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Infections of
the Brain and
Meninges
Mohamed Samir
Assist. LecturerEpisode 2 “The Good, The Bad and The Infectious”
Infections
Congenital / Neonatal Acquired
• Cytomegalovirus.
• Toxoplasmosis.
• Rubella.
• Herpes Simplex.
• HIV Infection.
• Enteroviruses.
• Meningitis.
• Pyogenic
Parenchymal
Infections.
• Encephalitis.
• TB & Fungal
Infections.
• Parasitic Infections.
Acquired:
♣ Non-Specific:
1- Meningitis.
2- Pyogenic Parenchymal Infections.
3- Encephalitis.
♣ Specific:
1- TB & Fungal Infections.
2- Parasitic Infections.
MeningitisMeningitis
• The most common form of CNS
infections.
• 3 General Categories.
1- Acute Pyogenic Meningitis.
2- Lymphocytic Meningitis.
3- Chronic Meningitis.
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Bacteria:
Acute Pyogenic Meningitis
• Neonates….
– Group B Streptococcus species (49%)
– Escherichia coli (18%)
• Children and infants ….
– Haemophilus influenzae (40-60%)
– Neisseria meningitidis (25-40%)
• Adults ….
– S. pneumoniae (30-50%)
– N. meningitidis (10-35%)
– Staphylococcus species (5-15%)
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Acute Pyogenic Meningitis
Routes of Infection:
1. Hematogenous spread.
2. Local extension from contiguous extracerebral
infection
3. Direct implantation of bacteria into the
meninges.
Clinical:
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Acute Pyogenic Meningitis
Classic triad (85% of patients with bacterial
meningitis)
• Fever
• Headache
• Stiff neck
Complications:
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Acute Pyogenic Meningitis
1. Hydrocephalus.
2. Ventriculitis.
3. Subdural Effusion.
4. Empyema.
5. Infarction.
6. Parenchymal abscess.
• Viral (Enteroviruses 50-80%).
• Mostly benign and self-limited.
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Acute Lymphocytic Meningitis
Imaging of Acute Meningitis
The most important role of CT in imaging
patients with meningitis is to evaluate for:
1.Contraindications to a lumbar puncture.
2.Complications of meningitis.
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CT:
Acute Meningitis
• NECT:
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CT:
 Normal (>50% of patients).
 Mild ventricular dilatation.
 Cerebral edema.
 Focal low-attenuating lesions.
 Effacement of sulci.
 Obliteration of the basal
cisterns.
Acute Meningitis
• CECT:
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CT:
Acute Meningitis
• Diffuse meningeal enhancement.
• Cerebritis.
• Abscess.
• Subdural fluid collection.
• Subdural empyema
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CT:
Acute Meningitis
CT scans may reveal the cause of
meningeal infection
Negative results on CT imaging
do not exclude the presence of
acute meningitis.
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MRI:
Acute Meningitis
The most sensitive modality due to increased
contrast resolution, and the absence of artifact
caused by bone.
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MRI:
Acute Meningitis
Obliterated cisterns and the distention of the
subarachnoid space with widening of the
interhemispheric fissure
T1WI:
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MRI:
Acute Meningitis
Cortical hyperintensities that
are believed to represent
edema
T2WI:
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MRI:
Acute Meningitis
•Diffuse enhancement of the
subarachnoid space.
T1WI+GAD:
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MRI:
Acute Meningitis
Empyema
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MRI:
Acute Meningitis
Cerebritis
Find 3
Differences
Parenchymal InfectionsParenchymal Infections
1. Bacterial (Pyogenic).
2. Viral.
Pyogenic Parenchymal InfectionsPyogenic Parenchymal Infections
Cerebritis.
Abscess.
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Pathology:
Four stages have been described in abscess
evolution:
1. Early cerebritis.
2. Late cerebritis.
3. Early capsule formation.
4. Late capsule formation.
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CT:
• CT manifestations of an intracranial
abscess depend on the stage of the
abscess formation
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CT:
• During early cerebritis, nonenhanced CT
scans may demonstrate normal findings or
may show only poorly marginated subcortical
hypodense areas.
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CT:
• Contrast-enhanced CT studies demonstrate
an ill-defined contrast-enhancing area
within the edematous region
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CT:
• During the early stage of a formed
abscess, the lesion coalesces, with an
irregular enhancing rim that
surrounds a central low-attenuating
area.
