Types of brain injury

Traumatic brain injury can cause structural damage of various types. Structural changes can be macro- or microscopic, depending on the mechanism of injury and the force of impact.

A patient with a less severe traumatic brain injury may not have major structural damage. Traumatic brain injury symptoms vary widely in severity and consequences. Injuries are usually classified as open or closed.

Pathophysiology of traumatic brain injury

With direct trauma (e.g., blow, wound), brain function can be disrupted immediately. Soon after the initial trauma, a cascade of processes can begin, leading to further damage.

Any traumatic brain injury may cause edema of the injured tissue. The volume of the skull is fixed by its bones and is almost entirely occupied by incompressible cerebrospinal fluid (CSF) and slightly compressible brain tissue; therefore, any increase in volume due to edema, bleeding, or hematoma has no free space for it and inevitably leads to an increase in intracranial pressure. Cerebral blood flow is proportional to the level of cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and the mean intracranial pressure. Thus, as intracranial pressure increases (or MAP decreases), CPP decreases and when it falls below 50 mmHg, cerebral ischemia begins. This mechanism can lead to ischemia at a local level, when pressure from local edema or hematoma impairs cerebral blood flow in the area of injury. Ischemia and edema may trigger the release of excitatory neurotransmitters and free radicals, further increasing edema and intracranial pressure. Systemic complications of trauma (eg, hypotension, hypoxia) may also contribute to the development of cerebral ischemia, which is often referred to as secondary cerebral stroke.

Excessive intracranial pressure initially leads to global impairment of brain function. If intracranial pressure is not reduced, this can lead to herniation of brain tissue into the foramen magnum and under the cerebellar tentorium with the formation of cerebral hernias, which significantly increases the risk of complications and death. In addition, if intracranial pressure is compared with the SBP, the IVD becomes zero, which leads to complete cerebral ischemia, which quickly leads to brain death. The absence of cerebral blood flow can be used as one of the criteria for brain death.

Open craniocerebral trauma

Open head injuries are injuries that penetrate the scalp and skull (and usually the dura mater and brain tissue). Open injuries are seen with gunshot wounds or injuries caused by sharp objects, but skull fractures that involve the tissues covering the skull as a result of forceful impact with a heavy blunt object are also considered open.

Closed craniocerebral injury

Closed craniocerebral injuries usually occur when the head hits an object or is subject to a sudden concussion, which causes instant acceleration and deceleration of the brain within the cranial cavity. Acceleration and deceleration can damage brain tissue at the site of the direct impact or in the area opposite it (counter-impact), as well as diffusely. The frontal and temporal lobes are most often affected. Tears or ruptures of nerve fibers, blood vessels, or both are possible. Damaged vessels become excessively permeable, which leads to the formation of contusion zones, intracerebral or subarachnoid hemorrhages, and hematomas (epidural and subdural).

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Concussion

Concussion is defined as a post-traumatic, temporary, and reversible change in the level of consciousness (eg, loss of consciousness or memory), lasting from a few seconds to minutes to a conventionally defined period of <6 hours. There is no major structural damage to the brain or residual neurological changes, although temporary functional impairment may be significant.

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Diffuse axonal injury

Diffuse axonal injury (DAI) occurs when sudden deceleration creates shear forces that cause generalized, widespread damage to axonal fibers and myelin sheaths (although DAI can also occur after minor trauma). There is no significant structural damage, but small petechial hemorrhages in the white matter of the brain are often seen on CT (and histology). Clinically, DAI is sometimes defined as loss of consciousness lasting >6 hours in the absence of focal neurologic deficits. Traumatic edema often increases intracranial pressure (ICP), leading to a variety of clinical manifestations. DAI commonly underlies the so-called shaken baby syndrome.

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Brain contusion

Brain contusion is possible with both open (including penetrating) and closed injuries. The pathological condition can disrupt a wide range of brain functions, depending on the size and location of the lesion. Large contusions can cause extensive brain swelling and a sharp increase in intracranial pressure.

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Brain hematomas

Hematomas (accumulations of blood in or around the brain tissue) are possible with both penetrating and closed injuries; they can be epidural, subdural, and intracerebral. Subarachnoid hemorrhage (SAH) is typical of craniocerebral trauma.

Subdural hematoma is a collection of blood between the dura mater and arachnoid mater. Acute subdural hematomas are often caused by the destruction of the veins of the brain or its cortex, or the rupture of the communicating veins between the cortex and the sinuses of the dura mater, and most often occur after falls and car accidents. As a result of compression of brain tissue by a hematoma, edema may develop with increased intracranial pressure, the manifestations of which vary. Mortality and complications after hematomas are significant.

Symptoms of chronic subdural hematoma may appear gradually, over several weeks after the injury. They are more common in older people (especially those taking antiplatelet drugs and anticoagulants), who may consider the head injury to be minor and even forget that it happened. Unlike acute subdural hematomas, swelling and increased intracranial pressure are not typical for chronic hematomas.

Epidural hematomas (accumulations of blood between the bones of the skull and the dura mater) are less common than subdural hematomas. Epidural hematomas are usually caused by arterial bleeding, classically due to rupture of the middle meningeal artery in temporal bone fractures. Without emergency intervention, a patient with a large or arterial epidural hematoma can rapidly deteriorate and die. Small, venous epidural hematomas are rare and have a low mortality rate.

Intracerebral hematomas (accumulation of blood in the brain tissue itself) are often the result of a progression of a contusion, so that clinically the boundary between a contusion and an intracranial hematoma is not clearly defined. Subsequently, increased intracranial pressure, herniation, and functional insufficiency of the brainstem may develop, especially with hematomas in the temporal lobes or cerebellum.

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Skull bone fractures

Penetrating injuries, by definition, are accompanied by fractures. However, even with closed head injuries, skull fractures are possible, which are divided into linear, depressed, and comminuted. Although severe and even fatal head injuries are possible without fractures, their presence indicates a significant force of the blow. Fractures in patients with diffuse head injury indicate a high risk of intracranial damage. Fractures in localized head injury (e.g., a blow with a small object) do not necessarily indicate a high risk of intracranial damage. A simple linear fracture is also usually not associated with a high risk unless accompanied by neurological symptoms or unless it occurs in an infant.

In depressed fractures, the risk of rupture of the dura mater and/or brain tissue is highest.

If a temporal bone fracture crosses the area of the middle meningeal artery, an epidural hematoma is likely to develop. Fractures that cross any of the large sinuses of the dura mater may cause massive bleeding and the formation of a venous epidural or subdural hematoma. Fractures that cross the carotid canal may lead to rupture of the carotid artery.

The bones of the occiput and base of the skull are very thick and strong, and their fractures indicate a high-intensity external impact. Fractures of the base of the skull that pass through the petrous part of the temporal bone often damage the structures of the outer and inner ear, and can impair the function of the facial, vestibulocochlear, and vestibular nerves.

In children, it is possible for the meninges to become trapped in a linear skull fracture, with subsequent development of leptomeningeal cysts and an increase in the primary fracture (“growing” fracture).