Author(s): Vincent Thieu, MD, Didem Inanoglu, MD, Simra Javaid, DO
Originally published: November 16, 2011 Last updated: January 3, 2024
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Note: See other PM&R KnowledgeNOW Topic, Mild to Moderate Pediatric Traumatic Brain Injury, for additional information

Disease/Disorder

Definition

Traumatic brain injury (TBI) is defined as brain pathology or alteration of brain function caused by an external force. The severity of TBI is classified using the Glasgow Coma Scale: mild (13-15), moderate (9-12), or severe (3-8). In children, severe TBI is associated with a high risk of mortality, neurologic morbidity, and acquired disability. TBI commonly results in impairments in mobility, cognition, language, swallowing, and performance of daily skills. In TBI, injuries may be primary due to impact, and secondary due to inciting events such as edema, seizures, and increased intracranial pressure (ICP).

Etiology

In children ages 0-17 years old, the leading cause of TBI-related deaths from 2018 to 2019 were motor vehicle crashes followed by homicide, as reported by the Centers for Disease Control and Prevention (CDC). However, in children ages 0-4, the most common mechanisms of TBI-related deaths were from homicide followed by unintentional motor vehicle accidents.1 Leading causes of TBI resulting in an emergency department (ED) visit from 2010 to 2014 in children 14 years old and younger include falls and nonaccidental trauma.2 Additionally, among children aged 0-17 years in 2016 and 2017, unintentional falls and motor vehicle crashes were the most common mechanisms of injury contributing to a TBI-related hospitalization.3 The most common cause for pediatric traumatic brain injury worldwide is motor vehicle collisions.

Abusive head trauma (AHT) is responsible for most child abuse-related deaths and is the most common cause of TBI in children less than 2 years of age. Potentially life-threatening conditions, such as subdural and epidural hemorrhages, can occur due to both accidental and abusive head trauma in children. While subdural hemorrhages are unusual consequences of mild TBI events in children, they can be found in almost 90% of cases of shaken baby syndrome. Among detected intracranial lesions, subdural hemorrhage is more common in AHT, whereas epidural hemorrhage is more common in accidental trauma.

Epidemiology including risk factors and primary prevention

According to the CDC, TBI is the leading cause of disability and death in children ages 0-4 and adolescents ages 15-19 years. In TBI, a bimodal age distribution is often described, with very young children (0-2 years) and adolescents (15-18) more commonly injured. Over 837,000 children ages 0-14 years sustain a TBI annually.

Of these children, about 812,000 visit the ED with over 23,000 hospitalizations and about 2,500 deaths (2014). TBI is the second most frequent cause of brain death in pediatric intensive care unit patients in the United States (behind hypoxic-ischemic injury due to cardiac arrest).2

Approximately 17,000 children are permanently disabled each year. Children who sustain a moderate-to-severe TBI before 7 years old have substantially worse short- and long-term outcomes than children who sustain a similar injury at an older age. The age-adjusted rate of TBI-related deaths in males is more than three times the rate of females. TBI most commonly occurs in the spring and summer. Studies indicate children with learning disorders and hyperactivity disorders are more likely to sustain a TBI. Prevention includes primarily educating caretakers on appropriate use of helmets and transportation seats with safety belts, and improved safety engineering of automobiles.

Patho-anatomy/physiology

TBI is comprised of primary and secondary mechanisms of injury. The primary injury is caused by direct damage and shear forces, which includes contusions or penetrating lesions, impact depolarization from increase in extracellular potassium and glutamate, and diffuse axonal injury (DAI). DAI is a result of acceleration-deceleration and rotational forces that cause shearing and damage of the axons. It most commonly affects the white matter of the corpus callosum and other midline structures.

Secondary injury results from the complications following the primary injury, including hypoxemia, electrolyte abnormalities, seizures, excitotoxicity leading to neuronal cell death and cerebral edema. The cerebral edema caused by increased cerebral blood volume and water content can lead to intracranial hypertension. The dangers of intracranial hypertension include cerebral ischemia, brain herniation, and death.

