Costovertebral Articulations (see Fig. 8-20A).

In the thoracic

area there are two sets of the articulations-that is, the joint spaces

between the heads of the ribs and the vertebral bodies, as well as

between the tubercles of the ribs and the transverse processes. The

costotransverse articulations lie posterior and lateral to the costover-

tebral articulations, the joints between the ribs and the vertebral

bodies, in a plane behind the articular pillar. Moreover, these ribs-like

ribs 11, 12, and occasionally 10-do not articulate with the transverse

processes.

Facet Joints (Fig. 8-27; see Figs. 8-21 and 8-22). Facet joints are

formed between the superior articular facet of the lower vertebra and

the inferior facet of the upper vertebra. In the cervical area they are

oriented in the oblique plane halfway between the axial and coronal

planes. The superior articular facet of the lower vertebra is always

anterior to the inferior facet of the upper vertebra. In the thoracic

region the facet joints are oriented approximately in the coronal plane.

The facet joints are oriented in a parasagittal plane in the upper lumbar

area but are more oblique in the lower lumbar area. The joint spaces

are narrow, with a range of 2 to 4 mm.'

The joint surfaces are lined with articular cartilage. The synovial

space extends medially just beneath the anterior margin of the liga-

mentum flavum. The facet capsule and the anterior portion of the

ligamentum flavum cannot be separately delimited on CT scans. The

articular cartilage is clearly visible on T1 and proton-density images,

which produce a moderately bright signal (see Fig. 8-27). The cartilage shows high signal intensity on T2
images. Gradient refocused
T2-weighted images are superior to spin echo T2-weighted images in

delineation of the cartilage of facet joints. With CT scans the joint

space appears outlined by the uniformly thick articular margins of the

adjacent articular processes. The dense cortex of the articulating facet

is easily separated by the low attenuation value of the facet joint space

(sce Fig. 8-21). Sagittal reconstruction of CT scan and sagittal MRIS

are useful for evaluation of the facet joints and their orientation.

Each facet joint receives innervation from the posterior primary

ramus of the posterior root ganglion at its level and the level above.

Thus the facet joint diseases may produce back pain, which should be

differentiated from the cause of disk herniation with nerve root

compression.

Ligaments

Anterior Longitudinal Ligament (see Figs. 8-22 to 8-26). This

ligament extends from the axis as the anterior atlantoaxial ligament to

the sacral segments, connecting the anterior aspects of the vertebral

bodies and disk spaces (see Fig. 8-26). On CT scans the ligament

cannot be distinguished from the bony structures and the disk space,

whereas T1 MRIs present it as a line of low signal, characteristic of

fibrous structures outlining the anterior aspect of the vertebral bodies

and disk spaces in the sagittal plane.

Posterior Longitudinal Ligament (see Figs. 8-24 to 8-26). This

ligament begins on the posterior surface of the axis and extends to the

sacrum. It widens and becomes adherent at the disk space and at the

posterior aspects of the vertebral body. In the cervical spine the poste-
rior longitudinal ligament extends cephalad to merge into the tectorial

membrane and dura mater. Anterior to this, just behind the dens, are the inferior and superior cruciate
ligaments, which merge to form the

transverse ligament. The posterior longitudinal ligament may serve as

a barrier to posterior disk herniation. It appears as a soft tissue density

on CT and as low signal intensity on T1 MRIs (see Fig. 8-26A).

Interspinous Ligament (see Fig. 8-26). This ligament connects the

spinous processes. It is easily seen on CT scans and T1 MRIs.

Nuchal Ligament. This ligament connects the base of the occipital

bone to the spinous processes of Cl to C7 (see Fig. 8-24).

Ligamentum Flavum. This ligament extends from the axis to the

sacrum and attaches at the ventral surface of the lamina of the upper

vertebra and at the dorsal superior surface of the lamina below. It has

both stretchability and retractability functions. It measures 3 to 5 mm

in thickness and appears as a higher attenuation value on CT scans (see

Fig. 8-21) and as a low signal intensity on T1 MRIs (see Fig. 8-23C).

