Imaging of infection of brain and its linings

MODERATOR: DR R.K. GOGOI
Presenter Dr CHARUSMITA CHAUDHARY

infection of brain and its linings 2
 There has been a significant decrease in the morbidity and mortality of
patients with intracranial infections with the advent of computed
tomography (CT) scanning and magnetic resonance imaging (MRI
Recent advances in technology
 positron emission tomography (PET)
 single photon emission computed tomography (SPECT)
 diffusion imaging
 proton magnetic resonance spectroscopy (MRS).
additional imaging modalities to use in the evaluation of intracranial
infection

Source
 Risk factoRs :
 diabetes mellitus
 alcoholism
 malignancy
 agammaglobulinemia
 radiation therapy and
chemotherapy
 steroids
 HIV 3
 Hematogenous spRead
 diRect extension
infection of brain and its linings

Forms of Intracranial
infections
Cerebritis
 Abscess
Empyema
Granuloma
 Encephalitis
Meningitis
Osteomyelitis
4infection of brain and its linings

Forms of Intracranial infections
CEREBRITIS: focal usually pyogenic
without capsule or pus formation
ABSCESS: pyogenic encapsulated pus containing
cavity
 EMPYMA: an abscess forms in an enclosed or
potential space epidural or subdural
GRANULOMA: : a focal, more or less encapsulated,
inflammatory lesion
usually chronic,
without pus formation

Forms of Intracranial infections
continue…..
Encephalitis:
direct infection of the brain,
usually viral and often diffuse
 Meningitis:
infection of the meninges, may be suppurative or
granulomatous

MENINGITIS

Leptomeningitis
The pachymeninges make up the dura mater,
which consists of the periosteum and a
meningeal layer.
The leptomeninges consist of the pia and
arachnoid

Leptomeningitis
 inflammation of the leptomeninges and the adjacent
subarachnoid space
 Characteristic pathogens
 Bacterial meningitis or purulent meningitis
 Non-bacterial meningitis often referred to as aseptic meningitis
Can be divided into
 acute pyogenic (bacterial),lymphocytic (viral), and chronic (TB)
meningitisThe diagnosis is usually made clinically.
 The role of neuroimaging is to exclude complications of
meningitis (e.g., abscess, ventriculitis, empyema)

Causative organism

Aseptic Meningitis
All non-bacterial causes of meningitis
Typically less ill appearing than bacterial
meningitis
Most common cause is viral
HSV
 type II
Enterovirus (coxsackie, echovirus)
 Affects all ages
 Generally self-limited illness

Aseptic Meningitis
 Other Viral
 HIV
 Lymphocytic choriomeningitis
virus
 Arbovirus
 Mumps
 CMV
 EBV
 VZV
 Adenovirus
 Measles
 Rubella
 Rotavirus
 Influenza and parainfluenza
 Other infectious
 Borrelia burgdorferi
 Mycobacterium tuberculosis
 Treponema pallidum
 Mycoplasma pneumoniae
 Rickettsia, erlichia, brucella
 Chlamydia
 Fungal
 Cryptococcus
 Coccidiodes
 Histoplasmosis
 Parasitic
 Angiostrongylus
 Toxoplamosis
 Medication
 NSAID’s
 Bactrim
 Pyridium
 Malignancy
 Lymphoma and leukemia
 Metastatic carcinoma
 Autoimmune
 Sarcoid
 Behcet’s
 SLE

Pathogens- Special Situations
VP shunts/penetrating head trauma- Staph epi
Neural tube defects- Staph aureus, enteric organisms
T-cell defects (HIV)- cryptococcus, listeria
Sinus fracture- Strep pneumo
Asplenia (HgB SS)- Neisseria, H. flu, S. pneumo
Terminal compliment deficiency- Neisseria

Clinical Presentation
 Clinical manifestations are due to local immune
response to bacteria
 Ensuing inflammatory response increases blood-
brain permeability
 Cerebral edema
 Increased ICP
 Local thrombosis and infarction

Clinical Presentation Con’t…

Pathological responses
 INITIALLY:
vascular congestion, edema, and minute hemorrhages
CT and MRI findings may be normal early in the disease process
 ONCE INFECTION PROGRESSES
NECT :obliteration of the basal cisterns. results from a combination of
hypervascularity in the acutely inflamed leptomeninges and exudate
in the subarachnoid space.
Diffuse cerebral swelling may be seen.
Contrast-enhanced CT scan : show enhancement in the basal cisterns
and sylvian fissure, regardless of the causative organism

Imaging continue…
Routine MRI scans :obliteration of the basal cisterns on
T1-weighted images.
 Fluid-attenuated inversion recovery (FLAIR) sequence
may show hyperintensity of the cerebrospinal fluid (CSF)
within the subarachnoid space in contrast to the
hypointense CSF in the ventricles. Abnormal cortical
hyperintensity may be seen on T2-weighted images.
 Contrast-enhanced MRI studies may show basal cisternal
and sylvian enhancement as well as enhancement deep
within the cortical sulci

