Head injury

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Head injury

In the UK, trauma is the leading cause of death in people under the age of 45, with head injury making a substantial contribution in more than 50% of cases. Approximately half of patients admitted to hospital with a serious head injury are under the age of 20, two-thirds are male and alcohol is frequently a contributing factor. Some head injuries are due to assaults, but the vast majority are accidental. Road traffic incidents are an important cause of more serious head injuries, accounting for 60% of fatal traumatic brain injury cases. Survivors are likely to be left with long-term physical and intellectual impairments and may require a prolonged period of neurological rehabilitation.

Clinical aspects

A distinction is made between primary and secondary brain damage. The term primary brain injury refers to direct (impact-related) damage which cannot be reversed. The main aim of medical treatment is to prevent or minimize secondary brain injury which is often due to hypoxia, ischaemia or infection. These complications develop in the hours or days after the initial injury and are usually associated with brain swelling and raised intracranial pressure.

Assessment and management

The best indicator of head injury severity is impairment of consciousness. This either reflects brain stem dysfunction or diffuse hemispheric damage. Level of consciousness is assessed using the Glasgow Coma Scale (GCS) which quantifies responses to verbal and painful stimuli in terms of eye opening, speech and movement (Fig. 9.1). The aggregate score ranges from a maximum of 15 (alert and orientated) to a minimum of 3 (comatose or dead).

Fig. 9.1 The Glasgow Coma Scale.
**(A)** Response to verbal and painful stimuli is assessed in terms of eye opening, verbal response and motor response. The minimum score is 3 (even in death) and the maximum score is 15 (alert and orientated); **(B)** Abnormal flexion to pain (an ‘M’ score of 3 out of 5) is also known as decorticate posturing, whereas abnormal extension to pain (an ‘M’ score of 2 out of 5) is called decerebrate posturing. From Teasdale, G and Jennett, B: LANCET (ii) 81-83: (1974) with permission.

A GCS score of 13–15 corresponds to mild head injury, accounting for the majority of cases. A total score of 9–12 represents moderate head injury, whilst a score of 3–8 signifies severe head injury. In addition to providing an initial assessment of severity, any reduction in the GCS score is a sensitive indicator that the clinical state has deteriorated. This may signify development of a secondary complication requiring urgent intervention. The role of imaging in the assessment of head injury is discussed in Clinical Box 9.1.

Clinical Box 9.1: Neuroimaging in head injury

Brain imaging is important in the assessment of moderate and severe head injury. The investigation of choice is computed tomography (CT), which is able to demonstrate lesions of the scalp, skull and brain. This can be supplemented by plain radiographs of the spine in cases with possible vertebral trauma. In severe head injury (GCS <9), significant focal lesions such as cerebral haemorrhages and contusions are identified in more than 50% of cases. The remainder often show small haemorrhages scattered throughout the white matter and at grey-white matter junctions. This is suggestive of diffuse axonal injury and is associated with increased morbidity and mortality.

The initial management of head injury is the same as for any other major trauma and begins with the ‘ABC’ of basic life support (airway, breathing, circulation). Attention is then directed to any potentially life-threatening pathologies in the chest, abdomen or pelvis. Once the patient has been stabilized they can be assessed for head and spinal injuries and any appropriate medical or surgical treatments initiated.

Outcome following head injury

The long-term outcome after moderate or severe head injury depends on the extent and severity of the damage, including any co-existing injuries. It also varies with the age and general health of the patient. Although the mortality rate is declining, around a third of patients with severe head trauma will ultimately die as a result of their injuries. Another third will eventually recover sufficiently to return to work, whilst the remainder will be left with at least moderate mental or physical disability.

A small proportion of people (less than 3%) enter a persistent vegetative state, in which there is partial arousal or apparent wakefulness without full conscious awareness; this is considered permanent if it lasts more than 12 months.

Factors that predict a less favourable outcome include increasing age (>60 years), an initial GCS score below 5, a fixed and dilated pupil, a prolonged period of hypotension/hypoxia or a haemorrhage requiring surgical decompression. Late complications may include hydrocephalus due to obstruction of CSF drainage pathways (see Ch. 2, Clinical Box 2.2) or seizures (Clinical Box 9.2).