Hypertrophy of the ligament results in narrowing of the canal poste-

riorly and laterally.

Epidural Space (see Figs. 8-20, 8-21, and 8-23). The epidural

space is formed between the dura and the spinal canal. It contains fat,

vessels, and neural elements. In the cervical area the spinal nerve can

be demonstrated by CT, owing of plenty of fat in the upper portion of

the neural foramen and in the perivertebral region. Within the space

is the internal vertebral venous plexus with no valve, thereby facilitat-

ing the spread of infectious processes and metastasis. The basivertebral

vein penetrates the vertebral body to join the internal venous plexus.
These veins cannot be identified as separate structures by nonenhanced

CT scans. Therefore dural and epidural venous enhancement by IV

injection of contrast medium may provide useful anatomic landmarks

and help evaluate extradural diseases.

In the thoracic region there is abundant epidural fat posteriorly

between the neural arch and the dura and laterally at the neural

foramen's but little anteriorly in the epidural space (see Figs. 8-20 and

8-23). The pattern of the thoracic epidural vein is similar to the pattern

in the cervical and lumbar areas, except that there is a possible link

between the anterior and posterior vertebral plexus with the intercostal

veins and the azygos system in the thoracic region.5 In the lumbar

area, epidural fat can normally be seen anteriorly and posteriorly at all

lumbar disk levels. Obliteration of fat in the epidural space is suggestive of an epidural process.
Therefore the fat within the epidural space and

the intervertebral foramina is helpful for evaluating disease processes

affecting the margins of the spinal canal. In addition, conjoined nerves,

two nerves exiting from the thecal sac at the same level, is an anomaly

seen in up to 1% of the population and most frequently involves the

L5 and S1 nerves.

Dura Mater, Intradural Space, and Spinal Cord. The dura mater

forms a sleeve around the subarachnoid space, covering the cord and

intracanal component of the nerve roots. It extends beyond the canal

to fuse with the perineurium of the spinal nerves (see Fig. 8-23B). The

cervical cord is slightly flat on the ventral surface, indented by

the anterior median fissure (see Fig. 8-23B). Its posterior surface is

indented by the shallow posterior median fissure. Because of the large

subarachnoid space in the cervical area, the cord can be seen on plain

CT scans (see Fig. 8-19). With intrathecal contrast, visualization of the

cervical cord and roots can be enhanced significantly (Fig. 8-28).

Eight pairs of dorsal and ventral roots arising from the cervical cord

unite lateral to the dural sheath to form the spinal nerves. The first and

second cervical spine nerves pass posterior to the atlantooccipital and

atlantoaxial joints. The remaining nerves pass through the interverte-

bral foramina.

In the thoracic area the cord appears round and is enlarged from

T9 to T12, terminating in the conus with rapid tapering in its diam-

eter. Its ventral surface is indented by an anterior median fissure. On

the dorsal cord surface the posterointermediate and posterolateral sulci

appear shallow and indistinct. In the upper thoracic region the cord

segment is about two levels lower in number than the corresponding

vertebra. The difference increases to three vertebrae in the lower

thorax.

In the lumbar area the dura terminates at the level of S2 and fuses

with the filum terminale to end at the coccyx. The lumbar canal con-

tains the conus, cauda equina, and filum terminale. The conus medul-

laris, continuous with the spinal cord, ends at the L1-L2 level with a

taper (see Fig. 8-26) and then becomes the filum terminale. Normally

the conus is above the mid-L2 level and the filum terminale is 2 mm

or less in thickness at the level of the L5-S1 interspace. Generally a

conus level below the mid-L2 in a person older than 12 years is referred

to as an anomaly. On T1 images the spinal cord is clearly seen because

of its isointensity surrounded by the low signal intensity of CSF (Figs.