Meningitis

complications
Early complications
abscess, subdural empyema, ventriculitis, and
infarction.
 Late complications
subdural effusion, encephalomalacia, hydrocephalus,
and atrophy

20
Contrast-enhanced MRI more sensitive than contrast-enhanced CT in
detection of meningitis and its complications
The MRI differential diagnosis includes only meningeal carcinomatosis

Grp b streptococcal meningitis
Leading cause of newborn meningitis in developed countries
Best diagnostic clue: Meningoencephalitis in anewborn

PACHYMENINGEAL ENHANCEMENT
may be seen as a normal finding
-- the dura mater does not produce a blood-brain barrier.
dural reflections of the falx and tentorium.
intracranial hypotension, meningiomas, metastatic disease,
lymphoma, and granulomatous disease]
Postoperative meningeal enhancement may be pachymeningeal or
leptomeningeal in appearance.

Subdural Effusion
irritation of the dura by the infectious agents or its by-products or by
inflammation of subdural veins with loss of fluid and albumin into the
subdural space.
H. influenzae is a common pathogen
On neuroimaging, effusions look similar to CSF and are frequently
seen in the frontal region.
 On contrast study , no evidence of abnormal enhancement
The subdural effusion usually resolves spontaneously

INTRACRANIAL EMPYEMA

Subdural empyema
 collection of pus between dura and leptomeninges
 as a complication of meningitis, paranasal sinusitis, otitis media,
osteomyelitis, or a penetrating wound of the skull
 Frontal sinusitis is the most common cause
 Route: retrograde fashion through a dural sinus or through bridging
veins
 even when small, usually cause focal neurologic deficits
 considered a neuro-surgical emergency because of its progressive
clinical course.
 Despite recent improvement in surgical technique and antibiotics,
mortality remains high (25% to 40%).
 Complications :venous thrombosis and infarction

CT scan
-hypodense or isodense crescentic or lenticular area adjacent to the inner table of
the skull
CECT
-enhancement of the medial rim may be seen
Enhancement of the margin of the empyema is characteristic
better visualized with MRI than with CT.

Epidural Empyema
collection of pus between the dura and calvaria,
 complication of otitis media, mastoiditis, sinusitis, or osteomyelitis of
the skull.
 not as toxic as that with subdural empyema.
Displacement of the falx and dural sinuses away from the inner table
of the skull, an important and useful sign indicating the epidural
location of a collection

Epidural Empyema

Epidural Empyema
 T2-weighted MR images , A hypointense rim,
representing inflamed dura, in an epidural, but not a
subdural, empyema
 , epidural empyema may extend into the subgaleal
space through emissary veins or adjacent
31
Epidural empyema, like epidural hematoma, can across the
midline but is limited by the sutures
. In contrast, a subdural collection of any kind cannot cross
the midline but is not limited by the sutures

Encephalitis
 refers to diffuse inflammation of the brain with a
parenchymal infiltration of inflammatory cells,
usually caused by virus.
 The brain damage is due to a combination of
intracellular viral growth and the host's
inflammatory response
 Common herpes simplex virus type 1 (HSV-1) and
type 2 (HSV-2

INTRODUCTION
unusual manifestation of human viral infection as
most viruses do not attack the human CNS.
Viruses vary in their potential to cause CNS
infections. some cause relatively benign infections,
others cause prominent neurologic symptoms
 Overall, viruses are the most common cause of
meningoencephalitis (3.5-7.4 per 100000 persons per
year in USA).

INTRODUCTION
Viral encephalitides can be divided into 4 types
acute viral encephalitis
postinfectious encephalomyelitis
slow viral infections of the CNS
chronic degenerative CNS disease of viral origin

VIRUSES THAT CAUSE
MENINGOENCEPHALITIS
 Herpes simplex virus (HSV-1, HSV-2)
 Other herpes viruses: varicella zoster virus (VZV), cytomegalovirus (CMV),
Epstein-Barr virus (EBV), human herpes virus 6 (HHV6)
 Adenoviruses
 Influenza A
 Enteroviruses, poliovirus
 Measles, mumps and rubella viruses
 Rabies
 Arboviruses—for example, Japanese B encephalitis, St Louis encephalitis virus,
West Nile encephalitis virus, Eastern, Western, and Venezuelan equine
encephalitis virus, tick borne encephalitis viruses, Chandipura virus, Dengue virus,
chikungunya, KFD.
 Bunyaviruses—for example, La Crosse strain of California virus
 Reoviruses—for example, Colorado tick fever virus
 Arenaviruses—for example, lymphocytic choriomeningitis virus
 Paramyxovirus – Nipah virus, hendra virus
Modified from Chaudhury and Kennedy Postgrad Med J. 2002;78:575

VIRUSES THAT CAUSE
MENINGOENCEPHALITIS cont.
Sporadic ;
HSV1 and 2, Mumps, EB, adenovirus, rabies etc
Epidemic;
Arboviruses, influenza, enteroviruses, emerging
viruses (Nipah).