Clinical Box 9.2: Post-traumatic epilepsy

Seizures occur in approximately 2–3% of patients with traumatic head injury (10–15% of those with severe injuries). Post-traumatic epilepsy is described as ‘early’ if it occurs within the first week or ‘late’ when the onset is beyond this point. Seizure risk is higher with penetrating trauma, depressed skull fractures and in the presence of an intracerebral haemorrhage. The focus may be an area of gliosis (glial ‘scarring’ ; see Ch. 8) resulting from a focal brain lesion. Individuals experiencing early post-traumatic seizures are at most risk of longer-term recurrent seizures.

Key Points

In the UK, trauma is the leading cause of death in people under the age of 45 and head injury makes a substantial contribution in more than 50% of cases.

A distinction is made between primary (irreversible, impact-related) damage and secondary brain injury (preventable, by avoiding complications such as hypoxia, ischaemia or infection).

GCS score indicates severity after head injury: 13–15 (mild); 9–12 (moderate); 3–8 (severe). Any subsequent reduction in GCS score is a sensitive indicator of deterioration in the clinical state.

Pathology of head injury

Most traumatic brain damage is caused by blunt-force trauma. This usually results in a closed head injury. Penetrating (or missile) trauma such as stab wounds and gunshot injuries are less common and carry the additional risk of infection (e.g. meningitis or brain abscess).

Contact (or impact-related) damage occurs when the head collides with a hard surface or object. The energy from the impact is rapidly dissipated, causing direct mechanical injury such as cerebral contusion (bruising) and laceration (tearing; from the Latin lacerāre, to tear).

In addition, acceleration–deceleration (inertial) injury occurs when the head is suddenly set in motion – or is moving at high velocity and comes to an abrupt halt. The brain slides forwards or backwards within the cranial cavity and strikes the inside of the skull, which is most likely to damage the frontal, temporal or occipital poles. Complex rotational (‘swirling’) movements are also generated within the brain, which has a very soft, gelatinous consistency. This leads to widespread compressive, tensile and shearing forces, causing diffuse damage to axons and blood vessels.

Three main patterns of traumatic brain damage are found at post-mortem examination in people who died as a result of serious head injuries (due to a mixture of contact-related and acceleration–deceleration injury): cerebral contusions, intracranial haemorrhages and diffuse axonal injury.

Cerebral contusions

Cerebral contusions (bruising) and lacerations (tears) are common in traumatic brain injury, occurring in more than 90% of fatal cases. Contusions are most pronounced at the crests of gyri in the frontal and temporal lobes, particularly in places where the brain comes into contact with the irregular contours of the skull base (Fig. 9.2). Cerebral contusions may be associated with haemorrhage into the overlying subarachnoid or subdural spaces and if blood continues to accumulate it will begin to act as an intracranial mass lesion. The combination of a cerebral contusion with an overlying subdural haemorrhage is called a burst lobe. This most often occurs at the frontal and temporal poles.

Coup and contrecoup lesions (Fig. 9.3)

Contusions that occur at the point of impact are referred to as coup lesions (from the French, meaning shock or blow). These result from direct mechanical trauma, often from small, hard objects. Contusions may also be present on the opposite side of the brain, well away from the point of impact. These are contrecoup lesions which may be more severe and extensive than those at the impact site. This phenomenon is particularly common at the frontal and temporal poles in association with a blow to the back of the head. The mechanism is not fully understood. It is sometimes said that the contrecoup lesion is due to ‘rebound’ of the brain against the opposite side of the skull, but this does not explain why it is often more severe (as the kinetic energy of the second impact would be less). Experiments suggest that it may be due to a pocket of negative pressure (a ‘vacuum’) caused by rapid separation of the brain from the overlying skull.

Fig. 9.3 Coup and contrecoup lesions. The direct (coup) lesion is impact-related. The contrecoup lesion, which is often more severe, is probably due to extreme pressure changes which may damage thin-walled blood vessels as the brain is violently wrenched away from the overlying skull.

Key Points

Most traumatic brain damage is caused by blunt-force trauma, often in association with a closed head injury. Penetrating (missile) injuries are less common and carry an additional infection risk.

Contact (impact-related) brain damage includes cerebral contusions, intracranial haemorrhages and lacerations (tears). The indirect (contrecoup) lesion may be more severe than the direct (coup) lesion.

Widespread shearing of axons and small blood vessels is caused by acceleration–deceleration (inertial) forces and complex rotational (swirling) movements in the gelatinous brain tissue.

