08 -CRANIOCEREBRAL TRAUMA .

Craniocerebral Trauma Classification, Etiology, and Frequency of Traumatic Brain Injury Classification of Brain Trauma Mechanisms of Traumatic Brain Injury Frequency of Traumatic Lesi

Craniocerebral Trauma

Classification, Etiology, and Frequency of Traumatic

Brain Injury

Classification of Brain Trauma

Mechanisms of Traumatic Brain Injury

Frequency of Traumatic Lesions

Primary Traumatic Lesions

Skull and Scalp Lesions

Diffuse Cerebral Edema

Vascular Manifestations and Complications of

Craniocerebral Trauma

Sequelae of Trauma

Head Trauma in Children: Special Considerations

In the United States, trauma is the leading cause of

death in children and young adults Head injury is

the major contributor to mortality in over half these

cases.1

Neuroimaging is fundamental to the diagnosis and management of patients with traumatic brain injury

Understanding the mechanisms underlying brain

trauma, their basic pathology, and their imaging

manifestations is therefore essential for the

practicing radiologist

CLASSIFICATION, ETIOLOGY, AND FREQUENCY OF TRAUMATIC BRAIN INJURY

Classification of Brain Trauma

Brain damage in head-injured patients has been classified in two major ways: focal or diffuse lesions and primary or secondary lesions We will follow the latter classification

Primary brain damage Primary traumatic

cranio-cerebral lesions arise directly from the initial

trau-matic event (see box, p 200) Skull and scalp lesions

are the least important of these and are therefore sidered only briefly (see subsequent discussion) The major primary intracranial manifestations of head trauma are extracerebral hemorrhage and a spectrum

con-of intraaxial lesions that includes cortical contusions, diffuse axonal injury, deep cerebral and primary brainstem injury, and intraventricular and choroid plexus hemorrhage

Secondary brain damage Secondary

manifesta-tions of craniocerebral trauma often develop and are frequently more devastating than the initial injury

(see box, p 200) These secondary effects include

herniation syndromes, ischemia, diffuse cerebral edema, and secondary infarctions and hemorrhages

Mechanisms of Traumatic Brain Injury

Projectile or penetrating wounds and nonmissile injury are the two basic mechanisms of traumatic brain damage

C H A P T E R

200 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Traumatic ischemia, infarction

Diffuse cerebral edema

Hypoxic injury

Projectile injuries Gunshot wounds to the head are the

most lethal of all violent injuries.1a Wounds are determined by projectile characteristics and the inherent nature of the affected tissues Some missile characteristics are intrinsic to the projectile itself (e.g., mass, shape, construction) and some are conferred by the weapon that delivers the missile (e.g., Iongitudinal and rotational velocity).2

Severity of a bullet wound is strongly influenced by missile orientation during its path through tissue and whether the projectile fragments or deforms Wounds are most severe when the missile is large, and traveling at high velocities and

if it fragments yaws early in its path through tissue (Fig 8-1).2Tissue crushing and stretching are the major mechanisms of injury in these cases Elasticity and tissue density, as well as thickness of the affected body part, strongly affect the wound produced.2

Imaging analysis in projectile injuries should include the following steps3:

1 Assess missile path

2 Determine extent of wound, including bone fragmentation and secondary or ricochet path

3 Detect presence of missile emboli

4 Localize intraarticular or intraspinal fragments

5 Determine if large vessels or (if abdominal wounds) hollow viscera have been traversed

Fig 8-1.For legend see p 201

Plain film radiography and fluoroscopy can be used

to determine bullet weight and caliber CT is best for

assessing the extent of soft tissue injury and

identifying entrance and exit wounds.3

Angiography is the diagnostic procedure of choice

for determining the etiology of missile-induced

trau-matic hemorrhage and delineating underlying vascu-

Chapter 8 Craniocerebral Trauma 201

lar abnormalities such as vessel laceration or matic pseudoaneurysm (Fig 8-2) Because half of all patients with gunshot wounds to the head have major vascular lesions' cerebral angiography should be considered in the evaluation and management of these cases.4

trau-Fig 8-1, cont’d Antemortem NECT scans in patient with a gunshot wound show typical abnormalities seen when the missle yaws and fragments early Entrance wound (A,

curved arrows) Bullet fragments at entry site and along path (arrowheads) Hemorrhagic brain (large arrows) Ricochet fragments from striking the inner table opposite entry site

(open arrows) Skull fracture at exit wound (F, black arrow)

I

Fig 8-2 Cranial gunshot wound A, Digital subtraction right internal carotid angiogram,

AP view, demonstrates multiple metallic bullet fragments The small traumatic middle

cerebral artery (MCA) aneurysm (large arrow) was initially overlooked Clinical

deterio-ration prompted repeat CT scan (not shown) that disclosed an enlarging middle fossa

hematoma B, Repeat angiogram shows the enlarging multilobed traumatic

pseudoan-eurysm (large straight arrows) Note medial displacement of the lenticulostriate arteries (small arrows) and elevation of the M1 segment and MCA genu (curved arrow) by the

expanding hematoma Also note the accompanying "square"-type anterior cerebral artery

shift (double arrows).

