Brain Injury

Brain injury is a broad term encompassing acquired insults to the brain that cause structural changes. Acquired brain injury may be traumatic (caused by an external force) or nontraumatic (caused by an internal force). Examples of traumatic brain injury (TBI) include injuries caused by falls, child abuse, or motor vehicle accidents. Examples of nontraumatic brain injury include injuries caused by stroke, infection, or hypoxia/anoxia. Traumatic head injury is covered in the section on Trauma in the Pediatric Emergency Medicine rotation guide. For more information on neonatal brain injury, see Neurologic Conditions in the Neonatal Care guide.

In this section, we cover the following pediatric brain injuries:

• Postconcussion Syndrome

• Hypoxic-Ischemic Brain Injury

Postconcussion Syndrome

The Centers for Disease Control and Prevention (CDC) describes concussion as a traumatic brain injury caused by a bump, blow, or jolt to the head or by a hit to the body that causes the head and brain to move rapidly back and forth, resulting in chemical changes and sometimes stretching and damaging cells in the brain. Postconcussion syndrome is the persistence of concussion symptoms beyond the normal period of recovery (typically, >4 weeks postinjury). However, the syndrome is a controversial entity because many of the symptoms are vague and present in the general population. An estimated one-third of children with concussion demonstrate postconcussive syndrome.

It is not uncommon for children who have had concussions to continue to experience neurologic symptoms after the expected period of recovery from the injury. The time frame for recovery from concussion is not well-defined, but the symptoms of concussions typically resolve within 2 weeks. Sports-related concussion tends to be associated with a more favorable natural history and shorter recovery time than does concussion caused by other mechanisms. For more on the management of acute concussion in children, see the section on Trauma in the Pediatric Emergency Medicine rotation guide.

Symptoms

Postconcussion syndrome refers to a constellation of the following symptoms occurring after the expected time frame for recovery of acute concussion:

• headache

• fatigue

• sleep disturbance

• vertigo

• depression

• irritability

• difficulty concentrating

• exercise intolerance

A thorough preconcussion history is essential to determine whether the symptoms noted in the particular patient were present before the trauma. In some cases, symptoms are an exacerbation of a preexisting condition such as attention deficit-hyperactivity disorder (ADHD), learning disabilities, depression, anxiety, and migraines. Postconcussion syndrome may also be associated with “unmasked” symptoms for which there was a preexisting risk factor (e.g., positive family history of migraine and postconcussion headaches). Persons experiencing multiple concussions may also be more prone to this syndrome. Cervical spine injuries (e.g., whiplash) can occur with concussion and contribute to symptoms including headache and vertigo.

Vestibular dysfunction is common after concussion and may lead to vertigo and imbalance. Eye movement abnormalities such as nystagmus provide evidence that the vestibular system has been affected. Vaguer complaints such as “dizziness” may have unclear implications. The vestibular system is a complex system involving the cortex, brain stem, cerebellum, inner ear, ocular system, and postural muscles. The vestibular system integrates information from head, eye, and limb movements to maintain balance and visual stability. Some specialists recommend vestibular rehabilitation to reduce symptoms of vertigo and improve balance after a concussion. Vestibular rehabilitation is an exercise-based treatment program that focuses on head movements with the goal of enhancing gaze stability, enhancing postural stability, and improving vertigo.

Oculomotor dysfunction is also common after concussion. Symptoms may include double or blurry vision, difficulty reading or using a computer, and headaches. Examination may reveal problems with saccades, smooth pursuits, vergence, and accommodation. Outpatient ophthalmology and/or neurology referral should be strongly considered if abnormalities in eye position or movement are identified. Acquired ocular malalignment should always be investigated comprehensively. The following oculomotor functions should be examined, and the presence or absence of abnormalities documented:

• saccades: the ability to quickly and accurately shift gaze from one target to the next

• smooth pursuits: tracking movements to keep a moving target centered on the fovea

• vergence: turning of the eyes toward or away from each other to maintain single binocular vision

• accommodation: the eye’s ability to adjust focal length and maintain focus at different distances

Evaluation

At the time of injury, clinicians should carefully evaluate the spine, neck musculature, balance, and eye movements. It is important to evaluate for cervical tenderness and muscle tightness on physical examination. During the postconcussive period, clinicians should consult initial physician notes and diagnostic test results. A thorough preconcussion history is essential.

Management

Treatment of postconcussion syndrome is individualized to the patient’s specific symptoms and can include the following:

• Education and reassurance: Often the most appropriate treatment is to educate and reassure patients that longitudinal studies show that symptoms will improve. Most symptoms do resolve with time and symptomatic support. To the extent that postconcussive symptoms may be amplified by anxiety, reassurance after a comprehensive neurologic examination may promote recovery.

• Other treatments may involve rest until symptoms improve, school intervention, neurocognitive rehabilitation, vestibular therapy, psychological training for coping techniques, and antidepressant medications. Of note, too much “brain rest” may lead to physical deconditioning and reduced coping mechanisms, which can worsen symptoms or prolong recovery. Exercise is safe if it does not cause major symptom exacerbation.

• Primary headache treatment: Postconcussive headaches may be treated with typical primary headache treatments (see Headache in this rotation guide).