8-25A and 8-26A). On T2 images these signals reverse, and the decreased signal cord and roots of the
cauda equina are outlined by

high-signal CSF (Figs. 8-25B and 8-26B). Unlike the thoracic spinal

nerves, the lumbar spinal nerves can be seen on plain CT scans, exiting

medial to the corresponding pedicles.

----------

CHAPTER 10

Computed tomography (CT) and magnetic resonance imaging (MRI)

have become indispensable for diagnosis, evaluation, and treatment of

intracranial infectious disease, contributing to significant decline in

morbidity and mortality of these patients. CT is useful as a rapid

screening tool to detect complications of intracranial infections such

as hydrocephalus, extraaxial collections, and mass effect. MRI is supe-

rior for assessment of intracranial infections and allows for a more

sensitive evaluation of parenchymal lesions and leptomeningeal

disease. CT angiography (CTA) is frequently used for detection of

vascular complications such as vasculitis and mycotic aneurysms, with

conventional cerebral angiography reserved for selected difficult cases

and endovascular interventions. Implementation of advanced MRI

techniques such as MR perfusion imaging, diffusion imaging, and

proton MR spectroscopy (MRS) has improved differentiation of neo-

plastic processes from intracranial infections and allowed for more

accurate characterization of these disorders. Functional MRI (FMRI)

and diffusion tensor imaging (DTI) have allowed for improved preop-
planning when surgical intervention is necessary.

There are four common routes of spread of infectious disease to

the intracranial compartment.

1. Hematogenous spread is the most common route, with patho-

gens from a distant site in the body disseminating to the choroid

plexus, meninges, and brain parenchyma. In cerebral paren-

chyma the pathogens usually lodge within small vessels, result-

ing in a subcortical distribution of such lesions. Anomalous

hemodynamics, such as those seen in children with cyanotic

heart disease, have a high incidence of intracranial infection

secondary to a right-to-left shunt. Retrograde venous spread

can also occur via anastomotic connections between superficial

veins of the face, scalp, and cortical veins.

2. Direct extension from an adjacent site of infection, such as mas-

toiditis, otitis media, sinusitis, or orbital infection is another

possibility.

3. Direct intracranial introduction of a pathogen may occur during

trauma or as a complication of surgery or lumbar puncture.

4. Retrograde spread to the central nervous system (CNS) via

peripheral nerves can occur in herpes simplex and rabies virus

infections.

Multiple coexisting conditions may increase the risk of intra-

cranial infections (e.g., diabetes mellitus, alcoholism, malignancy,

agammaglobulinemia, radiation therapy, chemotherapy, and steroid

therapy). Patients with acquired immunodeficiency syndrome (AIDS)

are particularly susceptible to intracranial infection; however, the

disease spectrum and imaging manifestations in these patients are

different.

A variety of infectious disorders involve the CNS. Pyogenic infec-

tion is discussed in detail in this chapter, with categorization according

to the anatomic site of involvement. Other infectious processes are also

discussed, including viral infections, granulomatous disease, spiro-

chete infections, fungal diseases, parasitic diseases, and inflammatory

disease.

LEPTOMENINGITIS

Three distinct layers of connective tissue known as the meninges sur-

round the brain within the intracranial compartment. The dura mater

layer is also referred to as the pachymeninges. The thinner inner arach-

noid and pial meningeal layers are referred to as leptomeninges.

There are two principal patterns of meningeal enhancement on

MRI: leptomeningeal and pachymeningeal enhancement. Because the

dura mater lacks the blood-brain barrier, normal pachymeninges

usually demonstrate only minimal discontinuous linear enhancement

except for dural venous sinuses. The leptomeninges usually demon-

strate no enhancement except for adjacent vascular structures.

Meningitis primarily involves the leptomeninges (pia mater and

arachnoid membrane) and the adjacent subarachnoid space, resulting

in a leptomeningeal pattern of enhancement. The diagnosis of

meningitis is frequently made by clinical history and cerebrospinal

fluid (CSF) analysis. Clinical presentation in adults may include the

classic triad of fever, neck stiffness, and altered mental status, as well

as headache and photophobia. CSF analysis in acute pyogenic menin-

gitis classically demonstrates high protein, low glucose, and neutro-

philic pleocytosis.