202 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Nonmissile head injuries All major traumatic brain

lesions can be produced by nonimpact inertial loading of

the head.5 The majority of nonprojectile traumatic brain

injury (TBI) is caused by shear-strain forces These are

mechanical stresses on brain tissue that are induced by

sudden deceleration or angular acceleration and rotation

of the head.6 Shear-strain injuries may be extensive and

severe, are often multiple and bilateral, and frequently

occur when there is no direct blow to the head

Rotationally induced shear-strain forces typically

produce intraaxial lesions in the following predictable

locations7:

1 Brain surface (cortical contusions)

2 Cerebral white matter (so called diffuse axonal

injury)

3 Brainstem

4 Along penetrating arteries or veins

Direct impact is significantly less important than

shear-strain forces in the genesis of most TBI With direct

blows there is localized skull distortion or fracture and the

underlying blood vessels and brain are damaged in a much

more focal fashion as the transferred energy dissipates

quickly The typical results are cortical contusions and

superficial lacerations localized to the immediate vicinity

of the calvarial lesion.8 Although some extraaxial lesions

such as epidural hematoma are frequently associated with

skull fracture (see subsequent discussion), significant

ex-tracerebral hemorrhage often occurs in the absence of

direct blows and is due to shear-strain forces

Frequency of Traumatic Lesions

Autopsy series The incidence of head injuries

en-countered in a recent series of postmortem examinations is

shown in Table 8-1.6 Twenty-five percent of cases with

fatal injuries do not demonstrate a skull fracture, although

the incidence of intracranial hematomas in patients who

have a skull fracture is much higher than in those who do

not.9 Intracranial hematomas, contusions, hypoxic brain

damage, and brain swelling are all more frequent in

postmortem series compared to surgical series or

imaging-based reports

Surgical and imaging series The approximate

in-cidence of traumatic injuries in patients who are imaged

or operated is listed in Table 8-2 Skull fractures and

extraaxial hematomas are less common than in autopsy

series, and shear-strain lesions such as diffuse axonal

injury are more frequently observed

PRIMARY TRAUMATIC LESIONS

Skull and Scalp Lesions

Scalp hematomas and lacerations Scalp lacerations

and subgaleal soft tissue swelling commonly accompany

head trauma (see Fig 7-15) Other than indicating impact

Table 8-1 Nonmissile Head Injury

(border zone; dif- fuse)

eral: bilateral, 2: 1)

From Adams JH: Pathology of nonmissile head injury,

Neuroimaging Clin N Amer 1:397-410, 1991

*More than one hematoma in some cases

Table 8-2 Craniocerebral Trauma in

Global/regional isch- 30% to 50% emia

edema

*Approximate; more than one lesion often present

site, these lesions may be cosmetically important but are usually clinically insignificant Exceptions are penetrating injuries that result in arteriovenous fistula or pseudoaneurysm These usually involve branches of the

superficial temporal or occipital arteries (see Fig 9-30)

Important extracalvarial soft tissue lesions are subgaleal extrusion of macerated brain through a comminuted skull fracture with dural laceration (see subsequent discussion)

Chapter 8 Craniocerebral Trauma 203

Skull fracture Skull fractures are present on CT

scans in about two thirds of patients with acute head injury, although 25% to 35% of severely injured pa- tients have no identifiable fracture at all.10 Therefore plain films obtained solely for the purpose of identi- fying the presence of a skull fracture have no appro- priate role in the current management of the head in- jured patient.11,12

Skull fractures can be linear (Figs 8-3 and 8-4), depressed, or diastatic and may involve the cranial vault or skull base Linear fractures are more often associated with epi- and subdural hematomas than are depressed fractures; depressed fractures are typically associated with localized parenchymal injury.10

Fig 8-3 Autopsy specimen of the calvarium in a patient who

expired from traumatic brain injury Endocranial view of the skull

shows a nondisplaced linear skull fracture (arrows) (Courtesy E

Tessa Hedley-Whyte.)

Fig 8-4 A, Axial nonenhanced CT scan with bone reconstruction

demonstrates a nondisplaced comminuted linear calvarial vault

fracture (arrows) The fracture crosses the superior sagittal sinus B

and C, Scans with soft tissue windows show a small epidural

hematoma (EDH) (arrows) with pneumocephalus, seen as multiple

very low density foci mostly within the epidural space Sudden neurologic deterioration 24 hours later prompted a repeat scan The

repeat CT scan (D) shows a large left occipital EDH (large straight

arrows) with hyperacute unclotted blood seen as low density foci (black arrows) within the EDH Note fluid-fluid levels (double white arrows); also, blood along the tentorium and straight sinus (open

204 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Extraaxial Hemorrhage

There are three types of extracerebral hemorrhage:

1 Epidural hematoma (EDH)

2 Subdural hematoma (SDH)

3 Subarachnoid hemorrhage (SAH)

Epidural hematoma

Incidence and clinical presentation Epidural

he-matomas are found in only 1% to 4% of patients imaged

for craniocerebral trauma, although EDHs represented

10% of fatal injuries in the Glasgow autopsy series (see

Table 8-1) A classic "lucid interval" between the

traumatic episode and onset of coma or neurologic

deterioration is seen in only half the patients with

EDH.13 Delayed development or enlargement is seen in

10% to 30% of EDHs and usually occurs within the first

24 or 48 hours.14,15 Late hematomas develop in 20% of

moderate to severely headinjured patients who do not

have signs of cerebral contusions on initial posttrauma

CT studies (Fig 84).16

Etiology A fracture that lacerates the middle

meningeal artery (MMA) or a dural venous sinus (Fig

8-4) is present in 85% to 95% of all cases with EDH16 ;

venous "oozing" or MMA tear without fracture accounts

for the remainder

Location Epidural hematomas are located between

the skull and dura As it forcefully strips the

Fig 8-5 Gross autopsy specimen of acute epidural

hematoma Note dural stripping from the inner table

forms a focal biconvex extradural collection (arrows)

that is filled with “currant jelly” fresh clot (Courtesy

B Horten.)

dura away from the inner table of the skull an EDH characteristically assumes a focal biconvex or lentiform configuration (Fig 8-5) EDHs may cross dural attachments but not sutures Ninety-five percent of EDHs are unilateral and occur above the tentorium The temporoparietal area is the most common site Five percent of EDHs are bilateral.13

Posterior fossa EDHs are relatively uncommon but have a higher morbidity and mortality rate than their supratentorial counterparts.17,17a

Outcome The overall mortality with EDHs is

ap-proximately 5% Poor outcome is often-but not variably- related to delayed referral, diagnosis, or operation.18,19 Occasionally, EDHs resolve spontaneously without surgical intervention, probably by decompression through an open fracture into the extracranial subgaleal soft tissues.20

in-Imaging (Table 8-3) On CT scans the typical EDH is

a biconvex extraaxial mass that displaces the gray-white matter interface away from the calvarium Two thirds of acute EDHs are uniformly high density; in one third, mixed hyper- and hypodense areas are present and indicate active bleeding (see Chapter 7) (Fig 8-6) The brain adjacent to most EDHs is severely flattened and displaced Secondary herniations with EDH are very common

MR scans of hyperacute EDHs demonstrate a lentiform-shaped mass that strips the dura away

Fig 8-6 Axial NECT shows a large acute right

frontal EDH (large arrows) Note the low density area (small single arrows) within the EDH This

so-called swirl sign represents active bleeding with unretracted liquid clot The gray-white matter

interface is displaced (open arrows) and there is

subfalcine herniation of the lateral ventricles

Subarachnoid pneumocephalus (double arrows) is

present

from the inner table The displaced dura appears as a

thin very low signal line interposed between the

calvariurn and brain (Fig 8-7) Acute EDHs are

isointense on T1WI but hyperintense on T2-weighted

studies Late subacute and early chronic EDHs are

typically hyperintense on both T1- and T2WI (Fig

8-13)

Subdural hematoma Traumatic acute subdural

hematoma is among the most lethal of all head

inju-ries Mortality rates range from 50% to 85% in some

reported series.21

Incidence and clinical presentation Subdural

hematomas (SDH) are seen in 10% to 20% of all

meningeal artery/dural sinus in 70% to 85%;

venous "ooze" or MMA tear without fracture

in 15%

Location Between skull and dura Between dura and arachnoid

Cross dural attachments but not sutures Cross sutures but not dural attachments 95% supratentorial (frontotemporal, frontoparie- 95% supratentorial (frontoparietal, convexity,

5% posterior fossa Interhemispheric parafalcial, bilateral SDHs com-

mon in child abuse

Displace gray-white interface Crescentic

2/3 hyperdense; 1/3 mixed hyper/hypodense 60% hyperdense, 40% mixed hyper/

hypodense May be isodense in coagulapathy or severe anemia

Subacute SDH May be nearly isodense with underlying cor- tex

Neomembrane, underlying vessels may en- hance

Chronic SDH Hypodense with enhancing membrane May be loculated

Rehemorrhage can cause mixed density 5% of chronic SDHs have fluid-blood den- sity levels

1% to 2% of very old SDHs may calcify

Chapter 8 Craniocerebral Trauma 205

cerebral trauma cases and occur in up to 30% of fatal injuries (see Table 8-2) A definite history of trauma may be lacking, particularly in elderly patients SDHs are common in abused children (see subsequent dis-cussion) Most patients with acute SDHs have low Glasgow Coma Scores on admission (Table 8-4); 50% are flaccid or decerebrate.21

Etiology Stretching and tearing of bridging cal veins as they

corti-cross the subdural space to drain into an adjacent

dural sinus is a common cause of SDH (see Fig 6-37,

C) These veins rupture because a sudden change in velocity of the head occurs.6 The arachnoid may also

be torn, creating a mixture of blood and CSF in the subdural space

206 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-7 Axial (A) T1- and (B) T2-weighted MR scans show a small acute right

posterior temporal EDH Note the very low signal displaced dura (black arrows)