TBIs can also be categorized into focal and diffuse injuries. Focal injuries are recognized by localized damage on imaging. Diffuse injury, as a result of DAI, is more readily visible on magnetic resonance imaging (MRI). A child’s head is relatively larger (head to body ratio) and has a thinner calvarium. The brain is often softer and less myelinated, thus increasing the susceptibility to DAI. Space-occupying hematomas are less likely in children. In general, clinical signs are less reliable in children due to limited vocabulary/communication, but gradually mirror adult symptoms as the child gets older. Typically, the presenting symptoms include headache, nausea, vomiting, seizures, lethargy, or drowsiness. Amnesia is often hard to elicit from a child. In neonates, clinical signs include hypotonia, listlessness, bulging tense fontanels, and sunsetting.

Mechanisms of recovery can occur in several ways. Neuroplasticity through neuronal regeneration and collateral sprouting can occur, along with activation of latent areas and change in synaptic communication.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Following a TBI, symptoms may include mental status changes, extremity weakness, headaches, cranial nerve deficits, and visual changes. Depending on injury severity, symptoms may progress due to cerebral edema, elevated ICP, seizures, and hydrocephalus. Management of medical issues may help determine recovery.

In the ED, the child’s airway, breathing, and circulation is assessed and managed. Glasgow Coma Scale (GCS) or the Pediatric GCS scores are obtained. Patients with a GCS of 8 or less are intubated for airway protection. The head and spine are evaluated and imaged as indicated. Patients are frequently assessed for signs of increased ICP, defined as ICP greater than 20 mm Hg, in which a monitor may be required. For patients with increased ICP, medical management may include positioning with elevated head of bed, hypertonic saline, the use of mannitol, and short periods of hyperventilation. A large multicenter study showed support for the use of 3% hypertonic saline as a first-line agent in the management of pediatric TBI compared to mannitol.4 The use of corticosteroids is not recommended to improve outcome or reduce ICP. If medical management fails, secondary methods are considered, including high-dose barbiturate therapy and decompressive craniectomy.

The main goal of the acute care hospitalization is prevention of secondary complications and secondary brain injury due to hypotension, hypoxia, or both. Once medically stable, a patient may be transitioned to the most appropriate rehabilitation setting.

Impairments may become more noticeable as the child recovers. All domains of functioning can be impacted, including motor, sensory, communication, cognition, and behavior. Rehabilitation is the next phase of recovery for patients with moderate to severe injury and even some with mild injury with ongoing symptoms. However, rehabilitation and recovery do not stop after discharge from rehabilitation centers. Cognitive and communication disorders are common and may persist – the more severe the injury, the worse the outcomes are across all cognitive domains.

Recovery is variable and may arrest at any stage of consciousness and cognition. Disorders of consciousness (DoC) are defined as a transient staging system to communicate these functional cognitive outcomes, including coma, unresponsive wakefulness syndrome (UWS), minimally conscious state (MCS), and confusional state. Patients in a coma lack a sleep wake cycle and eyes remain closed or cannot be aroused. In those who survive this phase, progression to an UWS usually happens within 2 to 4 weeks by the resumption of a sleep wake cycle and spontaneous opening of the eyes, but absence of environmental awareness. In this state, patients do not demonstrate language, comprehension of verbal/gestural cues, or purposeful movement. A retrospective study found the median time to recovery of consciousness to be 44 days, with recovery often signaled by reemergence of visual pursuit, reproducible command-following, and automatic movements.5

It is worth noting a controversy of the classification of permanent versus persistent categories within a vegetative state. Persistent is defined as one to three months, while permanent is defined as twelve months in traumatic cases. Patients who then advance into MCS exhibit environmental awareness, which is inconsistent but reproducible. Emergence from MCS is demonstrated by consistent command following and functional object use. This state is reliant concurrently on intact language and motor function. Individuals with moderate and severe TBI receiving inpatient rehabilitation have greater recovery of consciousness during acute care and absolute functional improvement by the end of inpatient rehabilitation.6 Longer time to recover from disorders of consciousness is predictive of worse prognosis after TBI, and some reports suggest that shortening the period of disordered consciousness may improve outcomes, partially to increase participation in rehabilitation treatment.