CT of the head should be obtained prior to lumbar puncture in

patients with suspected increased intracranial pressure, focal neuro-

logic deficits, or moderate to severe impairment of consciousness.

Imaging may also be used to confirm meningitis and evaluate for

complications such as abscess, ventriculitis, and subdural empyema.

Additionally, cross-sectional imaging may elucidate the origin of intra-

cranial infection, because CT and MRI are sensitive for sinusitis and

mastoiditis.

The infectious agents responsible for acute pyogenic meningitis

vary by age group and immune status. In neonates, causes include

group B Streptococcus and Escherichia coli. In infants and young chil-

dren, typical pathogens may include Haemophilus influenzae and

Neisseria meningitides. In immunocompetent adults, Streptococcus

pneumoniae and Listeria monocytogenes are the common causative

agents. In immunocompromised adults, causative agents for acute

meningitis include Klebsiella, Pseudomonas, E. coli, and fungal

organisms.

Initial CT and MRI of the brain may be normal in uncomplicated

cases of meningitis. Occasionally, in more advanced meningitis, non-

contrast CT may demonstrate basal cistern obliteration. This may rep-

resent increased attenuation of exudate in the subarachnoid space

and thickened, inflamed leptomeninges. Ventricular enlargement and

diffuse cerebral swelling may also be seen in more advanced cases of

meningitis. Postcontrast CT may show enhancement of leptomeninges

in the basal cisterns and sylvian fissures.

MRI is more sensitive for detection of meningitis, especially when

using fluid-attenuated inversion recovery (FLAIR) sequences. T2-

FLAIR is sensitive to subtle changes in CSF and may demonstrate

hyperintensity in the subarachnoid space (presumably due to exudate

and elevated protein in this region) even when T1-weighted images

may appear normal. However, T2-FLAIR sulcal hyperintensity may

also be seen in other subarachnoid space processes such as leptomen-

ingeal carcinomatosis and subarachnoid hemorrhage. Postcontrast

T2-FLAIR has been reported to have high sensitivity and specificity for

leptomeningeal enhancement.

T1-weighted images may show obliteration of the basal cisterns,

and T2-weighted images may show cortical hyperintensity. Postcon-

trast T1-weighted images may show linear continuous sulcal or cister-

nal enhancement, frequently involving the basal cisterns or sylvian

fissures and extending deep into the base of the sulci. Sulcal or cisternal

enhancement on three contiguous slices has been reported to correlate

with significant meningeal pathology (Fig. 10-1).

On postcontrast MRI and CT imaging, differential diagnosis of

abnormal subarachnoid enhancement includes meningitis, lepto-

meningeal carcinomatosis, and subacute subarachnoid hemorrhage,

although the clinical presentation is usually very different in these

entities. Contrast-enhanced MRI has been shown to be more sensitive

than contrast-enhanced CT in detection of meningitis and its compli-

cations. Leptomeningeal enhancement on postcontrast MRI is

seen in only 50% of meningitis cases.

Thin linear enhancement most evident along cerebral convexities

is typically seen in acute pyogenic or viral meningitis. Nodular thick

enhancement most evident in the basal cisterns is typically seen in

chronic meningitides such as tuberculous meningitis, fungal meningi-

tis, and sarcoidosis. Granulomatous disease may also result in pachy-

meningeal involvement.

Pachymeningeal thickening and enhancement may be seen in a

variety of disorders including intracranial hypotension, meningiomas,

metastatic disease, lymphoma, and granulomatous disease. Postop-

erative meningeal enhancement may be pachymeningeal or leptomen-

ingeal in appearance. Occasionally, pachymeningeal enhancement can

be seen in patients who had uncomplicated lumbar puncture."