Intracranial haemorrhage

Bleeding may occur at the moment of impact or as a secondary complication, leading to formation of a haematoma (blood clot) which acts as a mass lesion. If the haematoma becomes sufficiently large it may compress the underlying brain or cause a life-threatening rise in intracranial pressure. The three main types of intracranial haemorrhage are: extradural, subdural and intracerebral.

Extradural haemorrhage

This typically occurs when the middle meningeal artery is torn by a skull fracture in the region of the pterion, where the bone is thin and is closely related to the underlying vessel (Fig. 9.4). Arterial blood escapes into the extradural space (between dura and bone) and strips the tightly adherent dura from the inner table of the cranial vault (Fig. 9.5).

Fig. 9.4 The middle meningeal artery is closely related to the pterion, which is the thinnest part of the cranial vault.
The underlying vessel is therefore vulnerable to damage in association with a skull fracture.

Fig. 9.5 Extradural haematoma shown diagrammatically (A) and on CT scanning (B).
On brain imaging, the typical biconvex shape is due to the fact that the dura is firmly anchored to the overlying skull and the accumulating blood is not able to cross suture lines (between adjacent cranial bones). Note the considerable ‘midline shift’ caused by the expanding mass lesion. Courtesy of Dr Andrew MacKinnon.

An extradural haematoma occurs in around 10% of severe head injuries and this is associated with a skull fracture in four out of five cases. Classically, a brief loss of consciousness at the time of impact is followed by a lucid interval which may last minutes or hours. Later, there is a sudden deterioration in consciousness which may rapidly lead to death without urgent surgical intervention (the patient is said to ‘talk and die’). Extradural haematoma is therefore a surgical emergency.

Subdural haemorrhage is caused by tearing of bridging veins that pass between the cerebral cortex and dural venous sinuses (see Ch. 1). These vessels pass through a potential plane between the dura and arachnoid membranes. A subdural haematoma results from the accumulation of venous blood in this potential space, which is easily expanded by blood under venous pressure because the dura and arachnoid are only loosely attached to each other (Fig. 9.6).

Fig. 9.6 Subdural haematoma shown diagrammatically (A) and on CT scanning (B).
On brain imaging, subdural haematomas spread further over the surface of the brain and cause less mass effect. This is because the blood is able to track freely between the arachnoid and dura (within the subdural space). Courtesy of Dr Andrew MacKinnon.

Acute subdural haematoma usually follows an obvious head injury, is more common in younger people and is likely to require surgical evacuation. In contrast, chronic subdural haematoma is often seen in the elderly, particularly in those with some degree of brain atrophy and in many cases there is no recollection of a head injury.

Intracerebral haemorrhage

Traumatic intracerebral haemorrhage may occur at the time of impact or as a secondary complication. It is more likely in people with pre-existing vascular disease or high blood pressure. In some cases a spontaneous (non-traumatic) intracerebral haemorrhage leads to an accidental fall or road traffic accident, but it is not always easy to tell which came first.

Intraventricular haemorrhage is seen in a proportion of cases, mainly in association with severe head injury. It may be a primary event, due to rupture of vessels in the choroid plexus (within the ventricles) or it might be due to dissection of blood into the ventricular system from an intracerebral or subarachnoid haemorrhage.

Key Points

The three main types of intracranial haemorrhage are extradural, subdural and intracerebral.

Extradural haematoma is most often caused by rupture of the middle meningeal artery following a fracture in the region of the pterion. It is a surgical emergency with significant risk of death.

Subdural haematoma may be acute (e.g. as a result of head trauma) or chronic (more often encountered in older people, often with no recollection of a head injury).

Diffuse axonal injury

Perhaps the most significant pathological change in severe head injury is widespread damage to axons in the cerebral hemispheres and brain stem, termed diffuse traumatic axonal injury (TAI). Some axons are transected at the moment of impact (primary axotomy) whilst others degenerate later (secondary axotomy).

Diffuse axonal injury appears to be a major determinant of impaired consciousness in head injury across the full spectrum of severity and it is thought to be an important factor in determining long-term disability. Brain imaging in patients with diffuse axonal injury is sometimes normal or may show only non-specific changes such as generalized brain swelling, but neuropathological examination of the brain shows characteristic findings.

