Acta Radiologica

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Intracranial Infections: Clinical and Imaging

Characteristics

B. R. Foerster, M. M. Thurnher, P. N. Malani, M. Petrou, F. Carets-Zumelzu &

P. C. Sundgren

To cite this article: B. R. Foerster, M. M. Thurnher, P. N. Malani, M. Petrou, F. Carets-Zumelzu

& P. C. Sundgren (2007) Intracranial Infections: Clinical and Imaging Characteristics, Acta
Radiologica, 48:8, 875-893

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 REVIEW ARTICLE ACTA RADIOLOGICA

Intracranial Infections: Clinical and Imaging Characteristics

B. R. FOERSTER, M. M. THURNHER, P. N. MALANI, M. PETROU, F. CARETS-ZUMELZU & P. C. SUNDGREN
Department of Radiology, and Divisions of Infectious Diseases and Geriatric Medicine, Department of Internal
Medicine, University of Michigan Medical Center, Ann Arbor, Michigan, USA; Department of Radiology,
Neuroradiology, Medical University Vienna, Austria; Veterans Affairs Ann Arbor Healthcare System, Ann Arbor,
Michigan, USA; Geriatric Research Education and Clinical Center (GRECC), Ann Arbor, Michigan, USA

Foerster BR, Thurnher MM, Malani PN, Petrou M, Carets-Zumelzu F, Sundgren PC.
Intracranial infections: clinical and imaging characteristics. Acta Radiol 2007;48:875–
893.
The radiologist plays a crucial role in identifying and narrowing the differential diagnosis
of intracranial infections. A thorough understanding of the intracranial compartment
anatomy and characteristic imaging findings of specific pathogens, as well incorporation
of the clinical information, is essential to establish correct diagnosis. Specific types of
infections have certain propensities for different anatomical regions within the brain. In
addition, the imaging findings must be placed in the context of the clinical setting,
particularly in immunocompromised and human immunodeficiency virus (HIV)-positive
patients. This paper describes and depicts infections within the different compartments of
the brain. Pathology-proven infectious cases are presented in both immunocompetent
and immunocompromised patients, with a discussion of the characteristic findings of
each pathogen. Magnetic resonance spectroscopy (MRS) characteristics for several
infections are also discussed.
Key words: Infection; intracranial infection; meningitis; MR spectroscopy; neuroradiol-
ogy
Pia C. Sundgren, Department of Radiology, Division of Neuroradiology, University of
Michigan, Room B2A209D, 1500 E Medical Center Drive, Ann Arbor, MI 48109-0030,
USA (tel. +1 734 763 3253, fax. +1 734 764 2412, e-mail. sundgren@umich.edu)
Accepted for publication April 21, 2007

Intracranial infections include a wide range of Imaging modalities

different processes, each with unique clinical char-
acteristics. Many intracranial infections progress
rapidly and result in significant morbidity and
mortality if appropriate therapies are not initiated
promptly. Clinical presentations of intracranial
infection vary significantly. Common manifestations
include altered mental status, seizures, as well as
more subtle focal deficits, such as cranial nerve
palsies (10). In each case, the radiologist plays a vital
role in the diagnostic workup of these infections. By
interfacing with the clinicians who care for these
patients, the radiologist can help direct appropriate
testing and treatment, ultimately decreasing the
morbidity associated with these infections.
In this review, we will discuss several important
intracranial infections. We will briefly describe the
salient clinical features of specific infections and
offer guidance related to the utility of imaging
modalities in particular settings.
Computed tomography (CT) and magnetic reso-
nance imaging (MRI) are the two primary imaging
modalities used in the setting of suspected central
nervous system infection. While CT is widely
available and very useful for rapid assessment of
hydrocephalus, mass lesions, hemorrhage, or acute
brain edema prior to lumbar puncture, MRI is often
required to detect more subtle findings. MRI is
more sensitive, especially for cerebral spinal fluid
(CSF) involvement, leptomeningitis, empyema, ven-
triculitis, vasculitis, and infarctions (58, 61).
However, MRI is not as widely available and can
be logistically challenging to obtain in the acutely ill
patient.
Computed tomography (CT)
The standard pre- and post-contrast-enhanced CT
protocol of the head includes 5-mm-slice axial

