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Traumatic Brain injury

87

Table 6.5 Types of craniosynostosis (Continued)

 

 

 

Type

Fused suture

Shape of head

Remarks

 

plagiocephaly

premature fusion (or incomplete

asymmetrical (e.g., flattened

 

 

fusion) of a coronal suture

on one side)

 

 

 

often due to

 

 

 

 

 

 

 

 

asymmetrical

 

 

 

 

muscle tone in

 

 

 

 

cerebral palsy

 

Crouzon disease

mainly the coronal

(craniofacial

suture, and maxillary

dysostosis)

sutures in the face

trigonocephaly

metopic suture

broad skull and face, jutting

the airway

forehead, exophtalmos,

may be

hypertelorism, hook nose,

compromised

prognathism

 

pointed forehead

 

platycephaly

lambdoid suture

broad occiput

Traumatic Brain injury

Fundamentals

Traumatic injuries of the bony skull and the underlying brain can be of different types and varying severity, depending on the nature and intensity of the causative event. There may be a skull fracture affecting the cranial vault or the base of the skull, a brain contusion, an injury to larger sized blood vessels producing a traumatic hematoma, or any combination of these types of injury.

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). Open brain injuries are associated with the risk of early or late intracranial infection.

The scale of clinical severity of traumatic brain injury extends from a simple contusion of the bony skull to the concussion syndrome and the brain contusion syndrome. The leading clinical manifestation of a traumatic parenchymal injury is impairment or loss of consciousness, usually accompanied by memory impairment (retrograde and anterograde amnesia). A neurological deficit or epileptic seizures may also be present.

Large traumatic hematomas, or extensive damage to the brain parenchyma with accompanying edema, may lead to a rapid rise of intracranial pressure, caus-

blubber blubber

ing brain compression and possibly brainstem herniation.

Traumatic hematomas may be located within the brain parenchyma (traumatic intracerebral hematoma) or in the adjacent meningeal compartments (subdural and epidural hematoma). Traumatic subarachnoid hemorrhage is less common.

Frequent late complications of severe traumatic brain injury include neuropsychological deficits, personality changes, and symptomatic epilepsy.

Relevant Aspects of the Clinical History

and Neurological Examination

In the initial phase after trauma, the severity of injury is assessed, with particular attention 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);

the duration of amnesia for events that have occurred since the injury (anterograde amnesia, perhaps accompanied by confusion);

the duration of the entire period of amnesia, which is the sum of the durations of retroand anterograde amnesia;

Mumenthaler / Mattle, Fundamentals of Neurology © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.

6

Diseases of the Brain and Meninges

88 6

Diseases of the Brain and Meninges

 

 

 

 

 

 

 

 

early epileptic seizures;

extensive skull fracture, but no neurological deficit;

 

 

bleeding from the ear or nose (indicating a basilar

another patient may sustain a relatively minor blow to

 

 

skull fracture).

the head that ruptures a bridging vein and produces a

 

The depth of impaired consciousness or coma in a brain-

slowly growing subdural hematoma, which can com-

 

press the brain and ultimately cause coma and death. The

injured patient is graded numerically on the Glasgow

clinical state of the patient after traumatic brain injury

 

Coma Scale (Table 6.6).

can be classified as follows (in order of increasing sever-

 

 

Important aspects of the initial physical examination

ity):

 

are:

 

 

the patient’s level of consciousness (see above);

Skull contusion. Patients with the simple skull contu-

 

externally visible injuries, especially of the head;

sion syndrome have no evidence of a brain injury, i. e., no

 

bleeding and possibly flow of cerebrospinal fluid from

loss of consciousness or amnesia, a normal neurological

 

 

the nose or ears, or in the pharynx (a CSF leak is con-

examination, and normal intracranial findings on CT or

 

 

clusive evidence of an open brain injury, while bleed-

MRI (if performed). Some patients with this syndrome

 

 

ing is not);

have scalp lacerations, or even skull fractures, and head-

 

injuries of the cervical spine;

ache may be present. Adequate therapy consists of a tem-

 

 

periorbital hematoma; neurological findings (pupil-

porary restriction of activity and symptomatic medica-

 

 

lary reflexes, visual impairment, nystagmus, deaf-

tion, as required (analgesics, antiemetics).