The acute EDH and overlying subgaleal hematoma (curved arrows) are isodense

with brain on the T1-weighted study and mostly hyperintense on the T2WI

Table 8-4 Glasgow Coma Scale

Rating for Total

Ten percent to thirty percent of chronic SDHs show evidence of repeated hemorrhage.22 Rebleeding

usually occurs from rupture of stretched cortical veins

as they cross the enlarged fluid-filled subdural space

or from the vascularized neomembrane on the

calvarial side of the fluid collection

Location SDHs are interposed between the dura

and arachnoid (Fig 8-8) Typically crescent-shaped,

Fig 8-8. Gross autopsy specimen with acute

subdural hematoma (arrows) (Courtesy E Tessa

Hedley-Whyte.)

they are usually more extensive than EDHs and may cross suture lines but not dural attachments Eighty-five percent are unilateral Common sites for SDH are over the frontoparietal convexities and in the middle cranial fossa Isolated interhemispheric and parafalcial SDHs are common in cases of nonaccidental trauma Bilateral SDHs are also more frequent in child abuse (see subsequent discussion)

Chapter 8 Craniocerebral Trauma 207

Fig 8-9 Axial NECT shows a large acute right

subdural hematoma (SDH) The high-density

crescent-shaped fluid collection (large white

arrows) spreads diffusely over the underlying

hemisphere Note displacement of the gray-white

matter interface (open arrows) and the subfalcine

herniation of the lateral ventricles The left lateral

ventricle (black arrows) is obstructed secondary to

foramen of Monro occlusion

Imaging The appearance of SDHs on CT and MR

studies varies with clot age and organization (see

Table 8-3)

The classic CT appearance of an acute SDH is a

crescent-shaped homogeneously hyperdense

ex-traaxial collection that spreads diffusely over the

af-fected hemisphere (Fig 8-9) However, up to 40%

of acute SDHs have mixed hyper/hypodense areas

that reflect unclotted blood, serum extruded during

clot retraction, or CSF within the subdural

hematoma due to arachnoid laceration (Fig 8-10).23

Rarely, acute SDHs may be nearly isodense with the

adjacent cerebral cortex This occurs with

coagulopathies or severe anemia when the

hemoglobin concentration reaches 8 to 10 g/dl.24, 25

With time, subdural hematomas undergo clot

ly-sis, organization, and neomembrane formation (see

Chapter 7) The evolution of an untreated,

uncom-plicated SDH follows a predictable pattern

Subacute SDHs become nearly isodense with the

underlying cerebral cortex within a few days to a

few weeks after trauma (Fig 8-11).26 In such cases

the displaced gray-white matter interface, failure of

surface sulci to reach the inner calvarial table, and

comparison of the subtle extraaxial fluid collection

to density of the underlying white matter usually

permit detection of a subacute SDH Contrast

administration often

Fig 8-11 Axial NECT scan shows a nearly isodense

leftsided subacute SDH The border between the

extraaxial collection and underlying brain (black arrows) is barely discernible Medially displaced gray-white matter interface (white arrows) Compare

to the normal right side

Fig 8-10 Axial NECT scan in a head-injured patient

with rapid clinical deterioration A large right-sided

acute SDH is present (white arrows) Low density areas (black arrows) within the SDH could represent

unclotted blood, serum extruded during clot retraction, or cerebrospinal fluid from arachnoid tear Note subfalcine herniation of the lateral ventricles with foramen of Monro obstruction An actively bleeding SDH with unretracted liquid clots was evacuated surgically

208 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-12 Pre- (A) and (B) postcontrast axial CT scans of a subacute subduraI hematoma show the crescent-shaped extraaxial collection is nearly isodense with the

white matter but the corticomedullary interface displacement (A, arrows) is readily apparent The postcontrast study shows enhancing cortical veins (B, arrows) stretched

across the subacute SDH Rupture of these so-called bridging veins can easily occur (compare with Fig 6-37, C), although recurrent bleeding into subacute or chronic

SDHs occurs primarily from the vascularized neomembrane (see Fig 8-13, A)

eates an underlying membrane or demonstrates

cor-tical vessel displacement by the nearly isodense

ex-traaxial collection (Fig 8-12)

Chronic SDHs are encapsulated, often loculated

collections of sanguineous or serosanguineous fluid

in the subdural space These may be either crescentic

or lentiform (Figs 8-13 and 8-14) Uncomplicated

chronic SDHs are typically low attenuation (Fig

8-15) Recurrent hemorrhage into a preexisting

chronic SDH produces mixed density extraaxial col-

lections, seen in approximately 5% of cases (Figs 7-10, 7-11, and 8-15).27

The capsule of a chronic SDH is a capillary-rich membrane through which active exchange of solutes such as albumin and contrast material can occur.28 Both the neomembrane and the subdural collection may enhance following contrast administration Calcification

or ossification is seen in 0.3% to 2.7% chronic SDHs, usually when they have been present for many months

to years (Fig 8-16).29

Fig 8-13 For legend see p 209.

