Review Article

Imaging of Meningitis and Meningoencephalitis

in Children
Simay A. Kara1 Gagandeep Choudhary2 Unni K. Udayasankar2

1 Department of Radiology, Acıbadem University School of Medicine, Address for correspondence Unni K. Udayasankar, MD, Department
Istanbul, Turkey of Medical Imaging, University of Arizona College of Medicine, Tucson,
2 Department of Medical Imaging, University of Arizona College of AZ 85750, United States (e-mail: unniu@radiology.arizona.edu).
Medicine, Tucson, Arizona, United States

J Pediatr Neurol

Abstract Although central nervous system infections in children are rare, when suspected,
urgent diagnosis and treatment are mandated to prevent morbidity and mortality.
Inflammation of the meninges alone is termed meningitis; associated involvement of
the underlying brain leads to meningoencephalitis. CSF analysis remains the gold
standard in identifying the infectious agent. Imaging plays a vital role not only in

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Keywords
► meningitis
► cerebrospinal fluid
► subarachnoid space
► subdural effusion
► empyema
supporting the diagnosis of meningitis or meningoencephalitis but also in identifying
potential complications, monitoring treatment response, and follow-up. The pattern
of meningeal and brain involvement can vary depending on the infectious agent;
cerebral convexity meninges is commonly involved in acute bacterial infection,
basilar meninges in tuberculosis, and meningoencephalitis in viral infection. In this
article, we review the characteristic imaging appearances of common bacterial,
mycobacterial and viral agents, role of newer imaging technique, and list potential
complications.

Introduction age, as the subarachnoid space becomes more resistant to

The most common central nervous system (CNS) infection in
children is meningitis, and it is associated with high mor-
bidity and mortality, especially in the first 3 months of life.
Neonatal period is the most common age group for occur-
rence of meningitis in children. Incidence of neonatal me-
ningitis is between 0.3 and 6.1 cases per 1,000 live births per
year. Neonates have deficiencies in the immune system,
including cellular, innate, and humoral immunity, as well
as phagocytic function leading to a higher risk of meningitis
compared with other ages.1,2 A lack of specific clinical
findings in premature babies and neonates creates chal-
lenges to an early diagnosis. Most premature infants and
neonates survive with advanced medical treatment; how-
ever, meningitis continues to be a leading cause of neurologic
disability worldwide. Incidence of meningitis decreases with
infection in older children.3
Meningitis is the inflammation of the protective mem-
branes covering the brain, more commonly the leptome-
ninges (pia, arachnoid) and subarachnoid space. Bacterial
(pyogenic), viral (lymphocytic), and chronic granulomatous
are three main types of meningitis. Pathogenic microorgan-
isms can affect the meninges via hematogenous spread from
the choroid plexus, directly penetrating trauma, rupture of a
superficial cortical abscess, or extension from an adjacent
infection (secondary to sinusitis, mastoiditis, otitis, and
dental abscess). History of skull base trauma, spinal dysraph-
ism such as dermal sinus tract, and neuroenteric fistula are
also risk factors for infection.
Meningitis is diagnosed using a combination of patient
history, clinical symptoms, physical examination, laboratory
evaluation, and positive cerebrospinal fluid (CSF) findings.4