 

 

ness, weakness, pyramidal tract signs), general state

Concussion (= mild traumatic brain injury) is character-

 

 

of health, and, in particular, circulatory status.

 

Ancillary tests, to be performed as indicated by the

ized by a brief, transient loss of consciousness, usually last-

 

ing no more than a few minutes and sometimes followed

 

clinical situation, include cervical spine radiographs and

by a period of confusion. The periods of retroand antero-

 

a CT and/or MRI scan of the head. Skull radiographs are

grade amnesia are very brief. Headache, dizziness, nausea,

hardly ever indicated.

and (sometimes) vomiting are common accompani-

 

 

 

 

ments of concussion in the early phase. A standard neu-

 

 

 

 

 

 

Traumatic brain injuries are often accompanied by

rological examination reveals no deficit. In the past, it

! cervical spine injuries.

was generally assumed that concussion produced no

 

 

 

 

structural damage to the brain, but T2-weighted MR im-

 

 

 

 

 

 

 

 

ages do, in fact, reveal diffuse axonal injury in some

 

Grades of Severity of Traumatic

patients. Moreover, neuropsychological testing reveals

 

that some patients said to have sustained no more than a

Brain Injury

concussion actually have deficits of certain characteristic

 

 

 

 

types, collectively designated minimal brain injury. Oc-

 

The clinical grade of severity of traumatic brain injury is

casional patients suffer from persistent posttraumatic

 

closely correlated with the initially evident extent of

headaches. The clinical distinction between concussion

structural damage to the skull and brain, but the correla-

and brain contusion (see below) is not always easy to

 

tion is not absolute. For example, a patient may have an

draw.

Table 6.6 The Glasgow Coma Scale

Category

Points

 

 

 

Best verbal response:

 

 

none

1

 

unintelligible sounds

2

 

inappropriate words

3

 

disoriented

4

 

oriented

5

 

Eye opening:

 

 

none

1

 

to painful stimuli

2

 

to auditory stimuli

3

 

spontaneous

4

 

Best motor response:

 

 

none

1

 

abnormal extension

2

 

abnormal flexion

3

 

withdraws (pulls away from pain)

4

 

localizes (fends off painful stimulus)

5

 

follows commands

6

 

 

 

 

Patient’s overall score

. . .

 

 

 

 

The overall score is the sum of the scores in the three categories.

Treatment of concussion. As in the skull contusion syndrome, transient restriction of activity suffices (e. g., a few days of bed rest), combined with symptomatic medication as required (see above). The patient should on no account 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 within the next few days at latest. Rapidly mobilized patients tend to have less severe postconcussive symptoms with a lesser tendency toward chronification.

Brain contusion and penetrating injuries. By definition, these types of injury involve damage to the brain parenchyma. Compared with concussion, they produce considerably longer periods of unconsciousness and retroand anterograde amnesia; indeed, the patient may not remember anything for a period of several days surrounding the time of the injury. Examination in the acute phase often reveals neurological deficits, which may persist. Residual anosmia is common (p. 180). CT or MRI reveals foci of contusion (Fig. 6.2) or intracranial hemorrhage, e. g., an acute epidural hematoma. Parenchymal injuries can be found both directly underlying the site of the external blow (“coup” injuries) and at the diametri-

Mumenthaler / Mattle, Fundamentals of Neurology © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.

Traumatic Brain injury

cally opposite location in the brain (“contrecoup” injuries). Injuries of the latter type are due to the violent, tissue-distorting force transmitted across the brain to the other side at the moment of injury. The Pathoanatomical 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, if performed (generally contraindicated!), yields bloody or xanthochromic cereobrospinal fluid.

