Brain Contusion: Etiology, Classification, Clinical Presentation, Diagnosis, and Treatment

Traumatic brain injury is a condition characterized by damage to the skull and intracranial contents by mechanical energy.

The incidence of traumatic brain injury is 35% of the total body trauma, and the mortality rate from traumatic brain injury, according to various literature sources, can reach up to 60%.

Brain contusion is a form of focal traumatic brain injury where irreversible damage to the brain parenchyma occurs due to microvascular and macrovascular disorders. The injury is accompanied by the development of edema, the formation of contusion foci and intracerebral hematomas, leading to irreversible destruction of brain tissue.

Brain contusions of varying degrees occur in 17–50% of severe traumatic brain cases and can be both an independent form of traumatic brain injury and occur alongside other brain injuries. The mortality rate from brain contusions is 30–40% and directly correlates with the presence of concomitant brain injuries.

Etiology of brain contusions

The etiology of brain contusions directly correlates with the causes of traumatic brain injury in the adult and pediatric populations. The main causes of traumatic brain injury are commonly the following:

• Road traffic accidents;
• Falls;
• Violent injuries;
• Sports injuries.

Pathogenesis of brain contusions

The pathogenetic mechanism of brain contusions is described by the coup-contrecoup theory, which involves the direct transfer of mechanical energy to the rigid bony structures of the skull, causing a focus of brain trauma at the point of kinetic energy application.

Brain contusions, occurring directly at the site of contact with the injurious agent, are caused by the brain’s contact with the rigid bones of the skull. Subsequently, due to the dissemination of energy in brain tissue and the pressure gradient changes, an opposite contusion focus forms due to cavitation interactions (contrecoup point).

After forming the primary contusion focus, part of the nerve cells in the focus die, leading to lysis and the release of chemokines and interleukins, reactive oxygen species, and proteases by the cells. These substances violate the permeability of the blood-brain barrier, inducing brain edema development.

Released free radicals damage DNA and disrupt mitochondrial function of the cells, exacerbating cellular edema and subsequent death of neurons and neuroglia.

The formation of brain edema begins with vasogenic edema due to damage to the blood-brain barrier, developing about 12–24 hours after injury. This is followed by cytotoxic edema resulting from the glial cell and neuron edema due to the release of free radicals and their subsequent death. This process’s progression is observed over 7–10 days after the injury.

The most common contusions are noted in the lower and inferolateral parts of the frontal and temporal lobes of the brain. These areas are most vulnerable to contusion due to the anatomical features of the skull and the distribution of kinetic energy in the structures of the anterior and middle cranial fossae.

An additional factor is the local deformation of the skull since the orbital, temporal, and sphenoidal regions demonstrate more intensive vibrations upon impact in experiments.

Classification of brain contusions

From a morphological substrate and clinical presentation perspective, brain contusions are classified into mild, moderate, and severe contusions.

Mild brain contusion

For a mild contusion, the following is typical:

• Brief loss of consciousness lasting up to several minutes;
• Autonomic reactions;
• Mild neurological disorders in the form of coordination disturbances;
• Nystagmus.

In instrumental studies, mild contusions are visualized on computed tomography. They are characterized by an area of reduced density in brain tissue (approximate density 16–20 Hounsfield units).

Upon more detailed examination, performing magnetic resonance imaging, foci of microhemorrhages can be visualized in this area. These changes typically disappear two weeks after injury and do not leave any post-traumatic changes.

Moderate cerebral contusion

For a moderate contusion, the following is characteristic:

• Presence of small hemorrhagic foci clearly visible on neuroimaging, maintaining the differentiation of sulci and gyri.
• Loss of consciousness from tens of minutes to several hours.
• The entire spectrum of focal neurological disorders: mental impairment, motor function, sensory disturbances, etc.

In neuroimaging, such contusions are characterized by small foci of hemorrhagic soaking in the damaged brain tissue areas.

Severe cerebral contusion

A severe brain contusion is clinically characterized by loss of consciousness from several hours to several weeks, accompanied by significant neurological deficits with dominant brainstem symptoms.