received Issue Theme Neuroimaging of Pediatric Copyright © by Georg Thieme Verlag KG, DOI https://doi.org/
April 30, 2017 Infections; Guest Editor, Surjith Vattoth, Stuttgart • New York 10.1055/s-0037-1604235.
accepted MD, FRCR, DABR ISSN 1304-2580.
May 8, 2017
Meningitis and Meningoencephalitis Imaging Kara et al.
Neuroimaging is not necessary for diagnosis but is useful in
excluding contraindications for lumbar puncture, identifica-
tion of complications, and in cases where the diagnosis is not
straightforward. It is important for monitoring the response
to treatment. It is also a valuable tool in patients with
symptoms suggestive of increased intracranial pressure,
focal neurological deficits, and persistent seizures and a
helpful adjunct in patient whose recovery is slow.4–9 Mental
retardation, cerebral palsy, hydrocephalus, sensorineural
hearing loss, behavioral problems, speech and language
disorders, and impaired vision are the main long-term
complications of the neonatal meningitis.3 Diagnosis and
treatment of meningitis are very important, and imaging
studies help in early diagnosis and evaluation, thereby
decreasing the morbidity and mortality.
Magnetic resonance (MR) imaging with contrast is the
gold standard modality in imaging for evaluation of the
patient with meningitis.10 Diffusion-weighted imaging
(DWI) is very important in early diagnosis of meningoence-
phalitis, for follow-up, and for evaluation of complications.11
Diffusion tensor imaging (DTI) may show high fractional
anisotropy (FA) values in the affected cortical area.12
Meningitis can cause important complications, such as
arterial and venous thrombosis, stroke, ventriculitis, epen-
dymitis, hydrocephalus, cerebritis, abscess formation, sub-
dural effusion, and empyema.2 Infection can spread through
the perivascular spaces to the cortical vessels causing ne-
crosis of the vessel wall due to inflammation leading to the
formation of arterial or venous thrombosis and subsequent
infarction of the affected area.13 Fibrinopurulent exudate
formation in the subarachnoid spaces in cerebral convexity,
basilar cisterns, or foramina of Magendie and Luschka can
cause communicating or noncommunicating hydrocepha-
lus.3,14,15 Ventriculitis is a common complication occurring
in up to 30% of children, and its incidence is up to 92% in
neonates. Intraventricular debris, ventricular dilatation,
periventricular edema, intraventricular DWI restriction,
and enhancement of the ventricular wall can be seen.6
Ependymal inflammatory changes, thrombosis of the sub-
ependymal and periventricular veins, and parenchymal in-
jury are known complications.16
Bacterial Meningitis
Bacterial meningitis is diagnosed and primarily managed
based on a combination of clinical examination findings and
evaluation of the CSF. The causes vary with patient age. In
neonates, Streptococcus group B infections account for nearly
86% of cases, followed by Escherichia coli, Listeria, and Enter-
obacteriacae. In young infants, Haemophilus influenzae was a
major causative agent, but the incidence has decreased after
the introduction of Hib vaccine. Neisseria meningitidis, Strep-
tococcus, and Pneumococcus are the major pathological agents
in this age. In older children, Pneumococcus, N. meningitidis,
and staphylococci are the main causative agents.9 Almost
90% of neonatal meningitis is diagnosed within the first
24 hours of life.1,3 Premature rupture of membranes, pro-
longed membrane rupture more than 18 hours, antenatal
Journal of Pediatric Neurology
chorioamnionitis, premature birth, traumatic delivery, low
birth weight, male gender, low socioeconomic status, invasive
monitoring, and need for resuscitation are the major risk
factors in the early neonatal period. Diabetes mellitus, Cush-
ing’s syndrome, sickle cell anemia, and coma are the risk
factors for young infants. Patients with recurrent meningitis
should be evaluated for anomalies of neuroenteric canal, nasal
dermal sinus, and dorsal dermal sinus. Streptococci and gram-
negative bacilli are the most common agents in recurrent
meningitis.6 Sagittal and axial high-resolution T1- and T2-
weighted MR images can detect dysraphism of the spinal cord
or the presence of a dermal sinus tract. Contrast-enhanced
scan is not mandatory but may be helpful.
Patients present with fever, neck stiffness, and altered
mental status. Almost all patients have at least one of these
findings. Mortality rate may reach 30%, especially in patients
with pneumococcal meningitis. If bacterial meningitis is
clinically suspected, antibiotic treatment should be started
as soon as possible after the blood culture and CSF analysis in
patients presenting with seizures or altered mental status.
Antibiotic treatment before CSF culture can change the
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results,8 but treatment should not be delayed if there is a
delay in obtaining CSF.
Lumbar puncture regularly demonstrates a higher open-
ing pressure greater than 20 cm H2O. CSF proteins and
neutrophils are increased, whereas glucose is decreased
(less than 10 mg/dL). White blood cells count is greater
than 1,000 in CSF (106/L). Glucose level is generally low.
High protein level (>500 mg/dL) is recognized as a poor
prognostic factor.1 If the patient has accompanying neuro-
logic deficits or moderate or severe impairment of conscious-
ness, imaging is recommended before attempting lumbar
puncture.
On contrast-enhanced MRI, enhancement of meninges
can sometimes be seen in various patterns (►Fig. 1). This
could be almost symmetric, short segment, discontinuous,
very thin rim at sites with absent blood–brain barrier,
including parasagittal areas, inner table, falx, and the tentor-
ium cerebelli. Any meningeal enhancement seen in more
than three slices is considered abnormal. Additionally, dura
and venous structures normally enhance. Arachnoid is avas-
cular and pial enhancement is frequently subtle. Abnormal
enhancement is rarely symmetric and it extends into the
depth of the involved sulci.16,17 Suprasellar and ventricular
enhancement are not normal findings.
Computed tomography (CT) may be normal at the beginning
of the disease. Hyperattenuation and enlargement of the sub-
arachnoid spaces, sulcal effacement, and cerebral edema are
revealed in the later stages of the disease. An enhancement of
the leptomeninges can be detected on the contrast-enhanced
CT (CECT) scan when disease progresses. Enlargement of the
subarachnoid spaces and ventricles and increased density of
basal cisterns or sylvian fissures due to purulent exudates are
findings indicating an advanced stage of the disease on a
nonenhanced CT (NECT) study of the brain. Subdural effusion
or empyema is an occasional additional finding.
CT angiography (CTA) may be indicated to detect vascular
complications of meningitis. CTA can show arterial stenosis
 Meningitis and Meningoencephalitis Imaging Kara et al.

