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Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.
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Intracranial Infection andInflammation
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TchoyosonLim andMajdaM.Thurnher
6
Abstract
Although uncommon compared to traumatic and cerebro-
vascular disease, radiologists should recognize the typical
imaging features of meningitis, abscess, and encephalitis;
and be aware of autoimmune mimics. DWI, SWI, and
vessel wall imaging are useful advanced MRI techniques
for problem-solving.
Keywords
Meningitis · Abscess · Encephalitis · Virus · Bacteria
Tuberculosis · HIV · Parasite · Autoimmune encephalitis
Learning Objectives
• To review basic cranial MRI features of common
CNS infections.
• To recognize typical imaging patterns of meningitis, abscess, and encephalitis.
• To apply imaging features that may differentiate
different infections and non-infectious mimics.
• To identify imaging ndings in autoimmune brain
diseases.
• To evaluate the role of radiologists and the importance of multidisciplinary teams.
T. Lim (*)
Neuroradiology, Radiological Sciences Academic Clinical
Program, National Neuroscience Institute, Duke-NUS Medical
School, Singapore, Singapore
e-mail: Tchoyoson.lim@singhealth.com.sg
M. M. Thurnher
Section of Neuroradiology and Musculoskeletal Radiology,
Department of Biomedical Imaging and Image-guided Therapy,
University Hospital Vienna, Vienna, Austria
e-mail: majda.thurnher@meduniwien.ac.at
Key Points
• DWI, SWI, and vessel wall imaging are useful
advanced pulse sequences, whilst MR perfusion
and spectroscopy may be used judiciously for
problem-solving.
• Meningeal enhancement and subarachnoid pus collections are typical of infectious meningitis.
• Ring enhancing lesions with restricted diffusion on
DWI are characteristic of untreated pyogenic
abscess.
• Hippocampal swelling and increased signal may be
caused by herpes simplex virus type 1 encephalitis
or LGI1-antibody encephalitis.
6.1 Approach toCNS Infection
CNS infections are uncommon diseases (compared to
trauma, cerebrovascular disease) in the casemix of a typical
modern metropolitan hospital or university radiology practice. Radiologists infrequently receive imaging requests to
rule out or to assess complications in patients with the classic
clinical triad of fever, nuchal rigidity, and altered mental status characteristic of meningism. Often, CNS infection is an
unexpected differential diagnosis or missed diagnosis in
unsuspected patients being investigated for cortical swelling,
abnormal ring, or meningeal enhancement, where the clinical diagnosis is stroke, tumour, or other diseases. Finally, in
some instances, typical imaging features characteristic of
CNS infection may be caused by unexpected non-infectious
diseases, such as LGI1 autoimmune encephalitis being mistaken for herpes simplex virus type 1 (HSV-1) encephalitis.
Hence, radiologists should have a good grasp of typical
features and differential diagnosis of CNS infections;
although infections can be classied by taxonomy of causative organism (viral, bacterial, fungal), this chapter will
© The Author(s) 2024
J. Hodler et al. (eds.), Diseases of the Brain, Head and Neck, Spine 2024-2027, IDKD Springer Series,
https://doi.org/10.1007/978-3-031-50675-8_6
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T. Lim and M. M. Thurnher
focus on imaging patterns on CT and MRI.This broad sweep
is not exhaustive and includes a section on inammatory diseases, especially as they pertain to differential diagnosis of
infections. With the worldwide trends of warming temperatures, travel and migration, outbreaks of pandemic COVID- 19
and other organisms, we are reminded of the importance of
this topic.
6.2 MRI Technique
CT yields limited information, and MRI is more sensitive
and specic for features of CNS infection. Contrast injection
should be routine in suspected infection if there are no contraindications, and DWI (with high lesion to normal contrast
and sensitivity) can be routinely added to conventional T1-,
T2-weighted images, and FLAIR. High-resolution, thinsection 3D sequences such as constructive interference in
steady state (CISS), fast imaging employing steady state
acquisition (FIESTA), and FLAIR images allow visualization of small structures such as parasitic scolex, cranial
nerves, and capsule wall details. MR angiography and
venography can be included to assess ischemic and
thrombotic complications. More recently, during the COVID19 pandemic, susceptibility-weighted imaging (SWI) has
been helpful to detect tiny focal microhaemorrhages.
