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Neuroimaging of central nervous system

infections
Article in Seminars in Pediatric Infections Diseases May 2003
DOI: 10.1053/spid.2003.127321 Source: PubMed

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Neuroimaging of Central Nervous System

Infections
J. V. Hunter, MD, and M. C. Morriss, MD
During the past decade, advances have been made in the technology used to image
the pediatric central nervous system. Although computed tomography (CT) remains
the first line of imaging for the sick child admitted to the emergency room with fever
and altered mental status, magnetic resonance imaging (MRI) offers superior soft
tissue imaging of central nervous system (CNS) infections and advanced techniques.
MRI also is the standard of care for imaging spinal infections. CT remains superior for
the detection of calcification and bony detail. With the advent of new MRI sequences
such as T2-weighted fluid attenuated inversion recovery (FLAIR), diffusion-weighted
imaging (DWI), and magnetic resonance spectroscopy (MRS), we are able to detect
early and subtle abnormalities such as the vasculitis accompanying a meningitis and
to identify patterns of signal alteration that can help us be more specific about the
diagnosis in lesions with similar appearances.
2003 Elsevier Inc. All rights reserved.

entral nervous system (CNS) infections may not need

radiologic imaging, but when they do, computed tomography (CT) and magnetic resonance imaging (MRI)
scans offer exquisite detail about the location, extent, and
associated complications of infections in the brain and
spine. At times, the clinical workup is unclear, and neuroimaging studies are used to help confirm a clinical suspicion
of CNS infection. Imaging studies also may uncover a
source for recurrent meningitis in children, such as cerebrospinal fluid (CSF) leaks in the paranasal sinuses, skull
base, or ear; malformative connections to the CNS, including nasal and facial dermoid cysts (Fig 1); or sinus tracks in
the spine.13 Routine infections, such as rhinosinusitis or
orbital cellulitis, may lead to meningitis, empyema, or abscess (Fig 2), and these complications are diagnosed with
CT or MRI studies.4 In pediatric patients, several CNS
diseases often have clinical features similar to infection at
initial presentation. Immune-mediated acute disseminated
encephalomyelitis (ADEM), metabolic disease, lymphoproliferative disease, or CNS vasculitis may mimic CNS infection. Neuroimaging is a valuable part of the diagnostic
workup in these cases. Neuroimaging also is important in
diagnosing immunocompromised patients with fever, al-

From the Department of Radiology, Baylor College of Medicine, Texas

Childrens Hospital, Houston, TX.
Address reprint requests to J.V. Hunter, MD, Associate Professor of
Radiology, Baylor College of Medicine, Texas Childrens Hospital, 6621
Fannin Street, MC22521, Houston, TX 77030; e-mail: jvhunter@
texaschildrenshospital.org
2003 Elsevier Inc. All rights reserved.
1045-1870/03/1402-0012$30.00/0
doi:10.1053/spid.2003.127231

140

tered mental status, seizures, and other clinical signs and

symptoms of CNS infection. Altered immune responses
may present an unclear clinical picture, and neuroimaging
is useful in differentiating among the numerous CNS lesions seen in these patients.5 Children with spinal infections typically present with back pain, fever, and abnormal
laboratory studies, but in some cases, overlap exists with
symptoms caused by pyelonephritis, septic arthritis of the
hip, sacroiliitis or pyomyositis, or bone infarctions (Fig 3
A,B). MRI of the spine is used to diagnose diskitis and
osteomyelitis and the significant potential complications of
epidural abscess and cord compression.6

Imaging Tools for Evaluating CNS Infection

Magnetic Resonance Imaging
Radiologic technology in both CT and MRI has advanced at
a rapid pace during the past decade, with improvements
being made in image quality, faster scan times, and newer
types of imaging sequences. The most sensitive neuroimaging technique for intracranial and spinal infection is MRI
because of its superior soft tissue detail, sensitivity to subtle
inflammatory processes, vascular imaging techniques, functional imaging, and multiplanar imaging capabilities. Functional MRI techniques, such as diffusion imaging, aid in the
investigation of physiologic properties of tissues. Diffusionweighted imaging (DWI) acquires images with signal intensities of tissues dependent on the speed of water motion
within the tissues. DWI is used most commonly in stroke
imaging, but it also shows slowed water motion in abnormally proteinaceous or viscous tissues such as abscess cavities. Diffusion in abscess cavities typically is much slower
than in a cystic neoplasm, thus helping to differentiate
between these similar appearing lesions.7,8

Seminars in Pediatric Infectious Diseases, Vol 14, No 2 (April), 2003: pp 140-164

CNS Infections Neuroimaging

141

injury. The study described above can typically be performed in less than 45 minutes (not including MRS). Most
MRI centers in tertiary care facilities have advanced physiologic monitoring equipment for the seriously ill patient.

Positron Emission Tomography Scanning

Although its definitive place has yet to be determined,
fluorinated deoxyglucose (FDG) positron emission tomography (PET) has been demonstrated to have some valueadded in distinguishing tumefactive multiple sclerosis
(cold lesion) from abscess or glioma (hot lesion). PET
also has been demonstrated to be of value in the investigation of the adolescent with altered mental status and
normal or near normal MRI examinations in whom the
question of organic disease versus acute psychosis arises.
Similarly, a positive PET scan demonstrating either hot or
cold areas in the basal ganglia and striatum has proven very
useful in those children presenting with a choreo-athetoid
movement disorder. These patients often have a normal
conventional MRI but show evidence of altered glucose
metabolism on FDG PET. This detection can be especially
important in the early treatment of children at risk of
subsequently developing Tourette syndrome after having
group A beta hemolytic streptococcal infection.11
Figure 1. T1-weighted postcontrast sagittal MR image of a
nasal dermoid cyst (arrowhead) with a sinus track beneath
the nasal bones leading to the foramen cecum.

Magnetic resonance spectroscopy (MRS) is another advanced imaging technique that has had rapid development
during the past few years. MRS takes the MR radio frequency signal from tissues and converts it into a chemical
shift profile similar to an NMR spectroscopic study utilized
in basic chemistry. Several of the major metabolite peaks of
the brain have been localized. Resonance peaks associated
with diseased tissues such as lactate also have been identified. The MRS technique has been used to identify characteristic metabolite profiles in CNS tumors, metabolic disease, demyelinating disease, and hypoxic-ischemic injuries.9
Acetate, alanine, phenylalanine, and lactate- lipid peaks are
found in abscess cavities and have been identified on MRS
studies.9,10
A typical MRI study for a child with CNS infection
consists of T1 sagittal and axial, T2 and FLAIR axial images, diffusion-weighted images, and postcontrast images
in three planes. MRS adds 10 to 20 minutes to the study,
depending on the technique chosen, and should be added if
indicated. FLAIR images are T2-weighted images that show
suppressing signals from normal water such as CSF,
whereas water in diseased tissues shows bright signal. This
sequence is very sensitive to pathology in the brain, including abscess, gyral swelling, and inflammation in the leptomeninges. Diffusion images take less than a minute to
acquire and should be a routine part of every MRI study
because they may demonstrate unsuspected areas of infarction or demyelination and are very sensitive to early tissue

CT Imaging
In CT imaging, new generation multislice, multidetector
scanners allow for the critically ill patient to be scanned in
a matter of seconds. With a single injection of CT contrast

Figure 2. Axial postcontrast CT through the posterior

fossa in a child with mastoiditis, thrombophlebitis, and
epidural empyema containing air after surgical drainage
(arrowheads).