Fig. 1 A-3-year old girl with acute bacterial meningitis. (A) Coronal T2 FLAIR image shows linear abnormal high signal in the left posterior frontal
lobe along the parenchymal surface (arrow). Note the corresponding leptomeningeal enhancement on coronal (B) and axial (C) postgadolinium
images (arrows). FLAIR, fluid-attenuated inversion recovery.

or occlusion due to vessel inflammation. Empty delta sign on gradient echo, and T1-weighted images are highly sensitive

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CT venogram is the classic imaging finding described in cases
of dural sinus thrombosis. Venous sinus thrombosis affects
the cortical veins in the initial phase with extension into the
dural sinuses with disease progression.
MR imaging can show hyperintense sulci and cisterns on
fluid attenuation inversion recovery (FLAIR) sequences. This
finding may be secondary to increased protein concentration
in CSF; however, this finding in isolation is not pathogno-
monic of acute meningitis. Contrast-enhanced T1-weighted
sequence is the most accurate technique for detection of
acute meningitis. Complications, such as edema, infarction,
and abscess, can be detected on DWI, T2, and FLAIR se-
quences. Contrast-enhanced FLAIR images can detect subtle
leptomeningeal enhancement and has been shown to be
superior to the contrast-enhanced T1-weighted images
in some studies.18 Susceptibility-weighted images (SWI),
for any associated hemorrhage. SWI is the most sensitive
sequence for hemorrhage and also facilitates differentia-
tion of microhemorrhage from calcification. Thin, smooth
meningeal enhancement can be seen in bacterial or viral
meningitis, but if the enhancement shows thick and nodular
pattern, granulomatous diseases or carcinomatous meningi-
tis should be considered in the differential diagnosis.19
Focal parenchymal involvement (cerebritis) is seen as a
hypodense area when compared with normal parenchyma
on nonenhanced head CT. Ring-like enhancement and de-
layed central diffusion of contrast may be seen on postcon-
trast images. If capsule develops around the central necrosis
with subsequent abscess formation, an ill-defined hypo-
dense area with peripheral smooth enhancement is usually
identified (►Fig. 2). Enhancement in cases of well-defined
abscess formation does not diffuse to the center, and steroid

Fig. 2 Brain abscess in the left temporal lobe in a 29-month-old girl with hypoplastic left heart syndrome and new -onset seizures. (A) Axial NECT
shows an ill-marginated hypodense left superior temporal lobe lesion (arrow) with posteromedial vasogenic edema (arrowheads), left
hemispheric mass effect, and mild left-to-right midline shift. (B) Axial DW image shows layered restricted diffusion (arrow). (C) Axial postcontrast
T1W image shows a ring enhancing lesion (arrow) and surrounding vasogenic edema. DW, diffusion-weighted; NECT, nonenhanced head
computed tomography; T1W, T1-weighted.