DOI 10.1080/02841850701477728 # 2007 Taylor & Francis

876 B. R. Foerster et al.
images though the entire brain, including brain, soft
tissue, and bone windows. While contrast can aid in
the detection of small lesions and leptomeningeal
enhancement, it is not required to exclude findings
that may preclude lumbar puncture, such as a focal
mass. In many types of infection, CT findings can be
nonspecific or even normal, especially in early stages
(21).
Magnetic resonance imaging (MRI)
Conventional gadolinium-enhanced MRI of the
brain should include: 1) axial and sagittal pre- and
post-contrast T1-weighted images; 2) coronal post-
contrast T1-weighted images; 3) axial T2-weighted
and fluid-attenuated inversion recovery (FLAIR)-
weighted images; and 4) diffusion-weighted imaging
(DWI). MR spectroscopy (MRS) has also been
shown to be useful in the evaluation of infection,
since brain abscesses and certain pathogens are
characterized by specific resonances that are not
present in uninfected tissue. Table 1 summarizes MR
spectroscopy findings found in several pathogens.
Anatomic compartments
Bacterial meningitis
Meningitis, or inflammation of the meninges, is
among the most serious and morbid of all infec-
tions. A high index of suspicion, followed by rapid
diagnosis and treatment are essential to prevent
severe sequelae and death. Diagnosis requires an
abnormal number of white blood cells (WBC) in the
CSF. Classic clinical characteristics include head-
ache and neck stiffness, followed by mental status
changes. Microbiologic culture results from blood
or CSF remain the gold standard for diagnosis,
although this requires several days to complete.
In terms of basic pathophysiology, bacteria lodge
in the venous sinuses, creating inflammatory
changes that interfere with CSF drainage and
potentially causing hydrocephalus. Early in infec-
tion, the pia and arachnoid matter become con-
gested and hyperemic. Later, the leptomeninges
Table 1. Infectious MR spectroscopy findings
Infection
HSV Reduced N-acetyl aspartate, elevated choline, sometimes elevated lactate
TB granuloma Elevated lipid
HIV Decreased N-acetyl aspartate, increased choline and myo-inositol
Toxoplasmosis Elevated lactate and lipid
Mucormycosis Elevated lactate, decreased N-acetyl aspartate
Bacterial abscess Succinate, acetate, alanine, amino acids, and lactate peaks
Acta Radiol 2007 (8)
become thickened, and an inflammatory exudate
can cover the brain, particularly in the dependent
regions, such as the basal cisterns.
CT imaging is generally obtained prior to lumbar
puncture to exclude a mass lesion or other signs of
elevated intracranial pressure. In addition to helping
exclude other diagnoses, such a subarachnoid
hemorrhage, CT can also identify complications
from meningitis, as discussed below (58). Non-
contrast CT and MR imaging can be normal in
early cases of meningitis (14). Administration of
contrast may be helpful to detect diffuse meningeal
enhancement, with MRI being more sensitive than
CT (66); meningeal enhancement is not, however,
specific to the diagnosis of infectious meningitis and
can be seen in other diagnoses, such as leptome-
ningeal carcinomatosis (58). FLAIR MR imaging
can demonstrate high signal in the subarachnoid
spaces, which reflects high protein content in the
CSF (14, 30, 56). High signal in the subarachnoid
space is also nonspecific and can be seen with
leptomeningeal carcinomatosis and subarachnoid
hemorrhage. Fig. 1 demonstrates the CT and MRI
meningeal and subarachnoid findings that can be
seen in bacterial meningitis.
After excluding a mass lesion, the most important
role of neuroimaging is to identify potential
complications of meningitis, such as infarction,
hydrocephalus, ventriculitis, brain empyema, and
venous sinus thrombosis. Communicating hydro-
cephalus is a common complication, with the
inflammatory debris obstructing the flow and
reabsorption of CSF (58). Pyogenic ventriculitis is
a very severe complication of meningitis. Imaging
findings in this setting include periventricular high
FLAIR signal, ependymal enhancement, ventricular
debris, and fluid–fluid levels in the ventricles (11,
22). MRI is the method of choice for the detection
of venous thrombosis secondary to meningitis, with
a high signal intensity seen on spin-echo sequences
in the venous sinuses, reflecting thrombus forma-
tion. The subsequent venous thrombosis can lead to
infarctions that do not conform to well-defined
arterial territories and have accompanying hemor-
rhage (39).
Findings

Fig. 1. Bacterial meningitis. A. Pre-contrast CT is unremarkable. B. Post-contrast CT shows meningeal enhancement (black arrows). C.
Axial FLAIR MR imaging with high signal in the subarachnoid space (black arrows). D. Axial post-contrast T1-weighted MR image shows
extensive meningeal enhancement (black arrows).
Viral encephalitis
Encephalitis is distinguished from meningitis based
on the presence of abnormal brain function. Nuchal
rigidity is usually absent in encephalitis in contra-
distinction from meningitis. Patients can present
with focal neurologic deficits and seizures. Viral
encephalitis can be either primary or postinfectious.
In postinfectious encephalitis, an active virus cannot
be isolated and is secondary to an immune-mediated
process. MR is more sensitive than CT for the
detection of intracranial findings. The predominant
MR imaging characteristic of viral encephalitis is
parenchymal signal abnormality on T2-weighted
imaging.
Brain subdural empyema
Brain subdural empyemas are infected CSF collec-
tions in the potential space between the cranial dura
Imaging of Intracranial Infections 877
and arachnoid membranes that generally occur in
the setting of sinusitis or otitis media (3, 13). In
addition to fever, vomiting, and meningismus,
patients typically present with focal neurologic
signs, including hemiparesis. Since many of the
typical presenting symptoms overlap with those of
meningitis, the radiologist must diligently search for
extra-axial fluid collections, particularly in the
setting of paranasal sinus disease.
The pathogenesis includes phlebitic bridging veins
(from meningitis), hematogenous spread, and direct
extension of infection from adjacent structures.
Venous thrombosis or brain abscess develops in
more than 10% of patients. Delays in appropriate
antimicrobial therapy and surgical drainage result in
high mortality rates, as well as serious neurologic
sequelae in those who do survive.
In the early stages of the disease, small sub-
dural empyemas can be very subtle, particularly on
Acta Radiol 2007 (8)
878 B. R. Foerster et al.