In neuroimaging, these contusions are characterized by dense tissue foci with areas of reduced density, presented with brain debris.

Classification by CT foci type

There is also a classification of brain contusions reflecting purely neuroimaging patterns.

In this classification, contusions are divided into:

• Contusion type 1 is characterized by the presence of a brain CT focal area of decreased density (+18–25 HU).
• Contusion type 2 is characterized by the presence on a brain CT of small, scattered hemorrhagic foci with a density of approximately 50 HU.
• Contusion type 3 is characterized by the presence of the areas of heterogeneously increased density with compactly located hemorrhagic transformation foci of small and medium size fully around 64–76 HU.
• Contusion type 4 is characterized by single or multiple foci of increased homogeneous oval-shaped density, up to 76 HU.

Clinical Manifestations

The clinical presentation of brain contusions directly consists of non-focal and focal neurological symptoms.

Non-focal symptoms include:

• Headache;
• Dizziness;
• Nausea;
• Vomiting;
• Loss of consciousness.

Herewith, the loss of consciousness is a clinical criterion correlating with the severity of the brain contusion. Loss of consciousness after injury can last from a few seconds to a few weeks.

The manifestation of focal neurological symptoms directly depends on the localization of the contusion focus.

The most common brain contusion localizations are the frontal (40–50%) and temporal lobes (35–45%) of the brain.

In the case of frontal lobe contusion foci, the clinical picture can include:

• Mental disorders;
• Speech disorders in the form of motor aphasia;
• Gaze paresis;
• Anosmia.

Cortical damage may lead to:

• Mono- and hemipareses;
• Facial muscle paresis;
• Hypoglossal nerve paresis.

For damage to the temporal lobe of the brain, the following is typical:

• Sensory aphasia;
• Higher nervous activity function disorders (alexia, acalculia, agraphia);
• Homonymous hemianopsia due to visual tract damage.

The parietal lobe is a relatively rare site for brain contusions due to its superficial location and distance from the base of the skull. Contusions in this area are primarily developed due to the coup mechanism rather than the counter-coup mechanism. The clinical presentation of focal neurological symptoms of contusions in this area is characterized by sensory disturbances.

Occipital lobe brain injuries occur relatively rarely due to the cushioning properties of the cerebellar tentorium. Visual agnosia and homonymous hemianopsia, up to complete cortical blindness with injury to both occipital lobes, are often found when this lobe is damaged.

Contusions of the cerebellum are more often formed by the impact mechanism and are characterized by the development of unilateral or bilateral hypotonia and coordination disorders.

Diagnosis of brain contusions

Upon admission of the patient to the emergency room, the diagnostic algorithm for brain contusions consists of the following stages:

1. Assessment of consciousness level using the GCS (Glasgow Coma Scale)

This step allows for determining the patient’s level of consciousness and estimating the severity of brain structure damage, suggesting possible treatment options (surgical or non-surgical).

2. Medical history

It is necessary to specify the timing of injury onset, the mechanism of injury, and whether there was a loss of consciousness after the injury.

This step allows for understanding the dynamics of symptom progression and inferring possible injuries considering the injury mechanism. For certain injury mechanisms (e.g., fall from height), it’s essential to consider the possibility of combined head and body injuries, which may complicate the treatment prognosis.

3. Visual examination of the patient

Includes examination of the head area and checking for concomitant soft tissue damage in areas of the body other than the head.

This step helps highlight the location of soft tissue in head injuries, allowing inference of the brain contusion’s possible location. Additionally, this step is essential for patient care, treating soft tissue bruises, and performing primary surgical treatment if needed.

4. Neurological examination of the patient

Assessment of non-focal, focal, and meningeal symptoms is performed.

This stage enables preliminary topical diagnosis of brain injury to determine indications for neuroimaging studies. If the patient presents with non-focal, focal, or meningeal symptoms, neuroimaging is indicated.

