In more than half of all cases, traumatic brain injury occurs as a component of multiple trauma. The associated injuries commonly affect the face, limbs, spine, chest, abdomen, and pelvis (in descending order of frequency).
The main clinical manifestation of a traumatic brain injury is impaired consciousness, often associated with a memory deficit (retrograde and anterograde amnesia). These problems can be accompanied or followed by neurologic deficits and/or epileptic seizures.
Brain injuries are either closed (i.e., with the dura mater intact) or open (with a wound extending into the subdural compartment or deeper into the brain parenchyma). Their severity is judged clinically and rated numerically on the Glasgow Coma Scale (GCS). Traumatic hematomas can be located within the brain parenchyma (traumatic intracerebral hematoma) or in the epidural or subdural compartments.
Large traumatic hematomas, or extensive damage to the brain parenchyma with accompanying edema, may lead to a rapid rise of intracranial pressure (ICP), causing brain compression and possibly brainstem herniation.
Frequent late complications of severe traumatic brain injury include neuropsychological deficits, personality changes, and symptomatic epilepsy.
6.2.2 Clinical History and Neurologic Examination
In the initial phase after trauma, the recognition that a traumatic brain injury is present and its clinical and anatomic assessment (e.g., intracranial hematoma) are vital. The duration and type of the impairment of consciousness are especially important elements of the clinical history. Meticulous history-taking and directed physical examination point the way to proper diagnosis and treatment.
Relevant Aspects of the History
Particular attention must be paid to the following aspects of the history:
The duration of unconsciousness (as reported by eyewitnesses).
The duration of amnesia for events that occurred before the injury (retrograde amnesia) and after it (anterograde amnesia, perhaps accompanied by confusion).
Early epileptic seizures.
Bleeding from the ear or nose (indicating a basilar skull fracture).
Important aspects of the initial physical examination in the emergency room are:
The vital signs, especially pulse and blood pressure (is the patient in shock?).
The level of consciousness: the depth of impairment of consciousness (up to and including deep coma) is assessed numerically with the GCS ( ▶ Table 6.5). This assessment may need to be performed multiple times—in particular, with each change in the patient’s circumstances and surroundings (before and after intubation, transport, arrival in the hospital, etc.).
Cranial injuries: inspection and palpation of the skull, orbital rims, zygomatic arches, jaws.
Cervical spine injuries and other accompanying bodily injuries.
Bleeding and possibly flow of CSF from the nose or ears, or in the pharynx (a CSF leak is conclusive evidence of an open brain injury, while bleeding is not).
Periorbital hematoma, a sign of basilar skull fracture.
Neurologic deficits (impaired pupillary reflexes, visual impairment, nystagmus, deafness, weakness, pyramidal tract signs).
Table 6.5 The Glasgow Coma Scale
Best verbal response:
To painful stimuli
To auditory stimuli
Best motor response:
Withdraws (pulls away from pain)
Localizes (fends off painful stimulus)
Patient’s overall score
Note: The overall score is the sum of the scores in the three categories.
6.2.3 Assessment of Severity; Imaging Studies
Mild, moderate, and severe traumatic brain injury are distinguished on the basis of the type and duration of the impairment of consciousness.
Assessment of Severity
The severity of traumatic brain injury is assessed on the basis of the clinical manifestations and their classification on the GCS ( ▶ Table 6.6).
Loss or impairment of consciousness lasting less than 1 hour, EEG changes lasting less than 24 h
Loss or impairment of consciousness lasting 1–24 h
Unconsciousness for more than 24 h, and/or brainstem signs
Score on Glasgow Coma Scale
Possible neurologic findings
Confusion, amnesia (generally encompassing the traumatic event itself, a short period before it, and the period of posttraumatic confusion)
Depending on the site and extent of brain injury:
Mild traumatic brain injury In mild traumatic brain injury, consciousness is only mildly impaired (GCS score: 13–15) and the impairment lasts no longer than 1 hour. The patient may be confused. There may be amnesia for brief periods of time before and after the injury (retro- and anterograde amnesia).
Moderate traumatic brain injury The impairment of consciousness is somewhat more severe (GCS score: 9–12) and longer-lasting. The patient may have neurologic deficits, such as weakness or cranial nerve deficits, and/or epileptic seizures.
Severe traumatic brain injury The GCS score is 8 or lower and the patient is in coma for 1 day or longer. Neurologic deficits are generally seen, as well as signs of intracranial hypotension. Without appropriate treatment, transtentorial herniation of the midbrain and diencephalon may ensue (or, less commonly, herniation of the medulla through the foramen magnum).
Alternative classification An alternative classification of traumatic brain injury, based on pathophysiology rather than clinical severity, consists of the following categories:
Commotio cerebri (brain concussion).
Contusio cerebri (brain contusion).
Compressio cerebri (brain compression).
Depending on the clinical situation, the following imaging studies can be performed:
Head CT A head CT (often as a component of whole-body spiral CT) is generally obtained immediately on arrival of the injured patient in the emergency room for the prompt diagnosis of skull fractures, intracranial hemorrhage, brain contusions, cerebral edema, and intracranial air.
Cervical spine CT Cervical spine CT with multiplanar reconstruction is used to diagnose fractures and dislocations of the cervical spine.
Whole-body spiral CT A CT scan of the entire body is obtained in multiply and severely injured patients so that all of their injuries can be detected and classified according to the urgency of treatment.