Journal of Pediatric Neurology

Meningitis and Meningoencephalitis Imaging Kara et al.

Fig. 3 A 3-week-old neonate with group B streptococcal bacteremia and meningoencephalitis. (A) Diffusion-weighted axial image
shows peripheral areas of restricted diffusion in bilateral frontal and occipital regions (arrows) with corresponding ADC abnormalities.
(C) Postgadolinium axial T1-weighted images demonstrates abnormal leptomeningeal and brain surface enhancement (white arrows).
Additionally, nonenhancing subdural effusions are also present (black arrows). A lack of diffusion abnormality within the subdural fluid suggests
subdural effusion instead of a subdural empyema. ADC, apparent diffusion coefficient.

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treatment does not suppress the wall enhancement.20
Medial wall of the capsule is characteristically the thinnest
part, and it may rupture into ventricular system or a new
daughter abscess may form. Paramagnetic effects of the
bactericidal free radicals can manifest as hyperintensities
on T1-WI and hypointensities on T2WI. MR spectroscopy
shows elevated amino acid peaks at 0.9 ppm. Normal brain
metabolites, such as N-acetylaspartate (NAA), choline, and
creatinine, are not detected.21 MR spectroscopy can show
increased choline and mildly decreased NAA.
DWI is the most sensitive sequence for detecting abscess
and subdural empyema.22,23 It shows a central restricted
diffusion and the corresponding decrease in apparent diffu-
sion coefficient (ADC) value in the abscess. Restricted diffu-
sion aids in the differentiation of subdural empyema from
subdural effusion (►Fig. 3). Diffusion restriction can also be
seen in acute demyelinating lesions, neoplasms, and ische-
mia. Demyelinating lesions generally show peripheral and
often interrupted diffusion restriction. Neoplasms, however,
show more heterogenous restricted diffusion corresponding
to the areas of higher cellularity. Arterial spin labeling (ASL)
perfusion imaging can help demonstrating cerebral blood
flow changes in patient with meningitis; abnormal ASL
perfusion has shown a correlation with patient’s neurologi-
cal status.24
Subdural infection and abscesses are mostly associated
with pneumococcal meningitis but also seen in streptococcal
and staphylococcal meningitis (►Fig. 4). Ischemia as well as

Fig. 4 Acute subdural empyema in a 15-year-old boy with fever and seizures. (A) Axial NECT shows subtle, extra-axial, linear hypodensity with
mass effect along the parasagittal right frontal lobe (arrow). (B) Contrast-enhanced CT shows peripherally enhancing empyema and
leptomeningeal enhancement (arrow). (C) Contrast-enhanced T1W MR image shows shallow subdural hypointense collection along the anterior
frontal lobe with thickening and enhancement of the dural layers (arrow). Also note subtle right frontal leptomeningeal enhancement
(arrowheads). Images through the paranasal sinuses showed acute left maxillary and frontal sinusitis (images not shown). CT, computed
tomography; NECT, nonenhanced head computed tomography; T1W, T1-weighted.

