the general appearance of edema and hemorrhage

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43J.L. Creasy,Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses,

and Attorneys, DOI 10.1007/978-1-60761-250-6_2, Springer Science+Business Media, LLC 2011

Abstract This chapter begins with a discussion of the terminology and hardware of computed

tomographic (CT), magnetic resonance (MR), and ultrasound (US) imaging. This includes an intro-

duction to CT numbers and very basic MR image formation, sequence types, and sequence usages.

The remainder of the chapter is an introduction to edema and hemorrhage. The two basic typesof edema are cytotoxic and vasogenic. The appearance of these types of edema is presented on CT,

MR, and US. The general imaging of hemorrhage without following in detail the evolution of

these findings with time and the various spaces in which it occurs in the brain are discussed and

demonstrated on CT, MR, and ultrasound.

Keywords Computed tomography (CT) Magnetic resonance (MR) Ultrasound (US) Edema

Cytotoxic edema Vasogenic edema Hemorrhage

Introduction

This chapter will build on the anatomy and imaging findings of normal brain detailed in Chap. 1.

Knowing the normal appearance of brain is mandatory to make an intelligent assessment of the changes

in brain as a result of injury. In this chapter, we begin with a brief introduction on the basics of computed

tomography (CT), then magnetic resonance (MR) and finally, ultrasound (US) imaging of the brain.

Second, we will discuss the general topic of edema and how it appears on each of the three imaging

modalities. Finally, in a broad sense, we will introduce hemorrhage and its imaging appearance. In all

cases in this chapter, we will not discuss in detail the manner in which the basic findings change con-

siderably over time. That detailed discussion, including the most complicated topic of all the changing

appearance of hemorrhage over time on MR scanning is reserved for Chap. 4.

CT Scanning: The Absolute Basics

In any discussion of the pathology within the central nervous system (CNS the brain and spinal

cord), one should have an understanding of the basic underlying principles of the modality that is

used to image the brain, in addition to an anatomic understanding of the brain. Therefore, at this

point, we will provide an overview of the basic principles of CT scanning and, more specifically,

those principles that are directly applicable to imaging the CNS [1]. Once one understands CT

Chapter 2

The General Appearance of Edema and Hemorrhageon CT, MR and US (Including a General Introduction

to CT, MR and US Scanning)


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Fig. 2.1 CT scanner. A typical CT scanner. The table on which the patient lies, is at the front of the scanner. The

table then moves into the central bore of the CT scanner. Within the scanner gantry is a rotating ring with both the

X-ray tube and the detector array

2 The General Appearance of Edema and Hemorrhage

technology, we can move beyond that into the specific findings on CT that occur in the setting of

injury. Abnormalities are recognized in one of two ways: either anatomy is distorted (i.e., something

there that shouldnt be, or something not there that should be) and/or an alteration occurs in the

normal CT numbers of the tissue. CT numbers, as we shall see, are an essential component of the

information provided by a CT scan.

A CT scanner consists of the basic components of a patient table (on which the patient to bescanned lies); the scanner gantry (which contains the rotating portion that holds the X-ray tube

generator and detector array) and a computer system (for performing the necessary calculations to go

from measurements to a viewable image) (Fig. 2.1). The patient lies supine on the movable scanner

table as the portion of the body to be scanned passes through the middle of the opening in the gantry.

During the scan, the X-ray tube continually generates X-rays, which pass sequentially through the

patient and then on to an array of detectors. The computer begins with the detector-made measure-

ments of the radiation that is left over after passing through the patient and calculates what the

tissues in the body must have looked like to have produced the observed measurements.

The term density is often used to describe the distribution of matter that must have been

present to partially absorb the X-ray beam and produce the measured residual beam at the detec-tors. However, a more technically accurate description is that the scanner computes the amount

of radiation absorption that occurs at each scanned point in the body. Fortunately, a close

correlation exists between the density of a tissue and its ability to stop X-ray photons. For our

purposes we will, therefore, use the shorter term density, rather than the technically more

accurate (but much more cumbersome) phrase, relative ability to absorb X-ray photons, for the

remainder of this book.