VIRUSES THAT CAUSE MENINGOENCEPHALITIS
Indian scenario
 In India, most common cause for epidemic encephalitis
JE
 Other viruses cause sporadic meningoencephalitis
include herpes, mumps, measles and polio
 In children enterovirus 71, mumps, measles, and JE are
major causes. Others include herpes, varicella ,rubella
and dengue
 Emerging viruses with threat potential – Nipah,
chandipura, chikungunya
.

Pathogenesis
CNS access of the virus can be through two routes
 Hematogenous (eg. Arboviruses) –most common
 Intraneuronal ( eg. HSV, rabies, varicella zoster)
After hematogenous entry transient viremia→ →
seeding of reticuloendothelial system, replication→
secondary viremia seeding of CNS→ →

Pathology:
Gross: variable degree of meningitis, brain swelling,
congestion and hemorrhage.
Some viruses preferentially attack certain brain sites
 Herpes virus – temporal neocortex, pons
JE- thalamus, basal ganglia, substantia nigra, hippocampus
This may reflect as fairly characteristic imaging findings

Imaging
CT
Hypoattenuated
lesions affecting grey
matter, deep gray
matter and white
matter.
Focal or generalized
brain swelling
Focal hemorrhage
+- enhancement
MRI
More sensitive
T2 hyper and T1
hypo to isointense
single or
multifocal lesions
+- enhancement
+-hemorrhage
DWMRI
oIn acute
stage- DW may
show ↑ or equal
lesions
compared to
conventional
MR.
In later stages
may show less
lesions[1,2]

CONGENITAL CMV
Transplacental transmission of human herpes virus
Best diagnostic clue
o Microcephaly
o Cerebral calcification (40-70%)
• Periventricular (sub ependymal)
o Cortical gyral abnormalities
• Agyria ~ pachygyria ~ diffuse polymicrogyria ~
focal cortical dysplasia
o Cerebellar hypoplasia
o Myelin delay or destruction
Location: Dystrophic periventricular Ca++ has predilection for
germinal matrix zones

IMAGING
CT Findings
o Cerebral parenchymal Ca++ (40-70%)
• Periventricular (subependymal)
o Ventricular dilatation and WM volume loss
o Focal regions of WM low attenuation
o Cortical gyral abnormalities
o Cerebellar hypoplasia
MR Findings
• TIWI
 o Periventricular subependymal foci of Tl
shortening due to Ca ++
 o Ventricular dilatation and periventricular
WM volume loss

CONGENITAL HIV
Vertical HlV 1 infection early in-utero/late
pregnancy, at delivery or, by breast-feeding
Imaging Findings
• Best diagnostic clue: Basal ganglia Ca++, volume
loss
MRA: Fusiform vasculopathy
Image Interpretation Pearls
• Consider HIV if bilateral symmetrical calcifications
in BG are found in a child> than 2 months

CONGENITAL HIV
Scattered Ca++
• Hydrocephalus
Periventricular Ca++

Herpes
encephalitis

Herpes simplex encephalitis
most common endemic encephalitis in the USA (2 per
million) and causes 10-20% of all viral encephalitis.
 In India exact incidence is not known and it is under
diagnosed due to lack of awareness and diagnostic
facilities
Early diagnosis is important because AV therapy can
decrease mortality and morbidity.
HSV1 causes 95% of HSE. Most commonly occurs due to
virus reactivation. HSV2 causes 80-90% of neonatal
encephalitis
[1] Panagaria A. Neurol In. 49:360; 2001.

 Definitive diagnosis: PCR, intrathecal antibodies,
brain biopsy – take time and may be false negative in
early disease [1].
 Imaging helps in establishing an early diagnosis.
1) Akyldz BN Paeditr Emerg Care 24;377 :2008.

Usually bilateral
Hemorrhage and enhancement seen
Basal ganglia tend to be spared or involved in
contiguity with the TL.
Pons may be involved [Tien AJR:161,1993]
MR is more sensitive and shows lesions earlier than
CT or SPECT

Rare paraneoplastic syndrome
limbic system, often bilateral
Active seizures may disrupt BBB, cause
signal
abnormalities and enhancement

HSV 2
Both HSV1 and 2 are commonly prevalent in Indian
population. (Mixed=83%, HSV1=10%, HSV2=1%) [1]
HSV2 along with TORCH agents are major causes of
neonatal encephalitis.
Infections result from maternal birth canal or
transplacental spread
Unlike HSV1, HSV2 infection in neonates is
diffuse.
1.Shivaswami 2005. IJDVL 71:26

HSV 2
Imaging findings are nonspecific.
CT scans in early disease may be negative or show
subtle areas of low density
. Conventional MR and DWI show lesions better.
 Lesions may be multifocal involving almost any area of
brain or limited to temporal lobes brainstem and
cerebellum.
Watershed infarcts may be seen [1]
 In-utero infections can result in microcephaly,
encephalomalacia or calcification.
1)Vossough.2008. Neuroradiol 50:355

Axial T2WI MR shows areas of high signal in frontal lobes WM
due to acute H5V-2
Axial T1WI MR shows diffuse cystic encephalomalacia
and prominent CSF-containing spaces
Scattered Ca++, hydrocephalusPeriventricular Ca++,