Journal of Pediatric Neurology

 Meningitis and Meningoencephalitis Imaging
basal ganglia involvement has also been observed in strep-
tococcal meningitis. Extra-axial collection with symmetrical
prefrontal subarachnoid space dilatation is described in this
condition; however, subdural empyema and ventriculitis are
less common complications. Ventriculomegaly, ventriculitis,
and DWI-restricted extra-axial collections are more com-
monly found in E. coli meningitis. Multiple large intrapar-
enchymal abscesses can be seen as a complication in Serratia
meningitis. A specific parenchymal imaging abnormality
associated with meningococcal meningitis is gyriform occi-
pital cortical enhancement.13
Carcinomatous meningitis (neoplastic leptomeningitis),
leukemia, and Sturge–Weber syndrome are in differential
diagnosis of acute infectious meningitis. Presence of under-
lying CNS malignancy often points to the diagnosis of carci-
nomatous meningitis. Laboratory and clinical findings and
history of the patient can help to differentiate leukemic
deposits from meningitis. Patient with Sturge–Weber syn-
drome presents with seizure with or without cerebral atro-
phy depending on the disease stage. Unilateral contrast
enhancement of the leptomeninges are seen in the patient.
Calcification noted in the later stages of the disease is also a
useful imaging finding to diagnose chronic Sturge–Weber
syndrome.
Tuberculosis Meningitis
Mycobacterium tuberculosis is an intracellular microorgan-
ism, first isolated by Robert Koch in 1882.2 It is still the cause
of 1.6 to 1.7 million deaths per year. Small miliary tubercles
enter the meninges or brain parenchyma during hemato-
genous bacteremia. Mycobacterium may remain silent for a
long time before rupturing into the subarachnoid space and
causing meningitis.25
Increased cellularity (especially lymphocytic), increased
protein level, and decreased glucose level are characteristic
CSF findings. White blood cells count is in the range of 100
to 500  106/L, and more than 100 mg/dL protein is often
Fig. 5 Tuberculous meningitis in an 18-month-old girl. (A) Axial T2-weighted image shows diffuse dilation of the lateral and third ventricles
(arrow) and the cortical sulci with mild diffuse parenchymal atrophy. (B) Post gadolinium T1-weighted axial image shows diffuse leptomeningeal
thickening and enhancement (arrows).
Kara et al.
found within the CSF. Glucose level is approximately 10 to
45 mg/dL and generally less than 50% of blood sugar.1
Meningeal hyperdensity noted on NECT correlates with the
increased protein level in CSF with corresponding hyperin-
tensities on unenhanced T1-weighted and FLAIR MR
images.1,5
Imaging in patients with tuberculous basilar meningitis
typically shows thick and nodular enhancement (►Fig. 5).
Enhancement of the cisterns surrounding the middle cere-
bral artery and sylvian fissure is more common in children
with neurotuberculosis.26,27 The magnetization transfer
(MT) technique has shown to be superior to the conventional
spin echo sequences for imaging abnormal meninges. The MT
ratio in tuberculous meningitis is significantly higher than in
viral meningitis.28 Abnormal signal and enhancement of the
basilar meninges is not entirely specific for tuberculous
infections and can also be found in other granulomatous
diseases, such as fungal infection, sarcoidosis, or neoplasms
including lymphoma.
Tuberculoma is the most common parenchymal involvement
pattern of the disease. Homogenous nodular enhancement less
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than 2 cm is common in tuberculous meningoencephalitis. CT
shows solid or ring enhancing, hypodense or hyperdense, oval
or round nodules. Calcification is rare. On MRI, parenchymal
noncaseating tuberculoma is hypointense in T2-weighted
images with central hyperintensity compatible with liquefac-
tion or caseation necrosis.
MR spectroscopy may be valuable in the differential
diagnosis of tuberculous meningitis. MR spectroscopy shows
increased lipid peaks at 0.9, 1.3, 2.0, and 2.8 ppm. The lipid
peaks can be the result of the high lipid content of the
mycolic acid in the mycobacterial cell wall.25,29 Amino acid
peaks are generally not observed in contrast to pyogenic
abscess.
An important and common complication of tuberculosis
is ischemia of the small and medium vessels at the base of
the brain (►Fig. 6). Inflammation and vasospasm of the
vessels can cause hemorrhagic or nonhemorrhagic infarcts,
Journal of Pediatric Neurology
Meningitis and Meningoencephalitis Imaging Kara et al.

Fig. 6 Tuberculous meningitis, vasculitis, and infarct in a 19-month-old boy. (A) Axial diffusion-weighted image demonstrates a focus of
restricted diffusion in the right inferior/medial frontal lobe corresponding to a focal infarct (arrow). (B) Axial postcontrast T1-weighted image
shows diffuse basal meningeal thickening and enhancement affecting the prepontine cistern (black arrows) and suprasellar cisterns. Note
extension of the inflammatory process along the middle cerebral and anterior cerebral arteries (white arrows). (C) Sagittal postcontrast image
shows a communicating type hydrocephalus (white arrows) in addition to findings of basilar meningitis (black arrows).

