NEUROPATHOLOGY FOR MEDICAL STUDENTS
Presented by William I. Rosenblum, MD
CHAPTER 8--BRAIN AND SPINAL CORD TRAUMA
PRETEST: Answers will be found in the text of this chapter or click on link at end of questions
TRAUMA TO THE BRAIN
A blow to the head, or any other severe physical force, can deform, displace, and tear the tissues covering the brain and the brain itself. This may produce loss of function, necrosis, and hemorrhages. Head injuries can be classified as:
(a) Closed: when a blunt object damages the brain and its coverings without actually perforating the skull or dura.
(b) Penetrating: when the skull and brain are directly lacerated by an object, such as a bullet.
The closed type of injury constitutes the majority of civilian injuries. Extensive intracranial damage may result from an injury to the head which produces little damage to the outside. Instead, the force may be communicated through a rigid, bony vault (calvarium) to the soft tissue within.
When the head is struck, it often moves until it is abruptly brought to a stop against a solid object. At this moment, the brain continues moving for a brief instant until it hits the bony prominences inside the now stationary skull. Sometimes, the injury to the moving brain takes place at a site opposite the point at which the skull was initially struck. This type of injury is called "contra-coup," as opposed to a "coup" injury occurring on the same side as the initial impact (coup = blow, French; contra-coup = opposite the blow).
Traumatic lesions, whether they are the product of closed or penetrating injuries, and whether they are coup or contra-coup, may be said to have direct effects, and secondary effects as listed below.
A. DIRECT EFFECTS
2. Hemorrhages--epidural, subdural, intraparenchymal
3. Lesions to brain--contusion, laceration [ the most minor "lesion" has no identifiable gross or microscopic counterpart in human material and is the concussion which produces unconsciousness].
4. Diffuse axonal injury [DAI]
B. SECONDARY EFFECTS
1. Cerebral edema or swelling
2. Herniations of brain tissue
As a result of traumatic brain damage, there may be permanent localizing neurologic defects or post-traumatic epilepsy.
SPECIFIC TRAUMATIC LESIONS
The image below displays a large epidural hematoma in the temporo-parietal region. The epidural hemorrhage is outside the dura, and is located between the bone and the dura. The patient fractured the squamous portion of temporal bone and lacerated the middle meningeal artery. The brisk arterial bleeding produced a rapidly expanding mass of blood. This can produce rapid increase of intracranial pressure with consequent death. The patient may be awake at the beginning of the period of expansion and this interval is called the lucid interval and may fool the physician into believing that the trauma was benign.
A subdural hematoma is the accumulation of blood under the dura mater. This arises from rupture of the veins that course through the subdural space (bridging veins) as they pass from the cerebral hemispheres to the dural sinuses. These veins may be torn by any force suddenly applied to the head.
The natural history of subdural hematoma which finally resolves (organization) is as follows. Approximately two days after the hemorrhage, an outer membrane of fibroblasts begins to form under dura on the outer surface of clot. This membrane thickens over the ensuing weeks. Meanwhile, later in week one, an inner membrane of fibroblasts begins to form between arachnoid and inner surface of clot. During the following weeks, both membranes thicken. The clot between them organizes and thins; eventually the two thickened membranes become opposed. The resultant "membrane" varies in thickness, depending on size of original clot. It may be as thin as paper or it may be several mm thick.
The subdural hematoma just described is one which stopped bleeding, and often is not associated with clinical symptoms. However, a large subdural can cause acute symptoms because it acts as a space occupying mass. Sometimes these symptoms develop after an initial silent period. In such cases the subdural has continued to grow until it became symptomatic. These are often called chronic subdurals. We still do not understand why some subdural hemorrhages continue to grow.
In the image below the accumulation of blood in the subdural space is recent. The blood clot is soft, friable, and easily separated from the dural membranes. The dura mater has been reflected to demonstrate the extension and location of the blood clot.
In the image below the hemorrhage has become organized and largely resolved. A membrane, discolored by blood pigment is left adherent to the dura (arrows).
In the image below a microscopic whole mount of the cerebrum has been stained with a stain that colors collagen green. The old [organized] subdural hemorrhage consists of collagenous tissue seen here in the upper left portion of the figure adherant to dura and over the underlying brain.
The image below gives a low power microscopic view of the membrane itself stained with hematoxylin and eosin. Fresh hemorrhage is still present (A), Granulation tissue (B) grows from the inner surface of the dura. Thus, this subdural is still organizing.
A concussion is the temporary loss of consciousness with a variable period of pre- and post-traumatic amnesia, but without permanent detectable clinical or morphologic damage. The patient recovers consciousness within a few seconds or hours, and has no permanent residual ill effects.
A contusion is the superficial bruising and necrosis of brain tissue following its impact against a hard surface (bone or the dura mater). The necrosis may be the result of the vascular damage and edema that are products of the mechanical shock wave, as well as of the shock wave itself. Contusions of the brain are often confined to the crests of the gyri. The majority of contusions occur on the orbital surface of the frontal lobes and at the frontal pole of the hemispheres and the tips of the temporal lobes. They are usually areas of hemorrhagic necrosis.
The image below shows a lateral view of the brain with contusions (hemorrhagic necrosis) at the frontal poles, and along the temporal lobes.