New studies suggest minimal sensory stimulation may be beneficial even in the ICU.7 The Coma Recovery Scale-Revised designed by Aspen neurobehavioral conference for adults is commonly used to help with differential diagnosis, prognostication, and further management. It is applicable to Ranchos Los Amigo levels of Cognitive Function scales 1 through 4. Cognitive recovery as measured by the revised Rancho Los Amigos Levels categorizes patients into 10 levels ranging from no response to purposeful and appropriate behavior with modified independence. Remaining in vegetative states longer than 90 days following anoxic/traumatic injury has increased mortality rate in pediatric cases.

Neuroendocrine dysfunction is common in moderate to severe head traumas. An estimated 30% of traumatic cases will have some element of dysfunction in the first year following the injury. However, acute monitoring in the ICU for hyponatremia due to the frequency of syndrome of inappropriate ADH (SIADH) or hypernatremia from central diabetes insipidus (DI) is difficult. Due to the use of hyperosmolar substances such as mannitol and 3% normal saline as well as some sedative medications, the cause of Na abnormalities can be multifactorial. When other factors have been ruled out, small vessel inflammatory response more often than mechanical impact to the pituitary gland has been proposed as the cause for pituitary dysfunction. Unfortunately, MRI imaging only detects 30% of pituitary injuries, as specificity of identifying radiologic details in the pituitary stalk is difficult.

In addition to either SIADH or Central DI, chronic dysfunction in growth hormone, gonadotropin and hypothyroidism have been reported in children with TBI. Growth hormone deficiency is predicted to have an incidence of 20% with symptoms of fatigue, decreased exercise tolerance, depression, osteoporosis, hyperlipidemia, and atherosclerosis. Gonadotropin deficiencies are predicted to occur in 10-15% of cases with symptoms of decreased libido, muscle mass, and strength. Hypothyroidism is predicted to occur in 5% of cases.

Specific secondary or associated conditions and complications

Secondary complications may include:

  • Cerebral edema
  • Elevated ICP
  • Seizures
  • Electrolyte disturbances
  • Hydrocephalus
  • Depression8
  • Sleep disturbances9
  • Dysphagia
  • Hearing loss
  • Vision impairment
  • Extremity weakness
  • Joint/muscle contractures
  • Scoliosis
  • Speech impairment
  • Cognitive impairment
  • Attention-deficit/hyperactivity disorder10
  • Paroxysmal autonomic instability
  • Urinary and bowel incontinence
  • Heterotopic ossification
  • Neuroendocrine disorders

Essentials of Assessment

History

A detailed history includes the inciting event, use of protective gear such as helmet or seatbelt, duration of loss of consciousness, initial GCS score, and associated injuries. History of the child’s baseline function, developmental history, previous history of TBI, and social history are also obtained.

Physical examination

The physical examination varies based on injury severity. A detailed neurological and musculoskeletal examination includes mental status, cranial nerves (with smell), strength, sensation, reflexes, muscle tone, cerebellar testing, fine motor testing, balance, and active and/or passive range of motion. The initial examination may be limited by the child’s tolerance and medical stability and must be followed serially.

Functional assessment

Functional assessment will vary based on severity and age. The Functional Status Scale can be useful in tracking outcome measures for critically injured children with TBI during their acute hospital stay.11 For a child admitted to acute rehabilitation, the WeeFIM and Gross Motor Function Measure may be utilized.12 An age-appropriate assessment of alertness and orientation should also be conducted and monitored as needed. The Child Orientation and Amnesia Test (COAT) may be used in children ages 3 to 15. For children older than 16, the Galveston Orientation and Amnesia Test (GOAT) is utilized.

Laboratory studies

Electrolytes to evaluate for hyponatremia or hypernatremia and other laboratory abnormalities associated with dysfunction of the hypothalamic pituitary axis should be monitored. Symptoms may include polyuria, polydipsia, or decreased urine output. Other symptoms of axis dysfunction include fatigue, changes in mental status, and in the chronic phase, growth failure, precocious or delayed puberty, amenorrhea, and short stature.

Imaging

A computed tomography (CT) scan is initially performed in the ED to assess for bleeding or swelling. MRI may be obtained later to further assess injury to deeper structures and to evaluate for DAI. X-rays of the skull, neck, and limbs may be obtained to rule out additional injuries as indicated by physical examination.  Hematologic parameters, but not hypertension, are useful in predicting the presence of abnormal cranial CT findings in children with TBI in association with injury severity.13

In terms of complications such as heterotopic ossification (HO), a triple-phase bone scan is indicated since early HO does not appear on plain films.