Fig 8-13, cont'd Three autopsy cases with chronic

subdural hematomas (SDHs) A, This case

demonstrates acute (left side of photograph, large

arrows) and chronic (right side of photograph, small

arrows) SDHs The acute clot has a "currant jelly"

consistency and the older SDH consists of an

or-ganized membrane Note the fresh petechial

hemorrhages (double arrows) oozing from the

chronic SDH B, Second case demonstrates the

lentiform configuration that these chronic extraaxial

collections can assume Bilateral chronic SDHs are

present (arrows) C, Third case has small bifrontal

crescent-shaped organized chronic SDHs (arrows)

(Courtesy E Tessa Hedley-Whyte.)

Chapter 8 Craniocerebral Trauma 209

Fig 8-14 Combined venous phases of the right and left carotid angiograms, AP view, in a patient with bilateral chronic SDHs show the typical lentiform collections outlined by the displaced cortical veins

(arrows)

Fig 8-15 Axial contrast-enhanced CT scan in a

patient with bilateral chronic SDHs The left-sided

crescent-shaped low density collection is a classic

uncomplicated chronic SDH (white arrows) The

right-sided lesion is lentiform (arrowheads) and has

a fluid-fluid level (black arrow) that indicates

rehemorrhage into the preexisting chronic SDH

Fig 8-16 PA plain skull film demonstrates a

calcified chronic SDH (arrows)

210 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

The MR appearance of subdural hematomas and

hygromas is quite variable In general, SDHs evolve

in a pattern similar to intracerebral hemorrhage (see

Chapter 7) The exceptions are chronic subdural

he-matomas In these cases the extraaxial collections are

often iso- or hypointense on TIWI compared to gray

matter, and hemosiderin deposition is rarely observed

(Fig 8-17).30

Fig 8-18 Coronal (A) and axial (B) T1-weighted

MR scans show a uniformly hyperintense lentiform

chronic SDH (arrows) The fluid collection remains

hyperintense on T2-weighted scans (C)

Thirty per cent of chronic SDHs are iso- or hypointense on T1WI but most are hyperintense on T2weighted studies (Figs 8-18 and 8-19).31 If rehemorrhage into subacute or chronic SDHs occurs,

MR studies will show mixed signal intensities (Fig 8-20) Fluid-fluid levels are common with repeated hemorrhages (Fig 8-21) The neomembranes of subacute and chronic SDHs typically enhance following contrast administration

Fig 8-17 Coronal T1- (A) and axial T2-weighted (B) MR scans in a patient

with small bilateral chronic SDHs The crescentic extraaxial collections

(arrows) are isointense with cortex on T1WI and hyperintense on T2-weighted

scans (compare with Fig 8-13, C)

Fig 8-20. Coronal T1- (A) and T2-weighted (B) MR scans show bilateral

subdural hematomas The crescentic right-sided collection (small arrows) is a chronic SDH The left-sided chronic SDH (large arrows) contains a larger, lentiform subacute collection (open arrows)

Fig 8-21. Axial T1- (A) and T2-weighted (B) MR scans demonstrate large

mixed-age chronic SDHs (white arrows) with fluid-fluid levels (black arrows)

(Courtesy L Blas.)

Fig 8-19. Sagittal T1-weighted MR scan shows

diffuse chronic SDHs (arrows)

Chapter 8 Craniocerebral Trauma 211

212 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Traumatic subarachnoid hemorrhage and its

"mimics." Subarachnoid hemorrhage (SAH)

accom-panies most cases of moderate to severe head trauma

(Fig 8-22) On nonenhanced CT scans, acute SAH

appears as thin high density fluid collections within

the superficial sulci and CSF cisterns (Fig 8-23)

"Pseudo-subarachnoid hemorrhage" is seen in

cases of severe, diffuse cerebral edema when the

brain becomes very low in attenuation and dura and

circulating blood in the cranial vasculature appear

un-usually hyperdense compared to adjacent structures

Posterior parafalcine or interhemispheric

subarach-noid hemorrhage can mimic the "empty delta sign" of

superior sagittal sinus thrombosis and should not be

mistaken for dural sinus occlusion (see Fig 8-45,

B).32

Intraaxial Lesions

Diffuse axonal injury With cortical contusions,33

diffuse axonal injury (DAI, or "shearing," injury) has

been identified as the most important cause of

sig-nificant morbidity in patients with traumatic brain

injuries.7

Incidence and clinical presentation Diffuse

axonal injuries represent nearly half of all primary

intraaxial traumatic brain lesions34 (see Table 8-2)