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Hunter and Morriss

Figure 3. (A) T1-weighted postcontrast axial MR of the

lumbar spine shows a ring-enhancing abscess in the
paraspinous muscles on the right. (B) T2-weighted sagittal
MR of the cervical spine showing hyperintense signal in the
posterior spinous processes in a child with bone infarcts
(arrowheads).

material, the radiologist can evaluate brain perfusion for

areas of ischemia or infarction as well as for leptomeningeal
inflammation, abscess or empyema, or venous thrombosis.
Ultra-thin slice techniques, high-resolution bone detail, and
multiplanar reconstruction software are available in the
newest generation of CT scanners. The images available
from these machines render the diagnosis of lesions that
are associated with CNS infection more conspicuous. Fractures, bony dehiscences, and malformative craniofacial and
temporal bone anomalies are depicted in high-resolution
bone images from the newest generation of scanners.
As the initial screening study from the emergency department, nonenhanced CT of the brain is the appropriate
test unless the child has a neurological deficit. If the CT is
abnormal or the child has neurological deficits, then MRI
with contrast and diffusion-imaging should be performed.

Spinal Imaging
MRI is the standard for spinal imaging. The earliest imaging findings in diskitis and osteomyelitis are edema in the
disk, vertebral body, or both. These findings precede loss of
disk height and bone destruction seen on plain films and are
diagnosed inconsistently on nuclear medicine bone scans. A
routine MRI for evaluation of spinal infection should cover
the area of pain adequately and a generous number of
levels above and below the area of concern. In the case of
lower lumbar and sacral pain, the pelvis also should be
covered to adequately evaluate the sacrum, presacral space,

and hips. Imaging sequences typically consist of precontrast

T1-weighted and T2-weighted sagittal and axial images, T2
STIR sagittal images, and postcontrast T1-weighted images
in the sagittal and axial planes. If the infection is paraspinal, such as along the iliopsoas muscles or in the sacrum,
contrast-enhanced T1-weighted coronal images are helpful.
In the setting of infection, fat-suppression of the postcontrast images is essential. Enhancing epidural inflammation
blends in with the normally bright epidural fat on non-fatsuppressed T1-weighted images and may be missed. Also,
abnormal enhancement within infected vertebral bodies
may blend with normal bright marrow fat and be missed if
fat suppression techniques are not used. T2 STIR images
are T2-weighted images with a fat suppression pulse and
are very sensitive to edema in vertebral bodies or adjacent
paraspinous soft tissues including muscles.
Occasionally, a child suspected of having a spinal infection has a cardiac pacemaker or other MR-incompatible
implanted device. In that case, CT is the only available
modality. A contrast-enhanced CT is performed to diagnose
epidural or peri-vertebral infectious collections, bone destruction, or demineralization. Images reformatted into the
sagittal plane also may show disk space narrowing and bone
destruction. CT does not show vertebral or disk edema,
which are the earliest signs of infection. A CT myelogram
may be necessary before performing surgical decompression if spinal cord compression is suspected and the IV
contrast study does not demonstrate adequately the extent

CNS Infections Neuroimaging

143

Figure 4. CT and MR studies in a child with meningitis and

cerebritis. (A) Initial nonenhanced CT shows subtle sulcal
effacement in the left parietal lobe due to exudate and inflammatory swelling (arrowheads). (B) FLAIR MR coronal image
shows a focal area of hyperintense signal in the depths of the
sulcus in a developing focus of cerebritis (arrowhead). (C)
T1-weighted postcontrast axial MR shows enhancement in the
focus of cerebritis, as well as increased leptomeningeal enhancement in the sulci of the left parietal lobe.

or location of the epidural inflammatory mass. MRI always

should be performed in the setting of spinal infection unless
it is not available emergently or is contraindicated because
of an implanted biological device.

Imaging Patterns in CNS Infection

Certain recognized imaging patterns of CNS pathology
parallel the known biologic behavior of pathogens. Noninfectious CNS diseases may mimic infection, and careful

correlation of all imaging data, including advanced imaging

techniques, often is needed to distinguish infectious diseases from other lesions. Imaging studies rarely conclusively diagnose a specific pathogen, but they show patterns
of disease such as leptomeningeal inflammation/infiltration, encephalitic gyral swelling, subdural fluid collections,
abscess, or cerebritis that may generate a short differential
list. Spinal imaging generally is more specific in the diagnosis of infection versus other disease processes, but it also
usually is not specific for pathogens. Lesions mimicking
spinal infection include bone infarctions and neoplasms.

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In tubercular meningitis, abnormal enhancement usually is found in the basal cisterns.12 Thick enhancement is
seen in the suprasellar cistern and along the pial surfaces of
the brainstem and Sylvian fissures. When basal cistern
enhancement is present in the setting of suspected infection, tuberculosis must be considered as the leading diagnosis. Other lesions causing basal cistern enhancement in
children are disseminated neoplasm, sarcoidosis, and Langerhans cell histiocytosis.

Subdural Effusion and Empyema

Figure 5. T1-weighted postcontrast axial MR through the

parietal lobes shows abnormally increased leptomeningeal
enhancement in the left posterior frontal and parietal lobes
in a child with recurrent medulloblastoma.

Subdural fluid collections occur as sterile effusions or infected empyemas and are known complications of meningitis.13 On CT or MRI, effusions and empyemas appear as
extra-axial fluid collections with peripheral enhancement.
Sterile effusions are found commonly in children who have
meningitis in the first year of life. Diffusion-weighted imaging sometimes has been found helpful in distinguishing
between effusion and empyema. Empyemas are complex
collections of fluid and tend to have more restricted diffusion than do sterile effusions. However, these collections
typically occur over the top of the brain and are difficult to
evaluate with axial diffusion-weighted images. Empyemas
may be caused by an extension from a complicated sinusitis,
mastoiditis, or osteomyelitis of the calvarium. Adjacent
parameningeal sources should be investigated in the case of
empyema.

Leptomeningeal Disease
On imaging studies, meningitis demonstrates a wide variety of findings, including no abnormality, increased leptomeningeal enhancement, cerebritis, abscess, subdural effusion, empyema, hydrocephalus, infarction, diffuse edema,
and herniation. Meningeal inflammatory material fills the
sulcal spaces of the brain. On noncontrast CT studies,
meningeal inflammation is seen as a subtle loss of sulci.
The normal sulci are effaced in the area of inflammation
due to the inflammatory exudate and sulcal swelling (Fig 4
A). Other processes causing this same appearance on noncontrast CT include leptomeningeal neoplastic disease,
leptomeningeal sarcoidosis, gyral swelling caused by encephalitis or infarction, and postictal gyral swelling. On
contrast-enhanced studies, increased leptomeningeal enhancement may be present, but distinguishing it from the
normally enhancing leptomeninges often is difficult. Abnormally increased leptomeningeal enhancement also is seen
in pial vascular malformations (Sturge-Weber), sarcoidosis,
leptomeningeal dissemination of neoplasm, or postinfarction (Fig 5). Both pyogenic and aseptic meningitis may
cause leptomeningeal enhancement. Meningitis also may
cause venous thrombosis with hyperdensities on the surface
of the brain or along venous sinuses on noncontrast CT
scans. Magnetic resonance venography is used to confirm
venous thrombosis (Fig 6).