Advanced MRI techniques including perfusion-weighted
images (using DSC or ASL techniques) and MR spectroscopy may be helpful in problem-solving if used judiciously,
especially since patients that are recalled after an initially
ambiguous study can be hemodynamically unstable and
require sedation or monitoring in the MRI suite. Point-ofcare MRI using low-eld scanners has shown promise.
Radionuclide studies and PET have not been widely used in
clinical practice although 18F-uorodeoxyglucose (18F-FDG)
typically reveals that infections generally have lower metabolic activity than tumours.
(fungi cause very high opening pressure but normal glucose), and viruses usually cause lymphocytic pleocytosis
and normal glucose. Acute lymphocytic meningitis of
viral origin is usually benign and self-limited. Eosinophilic
meningitis, dened by >10% eosinophil or >10 eosinophils per cubic millimetre of CSF, is typically a marker of
helminthic parasite disease. Often, CT request to rule out
raised intracranial pressure before an LP is the result of an
abundance of caution, but this can also lead to a false
sense of security.
CT typically shows diffuse cereal swelling, effaced subarachnoid spaces (especially basal cisterns), and dilated ventricles. Unenhanced MRI more sensitively shows the
corresponding abnormal signal from elevated protein in
infectious exudates as increased signal on FLAIR images or
DWI (Fig. 6.1) [1, 2]. Sometimes, DWI may be the only
images that detect subtle, tiny amounts of pus within the subarachnoid space and ventricles.
Gadolinium contrast extravasation into the subarachnoid
space due to increased permeability of the blood–brain barrier, resulting in characteristic leptomeningeal enhancement
in meningitis. This is visible particularly in the depth of cerebral sulci and cisterns, sometimes extending to the larger cranial nerve surfaces as either thin, linear serpentine
enhancement (over cerebral convexity in typical viral/pyogenic bacterial meningitis) or thicker, irregular, nodular
enhancement (often involving the basilar cisterns in tuberculous meningitis). The difference between leptomeningeal
(extending into the sulcal depths and lling the subarachnoid
spaces and cisterns) and pachymeningeal (thick “felt-tip
pen” enhancement limited to the outer, dural surface either
focally or diffusely) features can be seen in Fig. 6.2.
Leptomeningeal enhancement is often better demonstrated
using post-contrast 3D T2-FLAIR than conventional
T1-weighted sequences (Fig.6.3) [3].
6.3.2 Dierential Diagnosis ofMeningitis
6.3 Meningitis
6.3.1 Imaging Features ofMeningitis
In patients with suspected meningitis, CSF analysis after
lumbar puncture (LP) is necessary to diagnose the responsible pathogen(s) and determine antimicrobial sensitivity
for bacterial meningitis; imaging is adjunctive, but does
not replace LP.Typical pyogenic bacteria result in neutrophilic pleocytosis, elevated protein, and low glucose
On MRI, with its multiple different tissue characterisation on
different pulse sequences, differential diagnosis can sometimes be difcult. Mimics of leptomeningitis include subarachnoid haemorrhage (which typically shows high signal
on T1-weighted images and low signal on gradient-recalled
echo/SWI), leptomeningeal carcinomatosis, administration
of oxygen and drugs. Differentials for pachymeningeal
enhancement include post-surgery and post-LP states, spontaneous intracranial hypotension, non-infectious granulomatous diseases, and tumours.
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Fig. 6.1 Diffusion-weighted MRI abnormalities in meningitis.
(Reprinted with permission from Thurnher, M.M., Sundgren, P.C.