HIV Encephalitis
Syndrome of cognitive, behavioral, and motor abnormalities
attributed to direct HIV effect on brain, in the absence of
opportunistic brain infections
Location: Bilateral periventricular and centrum semiovale WM, basal
ganglia, cerebellum, brainstem
56
Best diagnostic clue: Combination of atrophy and
symmetric, periventricular or diffuse white matter
(WM) disease suggests HIVE

Introduction
mosquito borne Flaviviral encephalitis.
 Pigs and heron like birds are main amplifiers.
leading cause of acute meningoencephalitis affecting
children and adults in the world.
JE is endemic to Indian subcontinent, particularly in
the NE state of Assam
Epidemics occur in the summer rainy season which
favor breeding of mosquitoes.
First recognized in India in 1955, Epidemics occur
every year in several Indian states since the first in
WB(1973).

Pathology
1)Tiroumourougane. Postgrad. Med. J. 2002; 78: 205
Some neurons have specific receptors with strong
affinity for JEV [1

Lesions of JE are most commonly seen in the thalami and
substantia nigra,
Basal ganglia, cerebral cortex, hippocampi, midbrain,
pons, medulla and cerebellum lesions are also seen.
Lesions hyperintense on T2 and FL and iso to hypo on T1
with local or generalized brain swelling.
No enhancement.
Hemorrhagic change has been reported from India [1].
MRI is the investigation of choice with reported sensitivity
of 89-100% compared to CT (38-55%) [1,2].
DWI has been reported to help in early diagnosis and in
assessing temporal evolution of lesions[1]
 Was helpful in making an early diagnosis in JE showing
additional lesions
1)Kalita. J Neurol Sci 2000; 174: 3
Imaging

Evolution of lesions in JE

Temporal lobe involvement in JE
Fairly characteristic pattern of TL involvement with
posterior hippocampal involvement and sparing of
anterior temporal lobe and neocortex. Insula
occasionally involved
Associated lesions characteristic of JE usually seen in
thalamus, SN, BG etc. Can help differentiate from
HSE [1]
1)Handique AJNR 2006 27:1027

T2 DWI
PATTERN 1 DWI>T2 [1]

Neurocysticercosis and JE
More than a casual relationship between NCC and JE
has been suggested by many studies in China and
India [1,2,3]
Co-infections have been advocated as prognosticator
of poor outcome[1]
1.Desai Epidemiol Infect 1997;118:165
2. Shankar. Ind J Med Res 1983; 78:431
3. Liu. Chinese Med J 1957;75:1010

Neurocysticercosis and JE
asymmetric with lateralization to the side of the brain
having maximum NCC or a cyst with edema.
were more florid with significantly higher amount of
abnormal CT scans and more abnormal MR imaging
more common in children.
Altered immune status in co-infections were
suggested by significantly lowered levels of JE IgM.

co-infection

Mumps, measles and varicella
Mumps, measles and varicella viruses may
occasionally cause acute encephalitis besides its
primary infectious manifestations.
 Acute measles encephalitis is much more common
than the more well known (amongst radiologists)
SSPE
In a study of VE in children from India, 10% was
caused by mumps, 7% by measles and 1.8% by
varicella [1]
(1) Karmarkar. Ind JPaediatr.2008;75:801

Mumps, measles and varicella
Very few large scale imaging studies exist for these
encephalitis as the findings are non specific.
Mumps encephalitis shows white matter and
brainstem lesions[1].
Measles shows lesions in the basal ganglia with
multifocal lesions in the gray and white matter,
thalamus (rare) with gyriform enhancement of gray
matter lesions [2].
Varicella shows multifocal cortical lesions[3]
(1)Koyama Int Med 2000 ;39:499 (2) Lee. Neuroradiol 2003; 45:100 (3) Tien AJR
19937; 161:16

Enterovirus 71
MRI revealed lesions in the brainstem and cerebellum
in 71% patients with rhombencephalitis. Anterior
horn cells showed lesions in patients with flaccid
paralysis [1]
In study from India lesions were also described in the
thalamus, basal ganglia, parieto occipital, frontal,
temporal lobes, substantia nigra besides brainstem
and cerebellar involvement [2]
1) Huang. New Eng J Med. 1999;341:936 (2) Karmarkar. Ind JPaediatr.2008;75:801

Dengue
Dengue is caused by a mosquito borne flavivirus like
JE. Neurologic manifestations in dengue fever,
hemorrhagic fever and Shock syndrome have been
thought to be due to encephalopathy
Recent reports have shown that dengue virus can
cause neuroinvasion and encephalitis [1,2]
(1) Lum. Am J Trop Med Hyg. 1996;54:256 (2) Muzaffar. Sing Med J 2006;47:975

Dengue
From. Muzaffar. Sing Med J 2006;47:975
Imaging studies
have shown cerebral
edema, lesions in
the hippocampus
and temporal lobes

Rabies encephalitis
Transmitted by bites of infected animals or by
transplants. 100% fatal.
In India rabies occurs in all parts of the country
except in Lakshadweep, Andaman and Nicobar
islands.