Figure 6. Magnetic resonance venogram (MRV) shows loss

of flow in the transverse sinus on the left (arrowhead) in a
patient with left transverse sinus thrombophlebitis.

CNS Infections Neuroimaging

145

Figure 7. Child with left temporal lobe abscess, meningitis, ventriculitis, and choroid plexitis. (A) T1-weighted postcontrast
axial MR through the temporal lobes shows an abscess with thick rim enhancement in the right temporal lobe (arrowhead).
There is diffuse leptomeningeal enhancement. (B) T2-weighted axial image shows the T2 hypointense collagenous wall of
the abscess. (C) Diffusion-weighted image shows diffusely dark signal in the abscess cavity consistent with restricted water
diffusion in the purulent abscess. Bright signal around the abscess is more unrestricted vasogenic edema in the white
matter. (D) T1-weighted postcontrast axial image at the level of the lateral ventricles shows enhancing ependymal lining
(large arrowhead) and debris in the occipital horn from ventriculitis, thick and enhancing choroid plexus (small arrowheads)
from choroid plexitis, and hydrocephalus.

Cerebritis and Abscess

The stages of progression from cerebritis to abscess formation in the brain are well-described.14,15 On imaging studies,

the lesion progresses from a nonspecific edematous focus of

cerebritis in the depth of a sulcus, with or without enhancement, to a conspicuous ring-shaped lesion with well-defined
rim enhancement and a necrotic center. Abscesses arise in

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Hunter and Morriss

Figure 8. Juvenile pilocytic astrocytoma of the posterior fossa (A) shows thick rim enhancement on postcontrast T1weighted MR, but diffusion-weighted images (B) show hyperintense signal (arrowhead) in fluid areas consistent with
astrocytoma.

white matter or at the gray-white matter junction, typically

in frontal, temporal, or parietal lobes and typically sparing
the basal ganglia and brainstem. During the cerebritis
stage, an unencapsulated inflammatory mass is surrounded by a hyperemic, edematous margin. It is seen on
imaging studies as a patchy focus of edema, with or without
ill-defined enhancement, in the depth of a sulcus. On CT,
the lesion is low density, and on MRI, it is a focus of
hyperintense (bright) signal on T2/FLAIR sequences (Fig 4
B,C). As the focus of cerebritis matures, it develops welldefined rim enhancement. In cerebritis and abscess, enhancement has been reported to be thicker along the cortical margin than along the ependymal margin, a reflection
of the better blood supply laterally. Neoplasms and tumefactive demyelinating plaques often have the opposite pattern, with thicker enhancement along the ependymal (medial) border.
The cerebritis phase typically lasts from 10 to 14 days,
with the progressive development of a central zone of softening and necrosis and a peripheral capsule. The capsule is
composed of layers of acute and chronically inflamed granulation tissue, peripheral edema, and gliosis. Fibroblasts lay
down collagen, making a thick wall to the abscess. Vessels
in the abscess wall lack a normal blood-brain barrier resulting in edema and contrast enhancement on CT and MRI
studies (Fig 7A). The collagenous wall is visible on noncontrast T2-weighted images as a hypointense (dark) wall that
is isointense to slightly hyperintense on precontrast T1weighted images (Fig 7B). Ring-enhancing cavities with

surrounding edema on imaging studies are typical findings

but are not specific for cerebral abscess, with the major
differential diagnostic imaging consideration in children
being cystic-necrotic neoplasms. Metastases, infarction, or
recent hemorrhage cavities also may have a similar imaging
appearance, but they are seen less commonly in children.
Cystic-necrotic neoplasm is the major diagnostic consideration, and diffusion-weighted imaging and spectroscopy are
helpful in distinguishing between cerebral abscess and cystic neoplasm. The central cystic region of an abscess tends
to have restricted water motion due to protein content (Fig
7C). Cystic neoplasms typically have more unrestricted
water motion (Fig 8). There are recognized MRS profiles in
abscesses and tumors (Fig 9).

Ventriculitis and Choroid Plexitis

Ventriculitis may accompany meningitis and commonly
is seen when an abscess ruptures into the ventricle. On
CT or MRI studies, ventriculitis is seen as abnormal enhancement of the ependymal surface of the ventricle, accompanied by edema in the adjacent periventricular white
matter (Fig 7D). A more reliable and consistent sign that
has been reported is debris within the ventricles.16 Pathologic enhancement should be distinguished from normal
enhancement of ependymal veins. Hydrocephalus also is
present commonly in children with ventriculitis. Choroid
plexitis is seen as an enlarged, enhancing choroid plexus
(Fig 7D).

CNS Infections Neuroimaging

Figure 9. Bone marrow transplant

patient with fungal abscess in the
right frontal lobe and lymphoproliferative mass in the basal ganglia on
the left. (A) T1-weighted postcontrast axial MR shows ring enhancement in the right frontal fungal abscess (small arrowheads) as well as
in the left basal ganglionic lymphoproliferative mass (large arrowhead). (B) Magnetic resonance
spectroscopy (MRS) with single
voxel centered over the right frontal
abscess shows large upright lipidlactate peak (arrowhead) and absence of significant choline peak.
(C) MRS with the single voxel centered over the lymphoproliferative
mass shows large choline peak (arrowhead), which is seen in cellular
masses or demyelination.

147

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Hunter and Morriss

Figure 10. Meningitis with basal ganglionic vasculitic infarctions in a neonate. (A) T2-weighted images show edema around
the caudate nuclei (arrowhead) and (B) abnormal diffusion signal (arrowhead) consistent with infarctions.

Hydrocephalus and Infarction

A significant percentage of children with meningitis develop hydrocephalus as a complication, with tubercular infections having the highest rate of postmeningitic hydrocephalus. The etiology is obstruction of CSF absorption
pathways, and obstruction of CSF outflow tracks with inflammatory debris. The onset of hydrocephalus may occur
days to months after infection develops. The imaging appearance of hydrocephalus usually is straightforward in
older children, with ballooning of the ventricular margins,
effacement of sulci, and edema around the ventricular margins. Inflammation in the ventricles may cause septation
formation and complex patterns of ventricular entrapment.
In infants and younger children, mild or early hydrocephalus occasionally may be more difficult to detect because of
their baseline larger sulci and ventricles. A combination of
clinical signs and symptoms, serial head circumference
measurements, and follow-up imaging may be necessary to
diagnose hydrocephalus in these cases.
Cerebral infarction is a serious complication of meningitis and can lead to devastating long-term neurologic deficits. Cerebral infarction is a recognized sequel of infectious
meningitis in as many as 30 percent of pediatric patients.17
Focal thalamic, pontine, or upper spinal cord infarction as
an early manifestation of meningitis has been reported.18,19
The etiology is an infectious vasculitis as a result of inflammation in the walls of vessels. Thrombosis, arachnoiditis,
and compression of the arterial blood supply at the skull
base secondary to herniation of the cerebellar tonsils are
contributory mechanisms, compounded on occasion by hypotension. Organisms may be bacteria, viruses, parasites,
or fungi. Aspergillus in particular may cause extensive
hemorrhagic infarctions and formation of an abscess.20