(2020). Intracranial Infection and Inammation. In: Hodler, J., Kubik-
Key Points
• Post-contrast 3D T2-FLAIR is very sensitive for
infectious leptomeningitis.
• Leptomeningitis and pachymeningitis show different enhancement patterns.
• Hyperintensity on DWI is sensitive to tiny amounts
of pus and is characteristic in untreated pyogenic
abscess.
• Radiologists should search for causes and complications of meningitis; MRA and MRV may be
helpful.
6.3.3 Causes andComplications
ofMeningitis
On MRI, features of causes and complications of meningitis
should be sought. Of the main routes of infectious spread,
direct inoculation from traumatic or iatrogenic injury/surgical interventions is often visible. Local extension into the
cranium from adjacent sinusitis, otitis media/mastoiditis,
Huch, R., von Schulthess, G. (eds) Diseases of the Brain, Head and
Neck, Spine 2020–2023. IDKD Springer Series. Springer, Cham)
dental, head and neck infection should be included in the
radiological search pattern, as well as along cranial nerves.
However, the most common source of spread is via hematogenous route, and a high index of suspicion is needed in
patients with a clinical history of immunosuppression, diabetes, alcoholism, congenital heart disease, pulmonary
arteriovenous malformation or abscess, intravenous drug
use, or bacterial endocarditis.
The most important complication of meningitis is cerebral abscess (see Sect. 6.4.1), which represents an important
change in management often resulting in surgical referral for
drainage for large lesions. Extra-axial uid collections may
also be seen, representing sterile subdural effusions or purulent empyema (which demonstrate diffusion restriction like
cerebral abscess); empyema can be life-threatening and
should be surgically drained. Hydrocephalus can result from
disturbed CSF resorption or mass lesions compressing normal drainage pathways and if severe, can lead to brain herniation; this is especially important in tuberculous meningitis.
Vascular complications including venous sinus thrombosis,
vasculitic occlusion, and subsequent infarction, typically
result from syphilis, tuberculosis, and angioinvasive aspergillosis (see Sect. 6.6.3).
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T. Lim and M. M. Thurnher
Fig. 6.2 Patterns of meningeal contrast enhancement (white outlines).
Normal meninges (a). Diffuse pachymeningeal (b). Diffuse leptomeningeal (c) and localized leptomeningeal (d). Gyriform cortical (e).
Ependymal (f). (Reprinted with permission from Duong MT, Rudie JD,
Mohan S.Neuroimaging Patterns of Intracranial Infections: Meningitis,
Cerebritis, and Their Complications. Neuroimaging Clin N Am. 2023
Feb;33(1):11–41)
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Fig. 6.3 Superiority of post-contrast 3D T2-FLAIR (top row) to postcontrast T1WI (bottom row) in the detection of leptomeningeal enhancement. (Reprinted with permission from Thurnher, M.M., Sundgren, P.C.
6.4 Brain Abscess
6.4.1 MRI Features ofDiagnosis ofBrain
Abscess
Mature pyogenic brain abscesses have a characteristic MRI
appearance. There is typically central high signal with a
smooth, thin, circumferential low-signal capsule on
T2-weighted images (central low signal with high-signal rim
on T1-weighted images), and prominent ring-like enhancement with surrounding white matter T2 prolongation from
vasogenic oedema. If cerebral abscesses are introduced via
hematogenous spread, they are typically located at the grey–
white junction within middle cerebral artery territories bilaterally. Although abscess is preceded by cerebritis (poorly
dened brain inammation with increased vascular permeability but without capsular neovascularization or angiogenesis), this is rarely detected by imaging studies. Left untreated,
a vascularized, collagenous capsule forms and is accompa-
(2020). Intracranial Infection and Inammation. In: Hodler, J., KubikHuch, R., von Schulthess, G. (eds) Diseases of the Brain, Head and Neck,
Spine 2020–2023. IDKD Springer Series. Springer, Cham)
nied by a central abscess cavity of purulent exudate and surrounding vasogenic oedema.
