Qam and Qnoon-can cause insomnia

Neurostimulants
Amantadine-Maximum doseage-200mg/day in children 12 and younger Side effectsinsomnia,hallucinations,irritability,nausea, vomiting, orthostatic hypotension May potentiate anticholinergic effects

Neurostimulants
Bromocriptine-Dopamine receptor agonist Potentiates post synaptic dopamine receptors/inhibits Prolactin secretion Conventional uses-galactorrhea,central fever,Parkinsons disease Improves focus and attention in children with TBI

Neurostimulants
Bromocriptine-appears effective in pediatric aphasia cases Dosing:Start low/Go slow Begin at 1.25mgQam.increase doseage every 2 to 3 days-BID-Qam and Qnoon Maximum doseage-20mg/day in children 12 and younger

Neurostimulants
Bromocriptine-Side EffectsOrthostatic hypotension,nausea,vomiting Caution in adoloscents-endocrine concerns Inhibition of Prolactin secretion Headaches also reported May be helpful in central fevertx

Neurostimulants
Ritalin[Methylphenidate] Increases catecholamine levels such as Norepinepherine-promotes alertness and arousal Useful in cases of low arousal and children who are minimally conscious Paradoxical effect in hyperactivekids

Neurostimulants
Ritalin-as before-Start low/Go slow Doseage:[0.5-1mg/kg/day] in kids Begin with Qam dosing as a test BID dosing-Qam and Qnoon Usual effective doseage-15-20mg/day Max doseage-60mg/day

Neurostimulants
Ritalin-SideEffectsinsomnia,anorexia,tachycardia Less common-thrombocytopenia,erythema multiforme,paradoxical reactions

Treatment Options
Pharmacologic choices are guided by treatment team input and experience Low arousal-goal is to ultimately increase epinepherine/norepinepherine transmission in certain areas of the brain [reticular activating center]-consider Ritalin/Provigil

Treatment Options
Poor focus/ideomotor apraxia-consider Amantadine/Bromocriptine Resistant Aphasia-Bromocriptine has shown promise Listen to the treatment team Encourage journal keeping

Clinical Notes
Remember-any change in status of these children needs immediate attention and work up-UTI/PNA/Dehydration can have devestating effects on the cognitive status of a child with a TBI-the slightest perturbation can manifest in dramatic clinical decline

Clinical Notes
Seizures-Early seizures tend to be of the Tonic-Clonic variety and are usually the result of a metabolic perturbation during the first week of TBI recovery Later-tend to be Partial Complex in nature and are usually anatomically related to damaged areas of the brain