Nipah virus encephalitis
paramyxovirus spread to man from fruit-bats or pigs
infected by fruit-bats.
 Subsequent spread from man to man occurs.
First identified in Malaysia and Singapore in 1988-89,
outbreaks have occurred in Bangladesh (2001-4,5)and
Siliguri (2001). Case fatality in India and Bangladesh
was 75%[1]
(1) Halder. Ann Ind Acad Neurol 2006;9:137

Nipah virus encephalitis
MR shows fairly
characteristic findings
with small T2
hyperintense white or
gray matter lesions with
transient T1
hyperintense punctate
cortical lesions in
subacute phase [1]
(1) Lim. Radiol 2002;222:219

Other emerging viruses
Chandipura virus is transmitted to humans possibly
by sandflies and primarily causes encephalitis in
children. Major outbreaks have occurred in Gujarat,
Andhra Pradesh, Madhya Pradesh and Maharashtra
with fatality rates of 50-80%.
Brainstem encephalitis has been reported.
 CT and MRI scans have showed no abnormality in
few (CT=5,MR=1)reported patients from India [1,2].
No large scale imaging studies available.
Other emerging viruses that ocassionally cause
encephalitis include Chikungunya and KFD.

ADEM acute Disseminated Encephalomyelitis
an immune response to a preceding viral infection or vaccination
neurologic signs and symptoms 5 days to 2 weeks later.
Both humoral and cell-mediated immunity
 A hypersensitivity reaction to a myelin .
Perivenous demyelination is the hallmark of the disease
The disease primarily involves white matter, but change may also be
apparent in gray matter and brain stem
The differential diagnosis includes multiple sclerosis, vasculitis, and
embolic infarction.
 In later stages of the disease, encephalomalacia, ventriculomegaly, and
atrophy may be seen.

Other Encephalitides
Creutzfeldt-Jakob Disease
human spongiform encephalopathy that results from an infection by a
prion
transmission has been traced to inoculations by injections of human
growth hormone, transplantation of corneas, and implantation of
cerebral electrodes
butchers and meat handlers are at greater risk of contracting the disease
variant ;bovine spongiform encephalopathy (so-called mad cow
disease).
The infective prion is a proteinaceous particle that contains little or no
nucleic acid.
The disease occurs in adults in their late 50s

 Cortical gray matter
involvement without cerebral
atrophy may represent an early
phase of the disease.
 [
In contrast to Creutzfeldt-Jakob
disease, wherein bilateral
involvement of the corpus
striata and thalami is seen on
the imaging studies, the bovine
spongiform encephalopathy is
characteristically demonstrated
by bilateral thalamic pulvinar
hyperintensity on T2-weighted
and FLAIR images
. A, FLAIR image demonstrates hyperintensity in both
thalami, in the periatrial white matter, and in the anterior
cingulated gyri. B, Diffusion-weighted image shows
restricted diffusion in both thalami and cingulated gyri

Subacute Sclerosing
Panencephalitis
measles virus
seen in children and young adults with previous
measles infection 3 to 9 years earlier
CT scans low-density changes in subcortical white matter as well as
in basal ganglia.
 MRI studies show hyperintensity in the periventricular white matter,
subcortical white matter, basal ganglia, cerebellum, and pons on T2-
weighted and FLAIR images.[
Abnormal signal intensity on T2-weighted and FLAIR images
involving the splenium of corpus callosum can occur.
 Atrophy is a late-stage finding.

Reye's Syndrome
disease of unknown etiology in children.
 It usually follows a viral infection such as type A or B
influenza and varicella
. Exogenous toxins, such as salicylates, and intrinsic
metabolic defects have been implicated as other
factors
CT scans show diffuse low density of the
supratentorial structures, a finding consistent with
diffuse cerebral edema.[124]

Encephalitis in Immunocompromised
Patients
Human
ImmunodefIcIency
VIrus
encepHalItIs
neurotropic virus
causes a subacute form of
encephalitis
CT scans low density in the
periventricular white matter.
 MRI hyperintensity in the
periventricular white matter on
T2-weighted and FLAIR images
Normal neuroimaging studies
do not exclude HIV
encephalitis.

Encephalitis in Immunocompromised
Patients
Progressive Multifocal
Leukoencephalopathy
a JC virus infecting the
oligodendrocyte
seen in immunocompromised patients.
 affects all parts of the brain, including
the cerebellum, and does not have the
propensity to involve the parieto-
occipital region, as previously describe

Progressive Multifocal Leukoencephalopathy
CT scans low-density lesions in
white matter.
 Early involvement -asymmetrical
pattern,
later disease -symmetrical and
diffusely confluent.
Contrast enhancement is usually
absent but may occur.[155
.
MRI shows a focal region of
hypointensity in the white matter
on T1-weighted images and
hyperintensity on T2-weighted
images
. Involvement of the subcortical U-
fiber is characteristic for PML, as
opposed to other HIV- related
encephalopathy.
. MRI is more sensitive than CT in
detecting abnormalities
T2-weighted image shows high
signal intensity in the parieto-
occipital white matter bilaterally.