On DWI, diffusion restriction is the hallmark feature of
untreated pyogenic abscesses: proteinaceous, purulent debris
comprising bacterial and inammatory exudate have high
viscosity, showing high signal on DWI and low signal on
ADC maps (this feature can be useful to distinguish abscess
from necrotic high-grade glioma, which typically do not
show diffusion restriction) (Fig.6.4). This feature becomes
less prominent after antibiotic treatment. Usually, the medial
or ventricular wall is thinner than the lateral wall due to
poorer blood supply, and predisposes to rupture into the ventricle, causing ventriculitis. SWI sometimes shows the “dual
rim sign” of concentric circles (hypointense outer layer and
hyperintense inner layer), which may be incomplete.
MR spectroscopic prole of pyogenic abscess includes
peaks representing branched chain amino acids valine, leucine,
isoleucine (at 0.9ppm), and succinate (2.4ppm). In anaerobic
abscesses, elevated acetate (1.9ppm) is often seen (Fig.6.5).
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T. Lim and M. M. Thurnher
Fig. 6.4 DWI in cerebral abscess. Post-contrast T1-weighted and T2-weighted images are similar in a patient with cerebral abscess (top row) and
another patient with metastatic cancer (bottom row). On DWI, high signal in the abscess cavity is distinguishable from low signal in metastasis
6.4.2 Dierential Diagnosis ofRing
Enhancing Lesions
Problem-solving in the assessment of ring enhancing lesions
can benet from history (immunocompromise, endemic/
travel history, primary cancer), physical examination (fever),
imaging features (incomplete ring, multiplicity, shape, and
location), and advanced MRI techniques. Although MR
spectroscopy can show elevated choline (at 3.2 pm) in neoplasms, necrotic tumours with predominant lipid and lactate
peaks (at 1.3 ppm) may not be easily distinguishable.
Decreased perfusion is usually seen in the central cavity and
capsule; rarely, high rCBV may be seen in the vascularized
abscess capsule, mimicking neoplasia; especially in granulomatous disease, which can mimic neoplasia on advanced
MRI techniques. A combined approach with multidisciplinary team conference would be most helpful for management decision-making.
Key Points
• Differential diagnosis of ring enhancing lesions.
– Pyogenic abscess.
– Tuberculoma/tuberculous abscess.
– Fungal abscess.
– Toxoplasmosis.
– Parasites (especially neurocysticercosis, see
Sect. 6.5.1).
– Metastatic tumour.
– Primary glioma, lymphoma.
– Subacute infarct.
– Contusion/hematoma.
– Demyelination.
bc
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a
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d
e
f
Fig. 6.5 Advanced MRI in cerebral abscess. Post-contrast T1-weighted
image shows typical ring enhancement (a), with increased signal on
DWI (b) and decreased ADC (c) and mixed increased signal on
T2-weighted images (d). Perfusion MRI (blue in e) shows decreased
relative cerebral volume in both the cavity and walls. MR spectroscopy
(f) with long echo time of 144ms shows low choline (Cho, 3.2ppm),
creatine (Cr, 3.0ppm), N-acetyl aspartate (NAA, 2.0ppm), and a large
inverted W lactate (Lac, 1.4ppm) and lipid (0.9ppm) peaks. Note the
acetate peak (arrow) at 1.9 ppm which is the anaerobic breakdown
product of NAA
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6.5 Parasitic Diseases
Although unicellular (amoeba, toxoplasmosis, see Sect.
6.6.1) and multicellular (helminths such as schistosomiasis)
parasites are uncommon in the developed world, these are
important diseases in endemic areas and can be seen with
increasing frequency due to travel and migration. Common
features of helminthic infection include eosinophilia and differing features according to parasite life cycle.
