Focal Injury
Lesions of the Scalp, Skull, and Dura
Lesions of the scalp, skull, and dura often provide a clue to the site and nature of the injury and alert the clinician to potential complications. For example, bruising at the back of the scalp is often associated with severe contu-sions of the frontal lobes, whereas bruising of the mastoid process may be associated with traumatic subarachnoid hemorrhage. A bruise in the temple may be associated with a fracture and the subsequent development of an extradural hematoma. In many instances, the laceration of the scalp is not of any great significance, but, if there is severe bleeding, the patient may become hypotensive, thereby adding a secondary insult to the already damaged brain. Furthermore, if there is an associated open, depressed fracture of the skull, a laceration of the scalp may be a potential route for intracranial infection.
In general, the more severe the brain injury, the greater the frequency of a fracture of the skull. For exam-ple, the frequency of skull fracture is 3% in those patients who present to emergency departments, 65% in patients admitted to a neurosurgical unit, and 80% in fatal cases (Jennett and Teasdale 1981). Fractures of the skull may be limited to the vertex, the base of the skull, or may affect both (Table 2–4). The majority of skull fractures are lin-ear, affecting the vault of the skull in 62% of cases, with extension into the base of the skull in 17%.
A fracture of the skull is not necessarily associated with underlying brain damage. For example, injury due to crush may result in extensive fractures of the skull with
little underlying brain damage, with the patient often re-maining conscious. More localized injury, as, for example, after an assault with a blunt object, may produce brain damage limited to the site of impact. Even under these circumstances, the fracture may be depressed, but brain function remains intact, there being only brief or limited loss of consciousness.
As a corollary, the absence of a skull fracture does not necessarily mean that the brain has not been injured. In-deed, a skull fracture is absent in some 20% of fatal cases. This is particularly true in pediatric patients be-cause the capacity of the skull to bend in children may prevent the development of fracture but nevertheless be associated with a considerable amount of underlying structural brain damage.
There is a strong association between the presence of a skull fracture and the development of an intracranial he-matoma (Cooper 2001; Mendelow et al. 1983), particu-larly if, after the injury, the patient has a depressed level of consciousness. For example, it has been determined that only 1 in 6,000 patients presenting to emergency de-partments who did not have either a depressed level of consciousness or a skull fracture subsequently developed an intracranial hematoma, whereas the risk becomes 1 in 4 if these clinical features are present. The site of the fracture is also important given that if it affects the squa-mous part of the temporal bone there is a possibility that an extradural hematoma may develop.
Surface Contusions and Lacerations of the Brain By definition, the pia-arachnoid is intact over surface contusions and is torn in lacerations. Contusions have been considered to be the hallmark of brain damage due to head injury (Table 2–5), and they have a characteristic distribution affecting the poles of the frontal lobes; the inferior aspects of the frontal lobes, including the gyri recti; the cortex above and below the operculum of the Sylvian fissures; the temporal poles; and the lateral and inferior aspects of the temporal lobes (Figure 2–1). Less commonly, they are seen on the underaspects of the cere-bellar hemispheres. They may extend into white matter, comprising a mixture of hemorrhage and necrosis at the margin of which is an area of swelling (Figure 2–2). Par-ticularly where there has been extensive damage, an actual hematoma may develop within the affected gyrus, and, if laceration of the pia-arachnoid has taken place, then there may be bleeding into the subdural space. The combina-tion of extensive contusion and an associated SDH is referred to as a burst lobe. Depending on the location of the lesion, there may or may not be an associated sen-sorimotor neurological deficit.
T A B L E 2 – 4 . Types of fracture of the skull Linear or fissure
Depressed if fragments of the inner table are displaced inward by at least the thickness of the diploe
Compound if depressed fracture is associated with laceration of scalp, and penetrative if there is also a tear in the dura Hinge if fracture extends across the base of the skull Coup at site of injury
Contre coup if fracture is located a distance from the point of injury
Growing fractures occur in infancy and are due to interposition of soft tissue between the edges of the fractures that may prevent healing
The surface contusions/lacerations and associated swelling may be sufficient to act as a mass lesion, with the subsequent sequelae of raised intracranial pressure (ICP).
Indeed, such a sequence of events was attributed to con-tusional injury alone in 6 of 66 patients who “talked and died,” 25% of whom did not have significant intracranial hematoma (Reilly et al. 1975).
Various types of contusion have been described. Ref-erence has already been made to fracture contusions that occur at the site of a fracture and are particularly severe in the frontal lobes and in association with fractures of the anterior fossae; coup contusions occur at the site of con-tact in the absence of a fracture, and contrecoup
contu-sions occur in brain tissue diametrically opposite the point of contact (Adams 1992).