Patients with DAI typically lose consciousness at the

moment of impact8 ; DAI is uncommon in the absence

of severe closed head injury

Etiology and pathology Axonal shear-strain

de-formations are induced by sudden

acceleration/decel-eration or rotational forces on the brain These

injuries

tend to be diffuse, bilateral, and occur in very predictable locations (Fig 8-24) The characteristic shearing injuries are microscopic axonal bulbs or "re-traction balls" (Fig 8-25).6 Disruption of penetrating blood vessels at the corticomedullary junction, corpus callosurn and internal capsule, deep gray matter and upper brainstem produce numerous small hemorrhagic foci that may be the only gross pathologic markers of DAI

Location DAI tends to occur in the following three

very specific areas (Figs 8-26 and 8-27)7:

1 Lobar white matter, particularly at the gray white matter interface

Imaging The initial CT scans in DAI are often

nor-mal despite profound clinical impairment Early im-

Fig 8-22 A, Gross autopsy specimen of severe closed head injury shows severe

traumatic subarachnoid hemorrhage (SAH) B, Coronal cut specimen shows

extensive SAH (large arrows) plus numerous cortical contusions (small arrows)

(Courtesy E Tessa Hedley-Whyte.)

Primary Neuronal Injuries

Diffuse axonal (shearing) injury Cortical contusions

Deep cerebral/brainstem injury

Chapter 8 Craniocerebral Trauma 213

Fig 8-23 Axial NECT scans in a patient with severe head trauma disclose acute

traumatic SAH (single arrows) Right frontotemporal contusion and a small SDH (open arrows) are also present

Fig 8-24 Coronal gross specimen demonstrates multiple small diffuse axonal

injuries (DAI), seen as petechial hemorrhages in the deep white matter and

corpus callosum (arrows) (Courtesy E Tessa Hedley-Whyte.)

Fig 8-25 Photomicrograph demonstrates the

"axonal retraction balls" characteristically seen in

DAL (Courtesy L Becker.)

Fig 8-26 Sagittal gross pathologic specimen

demonstrates severe shearing injuries of the corpus callosurn (compare with Fig 8-27, C) (Courtesy E Ross.)

214 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

aging evidence for acute DAI may be subtle or

non-existent; only 20% to 50% of patients with DAI have

abnormalities on initial CT examination.35, 36 Delayed

scans may demonstrate lesions not apparent on initial

examination Acute DAI is seen as small petechial

hemorrhages, particularly at the 3 pray-white junction

and corpus callosurn (Fig 8-28).37

The MR appearance of DAI depends on the

pres-ence or abspres-ence of hemorrhage and age of the

le-sions.8 T1-weighted studies are often unremarkable

On T2WI the most common finding is multifocal

hy-perintense foci at the gray-white interfaces or in the

corpus callosurn (Fig 8-29) The hyperintensity of

these lesions tends to diminish with time, although

shearing injuries are one of the numerous potential

causes of multifocal white matter lesions seen on

T2 weighted brain scans (see Chapter 17)

If shearing lesions are hemorrhagic, T1-weighted

studies may demonstrate blood degradation products

Multiple foci of diminished signal on T2WI and

gradient-echo scans can be seen for years after the

traumatic event (Fig 8-30) Occasionally lesions from

remote DAI can be identified only on gradient refo-

Fig 8-27 A to C, Anatomic diagrams depict

typical locations of diffuse axonal injury (DAI, or

"shearing," injury) Secondary midbrain (Duret)

hemorrhage is indicated (black area) in the

mesencephalon (C, arrow)

cussed sequences Nonspecific atrophic changes can

be late sequelae of DAI; on rare occasions they may occur in the absence of other identifiable parenchmal lesions

Cortical contusions Cortical contusions are the

second most common primary traumatic neuronal in

jury (see box, p 212)

Incidence and clinical presentation Cortical

con-tusions represent 45% of primary intraaxial traumatic lesions Compared to DAI, cortical contusions are less frequently associated with initial loss of con-sciousness unless they are extensive or occur with other abnormalities such as shearing injury or sec-ondary brainstem trauma.34

Etiology and pathology Contusions are typically

superficial foci of punctate or linear hemorrhages that occur along gyral crests6 (Fig 8-31) They are induced by brain striking on an osseous ridge, less often a dural fold, and occur when differential acceleration/deceleration forces are applied to the head.34 Focal contusions may also be associated with

a depressed skull fracture Petechial cortical contusions tend to co-

Chapter 8 Craniocerebral Trauma 215

Fig 8-28 Axial NECT scans in a patient with

severe closed head injury and a Glasgow coma score of 8 show a right frontotemporal scalp he-

matoma (curved black arrows), but no skull

fracture was identified Multiple shearing

injuries (large white arrows) are present A

choroid plexus hemorrhage is seen in the atrium

of the right lateral ventricle (B, curved arrow)

Subtle subarachnoid hemorrhage is present (A

and C, open arrows) Note that the only

subarachnoid blood visible in the suprasellar cistern lies in the foramen cecum of the

interpeduncular fossa (A, open arrow)