Supplemental assessment tools

An electroencephalogram (EEG) may be obtained to evaluate for seizures. Seizures are classified into immediate, early, and late posttraumatic seizures. Incidence of posttraumatic seizures is higher in children than adults. Depending on severity and presentation, additional studies may be utilized, including assessment of hearing, vision, and swallow function.

Outcomes

General Outcome

  • Children younger than 5 years of age with TBI have a greater mortality rate.
  • Longer length of coma, early coagulopathy, and subarachnoid hemorrhage are negative predictors of outcome.
  • Best motor response score on the GCS is the best acute predictor of outcome.
  • Longer duration of posttraumatic amnesia (PTA) and total duration of impaired consciousness have worse outcomes.
  • Survival rates: 63% of children in UWS, 65% of immobile, and 81% of mobile MCS children survived 8 years post injury.

Functional Outcome

  • In children with severe TBI and unconscious state lasting longer than 6 hours, approximately 75% regained physical independence within one year of injury.
  • Delay in initiation of comprehensive rehabilitation programs results in worse functional outcomes and diminished recovery and rehab efficiency in children with severe TBI.
  • Time to follow commands may be the best predictor of general functional outcome.
  • Volume and number of lesions on MRI correlate with severity and functional outcome.
  • Pupillary abnormality is a negative predictor of motor outcome.

Cognitive Outcome

  • Children with non-accidental brain injury have worse recovery based on the Glasgow Outcome Scale and have worse cognitive outcomes.
  • Age, time since injury to rehabilitation admission, and admission WeeFIM Cognitive DFQ (age-adjusted percentiles for WeeFIM scores) are significant predictors of cognitive functioning at discharge from inpatient rehabilitation.14

Environmental Management

As a patient evolves following moderate to severe TBI, he or she may go through a stage of confusion and agitation. During the agitation phase, environmental modifications may be necessary. This includes decreasing external stimuli and reducing demands on the patient by:

  • Reducing noise from TV and monitors if possible
  • Grouping vitals, medication administration, and cares to reduce interruptions
  • Limiting the number of visitors
  • Allowing for down-time
  • Providing frequent orientation
  • Identifying and treating pain

Social role and social support system

Following TBI, changes may be noted in a child’s emotional, behavioral, and social interactions. The most persistent negative impacts of TBI in children are behavioral changes and problems in adaptive functioning. Patient and family support is important through all phases after TBI. Specifically, family-level factors such as caregiver distress or depression and deterioration of family functioning as well as home environment factors such as parental responsiveness and negativity are critical social-environmental influences on outcomes for children following a TBI. In severe TBI, socioeconomic disadvantages have been associated with poor cognitive and academic outcomes. Social workers, psychologists, child life specialists, and educators may be necessary for coping, adjustment, and reintegration into society and school. Ongoing community support groups may be available as well.

Professional issues

If abuse is suspected, the child should be further evaluated by the medical team for signs of non-accidental trauma. Please see the PM&R Knowledge NOW topic on Physical Abuse (Non-Accidental Trauma) for further details regarding evaluation and reporting requirements.

Rehabilitation Management and Treatments

At different disease stages

New onset/acute

In the acute care setting, treatment will focus on the management of ICP and other injuries. Prevention of secondary complications of immobility such as contractures and skin breakdown should also occur. Acute care physical and occupational therapists can fabricate temporary splints for the extremities as needed to maintain range of motion. Medication management may be necessary for treatment of paroxysmal autonomic instability, electrolyte disturbances, seizures and spasticity or dystonia.

Subacute

The subacute management of TBI includes ongoing monitoring of range of motion and splinting as needed, management of spasticity or dystonia as it evolves, constipation and incontinence management, monitoring of nutritional status with appropriate assessment and supplementation, and assessment and treatment of swallow function as alertness improves.

