Author(s): Matthew McLaughlin, MD, Suzan Lisenby, BA, and Sumita Sharma, BS
Originally published: April 5, 2017 Last updated: April 5, 2017
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1. DISEASE/DISORDERS:

Definition

Mild traumatic brain injury (TBI) is defined as a disruption of brain function that can be characterized by: any loss of consciousness less than 30 minutes, loss of memory immediately prior to or after the injury not exceeding 24 hours, any altered mental status at the time of the event, or focal neurologic changes. However, in order to be characterized as a concussion, after 30 minutes the Glasgow Coma Scale (GCS) must be within 13-15 and structural imaging must be normal.1 Moderate brain injury requires a GCS of 9-12 with LOC being less than 6 hours.

Etiology

The most common causes are motor vehicle collisions (MVCs), falls, sports, recreational activities, and assault. Children with a history of attention deficit hyperactivity disorder (ADHD) are at a greater risk of sustaining a TBI.2

Epidemiology including risk factors and primary prevention

In 2010, the CDC estimated that approximately 2.5 million emergency department visits, hospitalizations, or deaths were associated with TBI, 75-90% of which are classified as a mild TBI.3

The CDC also noted that 50% of mild TBIs occur in those less than 24 years of age with a higher incidence in patients aged 0-4 and 15-19 years. An estimated 511,000 children sustain a TBI annually. There are approximately 475,000 emergency department (ED) visits, 35000 hospitalizations and 2000 deaths. Causes vary by age but are commonly due to falls, being struck by or against an object and MVCs. The incidence has increased in high school age athletes possibly due to more public education and rigorous concussion screening guidelines implemented in school districts.

Patho-anatomy/physiology

Mild to moderate TBI results from a mechanical insult generated by acceleration–deceleration and rotational forces. This subsequently leads to diffuse axonal injury commonly affects the corpus callosum, parasagittal white matter, and midbrain and results in the release of excitatory neurotransmitters that lead to a level of hyperalertness. The excess influx of calcium causes mitochondrial dysfunction and subsequent ATP depletion leaving the cell especially vulnerable to injury during times of brain healing.1,3-5

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

Following mild TBI symptoms can manifest immediately or up to 72 hours following injury and symptoms can be categorized into the following:1

  1. Physical: headaches, nausea, vomiting, fatigue, vestibular disturbance, blurry vision, photosensitivity
  2. Cognitive: difficulty thinking clearly, concentrating, or remembering new information,  feeling slowed down, difficult
  3. Emotional: irritability, sadness, increase sensitivity, nervousness, anxiety not explained by other psychological cause
  4. Sleep: increased or decreased amount of sleep, difficulty falling asleep

Certain symptoms to consider that may warrant further evaluation include: extremity weakness or numbness, differing pupil size, worsening headache, repetitive vomiting, acute onset confusion, increased irritability, decreased level of consciousness, or seizures.

Specific secondary or associated conditions and complications

Secondary conditions can be divided into two different categories:

  • Post-concussion syndrome can occur when symptoms last for great than 3 months.6 Symptoms range from headaches to mood or behavioral changes to difficulty with cognitive tasks.
  • Multiple mild TBIs or second impact syndrome patients may experience more severe deficits than patients with post-concussion syndrome, such as cumulative neurologic compromise, elevated intracranial pressure, subsequent brain herniation or death, if severe enough. Second impact syndrome is due to the metabolic cascade occurring after brain injury.5

2. ESSENTIALS of ASSESSMENT

History

A detailed history including inciting event, use of protective gear such as helmet or use of seatbelt, duration of loss of consciousness, initial GCS score, associated injuries. History of the child’s baseline function should also be obtained. If any red flags are observed, then the patient should immediately be evaluated in the ED.

Physical examination

The physical exam varies based on injury severity. Most importantly, a thorough and detailed neurological examination should be completed

  1. focused neurologic examination, including a Mental Status Examination (MSE), cranial nerve testing, extremity tone testing, deep tendon reflexes, strength, sensation, and postural stability (Romberg’s Test, dynamic standing)
  2. A focused vision examination including gross acuity, eye movement, binocular function and visual fields/attention testing
  3. A focused musculoskeletal examination of the head and neck testing for muscle strength, muscle tone, reflexes, passive and/or active range of motion.

