Head and spinal injuries
HEAD INJURY
The severity of head injury is often assessed using the Glasgow coma scale (Table 11.1). This yields scores of 3 (the worst score) to 15 (the best score) based on an assessment of ocular, verbal, and motor responses.
Table 11.1
| Best eye response (maximum = 4) | |||
| 1. | No eye opening | 3. | Eyes opening to verbal command |
| 2. | Eye opening to pain | 4. | Eyes open spontaneously |
| Best verbal response (maximum = 5) | |||
| 1. | No verbal response | 4. | Confused |
| 2. | Incomprehensible sounds | 5. | Oriented |
| 3. | Inappropriate words | ||
| Best motor response (maximum = 6) | |||
| 1. | No motor response | 4. | Withdrawal from pain |
| 2. | Extension to pain | 5. | Localizing to pain |
| 3. | Flexion to pain | 6. | Obeys commands |
| Coma score | Clinical correlate |
| 13 or above | Mild brain injury |
| 9–12 | Moderate brain injury |
| 8 or less | Severe brain injury |
From: Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81–84.
NATURE OF LESIONS IN HEAD INJURY
Type of head injury
Time course
Brain damage following trauma can be viewed as occurring in two phases (Fig. 11.1):
Progressive neurologic deterioration over many years has been noted in 15% of patients who have suffered severe head trauma (Fig. 11.2).
HEAD INJURY
NON-MISSILE HEAD INJURY
Laceration or bruising of the scalp is a common form of focal injury and a good indicator of the site of the trauma (Fig. 11.3).
FOCAL LESIONS OF THE SKULL
Contact with a flat surface tends to produce closed fissure fractures, which often extend into the base of the skull.
MECHANISMS OF PRIMARY DAMAGE IN NON-MISSILE HEAD INJURY
Acceleration or deceleration damage
Applying force to the head causes the skull to accelerate in a linear or rotational fashion. Due to inertia, the movement of the brain lags behind that of the skull and damage may result from the following mechanisms:
Contact of the inner surface of the moving skull with the stationary brain may produce contusions, particularly in places where the skull protrudes internally. When the moving head is abruptly halted, the brain continues briefly to move due to its inertia. Impact of the moving brain against the stationary skull may again produce contusions.
Traction on the bridging veins may cause them to tear, resulting in subdural hemorrhage.
The risk of intracranial hematoma is significantly increased in patients with skull fractures.
Fractures of the base of the skull predispose to:
Infection, as they often pass through the petrous temporal bone or the anterior cranial fossa and cause leakage of cerebrospinal fluid (CSF) through the ear, nose, or nasopharynx. These breaks in the integrity of the skull are also routes for the spread of infection.
Depressed fractures may tear the dura and associated blood vessels, leading to intracranial hemorrhage (see p. 274).
MACROSCOPIC APPEARANCES
Acutely, contusions appear as superficial hemorrhagic areas associated with some hemorrhage into the overlying leptomeninges and variable brain swelling (Figs 11.4–11.6). Over subsequent days and weeks their color changes to brown or orange, and involved gyri become indented or superficially cavitated as necrotic tissue is resorbed. In brain slices, old contusions often have a triangular shape, with the point in the depths of the cortex or underlying white matter and a wide base at the surface of the crest of the gyrus (Fig. 11.7, see also Fig. 11.31). Contusions can be distinguished from foci of old ischemic damage, which are almost invariably more severe within the depths of sulci.
11.4 Superficial contusions on the underside of the occipital lobes.
The contusions in the left occipital lobe are mostly superficial whereas those on the right are more hemorrhagic and involve the full thickness of the cortex.
11.5 Severe cerebral contusions.
Severe frontal and temporal lobe contusions associated with extensive hemorrhage into the overlying subarachnoid space.
11.6 Superficial contusions of orbital frontal cortex.
The contusions are more extensive in the right frontal lobe.