Therapy services include physical therapy, occupational therapy, speech therapy, and neuropsychological testing. The goals of therapy include preventing secondary complications, teaching strategies to compensate for impaired or lost function, optimizing the use of abilities as they return, and educating and supporting the family. In general, medical interventions center around improving delivery of rehabilitation by treating complications such as spasticity, dystonia, and arousal. The need for pediatric specific rehabilitation is determined by looking at general outcomes, family behavior, cognitive, speech, language, swallow, gross and fine motor skills, neuropsychology evaluations, and school reentry. When a rehab unit’s focus is pediatrics, the neuropsychology and cognitive outcomes are better. Also, both pediatric and CARF accredited rehabilitation units are better in achieving social reintegration and school reentry. During rehabilitation, behavioral psychology services may be necessary if the patient is agitated and may also be needed for coping and adjustment. A special educator should work with the team to facilitate school re-entry and creation of an Individualized Education Plan (IEP) as needed.

Chronic/stable

Impairments in all domains may continue long-term. The goal will be to decrease the effect of a chronic disability on growth and development. Following TBI, significant recovery may be seen over the first year and may continue at a slower pace over time with a recovery plateau. Children with severe TBI may demonstrate a secondary acceleration of worsening of symptoms around 24-36 weeks following the recovery plateau. Studies have shown that children with all severities of TBI do not fully recover to preinjury level of functioning even 3 years after injury. As a result, there is a need for longitudinal reassessment beyond 1-year postinjury.15 Ongoing monitoring of impairments and impact on the child’s functioning will be important. Splinting, therapy, and educational needs may vary over time.

Children who are younger at the time of injury may not show the true extent of their cognitive deficits until they reach school age and cognitive demands are increased. For adolescents and young adults, recommendations for a driving evaluation and vocational rehabilitation services may be appropriate.

Coordination of care

An interdisciplinary approach is required for individuals requiring inpatient and outpatient rehabilitation services.

Patient & family education

Patient education at an appropriate developmental and cognitive level is important to assist with coping and adjustment. Depending on injury severity, this may occur in the acute phase, subacute and/or chronic phase. Family education starts in the acute phase and is carried throughout all phases. Family-based problem-solving therapy has been shown to improve cognitive and behavioral outcomes in children with acquired brain injury.16 Education should be adjusted as the deficiencies become more apparent and require changing interventions. Important topics will include prevention of repeat injury, contact sports guidelines, transition to home and school, legal resources, educational resources, advocacy, and transition to adulthood.

Emerging/unique interventions

Non-pharmacologic treatments of disorders of consciousness include sensory or nervous system stimulation. Oftentimes, patients remain in ICUs with stimuli not conducive to improving arousal and awareness: lights off, noxious blood draws, excessive conversation, and limited interaction. Minimal Sensory stimulation may develop into a new frontier of therapy beginning as early as the ICU for patients in vegetative and minimally conscious states. While several protocols are being developed with an assortment of sensory inputs- requiring all five sensory inputs to be used at one time within a specific therapy session, current research suggests a three-week improvement in disorders of consciousness. The proposed benefits are based on the belief that the brain undergoes atrophy when deprived of stimulus. With stimulus, an increase in the reticular activation system increases awareness and arousal. Some imaging findings demonstrate an increase in brain activity when familiar tactile, olfactory, and visual stimuli are provided to patients. These new therapies are decreasing length of stay in ICU and duration of depressed consciousness. The limitation of studies is the absence of control groups making it difficult to differentiate results from a natural recovery.

Various other electrophysiologic stimulations are under investigation including non-invasive median nerve, dorsal column, transcranial direct current, magnetic stimulation, and deep brain stimulation. The proposed mechanism is to alter circuit-level neuronal signaling or stimulate cortical activation in aspects of the brain like the reticular activating system and basal ganglia. Finally, regenerative medicine has used fetal brain cells and liver cells to provide trophic factors and direct cell-to-cell communications helping to integrate new neuronal circuits. However, evidence for cell transplantation in children is limited to two case series, which showed significant improvement after transplantation with fetal brain cells and liver hematopoietic cells. Follow-up MRI brain imaging demonstrates reversal of early brain atrophy 6-months post-transplant and recovery of conscious state based on Glasgow Outcome Scale.