non-contrast CT (74). Subdural empyemas do not
cross the midline, distinguishing them from epidural
abscesses. Subdural empyemas, like subdural hema-
tomas, also tend to have crescent-like configurations
rather than lentiform configurations.
On CT, subdural empyemas appear as iso-
attenuation to low-attenuation extra-axial collec-
tions compared to brain parenchyma with rim
enhancement (65, 68). MRI is the study of choice
for detection of subdural empyema, as MRI has a
higher sensitivity for detection of small subdural
fluid collections. On MRI, subdural empyemas have
iso-intense signal on T1-weighted imaging (T1WI),
likely secondary to increased protein content and
high signal on T2WI (33, 39, 47). MRI can also help
to differentiate subdural empyemas from other
extra-axial fluid collections, such as sterile effusions
(usually low signal on T1WI) and chronic subdural
hematomas (usually high signal on T1WI). A thin
rim of enhancement may be seen, which is usually
more prominent along the inner table of the skull.
Fig. 2 illustrates some of these MRI findings in a
patient with a subdural empyema. DWI can be
useful in distinguishing between empyemas that are
bright with low apparent diffusion coefficient
(ADC) values and subdural effusions, which have
low signal and ADC values similar to CSF (75).
Brain epidural abscess
Brain epidural abscesses are usually caused by the
contiguous spread of infection from adjacent
structures, such as the mastoids or paranasal
sinuses, into the epidural space located between
the dura and the overlying bone. Compared to
subdural empyema, epidural abscess presents in a

Fig. 2. Subdural empyema. A. Coronal T2-weighted MR image shows hyperintense crescent-shaped subdural collection. B. On axial FLAIR
imaging, the subdural collection has CSF intensity in the anterior portion and iso-intensity in the posterior portion. In addition, high signal is
present in the subarachnoid spaces (black arrowheads). Pre-contrast (C) and post-contrast (D) T1-weighted MR images show peripheral
enhancement (white arrows), as well as meningeal enhancement (black arrowheads).

Acta Radiol 2007 (8)


more subtle fashion, usually with several days of
fever along with mental status changes and neck
pain.
Epidural abscesses can cross the midline, helping
to distinguish them from subdural empyema. In
addition, the adjacent brain parenchyma tends to
appear normal, whereas abnormal signal in border-
ing brain tissue can be seen in subdural empyema.
On CT, epidural abscess typically appears as a low-
attenuation extra-axial mass. On MRI, epidural
abscesses have iso-signal on T1WI and high signal
on T2WI, with enhancement of the thickened dural
surface (14). Two epidural abscesses with lentiform
configuration are shown in Fig. 3.
Brain abscess
Brain abscesses are a focal, intracerebral infection
that begin with a localized region of cerebritis,
evolving into a discrete collection of pus surrounded
by a well-vascularized capsule. Such infections result
from either hematogenous dissemination or local
extension from an odontogenic, sinus, or otic
source. The most common organisms involved in
brain abscesses include Staphylococcus and
Streptococcus species.
Imaging features of a brain abscess depend on the
stage at the time of imaging, as well as the etiology
of infection (10). Brain abscess development can be
divided into four stages: 1) early cerebritis (1 to 4
days); 2) late cerebritis (4 to 10 days); 3) early
capsule formation (11 to 14 days); and 4) late
capsule formation (w14 days) (26). The majority of
abscesses demonstrate considerable surrounding
edema, which generally presents during the late
Fig. 3. Epidural abscess. A. Coronal post-contrast T1-weighted MR imaging shows a lentiform, peripherally enhancing, extra-axial fluid
collection adjacent to the inferior right frontal lobe (white arrow). B. Axial post-contrast T1-weighted MR imaging depicts a lentiform,
peripherally enhancing, extra-axial fluid collection adjacent to the left frontal lobe (white arrow). Additional intraparenchymal abscesses are
also shown (black arrows).
Imaging of Intracranial Infections 879
cerebritis or early capsule formation stage, second-
ary to mass effect. Hematogenous abscesses, which
can be seen in the setting of endocarditis, cardiac
shunts, or pulmonary vascular malformations, are
usually multiple, identified at the gray–white junc-
tion, and located in the middle cerebral artery
territory.
In the earlier phases, a non-contrast head CT may
show only low-attenuation abnormalities with mass
effect. In later phases, a complete peripheral ring
may be seen. On contrast CT, uniform ring
enhancement is virtually always present in later
phases. MRI findings also depend on the stage of
the infection. In the early phase, MRI can have low
T1WI signal and high T2WI signal with patchy
enhancement. In later phases, the low T1WI signal
becomes better demarcated, with high T2WI signal
both in the cavity and surrounding parenchyma.
The abscess cavity shows a hyperintense rim on non-
contrast T1-weighted images and a hypointense rim
on T2-weighted images (26). As on CT, MRI
usually demonstrates a ring of enhancement sur-
rounding the abscess (58). Fig. 4 demonstrates an
abscess centered in the right occipital lobe.
Abscesses tend to grow toward the white matter,
away from the better-vascularized grey matter, with
thinning of the medial wall (29). However, the
enhancing-ring sign is nonspecific and must be
evaluated in the context of the clinical history.
Thickness, irregularity, and nodularity of the
enhancing ring are suggestive of tumor (majority
of cases) or, possibly, fungal infection (26). As seen
in Fig. 5, DWI may show restricted diffusion (bright
signal) that helps to differentiate abscesses from
Acta Radiol 2007 (8)
880 B. R. Foerster et al.