The development of a contusion index has allowed the depth and extent of contusions in different parts of the brain to be expressed quantitatively (Adams et al. 1985).
This index has shown that severe contusions are present in some 10% of fatalities, moderately severe contusions in 78%, and mild contusions in 6%. The index has con-firmed that contusions occur most commonly in the fron-tal and the temporal lobes, are more severe in patients with a fracture of the skull than in those without a frac-ture, are less common in patients with diffuse brain injury than in those with focal brain injury, and are more severe in patients who do not experience a lucid interval than those who do. More recently, a hemorrhagic lesion score has been derived that provides a finer discrimination of the distribution and severity of injury by including hem-orrhagic lesions involving the corpus callosum and deep grey and white matter (Ryan et al. 1994).
Intracranial Hematoma
Intracranial hematoma is the most common cause of clin-ical deterioration and death in patients who experience a lucid interval, the group who “talk and die” or talk and deteriorate after injury (Bullock and Teasdale 1990;
Klauber et al. 1989; Reilly et al. 1975; Rockswold et al.
1987). Indeed, it is the late recognition and treatment of intracranial hematoma that constitutes one of the most, if not the most, important avoidable factors in the manage-ment of TBI. Regardless of the severity of the brain injury, there is always the possibility that an intracranial hema-T A B L E 2 – 5 . Surface contusion and lacerations
Found in 96% of fatal adult brain injury, they are the most common source of bleeding into the subarachnoid space.
Characteristically affect crests of gyri.
Appear as punctate or streaks of hemorrhage at right angles to the cortical surface.
At vertex, are related to fractures and inferiorly correspond to irregular bony contours at base of skull.
In early infancy, they appear as tears in the subcortical white matter and in the inner layers of the cortex of the frontal and temporal lobes.
Healed contusions are found incidentally in 2%–5% of adult autopsies.
F I G U R E 2 – 1 . Acute contusions: 18-hour survival.
Base of brain to show hemorrhagic defects and associated sub-arachnoid hemorrhage on underaspects of frontal lobes and in relation to temporal poles.
F I G U R E 2 – 2 . Acute contusions: 48-hour survival.
Coronal section through frontal lobes to show distribution and extent of contusions.
toma may complicate the injury. The bleeding usually begins at the time of injury, and, by the time of admission to hospital some 3 to 4 hours later, there is a hematoma in between approximately 30% and 60% of patients admit-ted who are in a coma.
If the injury is mild, then loss of consciousness may be limited to a few minutes, but a secondary loss of con-sciousness may develop due to an expanding intracranial hematoma. This classical textbook description of a lucid interval followed by coma occurs in only a minority of cases, there being many more patients who are in a coma from the time of injury and in whom a hematoma pro-gressively develops.
Traumatic intracranial hematomas are usually classi-fied according to the anatomical compartment in which they develop (Table 2–6).
Extradural (epidural) hematoma. An extradural (epidu-ral) hematoma consists of an ovoid mass of clotted blood that lies between the bone of the vault or the base of the skull and the dura (Table 2–7) (Freytag 1963; Jamieson and Yelland 1968; Maloney and Whatmore 1969).
In two-thirds of cases, the extradural hematoma is caused by a fracture in the squamous part of the temporal bone; in the remaining cases, the hematoma may develop in relation to the frontal and parietal parts of the brain or even within the posterior fossa (Lewin 1949; McKissock et al. 1960), and, occasionally, they are multiple. Because the source of the bleeding is usually arterial, the hematoma en-larges fairly rapidly, gradually stripping the dura from the scalp to form a circumscribed ovoid mass that progressively indents and flattens the adjacent brain. In many cases, there is little associated underlying brain damage (Figure 2–3).
Small hematomas may become completely organized, although larger ones may undergo partial organization,
with their centers becoming cystic and filled with dark viscous fluid. After approximately 2 weeks, the hemato-mas become smaller and, in the majority of patients, are completely resolved by the fourth to sixth week after the injury (Bullock et al. 1985).
Intradural hematomas. Subarachnoid hematoma. S o m e degree of subarachnoid hemorrhage occurs in any serious brain injury. Most occur in association with surface con-tusions. In many cases, there is a thin layer of blood clot over the lateral and inferior aspects of the frontal and temporal lobes, but in approximately 10%–15% of patients, the amounts are larger and may constitute a sub-arachnoid hematoma. Under these circumstances, there may be associated constriction (vasospasm) of the cerebral arteries, and, if large amounts of subarachnoid hemor-T A B L E 2 – 6 . Types and frequency of
intracranial hematoma
Type Frequency (%)
Extradural (epidural) 4
Intradural 56
Subdural 13
Subarachnoid 3
Discrete intracerebral or intracerebellar hematoma not in continuity with the surface of the brain
15
The “burst” lobe—an intracerebral or intracerebellar hematoma in continuity with the related subdural hematoma.