Measurement of patient outcomes

Tools for measurement of outcomes include

  • Cognitive and Linguistics Scale (CALS): assess cognitive-linguistic skills and recovery during inpatient rehabilitation17
  • Child Behavior Checklist: caregiver report form defining child behavior
  • Child Health Questionnaire: internationally recognized scale to evaluate quality of life in children
  • Coma Recovery Scale- Revised (JFK Coma recovery scale): assess disorder of consciousness
  • Coma/Near Coma scale: developed to measure neurobehavioral changes in sustained TBI
  • Disorders of Consciousness Scale: tool used to detect subtle changes in neurobehavioral functioning during severe traumatic brain injury.
  • Functional Independence Measure for Children (WeeFIM): pediatric version of Functional Independent Measures: method for evaluating functional and cognitive outcomes
  • Functional Status Scale (FSS): assess pediatric functional impairment outcomes in severe TBI during acute hospital phase
  • Glasgow Coma Outcome Score: objective scale of patients with brain injury, in groups of cases for research purposes
  • Gross Motor Function Measure: tool to measure gross motor function over time, specifically designed for cerebral palsy population but has been adapted for TBI.
  • Pediatric Evaluation of Disability Inventory (PEDI): samples key functional capability and performance in children from 6 months to 7.5 years
  • Sensory Modality Assessment Rehabilitation Technique: valid and reliable assessment for vegetative state and minimally conscious state
  • Vineland Adaptive Behavior Scale: instrument for evaluating intellectual and developing disabilities
  • Western Neuro Sensory Stimulation Profile: a tool for assessing slow-to-recover head-injured patients
  • Post-Acute Level of Consciousness scale: for assessment of young patients in vegetative and minimally conscious state18

Cutting Edge/Emerging and Unique Concepts and Practice

Prognosis for recovery after TBI is predictably worse with longer time spent in a coma, vegetative or minimally conscious state. This data could possibly be due to the limited participation in therapy. Thus, shortening the period of disordered consciousness may improve outcomes, partly by improving participation in rehabilitation treatment.

In children more so than adults, pharmacological agents are promising to help shorten the time in a disordered consciousness state. Amantadine is the most well-studied medication for disorders of consciousness in the pediatric population. It has been associated with a greater increase in Rancho score, but no difference in length of hospital stay or length of post-traumatic amnesia.  There have been limited studies on dopamine agonists but are thought to increase attention and behavioral alertness. It has been proposed that GABA agonists, while thought to depress CNS function normally, may have useful paradoxical effects in traumatic brain injuries by inhibiting inhibitory GABAergic neurons that cause the condition of GABA impairment after TBI. These limited studies have shown improvement in Coma Near Coma scale and Ranchos Los Amigos.19

Non-invasive brain stimulation or (NIBS) has shown some promise in multiple points along acquired TBI pediatric cases. More classically investigated in neonatal cerebral palsy, it is beginning to be applied due to the similar pathophysiology between the two disorders. The principle relies upon an immature brain of a neonate/child less than two years old without fully mature myelination that can undergo neuronal migration, myelin formation, and dendritic/axonal remodeling. While several types of NIBS have been tested, repetitive transcranial magnetic stimulation (rTMS) using a parallel field coil has shown limited significance in predicting functional motor deficits and decreasing posttraumatic seizures. It is being investigated in altering behavioral/cognitive functions. Recent evidence suggests minimal risk of severe adverse effects like seizure, hearing damage, or pain in school-aged children. However, further investigation on the efficacy and safety of Transcranial Direct Current Stimulation (tDCS) and rTMS in children with standardized cohorts and methodology is needed to assess the impact on neurocognitive development.20,21

Recent studies are investigating biomarkers for predictability in outcomes. S100B, neuron specific enolase (NSE), and myelin basic protein all show promise in predicting severity of TBI when comparing the significantly increased concentration over time from initial presentation to rehabilitation setting. S100B is the most studied serum biomarker for both structural and functional brain damage in TBI and is proportional to the degree of brain damage. Sequential measurements of S100B may help diagnose pediatric TBI, assess brain damage, and predict clinical outcomes in pediatric patients when associated with the assessment of patients. The isolated measurement of S100B is not recommended. Increased sensitivity and negative predictive value can be achieved by evaluating S100B in association with CT. NSE has reasonable sensitivity for the diagnosis of moderate and severe TBI, but not as effective as S100B. Several studies have suggested an important role of GFAP as a single time point measure in the first evaluation of TBI. The different biomarkers vary mostly with length of time to peak and length of time to detection. More large-scale studies will need to be performed to investigate the biomarker use in predicting functional outcomes of TBI and support the use in clinical practice.22