Complications of meningitis include hydrocephalus, ventriculitis,

subdural effusions, subdural empyema, epidural empyema, cranial

nerve inflammation, cerebritis, abscess, and infarction due to arterial

or venous involvement. Hydrocephalus is the most common

complication and usually presents as transient communicating hydro-

cephalus due to subarachnoid space inflammation and secondary

decreased CSF resorption in pacchionian granulations. Noncommuni-

cating hydrocephalus may also occur, especially when meningitis is

complicated by ventriculitis.
Magnetization transfer (MT) sequences have been reported to

improve visualization of abnormal meninges by showing more promi-

nent enhancement on postcontrast images. These sequences may also

demonstrate basal cistern hyperintensity on noncontrast images in

tuberculous meningitis. MT ratio (MTR) may help determine the

cause of meningitis, with tuberculous meningitis reported to show

lower MTR than fungal and pyogenic meningitis and higher MTR than

viral meningitis.

Recent investigations of DTI have demonstrated high sensitivity

in detecting bacterial meningitis, showing increased fractional anisot-

ropy (FA) within enhancing and nonenhancing cortex. High FA is

thought to be due to increased orientation of inflammatory cells in the pia-arachnoid meninges closely
related to the cortical ribbon. FA of

the cortex has also shown a strong correlation with neuroinflammatory

markers in neonatal meningitis.

SUBDURAL EFFUSION

Subdural effusion is a sterile fluid collection between the dura and the

arachnoid. Reactive subdural effusions are common complications of

acule bacterial meningitis, especially in infants. S. pneumoniae and H.

influenzae meningitis are more frequently associated with this compli-

cation. These collections are similar to posttraumatic and postsurgi-

cal subdural effusions and may result from tears in the arachnoid

membrane and subsequent leakage of CSF into the subdural space.

Alternatively, subdural effusions may be caused by inflammation of

subdural veins or dural irritation.

CT and MRI demonstrate extraaxial collections with attenuation

and signal intensity similar to CSF, which are most frequently seen

as large bilateral fluid collections over the frontal and temporal con-

vexities. Subdural effusions may be isointense or hyperintense to CSF

on FLAIR images, depending on protein concentration of the fluid.

Lack of transiting venous structures within these collections on

T2-weighted images allows for differentiation from prominent sub-

arachnoid spaces. There is no diffusion restriction seen within these

collections, and typically they show no significant enhancement.

Occasionally, fibrin strands and membranes develop; they may enhance

and appear similar to subdural empyema. Subdural effusions regress

spontaneously and do not require intervention except when they are

large and result in significant mass effect.

SUBDURAL EMPYEMA

Subdural empyema is a purulent collection between the dura and the

arachnoid; it may arise as a complication of acute pyogenic meningitis,

mastoiditis, otitis media, paranasal sinusitis, trauma, or postsurgical

infection. The adjacent infection is thought to spread to the sub-

dural space via retrograde thrombophlebitis of the calvarial emissary

veins, bridging veins, or dural venous sinuses. More rarely, an infection

of a subdural effusion may occur, resulting in a subdural empyema.

These collections may cross the calvarial sutures but do not cross the

midline.

Subdural empyemas represent up to 15% of all extraaxial collec-

tions and are seen in 13% to 20% of all cases of intracranial

infection.
Subdural empyema may progress and result in multiple compli-

cations such as thrombophlebitis, dural venous sinus thrombosis,

infarction, cerebritis, and abscess formation. For this reason it usually

requires aggressive intervention, and early accurate diagnosis is

critical.

CT imaging usually demonstrates a hypodense to isodense crescen-

tic or lenticular extraaxial collection along the cerebral convexity or

falx, which frequently appears similar to a subdural effusion. MRI

is extremely useful when empyema is suspected, because it allows

for reliable diagnosis of this entity and evaluation of associated

complications.