25
T A B L E 2 – 7 . Extradural (epidural) hematoma Present in 5%–15% of fatal brain injury.
There is an associated skull fracture in 85% of adults; fracture is commonly absent in children.
There is a fracture in the squamous part of the temporal bone in 70% of cases; in remaining cases, fractures are frontal or parietal or even occur in the posterior fossa.
The hematoma reliably indicates the site of a fracture.
Hematoma is most common in young adults and is rarer in children.
In 5%–10% of patients, an extradural hematoma coexists with an intradural hematoma.
F I G U R E 2 – 3 . Acute extradural hematoma: 23-hour survival.
Coronal section through cerebral hemispheres at level of ante-rior thalamus. Note absence of acute contusions but consider-able distortion of right side of brain, with development of supracallosal and tentorial herniae, asymmetry of ventricles, and secondary hemorrhage in the brainstem.
rhage are present in the posterior fossa, acute obstructive hydrocephalus may develop. The entity of traumatic sub-arachnoid hemorrhage is well recognized as a result of damage to blood vessels in the posterior fossa (Harland et al. 1983) often in association with a fracture of the base of the skull (Vanezis 1979, 1986).
Subdural hematomas. A small amount of hemor-rhage within the subdural space is common in fatal brain injury. Because this blood can spread freely throughout the subdural space, it tends to cover the entire hemi-sphere, with the result that an SDH is usually larger than an extradural hematoma. The great majority of SDHs are due to rupture of veins that bridge the subdural space where they connect the upper surface of the cerebral hemisphere to the sagittal sinus. Occasionally, they are arterial in origin (Table 2–8).
SDHs large enough to act as significant mass lesions have been variously reported in between 26% and 63% of blunt head injuries (Freytag 1963; Maloney and What-more 1969) (see Figure 2–3). In approximately 8%–13%
of cases, the hematomas are pure with little evidence of other brain damage. However, most are associated with considerable brain damage, and, therefore, the mortality and morbidity are greater in subdural than in extradural hematomas. This is particularly true in cases with a
“burst” frontal or temporal lobe (Figure 2–4).
The current literature classifies SDH as acute when it is composed of clot and blood (usually within the first 48 hours after injury), subacute when there is a mixture of clotted and fluid blood (developing between 2–14 days af-ter injury), and chronic when the hematoma is fluid (de-veloping more than 14 days after injury) (Bullock and Teasdale 1990). Chronic SDH occurs weeks or months after what may appear to have been a trivial head injury.
However, a history of head injury is present in 25%–50%
of cases (Fogelholm and Waltimo 1975; Marshall et al.
1983). The hematoma becomes encapsulated and slowly increases in size, and may become sufficiently large to produce distortion and herniation of the brain (see Brain Damage due to Raised Intracranial Pressure). Chronic SDH is more common in older than in younger patients, in patients who are alcoholic, and in patients taking anti-coagulation therapy.
Intracerebral and intracerebellar hematomas. Intracer-ebral and intracerebellar hematomas are present in approximately 16%–20% of fatal brain injury cases. They are often multiple and occur most commonly in the fron-tal and temporal lobes (Bullock and Teasdale 1990). Less commonly, they occur in the cerebellum. Sometimes, traumatic intracerebral hematomas develop several days after the injury, and recognition of this possibility may have important medicolegal implications if the patient dies (Elsner et al. 1990; Nanassis et al. 1989). There is greater recognition of relatively small hematomas deeply seated in the brain as a result of computed tomography (CT) scanning and magnetic resonance imaging (MRI):
many hematomas are often rather small and centered on midline structures, including parasagittal white matter (a so-called gliding contusion), the corpus callosum, the structures in the walls of the third ventricle, and in the stri-atum (so-called basal ganglia hematomas). In the majority of these cases, the patients are in a coma, and the small hematomas are part of the clinicopathological entity of diffuse (traumatic) axonal injury (Adams et al. 1986;
Macpherson et al. 1986).
Sometimes, patients present with a history of possible brain injury so that the finding of a solitary hematoma re-quires consideration that it may be due to either a non-traumatic hypertensive bleed or the rupture of a saccular aneurysm. Interpretation of the autopsy findings can be difficult, and much depends on the site of the hematoma.