6.5.1 Neurocysticercosis
Cysticercal infection is endemic in many parts of Asia,
Africa, and Central/South America, and CNS cysticercosis is
Fig. 6.6 Neurocysticercosis:
Post-contrast T1-weighted
images shows a ring
enhancing left temporal lobe
vesicular-colloidal cyst with
surrounding vasogenic
oedema (arrow). A second,
non-enhancing vesicular
lesion without oedema is seen
in the right basal ganglia
(arrowhead)
the commonest cause of seizures and CSF eosinophilia
worldwide. Four classic stages can be seen; the vesicular
stage typically shows a non-enhancing cyst which is isosignal to CSF, with a T2 hypointense, FLAIR hyperintense,
and enhancing scolex visible on high-resolution thin-section
3D MRI FLAIR/CISS sequences. The vesicular-colloidal
stage (Fig.6.6) results in complex increased cyst signal on
T1-weighted and FLAIR images with ring enhancement and
surrounding oedema (often mimicking abscess or metastasis,
unless concomitant non-enhancing vesicular cysts or nonenhancing calcic nodular stages are recognized during
visual search). The cyst becomes smaller during the granular
nodular stages with signal changes from calcication; the
nal non-enhancing calcic nodular stage shows mineralization without surrounding oedema (Fig.6.7).
Fig. 6.7 Unenhanced CT
shows an isodense left frontal
lobe lesion surrounded by
vasogenic oedema. Multiple
concomitant chronic calcic
nodular lesions are seen in the
rest of the brain, consistent
with neurocysticercosis
infection in different stages
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6.6 HIV Infection andSpecic Organisms
HIV positive patients can present with a wide range of complications, including opportunistic infections, lymphoma,
progressive multifocal leukoencephalopathy (PML, see Sect.
6.7.3), CD8 encephalitis, and immune reconstitution inam-
matory syndrome (IRIS) [4]. IRIS is caused by an intense,
dysregulated inammatory immune response in situations
with a combination of successful antiretroviral therapy
(ART), improving CD4 and decreasing viral load. There is
paradoxical worsening of clinical and imaging features,
accompanied by orid enhancement on MRI. The clinical
course of IRIS is usually self-limiting, but radiologists
should rst rule out new opportunistic infection, drug toxicity, and other complications.
Key Points
• Patients living with HIV can present with opportunistic infections, primary HIV infection, inammatory reactions, and treatment effects.
• Opportunistic infectious agents include toxoplasma,
JC virus (PML), cryptococcus, cytomegalovirus,
tuberculosis, and varicella zoster virus.
• Primary HIV infection can result in acute meningoencephalitis, acute inammatory demyelinating
polyneuropathy (AIDP), chronic inammatory
demyelinating polyneuropathy (CIDP), HIVassociated neurocognitive disorder (HAND), myelitis, and cerebrovascular disease.
6.6.1 Toxoplasmosis
Toxoplasmosis is the most frequent opportunistic infection
in patients with HIV. MRI typically shows multifocal
enhancing nodules in the basal ganglia or frontoparietal
regions with vasogenic oedema and sometimes haemorrhage. Although the “eccentric target sign” has high specicity (but can also be seen in tuberculoma and metastasis),
unfortunately it is not very sensitive (Fig.6.8).
6.6.2 Aspergillosis
Immunocompromised patients (not only in HIV infection
but also in transplantation etc) are prone to angioinvasive
aspergillosis, which can occlude the perforating arteries and
result in basal ganglia, thalamic or brainstem infarction,
sometimes with blood products.
6.6.3 Tuberculosis
CNS tuberculosis (TB) can affect patients with and without
HIV infection: TB remains one of the major causes of mortality and morbidity worldwide and is an especially important health threat for people living with HIV.TB meningitis
results in especially orid enhancement with infection especially often involving the basilar cisterns (Fig.6.9) and can
be associated with dural thickening and enhancement from
concomitant pachymeningitis (TB is more common than
syphilis or Lyme disease in causing both leptomeningeal and
pachymeningeal infection). TB vasculitis can occlude the
Fig. 6.8 Toxoplasmosis:
Post-contrast T1-weighted
images showing characteristic
eccentric target sign of
enhancement
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