Fig. 4. Intraparenchymal abscess. A. Axial FLAIR MR imaging shows a high-signal lesion (black arrow) with surrounding edema and mass
effect. Axial pre-contrast (B) and post-contrast (C) T1-weighted MR images display a low-signal intraparenchymal lesion with peripheral
post-contrast enhancement.

necrotic neoplasms, which are not usually restricted
(18, 25), although not all abscesses follow this rule.
Fungal and tuberculous abscesses may have ele-
vated diffusivity and low signal on DWI (40).
Several studies demonstrate the utility of DWI to
differentiate between necrotic or cystic lesions and
brain abscesses (18, 25). The latter demonstrates
increased signal on the trace images and reduced
ADC, while necrotic neoplasms demonstrate
decreased signal on the trace image and high ADC
values. Initially, DWI was thought to be helpful in
differentiation of toxoplasmosis from lymphoma.
One study proposed an ADC threshold of 0.8,
where ADC ratios less than 0.8 would favor
lymphoma over toxoplasmosis; however, the study
showed a significant overlap in ADC values in
toxoplasmosis and lymphoma (50). The authors
concluded that, in the majority of patients, ADC
ratios are not definitive in making the distinction
between toxoplasmosis and lymphoma. DWI has a
high sensitivity to detect early acute ischemic
changes in cortical and deep white matter that can
occur in the setting of infectious vasculitis.
Intracerebral abscesses are characterized by spe-
cific resonances on MRS that are not detected in
normal or sterile pathologic human tissue. MRS has
been shown to be specifically beneficial in differ-
entiating between brain abscesses and other cystic
lesions (9), which can be used to expedite imple-
mentation of the appropriate antimicrobial therapy.

Fig. 5. Intraparenchymal abscess with restricted diffusion. A. Coronal post-contrast T1-weighted MR image shows a peripherally enhancing,
low-signal lesion (black arrow) in the left cerebellum. B. Diffusion-weighted imaging shows the abscess has restricted diffusion with bright
signal (black arrow).

Acta Radiol 2007 (8)


Metabolic substances, such as succinate (2.4 ppm),
acetate (1.9 ppm), alanine (1.5 ppm), amino acids
(0.9 ppm), and lactate (1.3 ppm), can all be present
in untreated bacterial abscesses or soon after the
initiation of treatment (32).
Specific pathogens
After localizing the infectious process to a specific
compartment, there may be certain distinguishing
characteristics that may help suggest a specific
pathogen. Of course, lumbar puncture, in most
cases, clinches the diagnosis, but certain infections,
in particular, require specific laboratory testing, for
example, the polymerase chain reaction (PCR) test
for herpes simplex virus. In addition, the immune
status of the patient must be considered, which
affects the differential diagnosis. Table 2 sum-
marizes some of the typical findings for different
infections, with a discussion of the clinical and
imaging features.
Herpes simplex virus encephalitis
Herpes simplex virus (HSV) is a common cause of
encephalitis. Both type 1 and type 2 HSV produce
encephalitis, with varying epidemiology, depending
primarily on patient age. The virus most often
invades the brain after reactivation of latent virus
that resides in the trigeminal ganglion. Clinical
features that distinguish HSV disease from other
intracranial infections include the findings of red
blood cells in the CSF. The gold standard for
diagnosis is either PCR or viral culture that
demonstrates HSV in the CSF. Treatment with
antiviral therapy is generally initiated any time there
is a suggestion of possible viral meningitis and/or
Table 2. Typical imaging findings of specific pathogens
Infection Anatomic predilection
HSV Temporal/inferior frontal lobes
West Nile virus Parenchyma
TB Basal cisterns
Cystercercosis Parenchyma, occasionally ventricles
Coccidioidomycosis Meninges and parenchyma
HIV White matter—frontal and parietal
PML White matter—asymmetric occipital
and parietal
Toxoplasmosis Basal ganglia, corticomedullary
junction
Cryptococcus Subarachnoid spaces infiltrating
basal ganglia
Aspergillus Basal ganglia and thalami
Mucormycosis Invades along cavernous sinus
VR spaces: Virchow-Robin spaces.
Imaging of Intracranial Infections 881
encephalitis. Many radiological findings offer sup-
port for a presumptive diagnosis.
CT findings are usually subtle, with lower-
attenuation areas in the temporal lobe and insular
cortex (51). Mass effect on the lateral ventricle can
sometimes be present (63). Petechial hemorrhage is
possible and may be more easily detected on MRI
than CT. On MRI, there is high signal on T2WI,
with a predilection for the limbic system (temporal
lobes, cingulate gyri, inferior frontal lobes).
Enhancement varies, and mass effect may persist
(58). Fig. 6 shows the typical asymmetric involve-
ment of the frontal and temporal lobes. HSV type 2
infection, more commonly seen in neonates rather
than adults, can demonstrate subtle regions of low
attenuation on CT in various regions of the brain,
with subsequent enlargement and meningeal and
gyriform enhancement. Thalamic hemorrhage is
possible, and calcification can be seen several weeks
after disease onset (63).
Metabolic alterations have been demonstrated in
HSV using MR spectroscopy, and are characterized
by reduced N-acetyl aspartate (NAA), elevated
choline compounds (Cho), and, sometimes, eleva-
tion of lactate (Lac) with normalization over time.
These findings correspond to histopathological
findings and are thought to reflect neuronal or
axonal injury (NAA), demyelination (Cho, Lip),
and anaerobic metabolism, or the presence of
macrophages (Lac) (36, 48, 62). In general, the
usual microbiologic diagnostic tests offer reasonable
sensitivity and specificity; thus, the routine use of
MR spectroscopy is limited.
West Nile virus encephalitis
West Nile virus (WNV) encephalitis is a potentially
fatal viral intracranial infection acquired from
CT MRI
Subtle low density High T2WI signal, variable enhancement
Negative Restricted diffusion, high T2WI signal
Poor visualization High FLAIR signal, enhancement
Off-center, spherical Enhancing cysts with variable signal
calcifications characteristics
Negative Dilated VR spaces, poorly visualized cisterns
Negative High T2WI signal
Negative High T2WI signal
Low- to iso-attenuation High T2WI signal, edema, and ring
nodules enhancement
Normal Dilated VR spaces, non-enhancing cystic
lesions
Varying attenuation Low T2WI signal, variable enhancement
Paranasal disease High T2WI signal in frontal/temporal lobes
Acta Radiol 2007 (8)
882 B. R. Foerster et al.