T A B L E 2 – 8 . Acute subdural hematoma In 70% of cases, injury is produced by a fall or an assault.
Approximately 70% of patients have a skull fracture, but in approximately 50% of these cases, the fracture is contralateral to the side of the hematoma.
Peak incidence of intradural hematoma is in the fifth and sixth decades of life.
Only 2%–3% of traumatic hematomas are in the posterior fossa, where intradural hematomas are as common as extradural.
An acute hematoma is associated with swelling of an ipsilateral cerebral hemisphere; such swelling often persists after the
hematoma has been evacuated. F I G U R E 2 – 4 . “Burst” temporal lobe: 37-hour survival.
Note extensive contusional injury to temporal lobes that at sur-gery was associated with a large acute subdural hematoma.
For example, if the hematoma is in the subfrontal or tem-poral region, it is more likely to be traumatic than not.
There are a number of risk factors for the development of intracerebral hematoma that include tumor, vascular mal-formation, and substance abuse. Patients receiving thrombolytic therapy are also at risk, and those receiving anticoagulants are at particular risk of developing intra-cerebral hemorrhage related to contusions.
Burst lobe. The term burst lobe describes an intrace-rebral or an intracerebellar hematoma that is continuous with a SDH. It is presumed to be due to damage to or lac-eration of superficial brain tissue. It is present in approx-imately 25% of fatal cases of brain injury and occurs most commonly in the frontal and temporal lobes.
Brain Damage due to Raised Intracranial Pressure ICP is frequently elevated in patients after brain injury due to the mass effects of contusions/lacerations, intra-cranial hematomas, and brain swelling occurring in what is essentially an enclosed space.
In a healthy adult, the ICP is usually in the range of 0 to 10 mm Hg. Pressures greater than 20 mm Hg are ab-normal, and when the ICP is greater than 40 mm Hg, there is neurological dysfunction and impairment of brain electrical activity. As the ICP continues to rise, the ability of the cerebral circulation to maintain autoregulation and the normal cerebral perfusion becomes compromised. An ICP greater than 60 mm Hg is invariably fatal, and there is increasing evidence that even pressures between 20 and 40 mm Hg may be associated with increased morbidity.
If unchecked, an increase in the ICP is likely to kill the patient as a result of deformation of tissue, shift of the midline structures, the development of internal herniae, and secondary damage to the upper brainstem. This mechanism is the most common cause of death in the neurosurgical intensive care unit, being present in ap-proximately 75% of brain-injured patients who die (Gra-ham et al. 1987).
A unilateral mass lesion causes distortion of the brain, a reduction in the volume of cerebrospinal fluid (CSF), and, in the closed skull, the formation of internal herniae.
Principal among these herniae are the displacement of the cingulate gyrus under the free edge of the falx (a subfal-cine or supracallosal hernia) and the medial temporal gy-rus downward through the incisura (a tentorial hernia). A mass lesion in the posterior fossa may result in herniation of the cerebellar tonsil through the foramen magnum (a tonsillar hernia). As these herniae develop, CSF spaces are obliterated, and pressure gradients begin to develop between the various intracranial compartments. Further progression is likely to mechanically deform blood vessels
sufficiently to cause vascular complications, such as hem-orrhage and/or infarction in the upper brainstem and variable degrees of ischemic damage within the territories of one or both posterior cerebral arteries. Less com-monly, there is infarction of brain tissue supplied by the anterior cerebral, anterior choroidal, and the superior cerebellar arteries (Graham et al. 1987). Infarction has also been recorded in the anterior lobe of the pituitary gland in approximately 45% of cases (Harper et al. 1986).
Other Types of Focal Brain Injury
In accidents causing hyperextension of the head on the neck, traumatic separation of the pons and medulla is a well-recognized cause of death (Lindenberg and Freytag 1970; Simpson et al. 1989). In many cases, there is an associated ring fracture at the base of the skull or disloca-tion and/or fracture of the first or second cervical verte-bra. Although complete tears are immediately fatal, patients with small or incomplete tears at the pontomed-ullary junction may survive for some time after injury (Britt et al. 1980; Pilz 1980; Pilz et al. 1982).
Almost any of the cranial nerves may be damaged at the time of injury. The frequency of injury to the cranial nerves has been underestimated, as demonstrated by MRI, which provides a much more sensitive means of identifying damage than was previously possible with CT (Gean 1994).
Damage can also occur to the hypothalamus and pitu-itary gland. Occasionally, the pitupitu-itary stalk is torn at the time of brain injury, but, more frequently, the stalk is in-tact, although there is infarction in the anterior lobe of the pituitary. A number of potential mechanisms have been suggested to explain this type of damage, including a fracture at the base of the skull that extends into the sella turcica; elevation of the ICP, leading to distortion and compression of the pituitary stalk; and hypotensive shock analogous to the situation occurring in postpartum ne-crosis of the pituitary.
