An Overview of Mild Traumatic Brain Injury

Mild Traumatic Brain InjuryMild Traumatic Brain Injury
Written by: Franco Cuevas
Franco Cuevas is a physician who graduated from the National University of Córdoba, Argentina. He practices general medicine in the Emergency Department at Sanatorio de la Cañada, Córdoba. His focus is on writing medical content to improve physicians' access to relevant medical information for daily practice. He has participated in some research projects and has a special joy in teaching and writing about medical concepts.
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Mild traumatic brain injury is a clinical syndrome caused by direct or indirect head trauma, classified with a Glasgow Coma Scale of 13-15. It is a common presentation in medical departments and is more frequent in males with a bimodal peak of presentation regarding age groups. Clinical manifestations may include headache, brief loss of consciousness, amnesia, focal or generalized neurological deficits, autonomic symptoms, psychiatric symptoms, and cognitive impairment.

Head computed tomography is the first line choice for evaluating patients with mild traumatic brain injury in the acute setting. Complete neurological evaluation, clinical judgment, and clinical decision rules are used in the diagnosis and management of patients with mild traumatic brain injury.

Introduction to Mild Traumatic Brain Injury

Mild traumatic brain injury (mTBI) represents a frequent concern for medical consultation in the acute medical setting. A significant proportion of patients having a mild head injury do not look for medical attention and thus may not be included in the epidemiological data available in the literature. Traumatic brain injury has a yearly prevalence of 1299 cases per 100,000 people in the US, while mTBI cases represent the majority among them (1).

Despite being a condition with low complication rates, its consequences affect individuals in many aspects of their lives, including cognitive, sensorimotor, psychiatric, and socioeconomic outcomes.

Diagnosis of mTBI is primarily clinical, and its management includes mainly clinical observation of subjects. Despite some unclear aspects of the management of this group of patients, ongoing research efforts are currently being made to develop appropriate tools to guide healthcare professionals facing this challenging condition.

This article aims to treat the general aspects of the condition and briefly describe diagnostic and management strategies for patients with mTBI.

Definitions and Classification of Mild Traumatic Brain Injury

Traumatic brain injury is classically stratified using the Glasgow Coma Scale (GCS) (2) in three different groups:

  • Mild traumatic brain injury: GCS 13-15.
  • Moderate traumatic brain injury: GCS 9-12.
  • Severe traumatic brain injury: GCS 3-8.

The GCS, first developed in the pre-computed tomography era, uses three clinical parameters to evaluate neurological function: ocular, verbal, and motor responses to external stimuli. (Table 1)
The patient should be assessed for the better response that is possibly elicited. The responses are ordered from best to worst and represent a continuous numeric score.

Eye-opening Verbal response Motor response
Spontaneous (4 pts) Oriented (5 pts) Obey commands (6 pts)
To verbal stimulus (3 pts) Confused (4 pts) Localize the pain (5 pts)
To painful stimulus (2 pts) Words (3 pts) Normal flexion (4 pts)
No response (1 pt) Sounds (2 pts) Abnormal flexion (3 pts)
  No response (1 pt) Abnormal extension (2 pts)
  No response (1 pt)

Mild Traumatic Brain Injury

Mild traumatic brain injury is an alteration of normal brain functioning produced by forces transmitted by direct or indirect trauma to the head. The definition includes at least one of the following manifestations: (3)

  • Any period of loss of consciousness of fewer than 30 minutes.
  • Altered mental status at the time of injury.
  • Any memory loss of the previous or posterior events related to the injury of less than 24hs.
  • Transient or permanent focal neurological deficit.
  • Glasgow Coma Scale 13-15.

Complicated mTBI refers to the presence of associated cranial or intracranial lesions (4) (e.g., basal skull fracture, cerebrospinal fluid (CSF) leakage, fracture of the cranial convexity, cerebral contusions, traumatic subarachnoid hemorrhage (SAH), subdural or extradural hematoma).

According to Williams et al. (4), patients with a complicated mTBI performed worse than those with a non-complicated mTBI in neurobehavioral performance tests. Katz et al. (5) found that patients with mild and moderate TBI recover in a similar pattern overall.

Concussion

A concussion is defined as a pathophysiological process produced by biomechanical forces, either directly or indirectly induced in the head, that involves transient neurological dysfunction with spontaneous resolution over a period of minutes to 7-10 days (3, 6, 7).

Concussion may involve one or more domains of clinical symptomatology, including somatic, cognitive, and emotional symptoms; physical signs, such as loss of consciousness or amnesia; behavioral changes; cognitive impairment; and sleep disturbances (7). A concussion is included under the spectrum of mTBI.

Despite efforts in defining terms, there are inconclusive aspects, including the fact that mTBI symptoms may be produced by concomitant pathologies, such as associated injuries, chronic disease decompensation, dehydration, and intoxications (5).

Epidemiology of Mild Traumatic Brain Injury

It is estimated that more than 64,000 TBI-related deaths are produced each year (8). mTBI presents a bimodal peak of the age of presentation, including males in the 15-24 years old group and both sex groups over 65 years old (9).

Among patients with mTBI, approximately 8% of the cases present with complicated mTBI, and around 1% require neurosurgical intervention (10). Only a small proportion of patients require delayed neurosurgical intervention, being acute subdural hematomas and epidural hematomas, the most frequent lesions encountered (11).

Pathophysiology of Mild Traumatic Brain Injury

Although complex and suspected under current investigation, mTBI pathophysiology involves a set of mechanisms that play a different but complementary role in the production of brain injury and pathology.