Microscopic appearances

Diffuse axonal injury can only be detected reliably by microscopic examination of the brain after death. This shows axonal swellings throughout the cerebral hemispheres and brain stem (Fig. 9.7). Large white matter bundles such as the corpus callosum and internal capsule are particularly vulnerable, together with the dorsolateral sector of the upper brain stem.

Fig. 9.7 Microscopic appearances of diffuse axonal injury.
**(A)** Axon swellings, demonstrated using silver staining. From Stevens and Lowe: Pathology 2e (Mosby 2000) with permission; **(B)** Antibody-labelling (immunohistochemistry) for beta-APP. From Prayson, R: Neuropathology 1e (Churchill Livingstone 2005) with permission.

Axonal swellings can be highlighted by silver stain preparations (Fig. 9.7A). They can also be demonstrated by immunohistochemistry (antibody-labelling) of proteins that are normally transported along axons, including beta amyloid precursor protein (β-APP). Positive labelling for β-APP can be seen within two hours of head injury (Fig. 9.7B).

In the most severe cases, axonal transection is accompanied by tears in small blood vessels, leading to microhaemorrhages. These form small haematomas at the junction between grey and white matter (Fig. 9.8). Confusingly, these small haemorrhages are known as gliding contusions.

Fig. 9.8 Gliding contusions.
Post-mortem photograph in a case of traumatic head injury. The upper and lower images show large gliding contusions in the parasagittal white matter, close to the overlying cortex. There is also severe contusion of the temporal lobe. From Ellison and Love: Neuropathology 2e (Mosby 2003) with permission.

Skull fracture

Head injury is often associated with damage to the scalp, skull and dura. The presence of a skull fracture does not necessarily imply damage to the underlying brain, but does give some indication of impact force. Conversely, there may be significant brain injury in the absence of a skull fracture.

Most are simple linear fractures of the skull vault, usually occurring at the site of impact (Fig. 9.9A). The term depressed fracture is used when a piece of bone becomes detached and is displaced towards the brain (Fig. 9.9B).

Fig. 9.9 Skull fracture.
**(A)** Simple linear fracture; **(B)** Depressed fracture.

A compound (or open) fracture is a depressed fracture that is associated with an overlying scalp tear; this poses an infection risk and requires antibiotic prophylaxis. Skull base fractures require much greater force and are considerably less common. They may be associated with cranial nerve damage or ascending infection from the ear or nose.

Key Points

One of the most significant pathological changes associated with impairment of consciousness and long-term neurological disability in severe head injury is widespread damage to axons.

This is called diffuse traumatic axonal injury (TAI) which is characterized by axonal swellings, accumulation of beta-APP and microhaemorrhages (‘gliding contusions’).

Skull fracture gives some indication of impact force but is not necessarily associated with brain injury. Conversely, there may be significant brain injury in the absence of a skull fracture.

Brain swelling and intracranial pressure

An important consequence of head injury is brain swelling. This includes generalized increase in brain water content (cerebral oedema) and focal swelling in association with haematomas or other lesions. Brain swelling is dangerous because it leads to raised intracranial pressure, which may in turn compromise cerebral blood flow or result in potentially fatal brain herniation (discussed below).

Raised intracranial pressure

The cranium is a rigid structure with non-compressible contents (Fig. 9.10A). Any increase in the total volume of the cranial contents will therefore lead to a steep rise in intracranial pressure, but this is initially prevented by compensatory mechanisms which modify the volume–pressure curve (Fig. 9.10B). These include redistribution of CSF from the ventricles to the lumbar subarachnoid space and compression of the dural venous sinuses (thereby reducing the total intracranial blood volume).

Fig. 9.10 Pressure–volume relationship with an intracranial mass lesion.
**(A)** The cranium can be regarded as a rigid box with non-compressible contents; **(B)** This figure illustrates the pressure–volume relationship with an expanding intracranial mass lesion.

Once the compensatory mechanisms have been exhausted (the point of decompensation) the volume–pressure relationship becomes linear and the intracranial pressure rises steeply. This may lead to brain shift and herniation.

In general, the impact of a space-occupying lesion is less if the rate of expansion is slow, since this allows more time for compensation. Individuals with some degree of brain atrophy (e.g. the elderly) are also more tolerant of an expanding intracranial mass, since there is more free space inside the skull.