Small vessels over the cerebral convexities or perforating

branches in the basal regions are affected. Infarctions may
be multifocal and extensive and typically show abnormally
restricted (slowed) water motion on diffusion-weighted images. Brain edema, large infarcts, hydrocephalus, extraaxial collections, and brain abscesses can be detected by
CT, but MRI with DWI is required to detect early infarction
and distinguish cytotoxic from vasogenic edema. This distinction is important in the young child in whom lack of
myelination renders detecting subtle hypodensity or alterations in signal intensity difficult. Acute cerebral infarctions show restricted diffusion and T2 hyperintensity with
edema (Fig 10). Infarctions typically progress during the
next two weeks to encephalomalacia with cystic change and
increasing water intensity (hyperintense T2 and hypointense T1 signal intensity). Diffuse cystic encephalomalacia
may result from severe widespread infarction with a near
water appearance to the brain. Within areas of ischemia
and infarction, abscesses may form due to the presence of
organisms.

Encephalitis Patterns
Viral infections of the CNS are not uncommon events in
children and often do not need neuroimaging. In severely
affected patients or patients who may have herpes infection, imaging may be helpful. Encephalitis is caused by
neurotropic viruses that reach the CNS either by the bloodstream or through nerves, as with rabies and herpes. The
findings on imaging studies with encephalitis are diverse,
due to the many agents involved. Cortical gray matter,
basal ganglionic, thalamic, and brainstem lesions may occur. Gyral swelling, edema, and occasionally hemorrhage
are findings in encephalitis (Fig 11). On T2/FLAIR studies,

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149

Figure 11. Child with PCR positive for HSV type 1. (A) FLAIR coronal MR shows bright signal (arrowhead) and swelling
in the hippocampus. (B) Diffusion MR images show restricted diffusion consistent with infarction (arrowheads).
the gyri are swollen and hyperintense and underlying white
matter edema may be present. DWI has shown areas of
cytotoxic edema in encephalitis and may be more sensitive
than are T2/FLAIR images in demonstrating acutely the
full extent of involvement.21 Herpes virus infections have
characteristic patterns of involvement of the brain depending on the type of virus. Type 1 is a reactivation disease with
trigeminal nerve involvement affecting the limbic system.
Swelling is seen in the hippocampus, cingulate gyri, insula,
and subfrontal regions. Herpes type 2 is a neonatal infection caused by viremia and is a diffuse process affecting
large areas of the brain. Herpes viruses may cause hemorrhagic necrosis on imaging studies. DWI has been reported
to show both restricted diffusion (cytotoxic edema with
ischemia/infarction) and less restricted diffusion (vasogenic
edema), suggesting that diffusion findings relate to the
timing of imaging in the course of the infection.22 Herpes
may result in significant cerebral parenchymal injury, volume loss, or extensive cystic encephalomalacia.
Mycoplasma childhood encephalitis deserves special
mention because it may show focal cortical lesions, deep
white matter lesions, and large areas of demyelination.
Ischemic lesions have been reported.23 Mycoplasma may
result in encephalitis resembling cortical encephalitis of
viral origin or may cause lesions more suggestive of ADEM
with areas of demyelination. Mycoplasma has been detected
in brain tissue and CSF of patients with encephalitis, indicating direct brain invasion in some cases. Mycoplasma also
may be responsible for immune-mediated ADEM type brain
lesions in children in whom it is found in the respiratory
tract but not CSF. Mycoplasma infection in children is,
thus, in the differential diagnosis of any brain lesion that
looks like ADEM or encephalitis.

Immunocompromised Patients
Imaging patterns in immunocompromised patients deserve
special consideration. Because of the common use of bone
marrow transplantation in hematology-oncology patients
and those with metabolic diseases, these patients commonly
present in the radiology department for workup of CNS
disease. Infections such as toxoplasma encephalitis and
cerebral aspergillosis occur in these patients, and imaging
patterns may differ from those of immunocompetent hosts.
In immunocompromised patients, the imaging pattern of
cerebritis and abscess is altered by the inability to mount a
normal inflammatory response, and thus the typical pattern
is less edema and less enhancement with a thinner capsule
wall. Encephalitis and meningitis also show less enhancement24

Mimics of CNS Infection

Because the brain responds to insults from any etiology in
a limited number of ways, certain diseases have similar
imaging features, though the clinical presentation and laboratory studies may be distinct. ADEM is an immunemediated disease process that is stimulated by a prior viral
infection (mumps, varicella, measles, influenza, EpsteinBarr, rubella, herpes), mycoplasma infection, or recent vaccination.25,26 The clinical presentation may be similar to
viral encephalitis, and some of the imaging features also
are similar. ADEM typically results in patchy multifocal
asymmetric areas of increased T2 signal at the gray-white
matter junction, with subtle corresponding areas of low
density on CT studies (Fig 12). The lesion burden typically
is underestimated by CT as compared with FLAIR or T2

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Hunter and Morriss

alitis and can be confused with ADEM or encephalitis.
The pattern of involvement in most metabolic diseases,
however, is symmetric, is bilateral, and often involves
descending tracks and the brainstem. MRS studies may
show elevated lactate or other peaks related to an altered
metabolic pathway.
Primary CNS vasculitis is a disease that has clinical
and imaging features mimicking CNS infections, although its diagnosis is rare and often elusive.27 Some
infections in the CNS such as Aspergillus result in a
vasculitis. CNS vasculitis usually is end-vessel disease
resulting in T2 hyperintense lesions at the gray-white
matter junction. Lesions also can occur in the cerebral
cortex, thalami, basal ganglia, or brainstem. The location
may mimic ADEM, cerebritis, or meningitic vasculitis. If
strong clinical suspicion for vasculitis exists, a conventional cerebral angiogram or arterial biopsy often is
required for confirmation. Vasculitis is seen commonly in
patients with Lupus and presents the dilemma of determining infection versus vasculitis or cerebritis in an
immunosuppressed patient.

Neuroimaging of Specific CNS Pathogens

Figure 12. FLAIR axial images in a child with ADEM show
hyperintense lesions in the white matter in the right frontal
lobe as well as in the internal capsule on the left.

Brain
Pediatric CNS infections can be divided into congenital
and acquired infections.