Cytomegalovirus Encephalitis
affect the immunocompetent as well as immunocompromised patients
cause meningoencephalitis or subacute encephalitis.
CMV can produce demyelination and necrosis within the white matter.
CMV is the most frequent cause of fetal and neonatal viral infection.
 calcifications are usually in the subependymal region, whereas in infants with
toxoplasmosis, calcifications are seen everywhere, including the periventricular
region.

 CT scans show low density in
the white matter, which may or
may not enhance with contrast
agents
. MRI shows high signal
intensity in the white matter on
T2-weighted and FLAIR images
and is more sensitive than CT in
detecting leukoencephalitis
Nonenhanced CT scans in
a newborn show
periventricular calcification
and ventricular dilatation
Cytomegalovirus Encephalitis

Cerebritis
and Abscess

most brain abscesses are bacterial
 streptococci accounting for the majority
haematogenous dissemination, penetrating
trauma or direct spread
 Blood-borne infection can occur anywhere in
the brain, but has a predilection for the territory
of the middle cerebral arteries
fever ,headache and focal neurological deficits.
Brain abscesses are multiple in 10–50 per

stages in the evolution of cerebral
abscess
there are four stages
1. Acute cerebritis (the first 4
to 5 days).
In early cerebritis, mild central
nodular enhancement may be
seen on contrast-enhanced CT
or MRI scans

2. Late cerebritis (at 7 to 10 days).
In the late cerebritis stage brain
enhancement on CT scans
Late cerebritis. A, Gadolinium-enhanced MRI
study shows thick, smooth, ringlike
enhancement with surrounding edema. B,
Gadolinium-enhanced MRI study (coronal
view) shows a second small, adjacent ringlike
enhancement

stages in the evolution of cerebral abscess
3. Early abscess (at 10 to 14
days). Formation of a
collagenous capsule by
fibroblasts is seen. The central
necrotic area is liquefied.
Surrounding edema persists.
4. Mature abscess (after 14
days). A decrease in
surrounding edema
gliotic reaction at outer margin
of the abscess capsule.
Usually, more than 2 weeks is required
to form a firm capsule
The wall of the mature abscess consists of
three layers: (1) an inner inflammatory layer
of granulation tissue containing
macrophages, (2) a middle collagenous
layer, and (3) an outer gliotic layer

Abscess treated
conservatively with antibiotics.

Abscess caused by gas-forming
organism.
The most distinctive feature of abscess on imaging is the presence of
a smooth, thin capsule with a moderate amount of cerebral edema.
[57]
 It is located at the corticomedullary junction and usually extends
into the white matter.
Nonenhanced CT scans show a low-density area with mass effect and
compression of the ventricular system.
 rupture of the abscess into an adjacent ventricle {medially into the
ventricular system because the medial wall is thinner than the lateral
wall

Differential diagnosis
 necrotic primary brain tumor, cystic metastatic tumor, infarction,
resolving hematoma, cysticercosis, and thrombosed aneurysm
Thick, nodular enhancing
wall typical
History of trauma or vascular
lesion
• Blood products present
Enhancement often
incomplete ring
• Thick, nodular
enhancing wall typical
Infarcts often show gyral enhancement, occasionally mimicking
ring enhancementThe MRI differential diagnosis of
abscess is similar to the CT diagnosis except for hematomas,
which can be recognized by their characteristic MRI signal
intensity patterns, depending on the age of the hematomas

Ependymitis
 Ventriculitis, or ependymitis, is an
inflammation of the ependymal lining of
the ventricular system
 rupture of periventricular abscess or
from retrograde spread of infection from
the basal cisterns by way of the fourth
ventricle
 Hydrocephalus may result from
intraventricular adhesions and septation
caused by organization of intraventricular
exudate and debris, resulting in blockage
of the interventricular foramina.
 A trapped fourth ventricle may result
from obstruction of its outlets and the
aqueduct because of ependymitis

 NECT scan -normal or may
show only slightly increased
density in region of affected
ependyma
 MRI -marginal ventricular
abnormality or only slightly
increased signal intensity in
the region of affected
ependyma
 proton-density-weighted
images. The fluid within the
ventricles may show slightly
increased intensity,.
 Contrast-enhanced CT or MRI
studies show uniform, thin
ependymal enhancement
Gadolinium-enhanced MRI
studies show thin, smooth
ependymal enhancement in an
AIDS patient with
cytomegalovirus ependymitis.


 The differential diagnosis on CT and MRI studies includes ependymal seeding of
intracranial neoplasm. The ependymal enhancement may be irregular or nodular if it
is secondary to seeding of neoplasm, the clinical history may be helpful in arriving at
the correct diagnosis
typically nodular
• Parenchymal disease usually present Ventricles typically not
enlarged

Granulomatous
Infection
99
Tuberculosis

Tuberculosis
Mycobacterium tuberculosis
 very young and very old persons are affected, with the highest
incidence in the first 3 years of life
Increased in incidence in immunocompromised patients, drug
abusers, and patients with AIDS
Tuberculous meningitis is the most frequent manifestation and
tends to involve the basal leptomeninges.