11.7 Old cerebral contusions.
(a) Old contusions over the lateral aspect of frontal, temporal and parietal lobes. These appear as brown or orange indentations in the crests of gyri. (b) Old contusions on inferior aspect of frontal lobes (c) Old wedge-shaped contusion of the left inferior temporal gyrus (arrow). There is also evidence of old diffuse axonal injury: the ventricles are dilated, the corpus callosum is thinned and yellow, and the temporal and right parasagittal frontal white matter show gray discoloration.
11.31 Long-term effects of DAI.
(a) Old trauma with contusions of the right middle and superior temporal gyri (arrows) and ventricular dilatation. Note the ill-defined gray discoloration of the white matter due to DAI. This is most marked in the temporal lobes (including the non-contused left temporal lobe), but also involves the corpus callosum and internal capsule. (b) Gray discoloration of the parasagittal white matter in the posterior part of the parietal lobes. (c) The gray-brown streaks in the parasagittal white matter in this brain are old gliding contusions.
Contusions may occur in the region of impact (a form of contact damage), particularly if this causes fracturing, but also occur elsewhere over the brain in a stereotyped distribution that tends to be much the same whatever the site of the original injury. The contusions involve the crests of gyri that come into contact with protuberances within the skull (Figs 11.8, 11.9). Contusions tend therefore, to be located in the following regions:
11.9 Common sites for contusions.
(a) Contusions of the orbital surface of the frontal lobes and tips of the temporal lobes. (b) Cut surface of brain showing contusions of the orbital surfaces of frontal lobes and tip of left temporal lobe. There is a hematoma in the right frontal lobe. (c) and (d) Contusions on either side of the sylvian fissure. (e) Contusions of the right cerebellar hemisphere. (f) A horizontal slice through the cerebellum shows that the contusions extend into the cerebellar white matter.
Contusions may also involve the cerebellar hemispheres (Fig. 11.9e,f).
Lacerations develop when the severity of trauma has been sufficient to cause tearing of the pia. This may occur in association with a depressed skull fracture. The most severe pattern of cerebral laceration is embraced by the term ‘burst lobe’. This is often associated with a skull fracture and most commonly involves the frontal and temporal lobes, which show confluent intracerebral and subarachnoid bleeding (sometimes even extending into the subdural or extradural space), associated with massive disruption of the affected lobe (Fig. 11.10).
11.10 Severe contusion.
(a) Severe contusion of the right frontal and temporal poles with blood clot over the frontal pole suggesting cerebral laceration. (b) Sectioning confirms laceration of the frontal lobe associated with severe contusional damage and extension of bleeding into the subarachnoid and subdural spaces. (c) Another common site of ‘burst lobe’ is the temporal region (as shown here).
MICROSCOPIC APPEARANCES
The appearance of contusions evolves with time through several stages:
Initially the contusion is visible as microscopic regions of perivascular hemorrhage (Fig. 11.11a) following the track of small vessels in the cortex and usually running perpendicular to the cortical surface. The hemorrhage occurs within seconds or minutes of the injury.
11.11 Microscopic appearance of early contusions.
(a) Early contusions with small perivascular hemorrhages. (b) Early contusions showing extravasation of blood into the cortex associated with acute degeneration of the surrounding neurons. (c) Later evolution leads to more extensive perivascular hemorrhages in the cortex and superficial white matter.
Over several hours blood continues to seep into the adjacent cortex, which shows local swelling and confluent hemorrhage. If the contusion is severe there is extension into the underlying white matter. During this phase, neurons in the immediate vicinity begin to degenerate (Fig. 11.11b,c). Blood vessels within the contused tissue may show margination by neutrophils (Fig. 11.12), which later infiltrate the adjacent parenchyma.
What remains eventually is a superficial, roughly wedge-shaped, region of neuronal loss and glial scarring (Fig. 11.13). Hemosiderin pigment is found in scattered residual macrophages and astrocytes. The remaining neurons may become mineralized. The subjacent white matter is rarefied and gliotic.