Congenital Infections
MRI. Lesions may enhance but usually do not demonstrate
restricted diffusion. However, some acute areas of demyelination from ADEM may show restricted diffusion similar to
that of acute MS plaques. Lesions from ADEM may affect
the thalami or basal ganglia or the cerebral cortex, and they
may be hemorrhagic and may grow to several centimeters
in size with significant mass affect and edema. Tumoral
ADEM usually is a large mass-like focus of demyelination
that may mimic a supratentorial neoplasm. ADEM also
may affect the spinal cord, and synchronous spinal and
brain lesions often help confirm the diagnosis. Multiple
sclerosis is the important differential diagnosis, and serial
MRI often is needed. Classically, no cropping or development of new lesions should occur in the 6-month period
after an episode of ADEM. The distinction between ADEM
and encephalitis on neuroimaging studies sometimes can be
very difficult to discern, but the most common presentation of
ADEM is patchy multifocal asymmetric lesions that predominate in the white matter. Encephalitis predominantly is more
cortical than white matter, and deep gray nuclear involvement
often occurs in the thalamus and is symmetric.
Metabolic disease in children is more rare than is
ADEM or encephalitis, but all these diseases will be seen
in large pediatric referral hospitals. Metabolic disease
usually has unique clinical features and lacks the laboratory features of CNS infection, but its imaging appearances can overlap those of ADEM or encephalitis. Mitochondrial diseases such as MELAS can present with areas
of gyral or deep gray nuclear swelling mimicking enceph-

Congenital infections have been given the acronym

S-TORCH (Syphilis,TOxoplasmosis, Rubella, Cytomegalovirus, Herpes Simplex type II, and HIV).
Syphilis. Congenital syphilis infection with a surviving
viable pregnancy results in generalized brain atrophy in the
child. Syphilis together with toxoplasmosis, parvovirus

Figure 13. Axial unenhanced CT in a microcephalic patient with congenital toxoplasmosis, demonstrating extensive periventricular and basal ganglionic calcification in the
presence of a simplified gyral pattern with hydrocephalus.

CNS Infections Neuroimaging

151

weighted and FLAIR) sequences. MRI is superior to CT for

detecting gyral abnormalities such as pachygyria and
polymicrogyria.
Rubella. Congenital rubella is a disease now rarely seen
owing to the implementation of immunization programs
around the world. Fetal infection results in both teratogenic
and destructive effects. As with other congenital brain infections, earlier infection results in a more severe encephalopathy and, a later onset of symptoms indicates less
severe brain injury than occurs in those who present at
birth.32 CT appearances in a single case report describe
diffuse brain hypodensity with dense basal ganglia calcification.33
Cytomegalovirus. Cytomegalovirus (CMV) infection occurs not only during pregnancy but can result from secondary infection as well. The entire brain may be involved with
an encephalitic process. Chronically, gliosis and calcification are present. As with toxoplasmosis, the calcification
can occur anywhere in the brain but has a predilection for
the periventricular zones. Differentiation between toxoplasmosis and CMV cannot be made with certainty by
imaging alone, although migration abnormalities have
been thought to occur more prevalently with CMV infection. CMV is included in the differential diagnosis of sub-

Figure 14. Axial unenhanced CT in a 20-day-old female

presenting with seizure activity and diffuse low attenuation
throughout the white matter. There was a maternal history
of genital herpes type II.

B-19, Listeria monocytogenes, as well as the genital mycoplasmas, Chlamydia trachomatis, HIV, and group B streptococcus,
all are purported causes of stillbirth.28
Toxoplasma gondii. Toxoplasma gondii is a ubiquitous
coccidian passed hematogenously through the placenta to
the fetus. Clinically significant abnormalities occur when
the fetus is infected before 26 weeks gestation. The earlier
the fetus is infected, the more severe the disease, with the
most severe disease occurring between 10 and 24 weeks of
gestation.29 31 The typical triad of findings is hydrocephalus, chorioretinitis, and intracranial calcification (Fig 13).
Hydrocephalus occurs commonly and most likely secondary
to infection with gliosis in the region of the aqueduct.
Calcification results from deposition of calcium salts in
areas of brain necrosis and classically occurs in a periventricular pattern of distribution. Generalized atrophy commonly is present with early severe infection. Focal areas of
brain infarction and even hydranencephaly also may be
seen.31 Neuronal migrational abnormalities occur when the
normal migration of the subependymal neuroblast is interrupted during the formation of the neurocortex.
Intracranial calcification is better delineated by CT than
by MRI. MRI is better at demonstrating demyelination
secondary to the infective insult on long TR (ie, T2-

Figure 15. Axial unenhanced CT in a 2-year-old boy with

congenital HIV and bilateral basal ganglionic calcification
in association with a mild degree of cerebral atrophy, all
noted incidentally during a workup for sinusitis.

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Figure 16. (A) Axial unenhanced CT through the basal ganglia in a young woman with lymphoma and new-onset dementia.
There are low attenuation areas within the left frontal lobe (small arrowhead) and left peritrigonal white matter (large
arrowhead) without mass effect or enhancement. PML was proven at biopsy and the patient died 6 months later. (B) Axial
T2-weighted image in a child with HIV infection demonstrating atrophy and patchy T2 signal hyperintensity in the bilateral
frontal (small arrowhead) and peritrigonal (large arrowhead) white matter. These appearances are consistent with HIV
encephalopathy.

cortical T2 hyperintense white matter signal abnormalities

on MRI.
Herpes I and II. Most congenital herpes simplex viral
(HSV) infection is caused by serotype II. It may infect the
fetus either hematogenously through the placenta or be
acquired through the vaginal canal. Transplacental infection that occurs during the first trimester results in microcephaly, cerebral atrophy, hydranencephaly, cerebral and
cerebellar necrosis, intracranial calcification, chorioretinitis, and multiple other cutaneous and systemic anomalies.34
CNS herpetic infection obtained from the birth canal presents within the first 3 weeks of life. CT findings of acute
HSVII encephalitis include focal or diffuse low attenuation
predominantly of the white matter with possible enhancement
of the meninges (Fig 14). The natural history of the disease is
the development of diffuse cerebral atrophy. Chronically, the
primary finding is multicystic encephalomalacia.
Children congenitally infected by the human immunodeficiency virus (HIV-1) demonstrate cerebral atrophy secondary to the encephalitis, with microcephaly and calcification of the basal ganglia (Fig 15).35 HIV-infected children
can present with secondary infection from a variety of

organisms, including Toxoplasmosis, progressive multifocal

leukoencephalopathy (PML) papovavirus infection (Fig 16),
and vasculitides from the HIV-1 organism itself.36,37

Acquired Infections
Bacterial infections. The screening and treatment of
pregnant mothers carrying streptococcus B and the introduction of vaccines for Streptococcus pneumococcus and Haemophilus influenzae type b have reduced significantly the
incidence of these bacterial CNS infections. H. influenzae
type b infection is associated with bilateral subdural effusions that usually are culture-negative, a result of increased
permeability of vessels.
In children older than 2 years of age and young adults,
the pathogen seen most frequently is Neisseria meningitidis.
As discussed above, bacterial infection of the brain can
present as meningitis, cerebritis, or frank abscess formation. Patterns of infection can vary depending on the mode
of entry of the organism. Pott puffy tumor describes the
extension of bacterial infection from the frontal sinus extending superficially to the soft tissues of the skin and
producing an osteomyelitis of the frontal bone while ex-