Fig. 6. Herpes simplex virus encephalitis. A. Axial T2-weighted MR imaging depicts asymmetric increased signal (leftwright) in the
frontotemporal lobes (white arrows). B. Axial post-contrast T1-weighted MR imaging shows low T1 signal in the same regions and meningeal
enhancement (white arrows).

infected mosquitoes. This infection has been the
source of several epidemics across the United States
during the past several years, beginning in 1999 in
New York City. The incubation time period of
WNV is estimated to range from 3 to 14 days. One
in 150 people infected with WNV will develop
meningoencephalitis, with the immunocompro-
mised, elderly, and very young at highest risk.
Symptoms include fever, headache, neck stiffness,
mental status changes, muscle weakness, and flaccid
paralysis. Death can occasionally result (7, 42).
Imaging findings with WNV infection have
generally been unremarkable. MR imaging findings
can be normal. Increased T2WI signal has been
reported in the lobar gray and white matter, as well
as the cerebellum, basal ganglia, thalamus, and
brainstem. Isolated restricted diffusion can also be
seen (Fig. 7); these patients have a better prognosis
than patients with T2WI signal abnormalities.
T1WI signal abnormalities and enhancement are
rarely present (1, 45).
Lyme disease
Lyme disease, or neuroborrelia, is a multisystemic
disorder caused by the tick-borne spirochete Borrelia
burgdorferi. The disease is seen worldwide, and is
common in Europe. The underlying pathogenesis is

Fig. 7. West Nile virus. A. Diffusion-weighted imaging with increased signal (black arrows) in the bilateral thalami in a patient with proven
West Nile virus. B. Corresponding ADC map confirms restricted diffusion in the bilateral thalami (white arrows). (Images courtesy of Nafi
Aygun, MD)

Acta Radiol 2007 (8)


poorly understood, and different etiologies such as
vasculitis, immune complex mechanisms, and post-
viral demyelination have been suggested. About 10 to
15% of patients with Lyme disease develop neurolo-
gic complications with cranial nerve palsies and
peripheral neuropathies being common.
MRI findings may vary from being normal to the
presence of extensive superficial and/or deep white
matter lesions that can be more discrete or confluent
in appearance. Some lesions may enhance after
contrast administration (2, 59). The lesions are not
characteristic and cannot be differentiated from
those seen in acute disseminated encephalomyelitis
(ADEM) or multiple sclerosis. Diagnosis is based on
clinical findings, CSF laboratory testing, and
response to antibiotics.
Tuberculosis
Tuberculosis (TB) remains one of the most
common and important infections around the
world, with millions infected annually and thou-
sands dying directly of complications related to TB.
HIV infection and issues of drug resistance add to
the importance of TB infection. Central nervous
system (CNS) involvement is a serious manifesta-
tion of chronic infection and includes meningitis,
intracranial tuberculoma, and spinal tuberculous
arachnoiditis. The mortality rate of those cases
remains high for these complications despite
effective treatment. For CNS TB, simple micro-
biology remains the method of choice for diagnosis,
since the areas of greatest prevalence generally lack
resources for widespread imaging, especially
MRI.
Tubercles (scattered tuberculosis foci) develop in
the CNS or adjacent bony structures during the
bacillemia that follows primary TB infection or late
reactivation of TB elsewhere in the body. Meningitis
most commonly occurs after primary infection in
infants and young children. Among adults with
intracranial infection, this develops from chronic
reactivation, almost always in the setting of some
type of immune deficiency (aging, malnutrition,
HIV, medications, alcoholism).
Tuberculomas are intracranial lesions that
develop from deep-seated tubercles acquired during
bacillemia. This complication of TB shows a
variable clinical course ranging from complete
resolution to rupture with associated meningoence-
phalitis. Patients typically present with confusion,
fevers, headache, lethargy, and meningismus.
Symptoms can progress to stupor, coma, decere-
brate rigidity, cranial nerve palsy, and stroke.
On CT, the basal and sylvian cisterns can be
poorly visualized without contrast secondary to
Imaging of Intracranial Infections 883
dense exudates, which can subsequently enhance
with contrast (13). On MRI, the basal cisterns can
have high FLAIR signal and meningeal enhance-
ment secondary to proteinaceous exudate. The
cisterns can enhance, with enhancement extending
over cortical surfaces. Hydrocephalus, either com-
municating or obstructive, is a common finding in
tuberculous meningitis. Fig. 8 demonstrates some of
the CT and MRI findings seen in tuberculous
meningitis. Infarction secondary to panarteritis
can also be seen in CNS tuberculosis.
Tuberculomas can appear as low- or high-
attenuation nodules on CT (4). On CT, tuberculo-
mas can also present with a ‘‘target sign:’’ central
calcification or a central region of enhancement, as
well as a peripheral ring of enhancement (67).
Tuberculomas have a varied clinical course, ranging
from complete resolution to rupture with menin-
goencephalitis. Noncaseating tuberculomas have
high signal on T2WI, with peripheral nodular
enhancement. The patient’s immune response then
creates a granulomatous reaction, with central
caseation and a solid center, and eventually,
progression to a liquid center (52). Caseating
tuberculomas with a solid center have low to
intermediate signal on T1WI and central low signal
on T2WI, with ring-like enhancement (6, 49, 58).
Caseating granulomas with a liquid center have low
signal on T1WI and high signal on T2WI, and can
be indistinguishable from true tuberculous
abscesses (seen in immunocompromised patients)
or pyogenic abscesses (6). Fig. 9 shows a patient
with multiple caseating tuberculomas. MRS typi-
cally shows an elevated lipid peak in tuberculosis
granulomas. This can be helpful in the differential
diagnosis from neurocysticercosis (27).
Cysticercosis
Cysticercosis results from infection by Taenia
solium, the pork tapeworm. This parasite is
endemic in Mexico, South America, Asia, Africa,
and Eastern Europe, and is generally acquired by
ingestion of undercooked pork. The larvae develop
into the tapeworm in the gastrointestinal tract and
then enter the blood stream to spread to other
regions, including the CNS. Patients are typically
asymptomatic until the larvae die, which incites an
acute inflammatory reaction. The larvae progress
through different stages, with varying degrees of
edema and enhancement. While most cases of
neurocysticercosis are asymptomatic, seizures, other
focal neurologic signs, and increased intracranial
pressure can result.
Acta Radiol 2007 (8)
884 B. R. Foerster et al.