Damage to blood vessels may also occur. It is possible to identify various vascular lesions by angiography, in-cluding dissection or occlusion of the internal carotid or vertebral arteries, traumatic pseudoaneurysm, traumatic arteriovenous fistula, and venous thrombosis and an as-sessment of vasospasm.
Imaging techniques after brain injury have shown that in many patients there are multiple lesions in the brain, some of which are hemorrhagic. MRI is particularly useful in the detection of these lesions, the principal neuropatho-logical correlates of which are lesions in lobar white matter, in the corpus callosum, and in the dorsolateral sector(s) of the rostral brainstem adjacent to the superior cerebellar
pe-duncles. These areas have become known as the shearing injury triad. However, such lesions are not restricted to these areas, being found also in periventricular structures, the hippocampal formation, the internal capsule, and, oc-casionally, deep within the cerebellar hemispheres.
Multiple petechial hemorrhages are not uncommonly found when patients die from severe brain injury. Al-though many of these may indeed have histological evi-dence of diffuse axonal injury (DAI) (see Diffuse Axonal Injury section), there are many others, including diffuse vascular injury (see Diffuse [Multifocal] Vascular Injury section), in which the hemorrhages can be ascribed to a number of causes that include ischemic damage in the ter-ritory supplied by the pericallosal arteries—usually sec-ondary to a supracallosal hernia, fat embolism, and a host of vascular and hematological abnormalities that consti-tute some of the medical complications of head injury.
Diffuse Brain Injury
Diffuse brain injury describes a number of pathologies, some of which are a consequence of acceleration/decelera-tion applied to white matter, whereas others are vascular in nature, and yet others are secondary to hypoxia. Although it is true that these pathologies are widely distributed and in some instances are diffuse, the overall generic term dif-fuse brain injury is somewhat of a misnomer, because in the majority of cases the pathology is multifocal.
Diffuse Axonal Injury
DAI is a type of brain damage that has many synonyms and was first described under the heading of diffuse degen-eration of white matter (Strich 1956). Since then, a variety of terms have been used that have helped to further char-acterize DAI (1) by mechanism (e.g., shearing injury) (Peerless and Rewcastle 1967; Strich 1961), (2) by loca-tion of the underlying pathology (e.g., inner cerebral trauma) (Grcevic 1988), or (3) by combination of mecha-nism and the location of the principal pathology (e.g., dif-fuse damage of immediate impact type [Adams et al. 1977]
and diffuse white matter shearing injury [Zimmerman et al. 1978]). There was international recognition for the term diffuse axonal injury (Adams et al. 1982; Gennarelli et al. 1982), but this has been superseded by the term trau-matic axonal injury (TAI).
In severe cases of DAI (Table 2–9), the hemorrhages in midline structures, including the brainstem, can usually be seen at the time of brain cutting (Figure 2–5). This is in contrast to the widespread damage to axons that can only be identified microscopically. The histological ap-pearances of the lesions depend on the length of survival after injury (Table 2–10). If the patient survives for only a
few days, midline structure lesions are usually hemor-rhagic, but over time these result in shrunken, often cys-tic, scars. However, the appearance of the important ax-onal lesions changes considerably over time. Thus, if survival is short (days), there are numerous axonal swell-ings and axonal bulbs that can be readily identified either as argyrophilic swellings in silver-stained preparations or by immunohistochemistry (Figure 2–6). The swellings and bulbs are most commonly seen in deep structures and, in particular, in the white matter of the parasagittal cortex, the corpus callosum, the internal capsule, and the T A B L E 2 – 9 . Pattern and frequency of
hemorrhages and tissue tears in severe cases of diffuse traumatic axonal injury
Pattern Frequency (%)
Dorsolateral sector of upper brainstem 95
Corpus callosum 92
Choroid plexus of third ventricle 90 Parasagittal (gliding) contusion 88
Hippocampus 88
Periventricular (third ventricle) 83
Interventricular septum 80
Cingulate gyrus 61
Thalamus 56
Basal ganglia 17
F I G U R E 2 – 5 . Traumatic diffuse axonal injury (DAI): 5-day survival.
Note absence of surface contusions and midline hemorrhages in the corpus callosum and in the left thalamus. Hemorrhages were also seen in the dorsolateral sector of the upper brainstem. Mi-croscopy revealed widely distributed axonal damage, with a se-verity grading of DAI 3.