Brain shift and herniation

The cranial cavity is incompletely divided into compartments by two dural partitions: the falx cerebri (in the midline) and the tentorium cerebelli (forming a roof over the posterior fossa) (see Ch. 1). A pressure gradient may be created by an expanding mass lesion, displacing part of the brain from one intracranial compartment to another. This is termed brain shift (or internal herniation).

Types of herniation (Fig. 9.11)

Displacement of the cingulate gyrus under the free edge of the falx cerebri is termed subfalcine herniation and usually results from a focal lesion in one cerebral hemisphere (see Figs 9.11a and 9.12a).

Fig. 9.11 Brain shift and internal herniation.
**(A)** Coronal section illustrating the main types of internal herniation; **(B)** Sagittal section of the posterior fossa showing tonsillar and central (diencephalic) herniation.

Fig. 9.12 Internal herniation after traumatic head injury.
**(A)** Coronal section showing subfalcine herniation of the right cingulate gyrus (arrow) with marked midline shift. There is also haemorrhage in the medial temporal region due to transtentorial herniation; **(B)** Displacement of the brain stem may lead to a fatal midline haemorrhages (Duret or ‘flame’ haemorrhages), shown here in the midbrain. From Ellison and Love: Neuropathology 2e (Mosby 2003) with permission.

Downward displacement of the medial temporal lobe (the parahippocampal gyrus and uncus) through the tentorial hiatus is referred to as transtentorial (or uncal) herniation (Fig. 9.11A). This may cause pupil changes due to compression of the oculomotor nerve (Clinical Box 9.3).

Clinical Box 9.3: Pupil reflexes in transtentorial herniation

Transtentorial herniation is often associated with compression of the oculomotor (III) nerve which runs alongside the free edge of the tentorium cerebelli. This results in a dilated pupil due to involvement of parasympathetic pupilloconstrictor fibres (see Ch. 3) which travel in the peripheral part of the nerve and are therefore vulnerable to compression. Reduction in GCS and sluggish pupillary light reaction on one side is therefore an early sign of a transtentorial herniation. At a later stage, the pupil will become fixed (unresponsive to light) and dilated.

Diffuse swelling of both cerebral hemispheres is likely to produce downward displacement of the entire diencephalon (thalamic region). This is called diencephalic (or central) herniation and may be associated with tearing of brain stem blood vessels, causing fatal haemorrhage (Fig. 9.12B).

Herniation of the cerebellar tonsils through the foramen magnum in the base of the skull is called tonsillar herniation (or coning). This can be rapidly fatal due to compression of the medulla oblongata, leading to respiratory arrest.

A sign of critical brain stem compression (compromising the cardiorespiratory centres of the medulla) is the Cushing response, consisting of (i) raised intracranial pressure, leading to (ii) arterial hypertension and (iii) bradycardia.

Secondary infarction

In addition to the direct effect of cerebral herniation, which damages the compressed brain tissue, obstruction of cerebral blood vessels may lead to secondary infarction (tissue death due to impaired blood flow; see Ch. 10). For instance, subfalcine herniation may be associated with compression of the anterior cerebral artery with consequent infarction of the medial frontal lobe, whereas transtentorial herniation may obstruct the posterior cerebral artery, with infarction of the occipital and inferior temporal lobes.

Key Points

Brain swelling (cerebral oedema) is an important consequence of primary and secondary brain injury. It may lead to raised intracranial pressure and brain shift or herniation.

An expanding intracranial mass can be tolerated for a short period of time due to compensatory mechanisms including CSF redistribution and reduced volume of the dural venous sinuses.

Beyond the point of decompensation the volume–pressure curve becomes linear and the intracranial pressure rises rapidly.

This may cause brain shift or internal herniation within the cranium. The main types of internal herniation are subfalcine, transtentorial, diencephalic and tonsillar.

Coning (medullary compression due to tonsillar herniation through the foramen magnum) is an important cause of respiratory arrest and death in patients with raised ICP.

Brain blood flow and ICP

The main factors determining cerebral blood flow (CBF) are illustrated in Figure 9.13. Blood flow to the brain is proportional to the cerebral perfusion pressure (CPP) and inversely proportional to the cerebral vascular resistance (CVR). The cerebral perfusion pressure can be thought of as the ‘driving force’ for cerebral blood flow.