Diffusion restriction is the most useful characteristic for diagnosis

of empyema, which is seen as very high signal on diffusion-weighted

images (DWI) and low values on apparent diffusion coefficient (ADC)

maps. In contradistinction, subdural effusions show signal intensity

similar to CSF on DWI. Empyemas are also typically slightly hyperin-

tense to CSF on T1-weighted images and usually demonstrate rim

enhancement (Fig. 10-2). The presence of adjacent cerebritis, abscess,

or infarction with associated parenchymal enhancement or diffusion restriction also supports the
diagnosis of empyema. Hyperintense

signal on T2-FLAIR and T2-weighted images compared to CSF is not

specific, because it may be seen in subdural effusions and empyemas.

EPIDURAL EMPYEMA

Epidural empyema, or epidural abscess, is a purulent collection

between the dura and the calvarium and usually occurs as a complica-

lion of olitis media, mastoiditis, sinusitis, or osleomyelitis of the

skull. Ten percent of epidural empyemas may be associated with

subdural empyema.

Epidural empyema is separated from the subarachnoid space and

brain parenchyma by the dura, which may act as a barrier to infection.

As a result this collection usually has a more insidious and benign

clinical course. Owing to its extradural location, this collection

usually has biconvex morphology and may cross and displace the dural

venous sinuses but does not cross the calvarial sutures. Typically an

avidly enhancing T2 hypointense rim is seen. Adjacent parenchymal

involvement is rare (Fig. 10-3). Imaging characteristics are otherwise

similar to subdural empyema.

EPENDYMITIS

Ependymitis or ventriculitis is inflammation of the ependyma along

the inner surface of the cerebral ventricles. Intraventricular infection

may result from intraventricular rupture of a cerebral abscess, hema-

togenous spread to subependyma or choroid plexus, retrograde spread

from extraventricular CSF spaces, trauma, or surgery. Staphylococcus

and Enterobacter are the most common causative agents. Imaging plays

an important role in diagnosis; signs and symptoms may be subtle.

Noncontrast CT frequently shows no significant abnormality,

although occasionally dependent debris or slightly hyperdense epen-

dyma may suggest the diagnosis. MRI findings include enhancing

thickened ependyma, T2 hyperintense ventricular walls, dependent

intraventricular debris, and ventricular enlargement. Dependent

debris is a characteristic finding in ventriculitis and usually demon-

strates diffusion restriction and hyperintensity on T2-FLAIR images

(Fig. 10-4). Intraventricular adhesions and septations may cause non-

communicating hydrocephalus or result in a trapped ventricle or seg-

mental dilatation.

CEREBRITIS AND ABSCESS

Cerebritis is a poorly defined regional acute inflammation of cerebral

parenchyma with increased local vascular permeability, which is

usually caused by pyogenic bacteria. Untreated cerebritis evolves into

a cerebral abscess, which is characterized as a focal parenchymal col-

lection of pus with a surrounding vascular collagenous capsule.

Britt and Enzmann divided the process of abscess formation into

four stages: early cerebritis, late cerebritis, early capsule formation, and

late capsule formation.5

1. Early or acute cerebritis (first 3-5 days). Bacteria invade the

parenchyma and trigger an immune response, with infiltration

by inflammatory cells, increased vascular permeability of the

blood-brain barrier, perivascular exudates, petechial hemor-

rhages, microthrombosis, early necrosis, and associated edema.

Imaging is rarely performed at this stage, because the patient

may still be asymptomatic. CT shows a poorly defined area

of parenchymal hypodensity, with mass effect and variable

enhancement, including no enhancement, mild nodular, or ring

enhancement. MRI is more sensitive for detection of cerebritis

and abscess. A poorly defined parenchymal area of edema with ~~~~~~~ T2 hyperintensity and T1 iso- to
hypointensity is seen with

variable ill-defined enhancement9.109 (Fig. 10-5).

2. Late cerebritis (second week). There is progression of necrosis

with formation of a large necrotic zone. Peripheral fibroblast

deposition occurs, with formation of reticulin matrix.