Fig 8-29 Axial T2-weighted MR scan in a patient

with closed head injury 3 weeks before study Small

right frontal and left temporal chronic SDHs are seen

as thin crescentic extraaxial fluid collections (straight

arrows) A highsignal focus in the corpus callosurn

splenium (curved arrow) is a classic shearing injury

216 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-30 Axial T2-weighted MR scans in a patient with severe closed head

injury 2 years before study Left temporoparietal encephalomalacia is secondary

to traumatic MCA infarct (A, large arrows) Some residua of hemorrhagic transformation are seen as gyriform low signal areas (A, open arrows) Multiple

old hemorrhagic shearing injuries are seen as low signal foci at the

corticomedullary junction (small arrows) The DAIs are particularly well seen

on the higher section (B)

Fig 8-31 A, Gross autopsy specimen demonstrates the

typi-cal frontotemporal contusions (arrows) seen with severe

closed head injury B, Close-up view of the frontal lobes in

another case with fatal closed head injury Note extensive

gyral contusions (arrows) (A, Courtesy Scott VandenBerg,

B, Courtesy J Townsend.)

alesce into larger hemorrhagic foci and often become

more evident 24 to 48 hours after the initial trauma.16

Location Because contusions occur when brain

contacts a dural ridge or bony protuberance, they occur

in very characteristic locations (Figs 8-31 and 8-32)

Nearly half of all cases involve the temporal lobes, most

frequently the temporal tip, inferior surface, and cortex

around the sylvian fissure One third occur in the frontal

lobes, particularly along the inferrior

surface and around the frontal poles Twenty-five per cent are parasagittal or "gliding" contusions (so-called because the convexities of each hemisphere are anchored to the dura by arachnoidal granulations

When the brain abruptly shifts at the time of impact,

the subcortical tissue "glides" more than the cortex).6 The inferior surfaces of the cerebellar hemispheres are less common sites of cortical contusion

Imaging Finding are variable because cortical

contusions tend to evolve with time Initially,

find-ings on CT scans may be subtle or absent (Fig 8-33,

A and B).33 Early findings include patchy, ill-defined

frontal or temporal low density lesions that may be

mixed with smaller hyperdense foci of petechial

hemorrhage (Fig 8-34)

CT scans obtained 24 to 48 hours after injury

of-ten show more lesions than are identified on initial

Fig 8-32 A to C, Anatomic diagram

depicts typical locations of contusional traumatic brain injuries

studies In 20% of cases, delayed hemorrhages velop in what previously appeared as nonhemorrhagic low density areas.34 Edema and mass effect typically increase in the first few days after the traumatic insult, then gradually diminish over time Cortical contusions may enhance following contrast ad-

de-ministration (Fig 8-35; see Fig 7-14, C)

Fig 8-33 Axial NECT scans in a patient with severe closed head injury A and B, Initial

scans show a subtle left frontal cortical contusion (A, arrow) and some traumatic SAH (B, arrows) Clinical deterioration 12 hours later prompted repeat examination

Continued

218 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-33, cont'd C, Cortical contusions are much more apparent and seen as patchy

hemorrhagic foci mixed with low density edema (arrows) D, Wider window also shows a small SDH (open arrows) that was difficult to see on the routine study (C)

because of the high density overlying calvarial vault

Fig 8-34 Axial NECT scan in a patient with severe

closed head injury A large tentorial SDH is present

(large arrows) The entire right temporal lobe and

much of the frontal lobe are severely contused The

contused brain appears as diffuse low density mixed

with more focal but patchy hyperdense areas of

petechial hemorrhage (small arrows) A small

"contre-coup" left frontotemporal contusion is also

present (curved arrow) There is subfalcine herniation

of the lateral ventricles with foramen of Monro

obstruction and enlargement of the entrapped left

lateral ventricle (open arrows)

Fig 8-35 A, Axial NECT scan obtained

immediately after trauma shows a high right frontal contusion (large arrows) and a small

interhemispheric acute SDH (small arrows)

Fig 8-35, cont'd B, Follow-up NECT scan 10 weeks later shows the contused

brain is now low density (arrows) The interhemispheric SDH has resolved C,

The contused gyri ,enhance (arrows) following contrast administration

MR is much more sensitive than CT in detecting

cortical contusions, particularly in the subacute

stage35,36 (Figs 8-36 and 8-37) Multiple superficial

areas of poorly delineated, hyperintense signal

abnormalities are seen on T2WI (Fig 7-14) The

lesions often appear inhomogeneous on T1- and

T2-weighted scans because hemorrhagic foci are

present

Fig 8-36 Axial T2-weighted MR scans abtained 4 days after traumatic brain

injury show extensive cortical contusions as multifocal low signal areas along

the gyral surfaces (open arrows) surrounded by high signal edema (large arrows) Numerous shearing injuries are also present (small arrows).