CNS Infections Neuroimaging

153

Figure 17. (A) Axial unenhanced CT in a 4-year-old female demonstrating soft tissue swelling overlying the right frontal bone,
without evidence of bony destruction but with subtle effacement of the right cerebral sulci. (B) Axial T2-weighted MRI just
above the lateral ventricles shows a shallow subdural mass (arrowheads) overlying the right cerebral hemisphere. (C, D)
Gadolinium-enhanced coronal MRI performed 3 days after the CT shows an enhancing scalp collection (C), (small arrowheads)
with an extra-axial collection adjacent to the superior sagittal sinus (D), (smaller arrowhead) which was a subdural empyema
at surgery, in association with an epidural collection laterally (larger arrowhead). Note the loss of normal bright fatty marrow
signal from the overlying calvarium consistent with early osteomyelitis.
tending deeply to involve the leptomeninges and produce
an underlying cerebritis (Fig 17).38 When the veins draining
the overlying soft tissues and bone get infected and thrombosed, extra-axial collections such as epidural abscesses and
subdural empyemas may form. A subdural empyema should

be considered a neurosurgical emergency because if it is left

untreated it may propagate rapidly, causing infarction and
infection of the underlying brain. The diagnosis is confirmed by contrast-enhanced CT, or MRI if readily available. Epidural or extra-dural collections require surgical

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Figure 18. Axial contrast-enhanced

CT images in a 20-year-old male with
dementia. There are multiple poorly
rim-enhancing, peripherally placed
lesions, which on biopsy proved to be
Whipple disease. The patient responded to tetracycline with complete recovery. Small bowel biopsy
was negative.
drainage, as well as appropriate antibiotic therapy, if they
are causing significant mass effect.
Aggressive infection of the orbits or paranasal sinuses can
result in bone destruction, allowing organisms to enter the
CSF, resulting meningitis. Meningitic vasculitis may occur if
the suprasellar cistern and the circle of Willis are involved.
Other portals of entry into the CNS include inner ear anomalies such as Mondini defects, dermoid cysts with dermal sinus
tracks, meningoceles, and posttraumatic CSF leaks. The latter
classically is associated with recurrent pneumococcal meningitis. In evaluating for CSF leaks, one sometimes must perform a cisternogram in which water-soluble iodinated contrast
is introduced into the CSF by lumbar puncture and refluxed
into the intracranial CSF spaces in an attempt to reproduce
the leak. A thin-section, high-resolution CT scan of the suspected region of the CSF leak (such as the temporal bone or
parabasal sinuses) is performed after the cisternography procedure is completed. A similar but less anatomically precise
procedure can be performed utilizing nuclear medicine radioactive isotopes. A small amount of literature suggests using
real-time digital subtraction techniques to identify the leak by
fluoroscopy at the time of cisternography. The single most
important clinical feature for the success of any of these
examinations is that the patient be actively leaking CSF at the
time the procedure is performed.
Cardiac sources of infection should not be forgotten as
being a cause of cerebral abscess. In the setting of congenital heart disease with systemic infection, reversal of blood
flow and right-to-left shunting through the heart bypasses
the natural filtering system of the lungs and can lead to the
delivery of infected emboli to the brain.
Whipple disease. Whipple disease of the CNS is an
uncommon chronic bacterial infection caused by the same
organism invoked in Whipple disease of the bowel, Tropheryma whipplei. Neurological manifestations include dementia (56%), abnormal eye movements (33%), and involuntary
movements (28%). The CT and MRI findings range from
normal to cerebral atrophy to poorly enhancing mass lesions, focal abnormalities, and hydrocephalus (Fig 18).

Figure 19. Axial unenhanced CT through the basal ganglia

in a child with seizures. There is low attenuation in the
right medial frontal and anterior temporal lobes with apparent sparing of the basal ganglia, with swelling and mass
effect on the Sylvian fissure and right frontal horn. Subtle
low density also is noted around the left frontal horn,
confirmed on follow-up MRI as bilateral frontotemporal
involvement. There is no hemorrhage. The PCR was positive for HSV I.

CNS Infections Neuroimaging

Figure 20. Coronal-enhanced MRI through the internal

auditory canal in a 7-year-old boy with a left peripheral
VIIth nerve palsy. There is inflammatory enhancement of
the facial nerve (arrowhead) in the internal auditory canal.

155

Small bowel biopsy not always is positive, but PCR is quite

sensitive. Long-term antibiotic therapy will halt neurologic
involvement in Whipple disease, although reversing established deficits sometimes is difficult.39
Viral infections. Herpes simplex type I infection classically spares the basal ganglia (Fig 19) but typically involves the frontal and temporal lobes bilaterally but asymmetrically, sometimes involving the hippocampus. Herpes
CNS infection will show evidence of restricted diffusion in
the acute phase of the illness. These children may go on to
develop mesial temporal sclerosis and partial complex seizures. Herpes is said to be one of the hemorrhagic encephalitides. Chickenpox (varicella) infection may be followed
by a primary vasculitis causing a pattern of basal ganglionic
infarction from a proximal middle cerebral artery lesion.40
Herpes zoster can cause a Bell palsy, as part of Ramsay
Hunt syndrome, which can be demonstrated on enhanced
MRI (Fig 20). The differential diagnosis of this appearance
would include demyelinating disease such as multiple sclerosis, idiopathic Bell palsy, and Lyme disease. Herpes zoster
ophthalmica is a description of orbital involvement by the
virus, usually seen in older and immunocompromised patients. Zoster also can be seen as a cause of transverse
myelitis in an immunocompromised patient who has spinal
involvement.
St. Louis encephalitis (arbovirus) presents as a hemorrhagic leptomeningeal process, and gradient echo imaging
on MRI can be used to identify the presence of altered blood
and blood products (Fig 21). Japanese encephalitis is caused
by another arbovirus and is described as typically demonstrating thalamic and basal ganglionic involvement with T2

Figure 21. Axial T1-weighted (A) and gradient-echo (B) MRI images through the lateral ventricles demonstrating T1
hyperintense signal (arrowheads) returned from the left parietooccipital gyri with blooming of abnormal signal on the
gradient-echo imaging consistent with hemorrhage. There is a second focus in the roof of the left lateral ventricle. St. Louis
encephalitis was proven with PCR in this 4-week-old baby.

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Figure 22. (A) Axial unenhanced CT in a 3-week-old term

infant with seizures. The CT shows no remarkable lesion.
(B) Axial diffusion images obtained 3 days after the CT
shows large areas of restricted diffusion (dark signal) consistent with infarction. Enterovirus was diagnosed. (C) Axial T1-weighted images obtained 15 days after presentation
show extensive cystic encephalomalacia, with areas of hyperintense signal and hemorrhage.
hyperintensity. Enteroviral infection is not an uncommon
occurrence in young children and may result in severe
parenchymal destruction (Fig 22). West Nile virus disease is
a tropical illness, and white matter hyperintensities and
isolated rhombencephalitis have been described on T2weighted imaging, but the final pattern of disease is not yet
determined. Mumps virus is said to have a predilection for
the posterior fossa, and Epstein-Barr virus also has been
implicated as a cause of isolated rhombencephalitis (Fig
23), as well as being seen in association with immunemediated ADEM.
Rasmussen encephalitis is another immune-mediated
disease thought to be triggered by a viral infection. On
imaging, a classic pattern of unilateral cerebral hemispheric involvement can be seen in children, with initial
swelling followed by atrophy. Rasmussen is accompanied by
intractable seizure activity, with a pattern of epilepsia partialis continuans on EEG. MRS may help in confirming the
extent of neuronal loss before performing surgery.41
Secondary hemophagocytic lymphohistiocytosis (HLH)

in children is seen after a variety of both viral and bacterial

infections as well as malaria.42 Its appearance in the brain
consists of calcifications with evidence of hemorrhage and
patchy, predominantly white matter signal abnormality
(Fig 24), the latter not unlike the appearance of ADEM.
Many viral encephalitides present in children with involvement of the deep gray nuclei on imaging studies in
which the organism is not found but presumed. With increasing utilization of PCR, physicians anticipate that more
definitive diagnoses will be made in the future.
Prion disease. Prion disease and the transmissible
spongiform encephalopathies include variant CreutzfeldtJakob disease (vCJD) associated with bovine spongy encephalopathy (BSE), also known as mad cow disease.
Imaging reports of young people describe a pattern of
signal abnormality in the pulvinar (dorsal) region of the
thalamus.43,44
Fungal infection. Fungal infection is seen most commonly in the immunocompromised patient who has undergone bone marrow or organ transplantation and in the