5. Neuroimaging studies

Computed tomography (CT) of the brain is the “gold standard” in diagnosing traumatic brain injuries, including brain contusions.

The advantages of brain CT over other studies (including MRI) include the speed of the study, the ability to clearly assess the location, extent, and nature of brain injuries, the ability to assess associated bony structure injuries, and the possibility of rapidly scanning other body parts to exclude associated injuries.

Brain contusions on CT have several typical features:

• Location of the contusion in cortical or basal brain regions;
• The size of the contusion ranges from small hyperdense areas in the brain cortex to massive hyperdense areas;
• Presence of a hypodense area around the contusion focus, which is explained by the initial formation of vasogenic edema followed by the addition of cytotoxic brain edema.

The characteristic density of hyperdense contusion foci on CT varies between 45–64 HU.

Magnetic resonance imaging (MRI) is generally not used in diagnosing brain contusions, though it may be applied to evaluate the progression of contusions. In brain contusions on MRI, the following are typical:

• T1-weighted images: hyperintense signal;
• T2-weighted images: hypointense signal;
• SWI images: hyperintense signal.

6. Laboratory diagnostics

A complete blood count, urinalysis, coagulation profile, blood biochemistry, blood group, and Rh factor are necessary.

These tests do not confirm or suspect brain contusions, but they allow for the assessment of the patient’s overall condition, accompanying coagulation system disorders, and preparation for potential surgery.

Treatment of brain contusions

Medical therapy

Non-surgical treatment of brain contusions primarily involves maintaining adequate cerebral perfusion pressure, which may vary due to increased intracranial pressure (ICP) from developing or established contusion foci.

The following must be provided at all stages:

• Maintaining vital functions of the body;
• Pain management (non-steroidal anti-inflammatory drugs, narcotic analgesics);
• Anticonvulsant therapy: anticonvulsants are recommended only if there are symptoms of seizures. These medications are not recommended for preventive purposes.

In all patients with a GCS score below 8 when there is a substrate on CT or without it (in the presence of decerebration neurological symptoms), the installation of an intracranial pressure (ICP) sensor is indicated.

In cases of persistent intracranial pressure increase, ICP monitoring is used, and the following treatment is provided:

• Sedative agents (in patients with traumatic brain injury, preference is given to propofol); Barbiturate derivatives in high doses are used only in case of refractory intracranial hypertension not responsive to non-surgical and surgical treatment;
• Osmotic diuretics are used without ICP monitoring in the event of reported signs of life-threatening brain herniations and progressing neurological deterioration;
• Hyperventilation;
• Hypothermia.

Surgical Therapy

Surgical treatment of brain contusions primarily aims to reduce intracranial pressure to ensure adequate cerebral perfusion and prevent life-threatening brain displacement syndromes.

Indications for surgical treatment of brain contusions with supratentorial localization:

• Contusion focus volume over 50 cm³;
• Axial displacement of midline structures of 5 mm or more;
• Compression of basal cisterns;
• Compression of the third ventricle.

In this case, surgery is limited to performing a craniotomy and resection of brain contusion foci.

The indication for surgical treatment with intracerebral hematoma formation may be the following:

• Hematoma volume of 40 ml in the frontal lobe of the brain;
• Hematoma volume of 20 ml in the temporal lobe of the brain;
• Axial displacement of 5 mm or more.

In this case, surgery also involves performing a craniotomy and resection of brain contusion foci.

In large contusions, progression of foci to surgically significant sizes, with an intracerebral hematoma volume of more than 140 ml, as well as with a patient consciousness level of less than 8 GCS points, decompressive craniotomy with resection of contusion foci is indicated.

Indications for surgical treatment of brain contusions with subtentorial localization:

• Presence of a cerebellar contusion focus with a volume greater than 20 ml;
• Signs of occlusive hydrocephalus;
• Displacement of the fourth ventricle.

Surgical treatment tactics involve emptying and removing the contusion focus by craniotomy. In the absence of regression of occlusive hydrocephalus, the placement of an external ventricular drain is necessary.