Traumatic Lesion 1 Head Trauma

The clinical picture of the effects of traumatic head injuries is defined in terms of the morphological damage inflicted on the brain and skull. Either an open or a closed head injury is diagnosed depending on the mechanism that mediated the trauma. An open head injury means that there is an open connection between the subdural and epigaleal space (i.e., between the CSF and the outside world). An open head injury usually results from penetrating brain damage (e.g., from a shooting incident or use of another weapon) but can also arise from a tearing of the dura (e.g., with ventricular fistula following basal skull fractures). An additional categorizatation of the morphology of skull and brain injury indicates the presence or absence of bone damage and whether intracranial lesions are focal or diffuse. The types of head injury are summarized in Table V in terms of the mode of accident, the clinical picture, and the damage as represented by imaging techniques.

Primary brain damage results from the effects of shear, stretch, and pressure on the tissue (including intracranial and intracerebral pressure gradients). Damage is usually a consequence of either extreme pressure on a particular point on the skull (contact injury) or a rapid acceleration/deceleration ofthe head and the brain mass. Primary damage occurs immediately at the site of the accident and consists of the breaking of the skin and scalp fracture, contusions and crushing of the brain tissue, intracranial bleeding, and/ or diffuse damage to the neuronal tissue and axonal network of the brain (Fig. 2).

Secondary brain damage appears with a delay. This manifests itself as a complication of the course and may be based on hypoxia, free radical formation, release of excitatory amino acids, ischemia, a swelling of the brain tissue, increased intracranial pressure, infection, or delayed (subacute) intracranial bleeding.

Table V

Classification of Traumatic Brain Injuries According to Biomechanical and Morphological Aspects0

Classification

Mechanism of injury Closed High speed (e.g., car accident)

Low speed (e.g., a fall with somatic injury)

Open Missile injury

Other penetrating injuries

Morphology of the injury

Skull fracture

Skull cap Base/basis

Along the length/cross-sectional with/without impression; open/closed

With/without CSF fistula; with/without facial paresis

Intracranial lesion

Focal

Diffuse

Epidural Subdural Intracerebral Diffuse axonal injury

"Modified from Keidel and Miller (1996).

Figure 2 Common types of traumatic brain injuries. (Top, left) Intracerebral hemorrhage. (Top, right) Intracerebral contusion of the right frontal lobe accompanied by an ipsilateral frontotemporal epidural hematoma (coup) and a left-sided temporoparietal epidural hematoma (contre). (Bottom, left) Right-sided temporoparietal epidural hematoma, soft tissue injury, and contralateral subdural hematoma. (Bottom, right) Left frontal traumatic hemorrhagic contusion.

Figure 2 Common types of traumatic brain injuries. (Top, left) Intracerebral hemorrhage. (Top, right) Intracerebral contusion of the right frontal lobe accompanied by an ipsilateral frontotemporal epidural hematoma (coup) and a left-sided temporoparietal epidural hematoma (contre). (Bottom, left) Right-sided temporoparietal epidural hematoma, soft tissue injury, and contralateral subdural hematoma. (Bottom, right) Left frontal traumatic hemorrhagic contusion.

An overview of primary and secondary brain damage is presented in Table VI.

2. Intracerebral Bleeding

Epidural hematoma is a collection of blood between the skull and the dura. It usually results from low-speed head injuries (e.g., from falls or impact with objects). It occurs most commonly in association with linear skull fractures that traverse meningeal vessels and tear them. In about half of the patients, after an initial short period of unconsciousness on impact, a lucid interval can be observed that is followed by a progressive loss of consciousness and contralateral hemiparesis. The underlying mechanism, the expanding mass-producing compression of the corticospinal tract, transten-torial herniation, and diencephalic derangement, is visible in computed tomography (CT) scans as a biconvex structure of the epidural hematoma bounded by dural insertion at cranial sutures (Fig. 2).

Table VI

Type of Lesion and Mechanism of Injury in Posttraumatic Primary and Secondary Cerebral Damage

Lesion Mechanism

Primary cerebral damage Scalp injury (acute manifestation)

Bruising or crushing of the brain Intracranial bleeding Diffuse axonal brain damage Acute intracranial hematoma

Secondary cerebral damage Hypoxia or ischemia (delayed manifestation)

Space occupying mass Delayed formation of hematomas Brain swelling Brain edema Hyperemia Hydrocephalus

Increased intracranial pressure Arterial vasospasm Infections

Cellular mechanisms

Phospholipid metabolism Lipid peroxidation, arachidonic acid

Prostaglandins, leukotrienes Platelet-activating factor Free oxygen radicals Excitotoxic mechanisms

Glutmate, acetylcholine Neuropeptides Endorphines Disturbances ofCa2+ andMg2+ metabolism Lactate acidosis

Disturbances of axonal transport

Long-lasting sequelae Focal scar formation

Secondary degeneration of the neuronal pathways and nuclei

Posttraumatic Demyelinization Brain atrophy Hydrocephalus internus

The subdural hematoma is a collection of blood between the dura and the underlying brain and frequently the result of torn veins draining into the dura or dural sinuses. It may be the result of high-speed impacts, such as occur in car accidents. Associated severe brain damage (contusions and edema) is common. In CT scans damaged areas are not bordered by sutures and can cover most of the hemisphere but do not cross the interhemispheric fissure (Fig. 2). The treatment of both types of hematoma is comparable and consists of neurosurgical interventions to reduce the effects of the expanding mass.

The term contusion describes necrotic cortex and white matter with variable quantities of petechial hemorrhages and edema. Traumatic contusions show a typical pattern of distribution, covering the poles of the frontal and temporal lobes, the orbital surface of the frontal lobe, and the inferolateral temporal lobes (Fig. 2). Due to the contact of the brain to bony or meningeal structures, several types of contusions can be distinguished: at the site of fracture, at the site of impact (coup), contralateral to the site of impact (contre-coup), or at the site of herniation. All these appear in CT scans as areas of variable densities (increased, decreased, or normal).

Diffuse axon damage commonly occurs in traffic accidents due to shearing injury. Since a strong acceleration or deceleration can elicit these shearing forces and pressure gradients, a direct impact on the skull is not necessary. Often, traumatic hematoma of the corpus callosum and necrotic hemorrhages of the dorsolateral brain stem are associated with diffuse axon damage. Furthermore, it can develop from a trauma-induced sequence of changes of tissue by neurotoxic mediator substances leading to the final breakdown of axonal function. The diagnosis should be considered if, in unconscious patients, no focal lesion is displayed in the CT scan, perhaps merely a small swelling is evident.

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