MRI MRI is more time-consuming than CT and thus plays only a limited role in the acute diagnostic evaluation of head-injured patients. It is a useful means of detecting intracranial hemorrhages and, in particular, diffuse axonal injury in the cerebral white matter, which may be present even in “mild” traumatic brain injury. MRI is preferable to CT for follow-up studies after the initial, acute phase of traumatic brain injury has passed.
Plain X-ray There is no current indication for plain X-rays of the skull in traumatic brain injury. These have been entirely supplanted by CT for the diagnosis of skull fractures. Plain films of the cervical spine and other parts of the skeleton may be useful for various indications and are usually obtained with a whole-body, skeletal and soft-tissue, low-dose X-ray scanner, also called Lodox.
6.2.4 Pathophysiology and Clinical Features
The main pathophysiologic types of traumatic brain injury and their manifestations will be presented in this section. Traumatic hematomas will be discussed separately.
The pathophysiologic effects of brain trauma are divided into primary and secondary brain injury, as outlined in ▶ Table 6.7.
Primary brain injury (immediate)
Secondary brain injury (delayed)
Mainly caused by arterial hypotension and hypoxemia as well as intracranial hypertension, leading to ischemia in brain tissue and, in turn, to:
Open versus Closed Head Injuries
A head injury is said to be open only if there is an opening in the dura mater through which the intradural space communicates freely with the outside world, generally with leakage of CSF. Such injuries carry a high risk of early and late infection (meningitis, cerebritis, brain abscess). If the dura mater is intact, the head injury is closed. Thus, a skull fracture directly under a scalp laceration is not necessarily an open injury; it is one only if there is an underlying dural tear.
Patients with simple skull contusions have no evidence of a brain injury, that is, no loss of consciousness or amnesia and normal findings on neurologic examination. Some patients with this syndrome have scalp lacerations, or even skull fractures, and they may suffer from headaches afterward. Adequate therapy consists of a temporary restriction of activity and symptomatic medication, as required (analgesics, antiemetics).
Diffuse Axonal Injury
Even mild head trauma can be associated with shearing forces that are strong enough to damage axons in the cerebral white matter and the blood vessels that supply them. Axonal shear injuries in various regions of the brain can lead to the degeneration of neural pathways; their clinical neurologic effects may only be noticed weeks or months after the traumatic event.
“Concussion” is often used as a near-synonym for mild traumatic brain injury. The concussion syndrome consists of a brief period of unconsciousness or impaired consciousness (generally no more than a few minutes), possibly followed by confusion. The periods of retro- and anterograde amnesia, if any, are only brief. Typical accompanying symptoms include headache, dizziness, nausea, and vomiting. There is no neurologic deficit, and it is thus often assumed that there is no underlying structural injury to the brain parenchyma. Nonetheless, T2-weighted MRI and diffusion tensor imaging (see section ▶ 4.2.3, ▶ 126.96.36.199) reveal evidence of axonal damage in some cases. Detailed neuropsychological testing may reveal subtle deficits even in patient who have “only” sustained a concussion; such deficits have been termed “minimal brain injury.” Posttraumatic headache after concussion generally subsides over time.
The clinical distinction between concussion and brain contusion (see later) is not always easy to draw.
The treatment of concussion resembles that of a skull contusion, with transient restriction of activity and symptomatic medication as needed. The patient should not be immobilized any longer than necessary: as long as there is no contraindication (such as hemodynamic instability), the patient should stand up and walk with assistance on the day of injury or in the next few days at latest. Rapidly mobilized patients have less severe postconcussive symptoms with a lesser tendency toward chronification.
Brain contusion is, by definition, a direct injury of the brain parenchyma. It is associated with a long period of unconsciousness and retro- and anterograde amnesia; indeed, the patient may not remember anything for a period of several days surrounding the event. Examination in the acute phase often reveals neurologic deficits, which may persist. Residual anosmia is common (see section ▶ 12.1).
CT or MRI reveals foci of contusion ( ▶ Fig. 6.7, ▶ Fig. 6.8) or intracranial hemorrhage, for example, an acute epidural hematoma ( ▶ Fig. 6.9) or an acute subdural hematoma. Parenchymal injuries can be found both directly underlying the site of the external blow (“coup” injuries) and at the diametrically opposite location in the brain (“contrecoup” injuries). Injuries of the latter type are due to the violent, tissue-distorting force transmitted through the brain tissue at the moment of injury. The pathoanatomic findings in foci of brain contusion include ischemic and hemorrhagic tissue necrosis, small hemorrhages, tears of brain tissue and blood vessels, and secondary brain edema. Lumbar puncture (LP), if performed (generally contraindicated!), yields bloody or xanthochromic CSF.
Fig. 6.7 Brain contusion (CT scan). There are extensive hemorrhagic contusions in both temporal lobes and smaller ones in both frontal lobes (arrowheads).
Fig. 6.8 Parenchymal defects 6 years after brain contusion. The T2-weighted MR images reveal cortical defects in the left temporal (a) and frontal lobes (b), accompanied by signal changes in the underlying white matter.
Fig. 6.9 Epidural hematoma (CT scan). There is an epidural hematoma on the right side (a) associated with marked extracranial soft-tissue swelling. (b) The bone window reveals a right-sided skull fracture over the hematoma as well as further fractures in the left frontal bone (arrows). This is the same patient seen in ▶ Fig. 4.1.