INTRACRANIAL HEMORRHAGES
Extradural hematoma
Extradural hematomas are relatively localized and may accumulate slowly over a period of hours because of the adherence between the dura and the inner aspect of the calvarium (Fig. 11.14). They are evident macroscopically as a biconvex accumulation of clotted blood between the skull and the dura (Fig. 11.15).
11.15 Extradural hematoma.
(a) Fracture of the right squamous temporal bone with an associated extradural hematoma. Extradural blood is visible through the dura in the left middle and anterior cranial fossae. (b) Extradural hematoma in right frontoparietal region. ((b) Courtesy of Professor Michael A. Farrell, Dublin, Ireland.)
LUCID INTERVALSubdural hematoma
Subdural hematoma usually results from tearing of bridging veins that cross the subdural space, especially those related to the superior sagittal sinus. Blood from the ruptured vessels spreads freely through the subdural space and can envelop the entire hemisphere (Fig. 11.16).
11.16 Subdural hematoma.
(a) Removal of the calvarium at necropsy reveals a left subdural hematoma that has compressed the underlying brain. The arachnoid surface of the left cerebral hemisphere is blood-stained and the gyri are flattened. (b) Indentation of the left cerebral hemisphere due to a subdural hematoma. Note the contusion, hemorrhage, and focal infarction in the underlying brain tissue. (c) Chronic subdural hematoma enclosed in a thin ‘membrane’ of granulation tissue. Although the hematoma was known to be more than 2 weeks old, it consisted of clotted blood. (d) Subdural hematoma showing compression of brain.
Chronic subdural hematomas become surrounded by a ‘membrane’ of organizing granulation tissue (Fig. 11.17). This is usually evident on the dural aspect of the hematoma within about 1 week, and later on its deep surface. Progressive enlargement of the hematoma may occur, mainly due to recurrent bleeding from friable blood vessels in the granulation tissue, although an osmotic effect of blood breakdown products may also contribute. Attempted dating of subdural hematomas by histologic examination of the ‘membranes’ has proven unreliable.
11.17 Chronic subdural hematoma.
(a) This hematoxylin-van Gieson-stained section through a chronic subdural hematoma illustrates the differing thickness of the outer (twin arrows) and inner walls (single arrow). The collagen within the hematoma walls is stained red. Very little blood (stained orange) remains within the hematoma cavity, which macroscopic examination had shown to contain a mixture of loose blood clot and turbid fluid. (b) A higher-magnification view of the outer wall (here stained with H&E) shows it to consist of collagenous connective tissue within which are numerous thin-walled blood vessels, some with adjacent microscopic foci of hemorrhage. The tissue also includes scattered lymphocytes and hemosiderin-laden macrophages. (c) The outer wall is much thinner and less vascular. In this case there has also been more recent hemorrhage into the underlying subarachnoid space (to the right of the image). (d) The accumulation of hemosiderin pigment in the outer membrane is well demonstrated in a section stained by Perls’ method.
Traumatic subarachnoid hemorrhage
There are several possible sources of subarachnoid bleeding:
Subarachnoid blood may derive from severe contusions and lacerations (Fig. 11.18, see also Figs 11.5, 11.10); the hemorrhage is usually localized to the region of cortical damage.
11.18 Traumatic subarachnoid hemorrhage.
Blood is present over the cerebral convexity and in the sylvian fissure.
Fractures of the skull base can tear large vessels at the base of the brain.
Even in the absence of basal fractures, cranial trauma occasionally causes rupture or dissection of the vertebral arteries, resulting in arterial occlusion or subarachnoid hemorrhage; the tear usually originates near where the arteries pass through the dura into the cranial cavity (Fig. 11.19). More rarely, subarachnoid hemorrhage results from a tear in the intraosseous part of the vertebral arteries within the cervical spine (Fig. 11.20).
11.19 Traumatic rupture of the vertebral artery in the region of entry into the cranial cavity.
(a) A pseudoaneurysm (arrow) is present at the site of vertebral artery rupture after head injury. The patient presented with delayed subarachnoid hemorrhage several days later. (b) The pseudoaneurysm is clearly visible in an elastic/van Gieson-stained section. (Courtesy of Dr Hugh White, North Bristol NHS Trust, UK.)