Functional assessment

The International Conference on Computational Science in Zurich in 2008 determined that cognitive testing is essential for diagnosis and management. A commonly used and well studied computerized neurocognitive assessment is Immediate Post-Concussion Assessment and Cognitive Test (ImPACT). This provides scores for 4 areas: verbal memory, visual memory, reaction time, visuomotor speed. Demographic information, history data, current concussion details and somatic and cognitive symptoms are also taken into account. ImPACT norms are available for ages 10 and above. There is also an adapted version for ages 5-12 years of age, termed Pediatric ImPACT. While useful and easily accessible, there is some concern about the use in patients in age groups for which the test has not been as well studied, sensitivity and validity of the test, interpretation in those with pre-existing cognitive issues (i.e. ADHD, learning disability, psychiatric diagnoses), and its use in non-sports related concussion.1

Laboratory studies

Currently, mild to moderate TBI is a clinical diagnosis. There are no laboratory studies or markers utilized in the diagnosis of Mild TBI, but researchers are working to discover markers that may be useful in the future for diagnosis and prognosis.

Imaging

Imaging may not be performed in all cases of mild TBI. A non-contrast CT scan should be used to evaluate cases of loss of consciousness, red flags, or if there are any abnormalities on neurologic exam to assess for bleeding or swelling. MRI may be performed if patient is not recovering at an anticipated rate to visualize any axonal injury or underlying pathologies that may be contributing to the patient symptoms. Currently, there is no evidence about the utility of other neuroimaging techniques such as functional MRI or PET scan. These methodologies, along with fiber tractography, are being explored as ways to develop more sensitive imaging tests that can be used clinically.7

Supplemental assessment tools

There are various supplemental tools that have been validated for the assessment of mild TBI. Two tools that can be used on the sidelines at sporting events to assess for concussion include the Sport Concussion Assessment Tool (SCAT-3) for ages 13 and above and the Child SCAT-3 for ages 5 to 12. These measure the patient’s memory, orientation, and concentration (reference: page 300 – acute evaluation) using a checklist and the assessment of cognitive performance. Physicians can use the results of these assessments to guide their management.

Early predictions of outcomes

The pediatric population is subject to prolonged recovery periods compared to adults because of the following:

  • Larger head-to-body ratios
  • Reduced neck and shoulder musculature, leading to increased force transmission to the head
  • Large subarachnoid space within brain
  • Decreased myelination within brain

However, despite this, youth often have a full and rapid recovery. Majority of patients who have a mild TBI will recover within 2 weeks. If symptoms last >3 months for any group, it is important to evaluate for other contributing conditions that may be prolonging the recovery or present as post-concussive syndrome.1

Other factors that predict a prolonged recovery include: previous concussions, female gender, mood disturbances (premorbid anxiety, depression, or PTSD), dizziness present at time of injury, retrograde amnesia, mental status change >5 minutes, poorer scores on ImPACT testing.1

Dizziness at 2 weeks post-injury is the single most predictive symptom for post-concussive syndrome.8

Social role and social support system

Following TBI, changes may be noted in a child’s emotional, behavioral and social interactions. Moreover, mild to moderate TBI may often lack a single treatment, it can sometimes be challenging for the patient and parents to understand. Patient and family support is important through all phases after TBI. Social workers, psychologists and educators may be necessary for coping and adjustment. 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 Knowledge NOW submission on Child Abuse for further details regarding evaluation and reporting requirements.

C. REHABILITATION MANAGEMENT and TREATMENTS

At different disease stages

Initial Recovery Phase Management

  • Rest for several days to 1 week
    • Full or relative physical and cognitive rest is thought to promote a quicker recovery if the brain is utilizing more energy to focus on healing as opposed to physical or cognitive tasks.9
  • Abortive headache medication (i.e. NSAID) may also be used
  • If sleep disturbances occur, melatonin may also be used
  • Monitor for mood changes
  • Neurocognitive testing (i.e. computer-based ImPACT testing)

Return to School

  • After acute symptoms improve, families and school faculty should facilitate school re-entry with creation of an Individualized Education Plan (IEP).
    • Some children may be able to resume full days of school with normal workload while others may start at half days with workload reduction and less time restrictions to complete assignments.1
  • Limit screen time due to risk of triggering vestibular symptoms

Return to Activity or Sport

  • Prior to return to play, the patient should:
    • Not to return to play on the day of injury,
    • Have normal physical examination,
    • Self-report being free of symptoms or at baseline,
    • Have returned to school with normal function, and
    • Have neurocognitive testing results that return to baseline (if testing was performed)

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, as able. Children who are younger at the time of injury may not show the true nature 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

For children with a mild injury a coordinated approach between involved care providers may provide the appropriate level of required services; however, an interdisciplinary approach is required for individuals requiring treatment for complex concussion where multiple providers may be providing care..