The next image shows a histologic section of an older contusion, which like any older area of previous necrosis, is now a cyst. The location at the crest of the gyrus helps us distinguish the contusion from an old infarct which generally has a less restricted distribution.
The zone of cystic degeneration extends into the white matter beneath the injured cortex. This is most likely the result of edema, which spread into the white matter at the time of injury. Though not shown here, old blood pigment (hemosiderin) often remains in macrophages in the old contusion.
As shown in the image below, hemorrhages are a common feature of head trauma. They arise from vessels torn by shearing forces within the brain tissue.
PENETRATING BRAIN INJURY
This coronal section of cerebral hemispheres demonstrates a penetrating brain injury. This was a gun shot wound. Note not only the extensive destruction of brain tissue in the path of the bullet, but also the ependymal lining tinged with blood, suggesting the presence of an intraventricular hemorrhage. When the bullet leaves the skull (exit wound), the skull defect may be larger than that at the point of entry. This is because the bullet wobbles as it passes through the brain and because bone fragments may be carried out of the skull with the exiting bullet. However this classical rule of thumb may not apply to modern high power weapons and modern explosive bullets or bullets with other than the old fashioned "bullet shape".
DIFFUSE AXONAL INJURY
This important concept explains both short and long term neurologic deficits in patients whose trauma did not produce either contusions, hemorrhages or lacerations sufficient to account for the deficits. Frequently, the latter lesions are minimal but the deficit is severe.
What has happened is that rotational and other movements of the brain during trauma has resulted in injury to numerous axons in both cerebrum and brain stem. This may be seen at autopsy following injury by many days. There will be many focal swelling or "balls" or "bulbs" visible on H&E stain [they will be eosinophilic--pink] and especially on silver stain. Sites where they may be most readily recognized are deep white matter and corpus callosum. In its most severe form--what many workers have called grade 3- there are not only swollen axons in the mid brain, but also focal "lesions" consisting of either small areas of hemorrhage or necrosis. These tend to be around the aqueduct or on the later margin of the dorsal midbrain or in the cerebellar peduncle. When hemorrhagic they should be distinguished from secondary brain stem hemorrhage caused by herniation. The secondary hemorrhages are generally more central [i.e. medial, along the midline] and ventral within the brain stem and are more likely to be present more caudally in the pons.Patients with grade three diffuse axonal injury are in coma fron the time of the injury and will not recover.
The presence of the diffuse axonal alterations may be recognized on autopsy when death occurs within hours of injury, but only with special staining techniques involving use of antibodies to the amyloid precursor protein. This is found to accumulate in the affected axons, often focally.
However stained, and at whatever time after death, the focal swellings of axons are now thought to be the result of metabolic alterations in damaged axons and ultrastructural changes that cause damming up of axoplasmic flow. This may or may not result in ultimate breakage or disconnection of the affected axon. Thus the large bulbs [cross section] or "torpedoes" [longitudinal section] seen with H&E or silver stains are not really the "retraction bulbs" resulting from a springing back of the proximal portion of disconnected axons as was though by the classical neuropathologists.
SPINAL CORD INJURIES
TRANSECTION OF CORD
Spinal cord injuries may result from fractures and dislocation of the vertebral column, from penetrating missile wounds, and from compression by tumors. The image below demonstrates an almost complete transection of the spinal cord at the level of the thoracic region (arrow). Naturally transection leads to paraplegia or quadraplegia (paralysis of limbs).
The image below shows a microscopic section at the level of the lesion. Note the extensive degeneration of almost the entire cord, with relative preservation of the posterior tracts. Only the latter are stained (arrows).
One consequence of cord transection is Wallerian degeneration (See also chapter on neuropathology of the neuron and its processes). The entire length of axons distal to the lesion [i.e. between lesion and tip of axons] die because they have been separated from their nourishing cell bodies. Above the lesion of the cord the affected tracts will be those ascending to the brain because the cell bodies from which they arise are in the dorsal root ganglia, from which the axons ascend to reach the sensory cortex. The image below shows a photomicrograph of a section of the spinal cord above the lesion stained with Weigert technique for myelin (black-brown color). Note the extensive paleness (degeneration, arrows) of the dorsal columns. This is Wallerian degeneration above the lesion
In the image below you are being shown the cord below the level of the lesion. Therefore the dorsal columns are intact and it is the descending tracts which have undergone Wallerian degeneration, since below the lesion it is these tracts that have been cut off from their nourishing cell bodies. These descending tracts are the lateral and ventral corticospinal tracts [arrows] cut off from their nourishing cell bodies above the lesion, in the motor cortex of the cerebrum.
SECONDARY EFFECTS OF BRAIN TRAUMA
As indicated earlier these include infection and infarction. Infection can occur if the infectious agent penetrates the brain at the site of a depressed fracture or missile wound. Infarction can occur as a result of cerebral edema, which itself is another secondary effect of trauma. The brain swelling can produce herniations as described in chapter concerning vascular diseases. The brain stem herniation is lethal. Edema can also cause infarction by causing compression of an artery adjacent to the edematous swollen lesion. Infarcts can also be produced if arterial flow is disrupted by thrombi in bruised or otherwise injured arteries and arterioles.