• Vestibular rehabilitation can help reduce symptoms of vertigo and improve balance after a concussion.

• Physical therapy: Cervical tenderness and muscle tightness can be treated with physical therapy.

Hypoxic-Ischemic Brain Injury

Hypoxic-ischemic encephalopathy (HIE) occurs in children after cardiac or respiratory arrest or after any condition that leads to decreased blood flow or oxygen to the brain (e.g., drowning or severe hypotension). Neurology is frequently consulted after hypoxic brain injury in children for electroencephalogram (EEG) monitoring, recommendation for neuroprotective measures, and prognostication regarding neurologic outcome.

The primary goal after cardiac arrest is to restore adequate cerebral blood flow while attempting to prevent secondary injury from reperfusion, cerebral edema, and excessive cerebral metabolic demand.

Neuroprotective Measures

We generally recommend the following neuroprotective measures after hypoxic brain injury. These recommendations also apply to children with traumatic brain injuries.

• Maintain normothermia:Fever is common after cardiac arrest and is associated with worse outcomes owing to increasing metabolic demand that promotes free radical production and other detrimental consequences. Therapeutic hypothermia is the standard of care after hypoxic-ischemic injury in neonates. In older infants and children, current data favor normothermia rather than hypothermia. The Therapeutic Hypothermia after Pediatric Cardiac Arrest Out-of-Hospital trial found no difference in neurologic outcomes in children receiving postarrest hypothermia to 33°C versus postarrest targeted temperature management to 36°C (normothermia). The American Heart Association (AHA) guidelines recommend targeting a temperature of either 32-34°C or 36-37.5°C for 48 hours, followed by 36-37.5°C for an additional 3 days.

• Maintain normal oxygen saturations and partial pressure of carbon dioxide in arterial blood (PaCO₂): Hyperoxia and hypoxia may both be detrimental to neurologic recovery after cardiac arrest. Current AHA guidelines recommend weaning oxygen as tolerated to target normoxemia. Cerebral-blood flow regulation depends on the PaCO₂. Hypocapnia results in cerebral vasoconstriction, and hypercapnia results in vasodilation. Postarrest care should target normal range PaCO₂ between 35 and 40 mm Hg.

• Maintain an adequate cerebral perfusion pressure: Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. CPP is defined as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). The formula is CPP = MAP - ICP.

  Cerebrovascular autoregulation is impaired after cardiac arrest and hypotension is associated with worse outcomes. Current AHA guidelines recommend keeping MAP above the 5th percentile for age and weight, although we typically strive for higher MAPs (<50th percentile) to maintain adequate CPP, as ICP is often elevated. Typical ICP is 5-15 mm Hg in healthy adults and lower in young children. The goal in management after brain injury is to keep ICP <20 mm HG. MAPs should be high enough that if ICP is elevated, patients can maintain CPP.

• Maintain normoglycemia: Hypoglycemia and hyperglycemia are both associated with increased mortality. In adults, suggested blood glucose goal is 120-180 mg/dL, and no evidence supports stricter blood glucose control. Data are limited in children, but typically the goal is to maintain blood glucose levels between 80 and 180 mg/dL.

• Avoid hyponatremia: Hyponatremia contributes to secondary brain injury by causing water to be driven from the extracellular compartment into brain cells, leading to cerebral edema and increased intracranial pressure.

• Control seizures: Seizures are a common complication of hypoxic brain injury after cardiac or respiratory arrest and may exacerbate neurologic injury by increasing metabolic demand and worsening excitotoxicity. These seizures are commonly nonconvulsive and require monitoring by electroencephalogram (EEG) for identification. After cardiac arrest, where available, continuous EEG monitoring is recommended to facilitate timely diagnosis and treatment of seizures.

Neuroprognostication After Cardiac Arrest

Approximately 5% of children who attain return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest and 15% to 45% who attain ROSC after in-hospital cardiac arrest have good neurologic outcomes, with no or limited long-term disability. Physical exam, EEG, and MRI findings can help neurologists predict neurologic recovery, but with many uncertainties. While no single factor has been found to have sufficient accuracy to predict outcomes, serial biomarkers associated with neurologic outcomes are being studied.

• Physical examination is unreliable in the first 72 hours in predicting neurologic outcome. After 72 hours, absence of pupillary response to light is considered an accurate indicator of poor prognosis.

• EEG: Continuous, reactive background on EEG with intact sleep architecture predicts good recovery, while discontinuous backgrounds are associated with worse recovery. A burst suppression pattern on EEG indicates guarded or poor prognosis.

• MRI and CT: On CT, early loss of gray-white matter differentiation is associated with worse recovery, while on MRI, basal ganglia injury and large areas of diffusion restriction are associated with worse recovery.

(Source: Electroencephalography (EEG): An Introductory Text and Atlas of Normal and Abnormal Findings in Adults, Children, and Infants. American Epilepsy Society 2016.)

Prognosis

When discussing prognosis with parents, it is important to remember that “poor” and “good” neurologic outcome is not a dichotomy. Although some outcomes, such as brain death or minimally responsive states, are universally considered to be poor outcomes, many children who have lesser degrees of neurologic disability can continue to live meaningful lives.