Fig. 8. Tuberculosis meningitis. A, B. Non-contrast CT shows dilated lateral ventricles with transependymal migration of CSF. The basilar
cisterns are not seen, and the fourth ventricle is patent (white arrow), indicating communicating hydrocephalus. C. Axial FLAIR MR imaging
shows increased subarachnoid signal (black arrows) seen with proteinaceous material. D. Sagittal post-contrast T1-weighted MR imaging
with enhancement of the basilar meninges (white arrow), as well as a ring-enhancing lesion.

The presence of calcifications, as well as non- Coccidioidomycosis

enhancing cysts and enhancing ring lesions
(Fig. 10), are typical findings in a patient with
appropriate exposure, and should suggest this
diagnosis (33). Characteristic calcifications are well
demonstrated on CT, and are slightly off-center and
spherical in shape. MRI can show multiple cysts,
with changing signal characteristics as the larvae
progress through different stages. In the early
vesicular stage, small non-enhancing cysts can be
seen, which are iso-intense to CSF on T1WI and
T2WI, with a mural nodule seen on T1WI. As the
larvae mature, a cyst wall becomes visible with
increasing T1WI signal within the cyst, relative to
CSF. Edema and ring-like enhancement can then be
visualized as the larvae die and incite an inflamma-
tory response. Eventually, the cysts decrease in size
and become calcified, and are best detected on CT.
Intraventricular cysticercal cysts occasionally
require surgical intervention if obstructive hydro-
cephalus occurs (31, 60, 73).
Coccidioidomycosis results from infection by the
dimorphic fungi of the genus Coccidioides (C.
immitis and C. posadasii). These are endemic fungi
present in the southwestern United States as well as
in Central and South America. The spore is inhaled,
setting up a primary pulmonary infection that can
then be hematogenously spread. While the clinical
manifestations are protean, meningitis is an impor-
tant complication that must be recognized and
treated aggressively. Without appropriate therapy
with systemic antifungals, the clinical course of
coccidioidal meningitis is fatal.
The initial head CT can be negative. Imaging
findings include dilated Virchow-Robin spaces,
poor visualization of basal and sylvian cisterns
secondary to dense exudates, and, occasionally,
hydrocephalus (20, 71). As seen in Fig. 11, enhan-
cing nodules that are nonspecific can also be seen.
Infarction can also be a common finding, which
may be secondary to direct invasion or vasospasm.

Acta Radiol 2007 (8)

 Imaging of Intracranial Infections 885

Fig. 9. Tuberculoma. A. Axial FLAIR MR image shows multiple central low-signal lesions with mild associated edema in the cerebellum. B.
Axial post-contrast T1-weighted MR image shows multiple ring-enhancing lesions with central low T1 signal.

Immunocompromised hosts
Intracranial infections are important manifestations
of disease in immunocompromised hosts, especially
in patients with HIV infection and those with
neutropenia related to hematologic malignancies
and/or bone marrow transplantation. Patients with
solid-organ transplantation are another group where
serious CNS infection is seen fairly often. Using
imaging to help narrow the differential diagnosis is
critical, as treatments differ for different infections.
In addition, therapies for many infections carry
significant toxicity, as well as drug interactions,
making prolonged empiric therapy impractical.
Human immunodeficiency virus (HIV)
Many HIV/AIDS-related intracranial manifesta-
tions seen frequently in the pre-retroviral era are
now rarely seen in areas of the world where patients
have access to highly active antiretroviral therapy
(HAART). Over time, HIV infection results in
subacute encephalitis and a syndrome of progressive
dementia, with cognitive, motor, and behavioral
abnormalities. Pathology shows microglial nodules
and multinucleated cells in the white matter. CT
imaging may show brain atrophy, but is typically
unremarkable. MRI findings include bilateral
patchy and confluent, moderately high T2WI
signal changes (Fig. 12) in the white matter,
predominantly affecting the frontal and parietal
lobes without contrast enhancement (8, 12, 70, 43).
Proton MR spectroscopy demonstrates metabolic
changes in HIV-infected brains. NAA reduction and
a low NAA/Cr can be seen in patients with early
disease, even before conventional MRI shows any
changes. Increases in Cho and myo-inositol (MI) are

Fig. 10. Cysticercosis. A. Non-contrast CT images show calcified lesions (white arrows), as well as fluid attenuation lesions, one with a
central calcification (black arrows). B. Contrast-enhanced CT shows no significant enhancement of the fluid attenuation lesions (black
arrows). (Images courtesy of Nafi Aygun, MD)

Acta Radiol 2007 (8)