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 should be started in the acute phase and carried throughout all phases. Education should be adjusted as the deficiencies become more apparent and the interventions require changing. Parents should be educated on important topics including: prevention of repeat injury, contact sport guidelines, transition to home and school, legal resources, education resources, advocacy, transition to adulthood, and symptoms to look out for that would warrant attention in the ED.

Emerging/unique Interventions

NA

D. CUTTING EDGE/EMERGING and UNIQUE CONCEPTS and PRACTICE

Cutting edge concepts and practice

States are beginning to pass laws regarding return to play following a concussion. Washington was the first state to implement a sports concussion safety law in 2009, which was known as the Zackery Lystedt Law. Since then, many states have followed suit. The law requires school districts to create specific concussion guidelines and educational programs. It also requires guardian and athlete signed consent, immediate removal of youth from practice or games if suspected to have a concussion, and written clearance by a physician before return to play (http://search.proquest.com.proxy.library.umkc.edu/docview/1642451104?pq-origsite=summon&accountid=14589). Screening tests to evaluate for suspected concussions may include the Post Concussion Symptom Checklist, the Sideline mental status test (SAC), and the Sport Concussion Assessment Tool-3 (SCAT-3).

E. GAPS in the EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

There is limited evidence to support which neuropharmacological agents are best for mild to moderate TBI recovery and whether biomarkers are useful in the evaluation of TBIs. At this time, biomarkers play only a limited role in the evaluation and treatment of mild to moderate TBIs. However, emerging research is working to introduce new blood tests that could be used in clinical practice. For example, S-100β may begin to be utilized across emergency departments in the future when deciding whether or not to obtain a head CT for the assessment of concussion. Optimal concussion management in kids, including return to sports, and extent and duration of cognitive rest needs further evaluation. Information on mechanisms underlying recovery and ability to predict specific long term outcomes is limited.

References

  1. Marcantuono N, Spohn J. Concussion Management and Rehabilitation. In: Alexander M, Matthews D, eds. Pediatric Rehabilitation: Principles and Practices. 5th ed. New York, NY: Demos Medical; 2015:298-306.
  2. Gerring JP, Brady KD, Chen A, et al. Premorbid prevalence of ADHD and development of secondary ADHD after closed head injury. Journal of the American Academy of Child and Adolescent Psychiatry. Jun 1998;37(6):647-654.
  3. Frieden T, Houry D, Baldwin G. Report to Congress: Traumatic brain injury in the United States: epidemiology and rehabilitation. Center for Disease Control; January 2016.
  4. Giza CC, Hovda DA. The Neurometabolic Cascade of Concussion. Journal of athletic training. Sep 2001;36(3):228-235.
  5. Signoretti S, Lazzarino G, Tavazzi B, Vagnozzi R. The pathophysiology of concussion. PM & R : the journal of injury, function, and rehabilitation. Oct 2011;3(10 Suppl 2):S359-368.
  6. Bigler ED. Neuropsychology and clinical neuroscience of persistent post-concussive syndrome. Journal of the International Neuropsychological Society : JINS. Jan 2008;14(1):1-22.
  7. Shin SS, Pathak S, Presson N, et al. Detection of white matter injury in concussion using high-definition fiber tractography. Progress in neurological surgery. 2014;28:86-93.
  8. Yang CC, Hua MS, Tu YK, Huang SJ. Early clinical characteristics of patients with persistent post-concussion symptoms: a prospective study. Brain injury. Apr 2009;23(4):299-306.
  9. Brown NJ, Mannix RC, O’Brien MJ, Gostine D, Collins MW, Meehan WP, 3rd. Effect of cognitive activity level on duration of post-concussion symptoms. Pediatrics. Feb 2014;133(2):e299-304.

Original Version of the Topic

Published in 2017

Author Disclosure

Matthew McLaughlin, MD
Nothing to Disclose

Suzan Lisenby, BA
Nothing to Disclose

Sumita Sharma, BS
Nothing to Disclose