Diffusion-weighted imaging (DWI) has been well associated with outcomes of diffuse axonal injury and is currently often used in clinical practice. This involves mapping of T2-weighted images to identify markers like lesions in multiple zones and lesion burden. As a result, there is potential for DWI use as a predictive value for long-term functional outcomes in pediatric patients.

Gaps in the Evidence-Based Knowledge

Research behind neuropharmacology and ability to predict specific long-term outcomes remain limited, especially in the pediatric population.

Definitive assessment tools and/or inter assessment reliability of disorders of consciousness continue to be discussed across the field. Research behind therapeutic interventions is progressing but limited due to natural progression of recovery in comparison to new interventions.

The use of assistive technology and augmentative and alternative communication can assist the cognitive-communication function following TBI, but more studies need to be completed.23 Virtual reality therapies have been increasingly adopted for brain injury rehabilitation. In a study with patients who had severe traumatic brain injury and upper limb paresis subjected to VR, there was documented volumetric increase of gray matter in multiple regions of the left brain hemisphere. However, future research is required to assess the effectiveness of virtual reality on psychosocial health in pediatric patients.24

References

  1. Centers for Disease Control and Prevention (2022). Surveillance Report of Traumatic Brain Injury-related Deaths by Age Group, Sex, and Mechanism of Injury—United States, 2018 and 2019. Centers for Disease Control and Prevention, U.S. Department of Health and Human Services.
  2. Centers for Disease Control and Prevention (2019). Surveillance Report of Traumatic Brain Injury-related Emergency Department Visits, Hospitalizations, and Deaths—United States, 2014. Centers for Disease Control and Prevention, U.S. Department of Health and Human Services.
  3. Centers for Disease Control and Prevention (2021). Surveillance Report of Traumatic Brain Injury-related Hospitalizations and Deaths by Age Group, Sex, and Mechanism of Injury—United States, 2016 and 2017. Centers for Disease Control and Prevention, U.S. Department of Health and Human Services.
  4. Kochanek PM, Adelson PD, Rosario BL, et al. Comparison of Intracranial Pressure Measurements Before and After Hypertonic Saline or Mannitol Treatment in Children With Severe Traumatic Brain Injury. JAMA Network Open. 2022;5(3):e220891. doi:10.1001/jamanetworkopen.2022.0891
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  7. Moattari M, Shirazi FA, Sharifi N, Zareh N. Effects of a sensory stimulation by nurses and families on level of cognitive function, and basic cognitive sensory recovery of comatose patients with severe traumatic brain injury:a randomized control trial.(2016) Trauma Monthly, 21(4)
  8. Durish CL, Pereverseff RS, Yeates KO. Depression and Depressive Symptoms in Pediatric Traumatic Brain Injury: A Scoping Review. J Head Trauma Rehabil. 2018;33(3):E18-E30. doi:10.1097/HTR.0000000000000343
  9. Yeo V, Phillips NL, Bogdanov S, et al. The persistence of sleep disturbance and its correlates in children with moderate to severe traumatic brain injury: A longitudinal study. Sleep Med. 2021;81:387-393. doi:10.1016/j.sleep.2021.03.013
  10. Asarnow RF, Newman N, Weiss RE, Su E. Association of Attention-Deficit/Hyperactivity Disorder Diagnoses With Pediatric Traumatic Brain Injury: A Meta-analysis. JAMA Pediatrics. 2021;175(10):1009-1016. doi:10.1001/jamapediatrics.2021.2033