886 B. R. Foerster et al.

Fig. 11. Coccidioidomycosis. A. Contrast-enhanced CT shows nodular meningeal enhancement in the right suprasellar region and adjacent
to the left sylvian fissure (white arrows) in a patient who had recently traveled to the southwestern United States. B. Coronal post-contrast
T1-weighted MR image shows nodular meningeal enhancement in the region of the left ambient cistern/choroid fissure (white arrow).

seen in virtually all cases of HIV infection in the
early stages, and a decrease in NAA occurs in HIV
encephalopathy (37, 38).
HIV patients can develop progressive multifocal
leukoencephalopathy (PML) caused by the JC virus.
The JC virus is a type of human polyomavirus that
primarily infects oligodendrocytes, resulting in a
demyelinating process. Unlike HIV encephalitis,
dementia is not the main feature in PML; rather,
patients characteristically present with rapidly
progressive focal neurologic deficits without signs
of increased intracranial pressure. Specific deficits
can include visual field deficits, ataxia, weakness,
and hemiparesis, as well as cognitive deficits.
Imaging findings include high T2WI signal in the
white matter that is typically asymmetric and
commonly affects the occipital and parietal lobes,
as depicted in Fig. 13. PML does not exhibit mass
effect and does not tend to show contrast enhance-
ment (12, 23, 28).
Toxoplasmosis results from Toxoplasma gondii,
an intracellular protozoan parasite. Reactivation of
latent infection is seen in advanced HIV, usually
when CD4 counts fall below 100 cells/ml. Typical
imaging findings include multiple abscess for-
mation with a propensity for the basal ganglia,
corticomedullary junction, white matter, and peri-
ventricular regions. CT can demonstrate areas of

Fig. 12. HIV encephalopathy. A, B. A 46-year-old, HIV-positive patient with clinical signs of dementia. Axial FLAIR MR imaging shows
severe atrophy and diffuse, increased signal abnormalities in the white matter without mass effect.

Acta Radiol 2007 (8)


low-attenuation or iso-attenuation nodules, both of
which can show varying degrees of enhancement
(24, 44). MRI features include multiple, high T2WI
signal lesions with vasogenic edema and ring or
nodular enhancement (19). Fig. 14 shows some of
the imaging findings seen in toxoplasmosis.
Clinically, toxoplasmosis and intracranial lym-
phoma are often indistinguishable. Newer imaging
techniques are sometimes useful in differentiating
between these processes. High-attenuation masses on
non-contrast CT, and periventricular lesions with
subependymal spread, suggest lymphoma. Thallium-
201 single photon emission computed tomography
(SPECT) has been shown to have increased uptake in
lymphoma, but not in toxoplasmosis; there is,
however, significant overlap, resulting in false
positives and false negatives (57). Fluoro-
deoxyglucose positron emission tomography
(18FDG-PET) can also be used to discriminate
between toxoplasmosis and lymphoma, as lym-
phoma exhibits increased 18FDG uptake (35). Some
studies suggest that MRS may help differentiate
between toxoplasmosis and lymphoma, whereas
other studies have suggested that MRS is less able
to discriminate between these two entities (15, 16, 54).
A previous report showed that lymphomas were
characterized by lower NAA/Cr and NAA/Cho
ratios, and by more frequent lipid signals, compared
to toxoplasmosis (55). Other studies have demon-
strated the presence of a lactate/lipid peak and the
absence of the other metabolites in toxoplasmosis,
while lymphoma shows increased choline levels
similar to those present in malignant tumors (15).
Fig. 13. Progressive multifocal leukoencephalopathy. Axial T2-weighted (A) and FLAIR MR (B) imaging shows asymmetric increased signal
in the bilateral occipital lobes without mass effect. C. Axial post-contrast T1-weighted MR image shows no associated pathologic contrast
enhancement.
Imaging of Intracranial Infections 887
Cryptococcus neoformans is an endemic fungus
that results in meningoencephalitis among patients
with AIDS. The diagnosis is made by staining the
organism from the CSF with India ink, detecting
cryptococcal antigen in the CSF or blood, or
growing the organism in culture. Clinically, the
patients present with elevated intracranial pressure
and often need repeat lumbar puncture in order to
improve clinical symptoms, such as pain and mental
status changes. Because the infection results in
relatively mild inflammatory changes, many patients
have normal contrast-enhanced CT scan (12). MRI
can also be normal.
Cryptococcomas can present as focal parenchy-
mal masses most commonly located in the basal
ganglia, thalamus, and midbrain. Leptomeningeal
nodules, with involvement of the choroid plexus and
spinal cord, can also be seen, although less
frequently (64). Some patients demonstrate mixed
findings, including dilated Virchow-Robin spaces,
focal masses, and leptomeningeal nodules (69).
Cryptococcosis can also present with basal ganglia
lesions (Fig. 15), with the differential diagnosis
including toxoplasmosis and lymphoma, which
more typically show enhancement relative to cryp-
tococcal infection (28).
Other immunocompromised hosts
Immunocompromised hosts, including those with
solid-organ transplants or neutropenia related to
hematologic malignancy and/or bone marrow
transplantation, can develop serious fungal
Acta Radiol 2007 (8)
888 B. R. Foerster et al.