When the CT scanner computer finishes its calculations for a single image, the result is a cross-

sectional image of the brain in which white represents structures that are more dense and dark

represents structures that are less dense. The CT image can be thought of as a density map, showing

the relative propensity of different portions of the image to absorb the X-rays that the CT scanner

beam sends through the patient. Within the scanner, it is the job of the computer to reconstruct and

calculate the density distribution which must have existed to produce the measured absorptions, and


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Table 2.1 CT numbers

Air 1000

Fat 100 to 50

Water 0

Most tissues 2040

Hemorrhage


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Fig. 2.2 MR scanner. Cut-away drawing showing the internal major components of an MR scanner. During a scan

the patient lies within the bore of the main magnet. Smaller gradient coils shape the larger field and allow imaging.

Radiofrequency coils send radio signals into the patient and listen to the emitted signals, which are used to create the

MR image

Table 2.2 MR pulse weightings

Image factor

Pulse sequence with this

weighting Best used for

T1 T1-weighted Depict anatomyT2 T2-weighted Depict pathology

T2 FLAIR Depict pathology

Proton density PD-weighted Seldom used

Magnetic susceptibility Magnetic susceptibility-

weighted

Detect calcium and

hemorrhage

Motion DWI (microscopic motion) Detect infarctions

Motion MRA (macroscopic motion) Evaluate vasculature

For each of the five components of an MR image (T1, T2, proton density, motion,

magnetic susceptibility) the table lists the different sequences that can have that

component as their primary weighting, and the main use of those sequences


However, while it is not possible to scan an image that is composed purely of any one of these

five, it is possible to scan an image in which one of these five becomes the predominant image

contrast in the final image. Such an image is said to be a weighted image. At least one type of imag-

ing examination corresponds to each of these five components of an MR image, including

T1-weighted images, T2-weighted images, proton density-weighted images, and magnetic suscep-

tibility-weighted images. Motion-weighted images have two types of sequences. The first empha-

sizes motion on the microscopic level (these are also called diffusion-weighted images); the second

weights motion on the macroscopic level and these are MR angiograms, or images of vessels within

the brain (Table 2.2 MR pulse sequence weighting). One of the greatest strengths of MR scanning

is that pathology can be detected by an abnormality of signal on a large number of different MR

sequences; and the appearance both of normal and abnormal tissues varies from sequence to

sequence.


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Fig. 2.3 Ultrasound (US) scanning. Diagram of hand-held, real-time transcranial ultrasonography of an infant.

The transducer is placed at the anterior fontanel and obtains coronal and sagittal images of the brain

US Scanning: The Absolute Basics

US Scanning: The Absolute Basics

An ultrasound machine utilizes high-frequency ultrasound to image patient anatomy and pathology.

High-frequency, ultrasonic sound waves are produced in a scanner placed on the patients skin,

directly over the area to be imaged. In order to produce an image, the sound waves must penetratethe patient. As the sound waves pass progressively deeper into the tissues of the patient, some are

selectively reflected back and received by the same transducer that generated them only a few mil-

liseconds earlier. This produces, in effect, a sonar image of the tissues of the body [3] (Fig. 2.3).

While CT and MR can be more helpful in the older child and adult, in specific clinical situations

neonatal head ultrasounds are extremely useful. It is often the case that the only images available of an

infants head in the first few days of life are ultrasound examinations, and only later are CT and/or MR

scans performed. The neonatal head can be scanned with ultrasound because of the presence of an open

anterior fontanelle, i.e., a normal developmental defect in the skull, anteriorly. However, by 1 year of

age the fontanelle is usually completely fused, and the previously usable acoustic window is no longer

available. From that time onward, MR and CT are the only means available for intracranial imaging.

However, in the initial days, weeks and first few months of life, ultrasound may provide an impor-tant adjunct or, in some cases, the only imaging evaluation of the intracranial contents. Consequently,

ultrasound needs to be considered in the discussion of the dating of neurologic injury by neuroradio-

logical imaging techniques. While, in general, some of the findings on ultrasound are perhaps not as

specific as the findings noted on CT and MR, in some clinical situations the ultrasound examination

may be a more sensitive test to early changes of injury to the brain parenchyma.