MRI and CT demonstrate thick, irregular, ring enhancement

around a central necrotic zone with a surrounding area of

edema. Central necrosis shows decreased attenuation on CT,

with T1 hypointensity, T2 hyperintensity, and diffusion restric-

tion on MRI. A rim may be seen around the necrotic zone on

MRI, which is T1 iso- to hyperintense and T2 iso- to hypoin-

tensc" (Fig. 10-6).

3. Early abscess early capsule formation (end of second week).

Granulation tissue forms at the periphery of the abscess. A thin

capsule is formed by fibroblasts, with reticulin matrix and scant

collagen. Liquefaction occurs in the central necrotic zone, with

reduction in surrounding edema.

CT frequently demonstrates iso- to slightly hyperdense

capsule interposed between the hypodense central area and sur-

rounding hypodense edema (Fig. 10-7). MRI demonstrates a

well-demarcated T2 hypointense capsule surrounding a central

T2 hyperintense area, demonstrating diffusion restriction. Typi-

cally there is well-defined avid enhancement of the capsule,

which may be thinner on the side closer to the ventricle (Fig.

10-8). Daughter abscesses may appear at this stage."

4. Mature abscess-late capsule formation (after second week). A

thick collagen capsule is formed, with surrounding gliosis. The

wall of the mature abscess consists of three layers: (1) an inner

inflammatory layer of granulation tissue containing macro-phages, (2) a middle collagenous layer, and (3)
an outer gliotic

layer.

The capsule may become thinner and better defined as sur-

rounding edema decreases. Over time and especially with treat-

ment, the capsule may become less T2 hypointense, enhancement

may decrease, and the abscess may gradually decrease in size."

Cerebral abscesses are caused by multiple mechanisms, including

direct spread from a local infection, hematogenous dissemination from

a remote infection, trauma, or postsurgical infection. Up to 30% of

cerebral abscesses are reported to be cryptogenic. Sources of direct

spread include sinusitis, otitis media, mastoiditis (Fig. 10-9), and

odontogenic infections, with pathogens invading the brain paren-

chyma via adjacent osteomyelitis or via emissary veins. 09

Sources of hematogenous seeding include endocarditis, pulmonary

abscesses, and abdominal infections. Congenital cyanotic heart disease

and pulmonary arteriovenous malformation patients are at high risk

for hematogenous dissemination of infections to the brain.

Presenting symptoms depend on size and location of the abscess

and may include headache, fever, nausea and vomiting, neurologic

deficits, and seizure. Absence of leukocytosis and normal CSF analysis

do not exclude cerebral abscess, and CSF cultures are often sterile.

Infectious agents include microaerophilic streptococci, anaerobic bac-

teria, Staphylococcus aureus, facultative gram-negative bacteria, and

polymicrobial infections. Nocardial abscesses have been associated

with high mortality.

There are three characteristic findings of a cerebral abscess on MRI:

(1) central liquefied cavity with diffusion restriction; (2) smooth, thin,

continuous capsular enhancement; (3) T2 hypointense signal in the

capsule. Frequently there is thinning along the medial wall of the capsule. The capsule is usually T1 iso-
to hyperintense compared to

gray matter (see Fig. 10-8). Usually only a moderate amount of edema

is seen surrounding a mature abscess. Gas-forming organisms may

result in gas accumulation within the central liquefied zone.

Typical T2 hypointensity of the capsule is thought to be due to the

presence of free radicals, which are generated by macrophages within

the wall of the abscess (see Fig. 10-8A). Satellite lesions associated with

an abscess also support the diagnosis (Fig. 10-10). Clinical improve-

ment is correlated

on CT and MRI.

Complications of cerebral abscess include hydrocephalus, menin-

gitis, subdural empyema, and thrombophlebitis. Ependymitis resulting

from rupture of an abscess into the ventricular system is a severe

complication with high mortality. The medial wall of the abscess is

often thinner owing to less extensive blood supply in periven-

tricular white matter, which predisposes an abscess to rupture medially

(Fig. 10-11).