Fig. 14. Toxoplasmosis. A. Non-contrast CT shows a low-attenuation lesion with a subtle peripheral ring in the left basal ganglia/thalamus
(black arrow). B. Axial FLAIR MR imaging re-demonstrates the lesion (black arrow) with surrounding edema. Axial pre-contrast (C) and
post-contrast (D) T1-weighted MR imaging demonstrates a low-attenuation lesion (black arrow) with peripheral enhancement.

infections of the CNS. Generally, these infections
begin in the respiratory tract or sinuses. Intracranial
involvement in this setting usually portends a poor
prognosis. While biopsy, along with culture, is
needed to definitively identify most infecting organ-
isms, imaging modalities offer a means to define the
extent of involvement and to track progression.
Imaging, along with clinical variables, helps suggest
the overall prognosis and is essential for medical
decision-making.
The Aspergillus species is an important pathogen
that can produce meningitis and meningoencepha-
litis among highly compromised hosts. Fungal
organisms gain entry to the CNS, either via direct
extension from the sinuses or, less commonly,
hematogenously. Patients may present with confu-
sion, fevers, headache, lethargy, and meningismus,
progressing to stupor, coma, decerebrate rigidity,
cranial nerve palsy, and stroke. Aspergillus invades
the vasculature walls, which can result in vascular
thrombosis, hemorrhage, infarctions, and propaga-
tion of the infection in the infarcted tissue.
Aspergillus has a predilection for the basal ganglia,
thalami, and corpus callosum (17). On CT, the
abnormalities are usually subtle, with varying
densities and minimal mass effect, poor contrast
enhancement, and no ring formation (41). On MRI,
the signs are nonspecific and include high-signal
lesions on T2WI and, at times, on T1WI, with
variable enhancement (5). However, involvement of
the basal ganglia, thalami, corpus callosum, and
other perforator artery territories are suggestive of
aspergillus infection in the immunocompromised
patient. Enhancing soft tissue in the sinuses can

Acta Radiol 2007 (8)


Fig. 15. Cryptococcus. Axial T2-weighted MR image shows patchy and more focal high T2 signal abnormality present in the bilateral basal
ganglia.
offer further support for the presence of an
intracranial aspergillus infection. MRI findings
from a patient with aspergillosis are shown in
Fig. 16.
Mucormycosis
Rhinocerebral mucormycosis is a devastating infec-
tion that results from zygomycetes. Such infection
carries a very grim prognosis and results invariably
in patients with altered cellular immunity, including
those with diabetes mellitus and hematologic
malignancies. Mucormycosis spreads from the
paranasal sinuses to the skull base or cribiform
plate into the orbits, frontal lobes, and basal
ganglia. Infection progresses rapidly, spreading
along vascular structures and often involving the
cavernous sinus. Infarction is seen frequently in
advanced disease.
Clinical symptoms associated with mucormycosis
include facial pain, bloody nasal discharge, chemo-
sis, exophthalmos, and cranial nerve palsy, progres-
sing rapidly to stroke, encephalitis, and death.
Orbital extension from the ethmoid sinuses
Imaging of Intracranial Infections 889
produces proptosis, chemosis, superior ophthalmic
vein thrombosis with extension, and subsequent
thrombosis of the cavernous sinus. The diagnosis of
mucormycosis must be made clinically. The pro-
gression of infection is often so rapid that imaging
does not offer much beyond demonstrating the
extent of involvement. Intracranial involvement is
almost invariably fatal in this infection. CT imaging
can demonstrate a rim of soft tissue along the walls
of the paranasal sinuses. On MRI, low intensity of
the sinuses may be present on T1WI and T2WI.
Intracranially, MRI findings can include high T2WI
signal in the basal portions of the frontal and
temporal lobes with mild mass effect; this likely
represents a combination of inflammation and
infarction secondary to vascular invasion (34, 46,
72). Fig. 17 shows a patient with intracranial
extension of paranasal sinus mucor.
Spectroscopy has also been studied for the
evaluation of mucor. In a previously published case
report, proton MRS showed markedly elevated
lactate, depleted NAA, and metabolite resonances
attributable to succinate and acetate. The spectro-
scopy profile is essentially similar to that of bacterial
Acta Radiol 2007 (8)
890 B. R. Foerster et al.

Fig. 16. Aspergillosis. A. Axial FLAIR MR imaging shows high-signal lesions in the bilateral white matter (black arrows). Axial pre-contrast
(B) and post-contrast (C) T1-weighted MR imaging demonstrates several low-attenuation lesions with peripheral enhancement (black
arrows).

Fig. 17. Mucormycosis. A. Coronal non-contrast sinus CT shows extensive opacification of the right paranasal sinuses, with destruction of
the nasal septum and cribiform plate (white arrows). B. Coronal post-contrast T1-weighted MR image shows enhancing, infiltrating lesion in
the right cavernous sinus (white arrowhead). C. Diffusion-weighted image shows restricted diffusion of the bilateral frontal lobes and right
basal ganglia. D. Magnetic resonance arteriography shows asymmetric decreased caliber of the cavernous portion of the right internal carotid
artery compared to the left internal carotid artery (black arrows). (Images courtesy of Stephen Gebarski, MD)

Acta Radiol 2007 (8)


abscess, but without the commonly seen resonances
of the amino acids valine, leucine, and isoleucine
(53).
Conclusion
The radiologist plays a central role in the diagnosis
and management of patients with intracranial
infections. Different imaging modalities offer dif-
ferent advantages in the diagnostic paradigm. CT is
helpful in rapidly excluding a focal mass lesion in
the acute setting, prior to lumbar puncture. MRI is
much more sensitive for defining the extent of
infection, and for identifying infection-related com-
plications, such as infected subdural effusions and
venous sinus thrombosis. Many investigators have
demonstrated the value of MR spectroscopy to aid
in the differentiation of abscesses and neoplasms. A
thorough understanding of the imaging patterns
associated with common intracranial infections
allows the radiologist to help narrow the differential
diagnosis and facilitate timely implementation of
appropriate therapies.
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