Subcortical gray matter (deep cerebral) and brainstem injuries Less common than DAI and

cortical contusions, these lesions nevertheless represent important manifestations of primary intraaxial traumatic injury

Incidence, etiology, and clinical presentation

Deep gray matter and brainstem lesions represent 5%

Chapter 8 Craniocerebral Trauma 219

220 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-37 A to B, Axial NECT scans obtained immediately after

severe closed head injury show cerebellar contusions (A, arrows) and choroid plexus hemorrhage (B, curved arrows) Some intra-

ventricular hemorrhage is present with a blood-CSF level in the

right occipital horn (B, double arrows) C and D, Axial

T1-weighted MR scans performed 10 days later show subacute

hemorrhagic cerebellar contusion (C, arrow) and temporal lobe shearing injuries (D, arrows)

to 10% of primary traumatic brain injuries.7 Most are

induced by shearing forces that cause disruption of

multiple small perforating blood vessels (Figs 8-37

and 8-38).6 Less commonly, the dorsolateral brainstem

strikes the tentorial incisura during violent excursions

of the brain (Fig 8-39).7 Sudden craniocaudal

displacement of the brain at impact may also result in

anterior rostral midbrain hemorrhage (Fig.8-40).38

Most patients with deep cerebral and brainstem juries have profound neurologic deficits, low initial

in-Glasgow coma scale scores, and a poor prognosis for

neurologic recovery.39

Imaging CT is often normal in these patients

Pe-techial hemorrhages can sometimes be seen in the

dorsolateral brainstem, periaqueductal region, and

deep gray matter nuclei (Fig 8-38) MR depicts these

brainstem lesions nicely (Figs 8-38 and 8-39)

Fig 8-38 Axial NECT scan in a patient with severe

deceleration closed head injury shows bilateral ocular

hemorrhages (double arrows) and a small hemorrhagic midbrain shearing injury (curved arrow) (From

Osborn AG: Secondary effects of intracranial trauma,

Neuroimaging Clin N Amer 1:461474, 1991.)

Chapter 8 Craniocerebral Trauma 221

Fig 8-39 Axial T2-weighted MR scans in a patient with closed head injury

shows a left dorsolateral midbrain contusion (arrows) No other abnormalities

were identified The lesion was probably caused by midbrain impaction against the tentorium during the traumatic episode

Intraventricular and choroid plexus hemorrhage

Incidence, etiology and clinical presentation IVH

is identified in 1% to 5% of all patients with closed

head injury.40,41 Traumatic IVH is thus relatively

un-common and usually reflects severe injury

Most cases of IVH are associated with other

manifestations of primary intraaxial brain trauma

such as DAI, deep cerebral gray matter, and

brain-stem lesions Prognosis is poor, although patients

with isolated IVH typically have a somewhat better outcome (Fig 8-41).41 Disruption of subependymal veins, shearing injuries, and basal ganglionic hem-orrhage with subsequent rupture into the adjacent ventricle are thought to cause most cases of traumatic IVH.41

Imaging CT manifestations oxcute IVH are high

density intraventricular blood with or without a fluid level (Fig 8-41) Occasionally, focal choroid

fluid-Fig 8-40 Axial (A) T1-and W T2-weighted MR scans in a patient with traumatic

anterior rostral midbrain hemorrhage (arrows), probably from peduncular contusion

against the tentorial incisura during sudden craniocaudal displacement at the time of impact

222 PART TWO Cerebral Vasculature: Normal Anatomy and Pathology

Fig 8-41 Axial NECT scans in a patient with isolated traumatic intraventricular

hemorrhage (arrows) No other lesions were present The patient recovered with

minor neurologic sequelae

plexus hematomas can be identified in the absence of

frank IVH (Fig 8-42) Most cases of traumatic ICH

have hemorrhagic foci in the adjacent deep gray

mat-ter nuclei or white matmat-ter Subarachnoid hemorrhage

is also commonly associated with IVH

SECONDARY EFFECTS OF

CRANIOCEREBRAL TRAUMA

The secondary effects of craniocerebral trauma are

sometimes of greater clinical import than direct

man-ifestations such as focal hematoma, contusion, or DAI

Most secondary injuries are caused by increased

intracranial pressure or cerebral herniations These

traumatic sequelae in turn cause compression of

brain, nerves, blood vessels, or a combination of all

three against the rigid, unyielding bony and dural

margins that comprise the cranial cavity.42

The major secondary effects of craniocerebral

trauma are summarized in the box Cerebral

hernia-tions, traumatic ischemia, infarction and secondary

hemorrhage, diffuse cerebral edema, and hypoxic

in-jury are all discussed here Vascular manifestations

and complications of craniocerebral trauma are then

specifically addressed

Cerebral Herniations

Pathology of cerebral herniations The cranial

cavity is functionally divided into compartments by

combinations of bony ridges and dural folds (Fig

8-43, A and B) Cerebral herniations are caused by

mechanical displacement of brain, cerebrospinal

fluid, and blood vessels from one cranial

compart-ment to another

Fig 8-42 Axial NECT scan shows a localized

hematoma in the left choroid plexus glomus (large arrows) Note subtle SAH (open arrow)

Major Secondary Effects of Craniocerebral Trauma

Cerebral herniations Traumatic ischemia, infarction, secondary hemorrhage

Diffuse cerebral edema

Hypoxic injury