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Fig. 2.4 CT scan of edema. (a) Extensive low density, representing vasogenic edema, is present throughout the high

right centrum semiovale, surrounding a several day old hemorrhage. (b) Extensive cytotoxic edema produces a

wedge-shaped region of low density in this patient with an acute left-sided infarction


Edema

Before proceeding further with a discussion of the appearance of edema on MR and CT, it is appro-

priate to discuss edema itself. Edema refers to swelling within a tissue due to the accumulation of

fluid. Edema occurs as the result of a variety of pathologic conditions. The brain experiences edemaas a result of almost any insulting agent it is seen in and around regions of dead or dying brain,

around metastases and abscesses, after traumatic injury, following hypoxic ischemic injury, and

around primary brain tumors. Greenfield describes five different types of edema vasogenic, cyto-

toxic, hydrostatic, interstitial, and hypoosmotic [4]. For our purposes, we will concentrate on the

vasogenic and cytotoxic types.

In vasogenic edema, the edematous tissue swells due to breakdown of the blood brain barrier. An

interesting feature of vasogenic edema is that it can spread to regions that are some distance from the

site of the brain abnormality. For example, an abnormal, disrupted blood brain barrier at point A can

lead to vasogenic edema in the brain, which can spread to point B, even though point B is several

centimeters away, and was otherwise normal brain. This spreading water within the tissues moves

more freely through white matter than through gray matter, and as a result it will often halt when itreaches the underside of the cortex. Vasogenic edema occurs around infectious processes like abscesses

and both benign (meningiomas) and malignant tumors (gliomas and metastases). Vasogenic edema

can also be seen peripherally around a central core of cytotoxic edema in cases of infarction.

Greenfield describes cytotoxic edema as cellular swelling associated with a reduced extracel-

lular space, but with an intact blood brain barrier (at least to macromolecules in the initial stages)

[4]. In cytotoxic edema, tissue swelling occurs because the tissue is severely injured, dying or dead.

Such an injury could occur, for example, if an arterial occlusion ceases all blood flow to a demar-

cated region of brain. Within that region, all the brain would be equally affected, whether it were

gray or white matter. Cytotoxic edema from an arterial infarct involves both white matter and over-

lying gray matter. Cytotoxic edema is more commonly associated with ischemic or hypoxic pro-cesses (Figs. 2.4 and 2.5 Vasogenic and cytotoxic edema on CT and MR).

Three effects of edema are visible on imaging: loss of gray-white matter differentiation, swelling

of sulci (shrinking of gyri) and mass effects [5]. The first effect, the loss of gray-white differentiation,


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Fig. 2.5 MR scan of edema. (a) Extensive vasogenic edema limited to the white matter on this axial FLAIR image,

posterior to a large tumor in the right hemisphere. (b) Wedge-shaped area of abnormal diffusion on a diffusion-

weighted imaging (DWI) in the right occipital pole, representing cytotoxic edema, consistent with acute infarct. In

this early infarction, the FLAIR and T2 scans were normal

Fig. 2.6 CT scan demon-

strating loss of gray-white

differentiation with fuzzy,

indistinct basal ganglia

Edema

is commonly seen in cytotoxic edema. This loss of the ability to discern gray matter from white

matter on MR or CT is seen between the gray matter of the cortex and the immediate adjacent

underlying white matter, and within the basal ganglia, obscuring the ability to visually isolate the

gray matter of the caudate, thalamus and lentiform nucleus from the white matter of the internal

capsules (Figs. 2.6 and 2.7 Loss of cortical G-W differentiation and fuzzy BG on MR and CT).

The second effect of edema on a region of the brain is to cause the involved gyri to expand and

the intervening sulci to decrease in size. As the brain continues to swell, not only do the sulcidecrease, but all of the CSF spaces of the hemispheres decrease as well. This includes the Sylvian

fissure, as well as the basilar cisterns containing CSF around the brainstem and posterior fossa

structures (Figs. 2.82.10 Brain edema effects on sulci and ventricles on CT, MR and US).