  • Traumatic axonal lesion, also known as diffuse axonal injury (DAI), is one of the processes involved in the production of brain pathology (12). DAI refers to the direct traction of axons producing edema and further Wallerian degeneration of white tracts, commonly located in the white-gray matter junction, corpus callosum, and brain stem; DAI involves a spectrum of severity, ranging from mild to life-threatening manifestations.
  • Altered cerebrovascular autoregulation plays a role in mTBI pathology, producing loss of normal arterial reflexes either focally or generalized, eliciting areas of hypo- or hyperperfusion (13, 14).
  • Excitotoxic cell damage and inflammation may induce apoptosis in neural structures and release of reactive oxygen and nitrogen species, contributing to symptomatology and neurological deficit (15). Further, if present, secondary brain lesions (contusions, extra-axial hematomas/hemorrhage, cerebral edema) contribute to symptom production and neurological deterioration (16).
  • Autonomic nervous system dysfunction may be involved in generalized neurological signs and symptoms (17).
  • Injuries associated with the cranial vault, such as skull fractures, may produce symptoms or clinical manifestations, including CSF leak, hemotympanum, raccoon eyes, Battle sign, vertigo, and dizziness (5).

Clinical Presentation

Patients present with a history of head or multisystemic trauma. In cases of poor recall by the patient, secondary anamnesis to close witnesses or Emergency Technician personnel should be performed.

The usual trauma survey should be applied to every patient encountering the acute setting, using the ABCDE approach systematically.

Full clinical history, vital signs, and systemic anamnesis should be reviewed.

The spectrum of clinical manifestations includes:

  • Headache or other pain syndromes (facial neuropathy associated with basal skull fractures, neck pain).
  • Autonomic dysfunction (altered heart rate variability, anxiety, perspiration, nausea, vomiting).
  • Sleep disturbances (insomnia, hypersomnia).
  • Emotional disturbances (anxiety, depression) and behavioral changes.
  • Cognitive dysfunction.

Diagnosis and Management of Mild Traumatic Brain Injury

The diagnosis of mTBI is made primarily clinically, based on a history of direct or indirect head trauma and accompanying signs and symptoms.

Further management relies on the decision of neuroimaging. Head computed tomography is the first line choice of study. Clinical decision rules help survey patients that might benefit from neuroimaging in the acute setting (10, 18). For this purpose, the New Orleans Criteria and the Canadian CT head rules have been developed.

The New Orleans Criteria

If 1 of the following criteria is found, head CT should be performed. These criteria are used only in patients with a GCS of 15. (19)

  1. Headache
  2. Vomiting
  3. Older than 60 years
  4. Drug or alcohol intoxication
  5. Persistent anterograde amnesia (deficits in short-term memory)
  6. Visible trauma above the clavicle
  7. Seizure

The Canadian Head CT Rules

If 1 of the following criteria is found, head CT should be performed: patients with a GCS of 13-15 who presented with witnessed loss of consciousness, amnesia, or altered mental status. (20)

High Risk for Neurosurgical Intervention

  • Glasgow Coma Scale score lower than 15 at 2 hours after injury
  • Suspected open or depressed skull fracture
  • Any sign of basal skull fracture
  • Two or more episodes of vomiting
  • 65 years or older

Medium Risk for Brain Injury Detection by Computed Tomographic Imaging

  • Amnesia before the impact of 30 or more minutes
  • Dangerous mechanism

*The rule is not applicable if the patient did not experience trauma, has a Glasgow Coma Scale score lower than 13, is younger than 16 years, is taking warfarin or has a bleeding disorder, or has an apparent open skull fracture.

Patients under anticoagulant or antiplatelet therapy, those with a history of bleeding disorders, patients with focal or generalized neurological deficits, or those with an evident skull fracture should also undergo head CT (18).

CT-scan Stratification

Patients with cranial or intracranial pathology (subdural hematoma, epidural hematoma, subarachnoid hemorrhage, skull fracture, cerebral/cerebellar contusion, cerebral edema) should undergo prompt neurosurgical evaluation (21).

Patients with normal head CT and the following characteristics should undergo clinical observation, preferably for 24 hours (21):

  • GCS < 15;
  • Focal neurological deficit;
  • Prolonged post-traumatic amnesia/agitation;
  • Severe headache;
  • Persistent vomiting;
  • Skull fracture;
  • CSF leakage;
  • Multi trauma;
  • Coagulation disorder;
  • Intoxication (drugs, alcohol);
  • Suspected non-accidental injury.

Finally, patients with an isolated mTBI, normal neurological evaluation, and head CT should be safely discharged home with appropriate information for returning to the emergency department and neurological follow-up (18). The latter should include information related to post-concussive symptoms.

Conclusions

Mild TBI represents a common presentation in acute setting medical facilities. Prompt clinical and neurological evaluation should be performed in order to evaluate and stratify patients, specifically those at risk for intracranial pathology. Ongoing research efforts are made to develop new tools for assessing and managing this widespread medical condition.

Disclosures:

The author does not report any conflict of interest.

Disclaimer:

This information is for educational purposes and is not intended to treat disease or supplant professional medical judgment. Physicians should follow local policy regarding the diagnosis and management of medical conditions.

See Also

Dyspnea Due to Respiratory Causes

Approach to Chest Pain

Acute Asthma Exacerbation

Lower Urinary Tract Infections

Acute Diarrhea in Adults

Acute Otitis

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