  11. Bennett TD, Dixon RR, Kartchner C, et al. Functional status scale in children with traumatic brain injury: a prospective cohort study. Pediatr Crit Care Med. 2016;17(12):1147-1156. doi:10.1097/PCC.0000000000000934
  12. Linder-Lucht M, Othmer V, Walther M, et al. Validation of the Gross Motor Function Measure for use in children and adolescents with traumatic brain injury. Pediatrics. 2007; 120(4):880-886.
  13. Eser P, Corabay S, Ozmarasali AI, Ocakoglu G, Taskapilioglu MO. The association between hematologic parameters and intracranial injuries in pediatric patients with traumatic brain injury. Brain Injury. 2022;36(6):740-749. doi:10.1080/02699052.2022.2077442
  14. Watson WD, Suskauer SJ, Askin G, et al. Cognitive Recovery During Inpatient Rehabilitation Following Pediatric Traumatic Brain Injury: A Pediatric Brain Injury Consortium Study. The Journal of Head Trauma Rehabilitation. 2021;36(4):253. doi:10.1097/HTR.0000000000000650
  15. Keenan HT, Clark AE, Holubkov R, Cox CS Jr, Ewing-Cobbs L. Trajectories of Children’s Executive Function After Traumatic Brain Injury. JAMA Network Open. 2021;4(3):e212624. doi:10.1001/jamanetworkopen.2021.2624
  16. Wade, Shari L, Eloise E Kaizar et al. Online Family Problem-solving Treatment for Pediatric Traumatic Brain Injury. Pediatrics (2018) 142
  17. Blackwell LS, Shishido Y, Howarth R. Cognitive recovery of children and adolescents with moderate to severe TBI during inpatient rehabilitation. Disabil Rehabil. 2022;44(7):1035-1041. doi:10.1080/09638288.2020.1788176
  18. Alvarez, Gabrielle, Stacy J Suskauer, Beth Slomine. Clinical Features of Disorders of Consciousness in Young Children. Archives of Physical Medicine and Rehabilitation (2019); 100: 687-94
  19. Evanson NK, Paulson AL, Kurowski BG. A Narrative Review of Pharmacologic and Non-pharmacologic Interventions for Disorders of Consciousness Following Brain Injury in the Pediatric Population. Curr Phys Med Rehabil Rep. 2016;4(1):56-70.
  20. Chung, M. G. Warren D. Lo. Noninvasive Brain stimulation: the potential for use in rehabilitation of pediatric acquired brain Injury. Archives of Physical Medicine and Rehabilitation, ACRM; 2015; 96 (4 Suppl 2); S129-37
  21. Di Sarno L, Curatola A, Cammisa I, et al. Non-pharmacologic approaches to neurological stimulation in patients with severe brain injuries: a systematic review. Eur Rev Med Pharmacol Sci. 2022;26(18):6856-6870. doi:10.26355/eurrev_202209_29789
  22. Marzano LAS, Batista JPT, de Abreu Arruda M, et al. Traumatic brain injury biomarkers in pediatric patients: a systematic review. Neurosurg Rev. 2022;45(1):167-197. doi:10.1007/s10143-021-01588-0
  23. Brunner M, Hemsley B, Togher L, Palmer S. Technology and its role in rehabilitation for people with cognitive-communication disability following a traumatic brain injury (TBI). Brain Injury. 2017;31(8):1028-1043. doi:10.1080/02699052.2017.1292429
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Haydel MJ, Weisbrod LJ, Saeed W. Pediatric Head Trauma. In: StatPearls. StatPearls Publishing; 2022. Accessed March 20, 2023. http://www.ncbi.nlm.nih.gov/books/NBK537029/

Kochanek PM, Tasker RC, Carney N, et al. Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Foundation Guidelines. Pediatric Critical Care Medicine. 2019;20(3S):S1. doi:10.1097/PCC.0000000000001735

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Original Version of the Topic

Melissa Trovato, MD. Pediatric Traumatic Brain Injury. 11/16/2011

Previous Revision(s) of the Topic

Nancy Yeh, MD, Melissa Trovato, MD. Pediatric Traumatic Brain Injury. 08/22/2016

Didem Inanoglu, MD, Simra Javaid, DO, Austin Henke, DO. Pediatric Traumatic Brain Injury. 4/10/2020

Author Disclosure

Vincent Thieu, MD
Ipsen Honorarium, Trainer for Dysport injection

Didem Inanoglu, MD
Nothing to Disclose

Simra Javaid, DO
Nothing to Disclose