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Fig. 2.8 CT scan showing the effect of brain edema on intracranial structures. In (a) a large infarction in the territory

of the right middle cerebral artery with marked low density, complete loss of gray-white differentiation within the

infarct, mass effect on the right lateral ventricle, and slight midline shift to the left. In ( b), a higher axial scan in a

different patient with a right-sided infarction shows complete absence (effacement) of the sulci on the effected side

Fig. 2.7 MR scan demonstrating abnormal DWI signal in the left basal ganglia in (a), and abnormal FLAIR signal

in the same region in (b)


The third and last effect edema produces is to cause the ventricles to decrease in size. The total

volume of the intracranial compartment is fixed, and composed of brain and all of the CSF-containing

spaces. As the brain tissues swell, in order for the total intracranial volume to remain constant, the

ventricles and extraaxial CSF spaces must decrease in total volume. As the amount of cerebral edema

worsens, more and more CSF is pushed out of the lateral, third and fourth ventricles into other CSF

spaces of the CNS beyond the cranium for example into the spinal canal. An excessive amount ofedema can cause mass effect which will result in both the displacement of normal ventricles and have

secondary effects on the ventricles. In addition to the ventricles being decreased in size, they can also

be displaced and moved, as can the normal midline structures of the brain. Severe edema can close


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Fig. 2.10 Ultrasonic demonstration of brain edema shows abnormally increased echogenicity in this patient bilater-

ally, more so on the patients right side, with early bilateral basal ganglia infarctions

Fig. 2.9 MR scan of the

effect of edema. The cortical

sulci are faced in the region

indicated by the arrowheads

the right lateral ventricle is

compressed and there is a

slight midline shift to the left

Edema

off the CSF drainage pathways and can cause portions of the ventricular system to increase in size

(Fig. 2.11 Additional effects of edema).

Edema on CT Scanning

As the brain swells (especially from cytotoxic edema), the comparative difference in appearance

between gray and white matter decreases on CT. As more and more water enters into the tissues,the relative density of both gray and white matter decreases, as does the difference in density

between the two tissues. Consequently, areas affected by cytotoxic edema can show the loss of

normal gray-white differentiation. This is manifested by an inability to see the difference between


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Fig. 2.11 Demonstration of various internal herniations. In (a) axial T2-weighted MR scan in a patient with a large

left-sided mass, surrounding vasogenic edema, and marked midline shift from left to right. In a different patient, in

(b) axial CT at level of midbrain showing loss of CSF spaces, consistent with tentorial herniation; and (c) axial CT

low in the posterior fossa showing very severe posterior fossa edema


gray and white matter in the region of affected brain, whether that involves the cortex and the under-

lying white matter, or whether that involves the deeper gray matter structures and their adjacent

white matter tracts (see Figs. 2.4, 2.6, and 2.8).

Edema on MR Scanning

On MR, the appearance of edema is similar to that of CT, though often, unlike CT, the underlyinganatomy is not completely obscured by the edema. MR can produce many different types of sequences

with very different weightings. However, of all these different types of weighting, the most sensitive

sequence for subtle degrees of edema is diffusion-weighted imaging (DWI) [6]. DWI can detect subtle

edema before it is seen on any other type of MR pulse sequence and, certainly, before it is seen on CT.

The ability to detect edema on MR scanning is due to a combination of two imaging findings.

The first is abnormal signal, most commonly noted on DWI but also seen on FLAIR and T2-weighted

imaging and, to a much lesser extent, on T1-weighted imaging; the second is due to morphologic

alteration (i.e., distortion) of the normal appearance of the tissues. While edema typically shows up

as bright signal on DWI, T2-weighting and FLAIR imaging, differences in the time, appearance and

duration of these signal abnormalities exist and will be discussed in much more detail in Chap. 4

(Figs. 2.5, 2.7, and 2.9 Edema on MR).