 

Large brain contusions and extensive traumatic hema-

 

tomas (see below), combined with the associated sec-

 

ondary brain edema, can cause very rapid and pro-

 

nounced increases in intracranial pressure, leading to

 

brain compression and herniation of the midbrain and

 

diencephalon through the tentorial notch, and/or of the

 

medulla through the foramen magnum. The clinical

 

signs of brainstem herniation are: progressive impair-

Fig. 6.2 Brain contusion (CT scan). There are extensive hemor-

ment of consciousness leading to coma; a dilated pupil,

rhagic contusions in both temporal lobes and smaller ones in both

initially only on the side of the expansive lesion; flexor

frontal lobes (arrowheads).

and, later, extensor spasms; and, finally, a loss of auton-

 

omic regulatory functions (breathing, temperature, car-

 

diac activity, vascular tone), bilaterally fixed and dilated

taken, including elevation of the patient’s head, hyper-

pupils, and death.

ventilation (in some patients), osmotherapy, or even

 

 

 

 

All patients with traumatic brain injury must be care-

craniectomy to relieve brain compression (p. 93). Recent

 

studies have shown a positive effect of therapeutic hy-

! fully clinically observed for signs of increasing in-

pothermia, in which the patient is cooled to ca. 34 °C.

 

tracranial pressure. In patients with a diminished level

If the patient survives, MRI may reveal a permanent in-

 

of consciousness, or coma, the width and reactivity of

 

jury to the brain parenchyma (Fig. 6.3). The late posttrau-

 

the pupils and other brainstem reflexes should be

 

matic symptoms resemble those of concussion, but they

 

checked regularly, so that intracranial hypertension

 

are more intense and usually persist longer. For further

 

can be detected at the earliest possible moment. In some

 

details, see p. 91.

 

patients, pressure-measuring devices will be implanted

 

 

 

intracranially for continuous, invasive ICP monitoring.

 

Treatment of the brain contusion syndrome. Depending on his or her clinical state, the patient may need to be observed in an intensive care unit or dedicated neurotrauma unit, with frequent checking of the vital signs and neurological functions, and possibly with invasive ICP monitoring. Extensive parenchymal injuries and the associated brain edema usually elevate the intracranial pressure; thus, ICP-reducing measures may need to be

Traumatic Hematomas

Traumatic hematomas come about when the traumatic injury tears a larger artery or vein (Fig. 6.4). They are classified as follows:

Intracerebral hematomas are usually found in the frontal or temporal lobe. They may exert considerable mass effect; combined with the surrounding edema,

89

6

Diseases of the Brain and Meninges

Fig. 6.3 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.

a

b

blubber blubber

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90 6 Diseases of the Brain and Meninges

they may cause sufficient pressure on the brain to produce a progressive decline of consciousness and increasingly severe neurological deficits. In such patients, neurosurgical evacuation of the hematoma should be considered, depending on its size and location.

Epidural hematomas (Fig. 6.5) are generally produced by traumatic tearing of a dural artery, usually the middle meningeal a. The tear itself is usually the result of a temporoparietal skull fracture, but sometimes occurs in the absence of a skull fracture. The blood collection lies between the periosteum and the dura mater. The arterial hemorrhage can compress the brain very rapidly: a patient who is initially comatose because of a coexisting brain contusion may fail to emerge from coma because of the development of an epidural hematoma in the minutes or hours after injury. On the other hand, an initially awake or only transiently unconscious patient may lapse into coma after a so-called “lucid interval” lasting minutes or hours. The side of the hematoma can often be ascertained by clinical examination: incipient uncal herniation compresses the ipsilateral oculomotor n. and causes dilation of the ipsilateral pupil, while the hemiparesis is contralateral to the hematoma. When an acute epidural hematoma is suspected, a CT scan should be performed immediately to confirm the diagnosis (not

Fig. 6.5 Epidural hematoma (CT scan).

plain films or MRI; see note, below). The hematoma is usually seen as a hyperdense, biconvex zone that is sharply demarcated from the adjacent brain tissue. Once diagnosed, it must be neurosurgically evacuated immediately to prevent brainstem herniation and death. Patients often make an excellent recovery if they

skull

intracerebral hematoma

acute subdural hematoma

 

 

epidural space

 

 

dura mater

 

 

subdural space

 

 

arachnoid

 

 

subarachnoid space

 

 

brain

 

 

chronic subdural hematoma

epidural hematoma

CSF fistula

rhinogenic posttraumatic meningo-

malresorptive hydrocephalus

posttraumatic focal epilepsy

encephalitis

 

 

Fig. 6.4 Traumatic brain injuries and posttraumatic complications (schematic diagram).

Mumenthaler / Mattle, Fundamentals of Neurology © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.

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