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CT:
• Scans obtained with a time delay
following contrast enhancement in
cerebritis may show contrast "filling
in" the central low-attenuating
region. A formed abscess will not "fill
in" the central portion of the abscess.
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CT:
• A relatively thin well-delineated capsule
marks the final stage of a fully formed
abscess.
• Peripheral edema results in considerable
mass effect with sulcal obliteration
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MRI:
1. Early cerebritis stage
The early cerebritis stage presents as an ill-defined hyperintense
zone that can be noted on T2-weighted imaging.
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MRI:
1. Early cerebritis stage
• Contrast-enhanced T1-weighted studies
demonstrate poorly delineated enhancing
areas within the isointense-to-mildly
hypointense edematous region
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MRI:
2. Late cerebritis stage
• During the late cerebritis stage, the central
necrotic area is hyperintense to brain tissue on
FLAIR and T2-weighted sequences.
• The thick somewhat irregularly marginated rim
appears isointense to mildly hyperintense on T1-
weighted images and isointense to relatively
hypointense on FLAIR and T2-weighted scans.
• The rim enhances intensely.
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MRI:
3 & 4- Early and late capsule stages
• The collagenous abscess capsule is visible prior to contrast
as a comparatively thin-walled isointense-to-slightly
hyperintense ring that becomes hypointense on T2-
weighted MRIs.
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MRI:
Diffusion-weighted MR may be useful in
differentiating abscess from necrotic tumor.
Diffusion-weighted echo planar images
demonstrate an abscess as a high signal
intensity with a corresponding reduction
in the apparent diffusion coefficient. The
brightness on DWI is related to the
cellularity and viscosity of the contents
within the abscess cavity.
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MRI:
MR spectroscopy is useful in differentiating ringlike
enhanced lesions that cannot be diagnosed correctly
using enhanced MRI alone. MR spectroscopy can help to
specifically differentiate tumor, radiation necrosis, or
abscess by identifying their different spectral profiles.
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MRI:
• 99m
TC HMPAO labeled leukocytes.
• Radiolabeled polyclonal immunoglobulins
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Nuclear Medicine:
Find 2
Differences
EncephalitisEncephalitis
•Diffuse non-focal brain parenchymal
inflammatory disease
• HSV TYPE 1 & 2
• Others; equine viruses. CMV, Parvoviruses, …..
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Agents:
Encephalitis
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Agents:
Encephalitis
• In adults, herpes simplex virus type 1 (HSV-1) accounts
for 95% of all fatal cases of sporadic encephalitis and
usually results from reactivation of the latent virus.
• In children and neonates, herpes simplex virus type 2
(HSV-2) accounts for 80-90% of neonatal and almost all
congenital infections.
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Agents:
Encephalitis
• In the typical adult infected with HSV-1, the neuronal
spread of the latent virus occurs from the peripheral
neuron in retrograde fashion to the brain, usually
through the trigeminal or olfactory tract.
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Pathology:
Encephalitis
• Fulminant hemorrhagic and necrotizing
meningoencephalitis. Typical gross findings include
severe edema and massive tissue necrosis, with
petechial hemorrhages and hemorrhagic necrosis.
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Pathology:
Encephalitis
• The virus has a predilection for the limbic system,
involving one or both temporal lobes, and often
involving the hippocampus, parahippocampus, and
amygdala. Frontal and parietal spread also can occur.
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CT:
Encephalitis
• CT classically reveals hypodensity in the temporal lobes either unilaterally or
bilaterally, with or without frontal lobe involvement.
• Hemorrhage is usually not observed.
• A gyral or patchy parenchymal pattern of enhancement is observed. Contrast
enhancement generally occurs later in the disease process.
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CT:
Encephalitis
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MRI:
Encephalitis
• T2-weighted MRI reveals hyperintensity corresponding to
edematous changes in the temporal lobes, inferior frontal
lobes, and insula, with a predilection for the medial
temporal lobes.
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MRI:
Encephalitis
• Foci of hemorrhage occasionally can be observed
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MRI:
Encephalitis
• Restricted diffusion in herpes encephalitis exist with
corresponding T2 hyperintensity reflecting edema
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MRI:
Encephalitis
• MR spectroscopy using proton
spectroscopic MRI has demonstrated a
reduction of the N-acetylaspartate (NAA)-
to-choline ratio.
Find ANY
Difference !!!!!
THANK YOU

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