CNS Infections Neuroimaging

157

Figure 23. (A) Sagittal unenhanced T1-weighted image in a 7-year-old boy presenting with a headache. There are low-lying
cerebellar tonsils (arrowhead) in association with a dilated supratentorial ventricular system concerning for tonsillar
herniation. (B) Axial T2-weighted MRI through the posterior fossa demonstrates increased signal in the cerebellar
hemispheres, with mediolateral compression of the brainstem. The appearances are consistent with cerebellitis proven at
postmortem.

Figure 24. (A) 12-month-old female with hypotonia and loss of milestones. Axial unenhanced CT scan through the basal
ganglia demonstrating multifocal areas of low attenuation throughout both cerebral hemispheres (small arrowheads) in
addition to parenchymal calcification with surrounding low attenuation (large arrowhead) in the right peritrigonal region.
There is low density in the corpus callosum and mild atrophy. (B) Axial FLAIR images performed 12 hours later show
extensive white matter lesions in the basal ganglia (small arrowhead) and splenium of the corpus callosum (large
arrowhead). The calcium is not seen on the MRI. Hemophagocytic lymphohistiocytosis (HLH) was diagnosed on bone
marrow aspiration.

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Figure 25. (A) Axial T2-weighted image in a young child undergoing therapy for acute lymphatic leukemia. There are two
large areas of hyperintense T2 signal in the perirolandic regions of the parietal lobes. (B) Axial T1-weighted postcontrast
images show enhancement at the gray-white matter junction of the right-sided perirolandic cortex (large arrowhead). The
child subsequently was proven to have aspergillus infection and died.

Figure 26. CNS tuberculosis in children. (A) T1-weighted postcontrast MR shows thick enhancement in the basal cisterns
typical for tuberculosis meningitis. (B) Axial postcontrast CT in a child with tuberculomas shows numerous small, rounded
enhancing tuberculomas (arrowheads).

CNS Infections Neuroimaging

159

Figure 27. (A) Axial FLAIR image through the lateral ventricles in an 11-year-old boy with seizures and syncope. There is
a well-defined solitary hypointense ring (small arrowhead) with surrounding hyperintense edema (large arrowhead) in the
left parieto-occipital region. This finding is consistent with the second stage of larval development of parenchymal
neurocysticercosis and inflammatory reaction with edema. (B) Sagittal postcontrast T1-weighted images show a well-defined
ring-enhancing lesion in the left parietal lobe (small arrowhead) consistent with a dying scolex.

patient with AIDS. Because these patients do not mount a

normal response to infection, they can have an atypical
imaging appearance as discussed above. MRI is the modality of choice, and administration of gadolinium chelate
contrast administration is essential to identify areas of
enhancement that may be subtle in these patients. Common organisms include the ubiquitous Aspergillus (Fig 25),
and Candida. Aspergillus accounts for the vast majority of
fungal disease seen in boys with chronic granulomatous
disease (CGD).
Cryptococcus neoformans is the most frequent cause of
fungal meningitis and the second most frequent CNS fungal infection. Cryptococcal meningitis is seen in immunesuppressed patients and described in systemic lupus erythematosus, HIV infection, and AIDS, as well as in patients receiving chemotherapy for underlying malignancies
such as Hodgkin disease.45 It can cause basal meningitis
such as Mycobacterium tuberculosis, with T1 shortening of CSF
in the basal cisterns and enhancement of loculated fluid
collections after gadolinium administration. Ventriculitis
and choroid plexitis causing mass lesions have been described.46
Mycobacterium tuberculosis in the brain can present as a
cerebritis with mass effect, swelling, and enhancement
caused by breakdown of the blood-brain barrier; as a basal
meningitis with highly proteinaceous CSF (bright signal on
T1-weighted imaging) that can be complicated by a basal
vasculitis with infarction of the basal ganglia (Fig 26); and
as enhancing small parenchymal granulomas that may go

Figure 28. Axial nonenhanced CT in a Latin American

child who fished in fresh water at the end of a pier. There
is the soap-bubble-appearing mass lesion (large arrowhead) in the left parietooccipital region with left occipital
horn effacement, midline shift and hydrocephalus. Edema
and low attenuation are found in the left frontal lobe.

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Figure 29. Sagittal lumbar

spinal MR images in a young
child with diskitis. (A) T1weighted precontrast images
show dark marrow signal due
to edema in vertebral endplates around the L3-L4 posterior disk space (arrows).
(B) T2-weighted, nonfat suppressed images show subtle
widening of the posterior disk
annulus and vertebral edema
(arrowheads). Without fat
suppression, vertebral edema
is obscured on T2 images.
(C) T1-weighted postcontrast images with fat suppression show corresponding
abnormal enhancement in
the posterior disk and mild
vertebral body enhancement
(arrowheads).

on to calcify or as parenchymal or subarachnoid abscesses.

Large calcified tubercular abscesses also known as antibiomas historically were seen after successful therapy of advanced intraaxial disease. Communicating hydrocephalus is
another common feature of tubercular meningitis.
Tuberculosis of the spine is addressed in another part of
the article. Atypical mycobacteria are seen in the head and

neck, where they produce lymphadenopathy with a violaceous hue of the overlying skin.
In patients with AIDS, toxoplasmosis is an organism
commonly found in brain infection. Because of the muted
immune response secondary to low CD4 counts, distinguishing it from lymphoma on imaging sometimes can be
difficult. An empiric trial of medical therapy for toxoplas-