The classic ring enhancing appearance of cerebral abscess is not

specific. CT and MRI imaging differential diagnosis includes high-

grade primary CNS neoplasm, metastasis, nonpyogenic infection,

radiation necrosis, demyelinating lesion, thrombosed aneurysm, sub-

acute infarct, and resolving hematoma. Hematoma demonstrates

typical MRI signal patterns of blood products, and infarcts demon-

strate gyriform enhancement or cortical laminar necrosis, leading to

the correct diagnosis. Neoplasms and granulomatous diseases typically

have thicker and more nodular enhancement. Generally the presence

of characteristic imaging features of cerebral abscess offers high speci-

ficity and sensitivity for this diagnosis. The presence of central diffusion

restriction (hyperintensity on DWI and low values on ADC map) is

particularly important in differentiation of abscess from other pathol-

ogy and has been reported to have sensitivity of 95.2% and specificity

of 95.7%68 (Fig. 10-12; see also Fig. 10-8). In contradistinction, necrotic

tumors usually demonstrate central diffusion facilitation.

Diffusion restriction within a liquefied center of an abscess is now

thought to be primarily due to high density of viable inflammatory

cells in pus, with high viscosity, macromolecules, and necrotic debris

as possible secondary contributors.6 Recent investigations suggest that

diffusion imaging may be helpful to follow up evaluation of treatment

response, with high ADC reported in treated abscesses and low ADC

after therapy reported in treatment failure.,38

The features of abscess tend to differ in immunocompromised

patients receiving steroids. In these patients, edema may be minimal

and the abscess capsule may be thick and irregular. Hypointensity

of the capsule seen on T2-weighted images may not be obvious.

Extraparenchymal spread into the ventricles and meningitis are more

common. 141
Thallium-201 has been investigated for differentiation of abscess

from necrotic tumor. However, a report of a false-positive result with

uptake in a brain abscess suggests that this technique may not be reli-

able." However, this technique has been shown to be useful in differ-

entiation of CNS lymphoma from Toxoplasımosis gondii infection in

HIV patients.

Advanced MRI imaging techniques such as 'H MRS, DTI, and MR

perfusion have been recently employed to assist in differentiation of

cerebral abscess from other lesions such as neoplasms with central

necrosis.

The most characteristic MRS findings within the liquefied nonen-

hancing center of a mature cerebral abscess include presence of cyto-

solic amino acids (valine, leucine, and isoleucine) at 0.9 ppm, lactate

at 1.3 ppm, and absence of normalmetabolites such as N-acetylaspartate

(NAA), choline, and creatine. Acetate at 1.9 ppm and succinate at

2.4 ppm may also be present. Lipid and lactate are not specific and

may be seen in tumors and abscesses. Detection of amino acids is

the most useful finding for diagnosis of abscess; these metabolites are

not detected in vivo in necrotic or cystic neoplasms.23.50 Amino acids

are generated during protein breakdown in pus owing to release

of proteolytic enzymes by neutrophils. Amino acids, acetate, and

succinate are generated during glycolysis and may be detected in

abscesses caused by anaerobes or facultative anaerobes..97 Amino

acids, acetate, and succinate have been reported to become undetect-

able after treatment."

69,97

Investigation of MR perfusion by Chiang et al. demonstrated lower

mean relative cerebral blood volume (1CBV) in the enhancing wall of

an abscess when compared to the enhancing rim of a necrotic tumor;

this is due to the relatively poor vascularity of the abscess wall.2"

Recent studies using DTI in brain abscess showed increased frac-

tional anisotropy (FA) within the abscess's liquefied center. High FA is

thought to be due to organized orientation of inflammatory cells,

caused by neuroinflammatory molecules in pus, which may assist in

differentiation from a necrotic tumor." Additionally DTI may be

useful for evaluation of treatment response, because FA has been

reported to decline during treatment, while mean diffusivity (MD) was

relatively unchanged.