Best diagnostic clue
o Basilar meningitis + extracerebral TB (pulmonary)
o Meningitis + parenchymal lesions highly suggestive

TBM pathology
Penetration of meningeal vessel walls by
haematogenous spread
• Rupture of subependymal or subpial granulomata
into the CSF

Tuberculous meningitis
 involve the basal leptomeninges.
 CT shows -
 obliteration of the basal cisterns by isodense or slightly
hyperdense exudate, which shows diffuse enhancement with IV
contrast medium
 The most useful CT criteria of abnormal basal meningeal
enhancement are:
 (A) linear enhancement of the middle cerebral artery cisterns;
 (B) obliteration by contrast of the CSF spaces around normal
vascular enhancement;
 (C) Y-shaped enhancement at the junction of the suprasellar
and middle cerebral artery cisterns and
 (D) asymmetry of enhancement

 MRI depicts the basal meningeal enhancement,
hydrocephalus and basal ganglia infarcts with
greater sensitivity than CT
 Late sequelae of tuberculous meningitis include
hydrocephalus, infarction, syringobulbia, and
syringomyelia.

Tuberculous meningitis
differential diagnosis includes fungal
meningitis, sarcoid and carcinomatous
meningitis

tuberculoma
found in any portion of the intracranial compartment
When tuberculoma and tuberculous meningitis are seen together, the
diagnosis of tuberculosis is easily made.
105
Tuberculoma pathophysiology
• Hematogenous spread (GM-WM junction lesions)
• Extension of meningitis into parenchyma via cortical
veins or small penetrating arteries

106
 NECT scans isodense, hyperdense, or of mixed density
 CECT- ringlike enhancement[152]
or, less likely, areas of nodular
enhancement
 A central nidus of calcification with surrounding ringlike
enhancement, known as the target sign, suggests tuberculoma.
 Gadolinium-enhanced MRI studies show enhancing patterns similar to
those on contrast-enhanced CT scans

107
T1-weighted image shows isointense to hyperintense capsules with central pus and
debris and surrounding edema. B, T2-weighted image shows the abscess capsules
with an inner ring of hypointensity and an outer ring of hyperintensity; pus shows
hyperintensity, and debris shows hypointensity. C, Gadolinium-enhanced MRI study
shows smooth, ringlike enhancement of the abscess capsule

Neurosyphilis
meningovascular
syphilis
syphilitic gumma
 widespread thickening of the
meninges, with lymphocytic
infiltration involving the
meninges and around the small
vessels
 CT shows multiple low- density
areas involving both gray and
white matter.
 Contrast-enhanced CT scans
show linear, nonhomogeneous
enhancement.
 Contrast-enhanced MRI studies
may demonstrate meningeal
enhancement in addition to a
gyriform pattern of enhancement
 consist of masses of granulation tissue
and are rare
 originate in the meninges and blood
vessels and spread into the brain
parenchyma.
 On CT scans, gummas are well-
delineated masses with ringlike or
nodular enhancement.
 On contrast-enhanced MRI, gumma
shows nodular or ringlike enhancement.
Cerebral atrophy may develop in patients
with neurosyphilis

Fungal infection
involve intracranial blood vessels, leptomeninges, and brain
parenchyma. Intracranial infection is frequently secondary to
pulmonary disease
HIV, diabetes, pregnancy, and malignancy.
CNS fungal infection displays neuroimaging features similar to those
seen with tuberculosis
The fungi of yeast forms tend to spread
hematogenously to the meningeal microcirculation,
with resultant leptomeningitis attributable to their
smaller size;
the larger hyphal form more commonly involves the
brain parenchyma, with resultant cerebritis or
encephalitis

Aspergillosis
Aspergillus fumigatus infection is seen predominantly
in immunocompromised patients
hematogenous spread of pulmonary disease and less
commonly caused by direct extension of disease in
the nasal cavity and paranasal sinuses
produces meningitis and meningo-encephalitis.

Patho physiology

Imaging
CT scans low-density areas with little
or no contrast enhancement and mass
effect, representing areas of infarction
 Incomplete ringlike contrast
enhancement may be seen
MRI studies demonstrate a peripheral
ring of low signal intensity
The ring of low signal intensity
corresponds to a dense population of
Aspergillus hyphal elements and small
areas of hemorrhage histologically.

Cryptococcosis
Cryptococcosis is the most
common fungal infection in
patients with AIDS
. a yeast with a polysaccharide
capsule
CNS infection is usually
secondary to pulmonary infectio
nmeningitis,
meningoencephalitis, or
cryptococcal mass
. Meningitis is the most
common presentation.
Ocular symptoms are common
in patients with cryptococcal
meningitis.

