Traumatic Brain Injury: Definitions and Nomenclature

Kristine O’Phelan

Traumatic brain injury (TBI) has a broad spectrum of severity, pathology, physiology, and sequela. This chapter will present pertinent definitions, nomenclature, and concepts relevant to the discussion of TBI.

PRIMARY VERSUS SECONDARY INJURY

The distinction is somewhat arbitrary and the specific combination and magnitude of secondary injury is to a great extent determined by the nature of the primary injury. This description is useful, however, in order to aid clinicians in identifying potential preventable or reversible causes of secondary brain injury. (See Chapter 2 for further details.)

• Primary injury—the physiological or anatomical insult, often but not exclusively the result of direct trauma to head. The primary injury may be associated with structural changes resulting from mechanical forces initially applied during injury. These forces may cause tissue distortion, shearing, and vascular injury as well as destabilization of cell membranes and frank membrane destruction.

• Secondary injury—systemic or local changes, which increase tissue damage. Many secondary insults result directly from the primary injury and some are caused by discreet systemic or local phenomena. Secondary injury mechanisms include generation of free radicals, excitotoxicity, disturbance of ionic homeostasis, disruption of the blood–brain barrier, generation of nitric oxide, lipid peroxidation, mitochondrial dysfunction and energy failure, inflammation, secondary hemorrhage, axonal disruption, apoptotic cell death, and ischemia. Ischemia may be due to microvascular changes, systemic hypotension or hypoxia, or elevated intracranial pressure.

CLASSIFICATION OF TBI BY MECHANISM

This classification is useful because injuries produced by different mechanisms are distinct in their pathophysiologies and natural courses.

• Closed/blunt force—injury caused by direct force to head, acceleration–deceleration, or rotational forces. Common causes include falls, assaults, and motor vehicle collisions.

• Blast injury—injury caused by overpressure waves generated from high-grade explosives. A large amount of thermal, mechanical, and electromagnetic energy is transferred to the brain. Energy can come directly through the cranium or be transmitted indirectly through oscillating pressures in fluid-filled large blood vessels. This may cause damage to the blood–brain barrier or gray–white matter junction, and can cause cerebral edema, axonal injury, apoptosis, and tissue degeneration.

• Penetrating injury—injury induced by an object that penetrates the cranial vault. Common causes include gunshot wounds, shrapnel, and knife wounds.

CLINICAL CLASSIFICATION OF TBI

The Glasgow Coma Scale (GCS) [1] (Table 1.1) is central to clinical classification of TBI. Clinical/injury severity classification is the most commonly used classification system in the clinical care of patients with TBI as well as in clinical neurotrauma research. (See Chapter 3 for further discussion of this topic.)

• Mild TBI (MTBI)—GCS 13 to 15, the majority of patients with cranial trauma fall in this group. Patients are awake, and may be confused but can communicate and follow commands.

• Moderate TBI—GCS 9 to 12, these patients are generally drowsy to obtunded but not comatose. They can open their eyes and localize painful stimuli. They are at high risk of clinical deterioration and must be monitored carefully.

• Severe TBI—GCS 3 to 8, these patients are obtunded to comatose, they do not follow commands and may exhibit decerebrate or decorticate posturing. They have significant structural and metabolic brain dysfunction and are at high risk of secondary brain injury and deterioration.

TABLE 1.1 Glasgow Coma Scale

Eye Opening

Spontaneous 4

To speech 3

To pain 2

None 1

Best Verbal Response

Oriented 5

Confused conversation 4

Inappropriate words 3

Incomprehensible sounds 2

None 1

Best Motor Response

Obeys commands 6

Localizes pain 5

Withdrawal 4

Abnormal flexion (decorticate) 3

Extension (decerebrate) 2

None 1

STRUCTURALLY BASED DESCRIPTIONS OF TBI

Structural descriptions incorporate information from imaging studies. They often aide in selection of patients who may benefit from a specific therapy such as surgical evacuation of a hematoma.

• Epidural hematoma (EDH) (Figure 1.1)—an extradural collection of blood. It is often associated with a skull fracture and typically has an arterial origin. Margins of the hematoma do not cross the skull suture lines and often appear convex on imaging studies. If an EDH is evacuated in a timely fashion to reverse mass effect or if the hematoma is small in size, patient outcomes are usually good.

• Subdural hematoma (SDH) (Figure 1.2)—a collection of blood in the subdural space. SDHs may be chronic or acute, and are caused by venous bleeding from cortical bridging veins. Bleeding may extend over the entire hemisphere. Acute SDHs are significantly associated with seizures. Acute SDHs are also associated with significant alteration of cerebral blood flow and metabolism of the underlying hemisphere and generally have a worse outcome than EDHs.

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