Edema on US Scanning

Edema on ultrasound in the neonate usually occurs around the ventricles in the periventricular white

matter. Because this is a watershed territory in newborns, the area around the ventricles and its associated

white matter is often involved by ischemic events. The initial examination can be normal. However, in

sonography the first detectable abnormality is areas of increased echogenicity around the ventricle. Over

time, cysts can develop, normally in 24 weeks. At longer time intervals, the cysts can either coalesce or

disappear such that they are no longer visible on ultrasound but the gliotic changes are still visible on

MR scanning. An initially normal ultrasound can become abnormal after weeks or months; hence, fol-

low-up imaging, even after an initial normal scan, is indicated (see Fig. 2.10).


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Fig. 2.12 CT scans of subarachnoid hemorrhage in (a), subdural hemorrhage in (b), and epidural hemorrhage in (c)

The General Appearance of Hemorrhage

In addition to the changes seen around the ventricles from paraventricular leukomalacia, more

global insults affecting larger areas of brain occur in the setting of global anoxia. This injured anoxic/

ischemic brain is diffusely echogenic with poorly defined sulci. The sulci may be lost in the overall

increase in echogenicity of the remaining brain parenchyma, the so called silhouetting of the sulci.

Another pattern which may be seen on ultrasound is damage to the basal ganglia, which can

occur with acute, near-total intrauterine asphyxia. Finally, while focal geographic parenchymalinfarction is uncommon in the neonate, it can occur due to underlying causes such as emboli from

heart disease or meningitis. In these cases, the region of brain that is affected shows focally

increased echogenicity.

In summary, the sonographic signs of cerebral infarction include echogenic parenchyma, mass

effect from edema, a pattern of injury which is that of an arterial territory and decreased definition

of the sulci [7].


Hemorrhage occurs when blood enters a portion of the brain that is not within the normal vascular

system. Hemorrhage can occur in the brain in three different space categories. It can occur within

the brain parenchyma (intraparenchymal hemorrhage), within the ventricles (intraventricular hem-

orrhage) or in the extraaxial spaces around the brain. Alluding to the earlier discussions of the layers

of the scalp, skull, and meninges in Chap. 1, extraaxial hemorrhage can occur in the subarachnoid

space, the subdural space or the epidural space (Figs. 2.12 and 2.13 Subarachnoid, subdural and

epidural hemorrhages on CT and MR).

Hemorrhage occurring into the brain parenchyma itself is usually the result of a closed head

injury or of bleeding from a vascular lesion such as a malformation, a malignancy, or hypertension.

Infarctions can also hemorrhage, as can intrinsic brain gliomas. These intraparenchymal hematomas

can be discrete, well-circumscribed collections that consist entirely of blood, or can be areas of

brain that are in effect bruised and are regions of brain where hemorrhage is interspersed among

the normal cellular elements (also called contusions) (Figs. 2.14 and 2.15 Intraparenchymal hem-

orrhage on CT and MR).

Blood in the ventricles can occur from a trauma which ruptures the small vessels that line the

ventricular wall. Alternatively, bleeding can occur initially into the brain adjacent to the ventricles,

and then rupture into the ventricles secondarily (Fig. 2.16 IVH on CT and MR).


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Fig. 2.13 MR scans of subarachnoid hemorrhage in (a) (arrows), subdural hemorrhage on FLAIR in (b), on T2 in

(c) and with GE in (d)


Blood in the extraaxial spaces tends to be caused by a short list of etiologies. The most common

cause of subarachnoid hemorrhage is trauma. If trauma is eliminated, in 8090% of cases the most

common cause of subarachnoid hemorrhage is rupture of an intracranial aneurysm. Subarachnoidhemorrhage can also occur from the rupture of a vascular malformation or from bleeding from a

CNS tumor. Bleeding into the subdural space is almost always traumatic in nature. However, if the

jet of leaking high-velocity blood is aimed directly at the dura, a previously-ruptured aneurysm that

has developed scar about its dome and ruptured again can rupture all or partially into the subdural

space. Epidural hemorrhages are almost always traumatic in nature.