CNS Infections Neuroimaging

mosis can be helpful because resolution of signal abnormality in the basal ganglia helps exclude malignancy. MRS
similarly can be a useful tool because a markedly elevated
choline in the presence of a marked reduction in N-acetyl
aspartate (NAA) is suspicious for tumor rather than abscess. In abscesses, a lipid lactate peak or succinate and
alanine peaks are more likely to be found.
Parasitic infections. With the increasing mobility of
populations, a wider variety and number of exotic parasites
are being seen. Cysticercosis is a common parasitic disease
caused by the larval pork tapeworm (Taenia solium). It enters the human CNS as a result of poor oral-fecal hygiene.
It is endemic in Mexico and South America. Neurocysticercosis most frequently involves the brain parenchyma. Cysticerci tend to lodge at the gray-white matter junction. As
they grow, a fluid bladder forms and appears dark on T1weighted imaging and bright on T2-weighted imaging.
Without edema and without contrast enhancement on CT
or MRI, at this stage, the larva appears as a round cyst with
a mural nodule (scolex or head of the larva). The larva then
begins to degenerate, at which point host inflammatory
responses produce edema around the cyst and result in
brain swelling. The fluid within the cyst now appears
brighter than CSF on T1-weighted imaging, and on T2weighted imaging, the surrounding edema is bright relative
to the hypointense scolex and cyst wall (Fig 27). In the third
stage, the larva undergoes retraction and calcifies. At this
time, the lesion becomes isointense to normal brain on
T1-weighted imaging and isointense to hypointense with or
without central high intensity on T2-weighted imaging. On
contrast-enhanced T1-weighted images, the dying scolex
appears as an enhancing nodule or micro ring-enhancing
lesion with or without surrounding edema, mimicking other
granulomata, small abscess, or metastasis. On CT at this
stage, only a calcified superficial nodule may be appreciated.
A second form of neurocysticercosis that may coexist
with the parenchymal form is racemose cysticercosis. In this
form, the cysticerci live in the subarachnoid space, basal
cisterns, and within the ventricles where they may cause
obstruction to flow of the CSF at the level of the aqueduct
and result in hydrocephalus. This form of the disease is
significantly more difficult to treat. It is diagnosed on contrast-enhanced imaging by the presence of nodules and
enhancement and on FLAIR imaging that distinguishes the
cysts from CSF by the absence of CSF pulsation and the
higher protein content of their fluid. Cysticercosis involving
the spinal canal is a relatively uncommon occurrence.
Human echinococcus occurs by ingestion of contaminated dog feces containing ova of a dog tapeworm. After
being ingested, the ova hatch in the gastrointestinal tract,
and embryos enter the circulatory system. The embryo
develops into a cystic larva called a hydatid cyst. This event
usually occurs in the liver and lung, but approximately 2 to
5 percent of all patients are said to develop a lesion in the
brain.47 The cyst usually is solitary, very round, and posterior; it can grow quite large, demonstrating little surrounding enhancement. When the cyst in the brain ruptures, it
causes extensive inflammatory change.

161

Figure 30. T2-weighted sagittal MR of the cervical spine

shows diffuse spinal cord swelling and bright T2 signal in a
patient with transverse myelitis.

Paragonomiasis is a lung fluke endemic in East and

South-East Asia, West Africa, and Latin America. Paragonomias westermanii is the most important species, and human
infection occurs by ingestion of undercooked freshwater
crabs or crayfish infected with the encysted larvae. The
larvae penetrate the bowel and diaphragm to enter the
pleural cavity. Some larvae may bypass the lung and penetrate the meninges at the skull base to invade the brain,
usually the posterior aspects of the cerebrum. The appearance produced is described as soap bubbles that ultimately
may calcify and demonstrate evidence of rim enhancement
after administration of contrast agent (Fig 28). Spinal involvement rarely occurs.
Schistosomiasis is a species of blood fluke that can seed
the brain and cause focal granulomas with surrounding
edema and contrast enhancement. MR findings in schistosomal myelitis have been reported.48

Spine
Spinal infections are considered briefly. In general, spinal
infections occur in the vertebral column, disk space, and
paraspinous soft tissues as diskitis and osteomyelitis; in the
epidural space as epidural abscess; and in the thecal sac as
meningitis and spinal cord abscess. Spinal infections may be
pyogenic or nonpyogenic. Diskitis and vertebral osteomyelitis are distinct entities in children because of the unique
arterial supply of the subchondral region of vertebral body
endplates and the adjacent disk space in toddlers.49,50 The
vascular supply to the disk regresses to an adult form with
a relatively avascular disk later in childhood. The initial site
of infection in the vertebral column in older children and

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Figure 31. Child with Guillain-Barre

syndrome. T1-weighted postcontrast
sagittal (A) and axial (B) MR shows
thickened, enhancing nerve roots in
the cauda equina which is consistent
with Guillain-Barre.
adults is the metaphyseal region of the vertebral body,
where the penetrating branches of the spinal arteries deliver organisms, resulting in the typical pattern of vertebral
ostemyelitis. In toddlers, however, the primary site more
commonly is the disk space, resulting in primary diskitis
with secondary vertebral endplate involvement. The cause
of diskitis remains controversial because of varying results
on aspiration and biopsy, but Staphylococcus aureus is the
most frequent organism isolated on aspiration in some
studies.50 The imaging appearance of diskitis usually is
characterized by abnormal disk space enhancement,
edema, and loss of disk height. The adjacent vertebral
bodies usually are involved, with edema and abnormal enhancement along the endplates (Fig 29). Edema is seen on
low T1 signal precontrast and increased T2 signal. Paraspinous collections may be present.
Epidural abscess usually is caused by Staphylococcus aureus
and is seen as a rim-enhancing epidural mass with a fluid

intensity central region.51 When small, these collections

may blend in closely with the thecal sac. As discussed above,
fat-suppression MRI techniques are essential for delineating fluid collections in the epidural space. Spinal cord abscess is a very rare occurrence in children and may be seen
with dermal sinus tracks or other malformative dysraphic
connections between the skin and the spinal cord.
Nonpyogenic, granulomatous infections of the spine in
children may be tubercular, fungal, or Brucellar.52,53 Tubercular spondylitis typically involves vertebral bodies, with
sparing of the intervening disk space. Subligamentous
spread of organisms may lead to involvement at multiple
levels. Significant bony destructive changes and kyphotic
deformities may result, and large paraspinous masses also
may be seen. Brucellosis has many features on imaging
studies that are similar to those of tuberculosis, with disk
space sparing and subligamentous spread to other vertebral
bodies being found in some cases. Brucellosis may remain

CNS Infections Neuroimaging

confined to a single vertebral body or be multifocal.54 Coccidioides, Aspergillus spp., or Candida spp. also may cause
granulomatous fungal infections of the spine.
Postinfectious lesions in the spinal cord and nerve roots
include myelitis and Guillain-Barre syndrome. Myelitis in
the spinal cord often is associated with intracranial ADEM.
Lesions present as areas of spinal cord swelling and increased T2 signal that may enhance along the leading edges
of the lesion due to demyelination (Fig 30). Guillain-Barre
syndrome is an idiopathic polyneuritis that usually develops
after an acute infection or other inciting event but may be
idiopathic. Patchy demyelination of ventral and dorsal
roots, dorsal root ganglia, and peripheral nerves is
present.55 Cranial and spinal nerves are involved, usually
with greater proximal than distal nerve involvement.54 Imaging studies show thickened and enhancing nerve roots in
the cauda equina (Fig 31).

Summary
Neuroimaging plays an important role in the care of children with CNS infections. In children with atypical clinical
courses or neurological deficits or in cases for which the
clinical workup is unclear, CT and MRI studies may add
significantly to the diagnostic workup. On imaging, many
CNS diseases have complex and variable patterns, some of
which are pathognomonic and some of which show considerable overlap. The application of newer imaging techniques, however, will continue to narrow the differential
diagnosis.

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