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especially in internal capsule and basal ganglia.30 Middle
cerebral artery and lenticulostriate and thalamoperforator
arteries are commonly involved. DWI can be used for evalua-
tion of ischemic parenchymal abnormality secondary to
vascular involvement. Communicating hydrocephalus can
be seen. Spread of infection to the dura mater and bone is
rare.15
hyperintensity in cortex, thalamus, and basal ganglia as a
result of perivascular demyelination and inflammation. Sub-
acute sclerosing panencephalitis develops with virus reacti-
vation years after the initial infection, often with poor
prognosis. Involvement of asymmetrical parietal and tem-
poral lobes is common. Multifocal T2 hyperintensity in
periventricular and subcortical white matter and involve-
ment of brain stem (later finding) may be seen.33,34

Aseptic Meningitis, Meningoencephalitis

Aseptic meningitis and meningoencephalitis are mostly
caused by viral agents. No specific imaging features are
described, and imaging is often normal in these cases despite
severe clinical symptoms.
Human Herpesvirus 6
Human herpesvirus 6 (HHV6) infection usually presents as a
febrile illness with cutaneous lesions in early childhood. The
virus may remain latent in the body; it can reactivate in
immunosuppressed patients and may rarely cause menin-
goencephalitis.31 Clinical findings can change from benign
infection to long-term neurologic deficits. No specific ima-
ging findings are described.
Measles Virus
Measles encephalitis can show multifocal hyperitensity in
both cerebral hemispheres, with swelling of the cortex, and
symmetrical bilateral involvement of putamen and caudate
nucleus on T2-weighted images. Focal gyral hemorrhage may
also be seen. Bilateral striatal necrosis, transient pseudoa-
trophy, and cerebral vein thrombosis have also been de-
scribed in some cases.32
Postinfectious encephalitis, progressive infectious ence-
phalitis, and subacute sclerosing panencephalitis are the
main types of measles infection of CNS. Postinfectious en-
cephalitis is an autoimmune process and presents with T2
Enterovirus 71
Enterovirus (EV) include more than 60 viral serotypes within
the picornavirus family, such as echovirus, poliovirus, cox-
sackieviruses, EV68, and EV71. EV infection is diagnosed in
approximately 12% of neonatal sepsis and aseptic meningitis
cases. EV71 causes hand-foot-mouth disease (HFMD) in
young children. Enteroviruses generally affect children un-
der the age of 5 years.
EV71 virus may be neurotropic, and when affected, pre-
sents with the severe neurologic symptoms.35 It can be
detected with polymerase chain reaction in CSF. Encephalitis,
seizure, and focal neurological defects are known presenting
features. Fever is often biphasic; the first peak is the cause of
systemic affect and the second one occurs with meningeal
signs. Encephalitis generally involves the brainstem. Myoclo-
nus and tremors are more common clinical symptoms. Dorsal
pons, medulla, dentate nucleus, midbrain, hypothalamus, and
thalamus are other regions involved. If it involves the dorsal
medulla, the virus affects the dorsal nucleus of vagus, fasci-
culus longitudinalis medialis, and reticulate body resulting in
respiratory and circulatory dysfunction. Parenchymal involve-
ment is seen as iso- to hypointense signal on T1-weighted
and iso- to hyperintense on T2-weighted images. Enhanced-
MRI is essential for diagnosis, as MRI without contrast media
may not detect the parenchymal changes. Neonates can pre-
sent with additional major systemic involvement, such as
myocarditis, hepatic necrosis, and necrotizing enterocolitis.

Journal of Pediatric Neurology


Morbidity and mortality because of systemic involvement
could be as high as 70%.36
Enterovirus meningitis is rarely fatal in older infants and
children. Febrile seizures and the syndrome of inappropriate
antidiuretic hormone (SIADH) can be seen in meningitis
patients without parenchymal CNS involvement. Enterovirus
can also cause chronic meningitis and fatal outcome in
patients with certain immunosuppressive conditions such
as hypo/agammaglobulinemia.
Funding
None.
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