Cerebral and cerebellar hematomas
Superficial lobar hematomas are generally related to overlying contusional damage and are mainly seen in the frontal and temporal lobes (Fig. 11.21). They also occur in association with contusions in the cerebellum (Fig. 11.22). Deep hematomas tend to be related to the basal ganglia and thalamus (Fig. 11.23, see also Fig. 11.30a) and are often associated with diffuse axonal injury.
11.21 Cerebral hematomas.
(a) Hematomas in the white matter of the frontal lobe associated with severe contusions. (b) Superficial lobar hematoma in the posterior frontal region. The hematoma was related to a cortical laceration associated with a depressed skull fracture.
11.22 Cerebellar hematoma.
Hematomas in the cerebellum are usually associated with severe contusional damage to the cerebellar hemispheres, which is often related to a skull fracture in the posterior fossa.
11.23 Hematomas of the basal ganglia and thalamus.
(a) Traumatic hematoma in the right basal ganglia associated with mass effect and compression of the ventricular system. The appearance resembles that of a primary intracerebral bleed. Histologic examination revealed diffuse axonal injury in a wide distribution. (b) A cluster of hematomas in the left thalamus caused by head injury. There is other damage in the form of cortical contusions, and a small hematoma in the hippocampus. A hemorrhagic lesion in the corpus callosum is indicative of diffuse axonal injury.
11.30 Gliding contusions.
(a) Bilateral gliding contusions in the parasagittal white matter. The one on the left is no more than a perivascular streak of hemorrhagic white matter discoloration. The one on the right includes several hemorrhagic foci and a larger hematoma. There are also typical DAI-related lesions in the corpus callosum, contusions of both unci, and several other hematomas, including one in the right putamen. (b) Large lesions extending through the parasagittal white matter towards the corpus callosum. In this case there is also severe contusion of the temporal lobe and petechial hemorrhages are present in the corpus callosum in the lower slice.
DISTINGUISHING PRIMARY AND TRAUMATIC INTRACEREBRAL HEMATOMAS
UNCOMMON TYPES OF FOCAL BRAIN DAMAGE
Uncommon types of focal brain damage include:
Ischemic brain damage due to traumatic arterial dissection and thrombosis resulting from stretching of the vertebral or carotid arteries by hyperextension of the neck (Fig. 11.24).
11.24 Traumatic arterial dissection.
Traumatic dissection and associated thrombosis of the vertebral artery in a patient who developed brain stem infarction after head injury.
A pontomedullary rent resulting from severe injury associated with hyperextension of the neck (Fig. 11.25).
11.25 Pontomedullary rent.
Tearing of the brain stem at the junction between the upper medulla and lower pons has produced a hemorrhagic lesion termed a pontomedullary rent. In this case the injury resulted from a high-speed motor-cycle collision in which the patient suffered a hyperextension injury to the neck. At necropsy there was a large quantity of subarachnoid blood in the posterior fossa, but no clear site of origin of the hemorrhage. Once the brain had been fixed and sliced it became clear that the site of bleeding had been this injury to the brain stem.
INFECTION
Infection is predominantly a complication of skull fractures:
Fractures of the calvarium or skull base can provide a route for bacteria to pass from the major air sinuses into the subarachnoid space and cause meningitis. Such fractures are often associated with a leakage of CSF or the formation of an aerocele.
The incidence of brain abscesses is, however, increased even after closed head injuries, presumably because the devitalized tissues are prone to colonization in the event of a transient bacteremia (see Chapter 15).
NON-ACCIDENTAL INJURIES IN CHILDREN
Non-accidental injuries in children are associated with distinct patterns of head injury, reflecting the types of trauma (often involving shaking, with or without impact), the flexibility and thinness of the scalp and skull, the immaturity of the brain, the relative size and weight of the head (12.5% of the weight of a young infant compared with 2.5% of that of an adult), and relative weakness of the neck muscles in infants.
There may be impact damage, with focal lesions of the scalp and skull.