Hemorrhage on CT Scanning

Regardless of the location of the hemorrhage, the appearance of the blood follows a fairly predictable

time course such that over days or at most weeks, hemorrhage decreases from its initial density of

4080, to a density range equal to that of gray or white matter, and finally to that of cerebrospinal

fluid [8]. This ordered, sequential progression of density changes over time occurs for any blood


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Fig. 2.14 CT of a small

intraparenchymal hemorrhage

in the left frontal brain


collection but the time each step takes varies with the exact location of the hemorrhage (be it

intraventricular, within the brain substance, or outside the brain). As the hemorrhage is resolved or

resorbed over time, its size also decreases, as does the amount of surrounding edema. The details of

this time course change will be discussed in much more detail in Chap. 4.

Hemorrhage on MR Scanning

The appearance of hemorrhage on MR scanning is very complex. Unlike CT scanning which

shows a progressive decrease in density over time, the MR appearance of hemorrhage varies mark-

edly over time and is different on each pulse sequence. In fact, on each of several different pulse

sequences the image appearance of hemorrhage may change several times over the initial23 week period following its occurrence. It is, therefore, not possible to state that hemorrhage

looks a specific way without also addressing and discussing the changes that hemorrhage takes on

over time on the different pulse sequences. Therefore, this complex topic will be discussed in much

more detail in Chap. 4.

Hemorrhage on Ultrasound

As with the ultrasonography of cerebral edema, the ultrasonography of cerebral hemorrhage is also

a discussion which is limited to patients under 1 year of age; ideally, even in the first few weeks and

months. After that period of time it becomes increasingly difficult to sonographically view the

intracranial contents.


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Fig. 2.15 MR of bilateral temporal lobe intraparenchymal hemorrhages. (a) T1-weighted axial image, (b) T2-weighted

axial image, (c) FLAIR and (d) gradient echo image all at the same level


The most common site for neonatal intracranial hemorrhage is the subependymal region, a spe-

cial portion of the lateral ventricles in neonates which houses the germinal matrix in the thalamo-

caudate groove. This is a frequent site of hemorrhage, which can remain subependymal or rupture

into the ventricles. In either case, these hemorrhages initially appear as hyperechoic structures,

either limited to the immediate subependymal brain or extending into the ventricle. Whereas, the

initial appearance is uniformly hyperechoic throughout, with time (12 weeks) the central portions

of the clot can become more sonolucent. Additional signs of intraventricular hemorrhage include a

clot that forms and makes a cast of the ventricle, a thickly echogenic choroid plexus, low-level

echoes floating within a ventricle, and CSF-blood fluid levels [9].

In a similar fashion, ultrasound can rather easily locate intraparenchymal hemorrhage. Thesehemorrhages, again, begin as hyperechoic structures which eventually have more echolucent centers.

The final resolution can be complete disappearance of the clot so that no sonographic appearance


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Fig. 2.16 Intraventricular hemorrhage on CT in (a). MR images of intraventricular hemorrhage sagittal T1 in (b),

axial T2 in (c), axial gradient echo in (d). US of IVH in (e)

Chapter Summary

remains. Alternatively, a small cyst or slit-like hole at the site of the prior hematoma may persist [10].

While hemorrhages can be detected noninvasively on ultrasound, both CT and MR scanning have

been found to be more sensitive exams [11, 12].

Chapter Summary

We began this chapter with an introduction to the three imaging modalities of CT, MR, and US. The

usefulness of US is limited to the first year of life. In contrast, CT and MR can both be used to image

brain injury throughout life. We presented the general imaging findings on CT and MR, but made

no attempt to describe how the imaging appearance of hemorrhage or infarction changes with time.

Those detailed discussions are reserved for Chaps. 4 and 5.

Regions of both infarction and hemorrhage are shown as areas of brighter signal (increased

echogenicity) on US. On CT, regions of hemorrhage begin as high density (whiter) and then

decrease in density (become darker) with time, while regions of edema are initially similar in

density to brain and then (if infarction occurs) become progressively less dense, eventually

approaching the density of water. On MR, regions of edema tend to have abnormally increased

(whiter) signal on DWI, FLAIR and T2-weighted sequences. The MR appearance of hemor-

rhage is quite complex, and is the reason why a significant portion of Chap. 4 is devoted to

that topic alone.


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58 2 The General Appearance of Edema and Hemorrhage

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