Mucormycosis
114

Candidiasis
-most common cause of
human fungal infection
and represents 75% of the
fungal infections in
patients with neoplasm
present as meningitis,
granuloma, or
microabscess
T1-weighted image reveals a hyperintense area in the left thalamus, consistent with focal hemorrhage. B, FLAIR
image demonstrates abnormal hyperintense areas in the corpus striati bilaterally and in the left thalamus. C,
Postcontrast image demonstrates patchy abnormal enhancement in the corpus striati bilaterally as well as in the left
thalamus

Cysticercosis
one of the most common parasitic diseases involving the brain
ingesting the ova of the pork tapeworm (Taenia solium), usually
on unwashed, fecally contaminated vegetables or water
By ingesting poorly cooked pork infected with cysticercosis, the
human becomes the definitive host for T. solium
through the anus-finger-mouth route.
117
Best diagnostic clue: Cyst with "dot"
inside
intracranial compartment is involved in 60% to 90% of patients with
cysticercosis
meningobasal, parenchymal, intraventricular, or a combination of
these sites
Convexity subarachnoid spaces most common
( cisterns> parenchyma> ventricles)

STAGES:
Escobar, has identified four stages that the parasite
undergoes within the brain parenchyma
Vesicular stage (viable larva)
Colloidal vesicular stage (degenerating larva)
:Granular nodular (healing) stage
Nodular calcified (healed) stage

119
STAGES .
.
VESICULAR STAGE
 the tiny (4- to 5-mm) live spherical larva
 Smooth, thin-walled CYST , isodense to CSF, no edema
 • Hyperdense "dot" within cyst = proto scolex
 No (or mild) wall enhancement
 COLLOIDAL VESICULAR STAGE.
 Hyperdense cyst fluid with surrounding edema The cyst wall may show enhancement
 The cyst fluid may show increased density with CT and intensity with MRI. The scolex begins to
degenerate and shrink

 GRANULAR NODULAR STAGE
Mild edema calcification may be
identified within the scolex and
along the cyst wall on CT scan
 NODULAR CALCIFIED STAGE,
 granular material appears
completely mineralized, with the
lesion having shrunk to one half or
one fourth of the size of the original
 Calcification is much better
demonstrated on CT than on MRI

Intraventricular
cysticercosis
potentially lethal
The cysts can be identified by CSF density or signal
intensity
A thick, ring like enhancement associated with
intraventricular cysticercosis

Echinococcosis
CNS involvement is rare
Hydatid disease, or echinococcosis, is the larval stage of Echinococcus
granulosus
definitive host of E. granulosus is the dog, intermediate hosts are
sheep, cattle, and camels.
Seizure, focal neurologic signs, and increased intracranial pressure are
the usual clinical presentations
. Extradural cysts have been reported

 NECT or MRI appear as large intraparenchymal cystic lesions with
sharp margins
 Cyst fluid is of CSF density or signal intensity.
 The lack of surrounding edema is an important feature differentiate
this lesion from cerebral abscess.
 Contrast enhancement may be seen partially or completely involving
the wall. Calcification MAY SEEN

Toxoplasmosis
 Toxoplasma gondii, a protozoan
 immunocompromised patients or
in patients with AIDS
 meningoencephalitis or as
granulomas
 Granuloma site corticomedullary
junction, in the deep gray matter,
or in the periventricular areas
 NECT- show multiple low-density
areas.
 MRI studies are more sensitive in
detecting the Toxoplasma lesions
than contrast-enhanced CT scans

Rasmussen's Encephalitis
childhood disease.
 severe epilepsy and progressive neurologic deficits
Characterized by hemispheric volume loss and difficult to control
focal seizure activity
partial motor seizure type and tend to be intractable
Early in the disease process, CT and MRI findings may be normal.
MRI may reveal hyperintensity in the white matter and putamen on
T2-weighted images.[143]
 PET imaging using 18
FDG may show decreased hemispheric activity.

(parieto-occipital
most commonHemispheric infarction

Acute Necrotizing Encephalitis
infants and children between 6 and 18 months of age
history of mild antecedent illness
elevated liver enzymes
no focal neurologic or meningeal signs.
 Etiology is unknown;
 it may be postinfectious (HSV-6 or influenza A and B), immune
mediated, or metabolic.
 Prognosis is usually poor; less than 10% of patients recover
completely.
 Focal neurologic deficits are common sequelae

Acute Necrotizing
Encephalitis
 Thalamic lesions almost
always become
hemorrhagic
 Enhancement in the
margin of the thalami may
be seen.
 MRS may show elevated
lipids,
glutamate/glutamine
complex, and lactate A, T1-weighted image reveals bilateral
thalamic hemorrhage. B, FLAIR image
demonstrates hyperintensity in both
thalami with adjacent edema.

Intracranial infections take the following forms
Cerebritis
Abscess
Empyema
Granuloma
Encephalitis
Meningitis
Osteomyelitis

132
Even with appropriate antibiotics, mortality rate for bacterial
meningitis is significant
imaging can help in establishing a working diagnosis of viral
encephalitis, and differentiate from other conditions such as
ADEM and TBM.
Keeping in mind the age, geographical location, climate and host
immune status, imaging findings can help arrive at an etiological
diagnosis of viral encephalitis.
HSV encephalitis can be identified early for early AV therapy
In epidemic situations the alert radiologist can point to the
possible etiological agent eg. in JE, NVE and EV71E
Can help in prognostication and identification of associated
disease such as NCC with JE

Imaging of infection of brain and its linings

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