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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
5infection of brain and its linings
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
6infection of brain and its linings
MENINGITIS
7infection of brain and its linings
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
8infection of brain and its linings
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)
9infection of brain and its linings
Causative organism
10infection of brain and its linings
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
13infection of brain and its linings
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
14infection of brain and its linings
Clinical Presentation Con’t…
15infection of brain and its linings
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
16infection of brain and its linings
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
17infection of brain and its linings
Meningitis
18infection of brain and its linings
complications
Early complications
abscess, subdural empyema, ventriculitis, and
infarction.
 Late complications
subdural effusion, encephalomalacia, hydrocephalus,
and atrophy
19infection of brain and its linings
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
infection of brain and its linings
Grp b streptococcal meningitis
Leading cause of newborn meningitis in developed countries
Best diagnostic clue: Meningoencephalitis in anewborn
21infection of brain and its linings
22infection of brain and its linings
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.
23infection of brain and its linings
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
24infection of brain and its linings
Imaging of infection of brain and its linings
infection of brain and its linings 26
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
27infection of brain and its linings
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.
28infection of brain and its linings
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
29infection of brain and its linings
Epidural Empyema
30infection of brain and its linings
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
infection of brain and its linings
32infection of brain and its linings
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
33infection of brain and its linings
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).
34infection of brain and its linings
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
35infection of brain and its linings
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
36infection of brain and its linings
VIRUSES THAT CAUSE
MENINGOENCEPHALITIS cont.
Sporadic ;
HSV1 and 2, Mumps, EB, adenovirus, rabies etc
Epidemic;
Arboviruses, influenza, enteroviruses, emerging
viruses (Nipah).
37infection of brain and its linings
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
.
38infection of brain and its linings
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→ →
39infection of brain and its linings
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
40infection of brain and its linings
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
infection of brain and its linings 41
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
42infection of brain and its linings
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
43infection of brain and its linings
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
44infection of brain and its linings
CONGENITAL HIV
Scattered Ca++
• Hydrocephalus
Periventricular Ca++
45infection of brain and its linings
Herpes
encephalitis
46infection of brain and its linings
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.
47infection of brain and its linings
Herpes simplex encephalitis
 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.
48infection of brain and its linings
Herpes simplex encephalitis
49infection of brain and its linings
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
infection of brain and its linings 50
Herpes simplex encephalitis
51infection of brain and its linings
Herpes simplex encephalitis
Rare paraneoplastic syndrome
limbic system, often bilateral
Active seizures may disrupt BBB, cause
signal
abnormalities and enhancement
52infection of brain and its linings
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
53infection of brain and its linings
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
54infection of brain and its linings
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++,
55infection of brain and its linings
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
infection of brain and its linings
57infection of brain and its linings
Imaging of infection of brain and its linings
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).
59infection of brain and its linings
Pathology
1)Tiroumourougane. Postgrad. Med. J. 2002; 78: 205
60infection of brain and its linings
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
61infection of brain and its linings
Imaging
Evolution of lesions in JE
62infection of brain and its linings
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
63infection of brain and its linings
infection of brain and its linings 64
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
65infection of brain and its linings
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.
66infection of brain and its linings
infection of brain and its linings 67
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
68infection of brain and its linings
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
69infection of brain and its linings
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
70infection of brain and its linings
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
71infection of brain and its linings
Dengue
infection of brain and its linings 72
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.
73infection of brain and its linings
infection of brain and its linings 74
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
75infection of brain and its linings
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
infection of brain and its linings 76
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.
77infection of brain and its linings
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.
78infection of brain and its linings
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
79infection of brain and its linings
infection of brain and its linings 80
 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.
81infection of brain and its linings
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]
82infection of brain and its linings
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.
83infection of brain and its linings
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
84infection of brain and its linings
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.
85infection of brain and its linings
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.
86infection of brain and its linings
 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
87infection of brain and its linings
Cytomegalovirus Encephalitis
Cerebritis
and Abscess
88infection of brain and its linings
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
infection of brain and its linings 89
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
infection of brain and its linings 90
infection of brain and its linings 91
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.
infection of brain and its linings 92
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
infection of brain and its linings 93
Abscess treated
conservatively with antibiotics.
infection of brain and its linings 94
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
95infection of brain and its linings
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
infection of brain and its linings 96
infection of brain and its linings 97
 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
98infection of brain and its linings
Granulomatous
Infection
99
Tuberculosis
infection of brain and its linings
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
100infection of brain and its linings
TBM pathology
Penetration of meningeal vessel walls by
haematogenous spread
• Rupture of subependymal or subpial granulomata
into the CSF
101infection of brain and its linings
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
102infection of brain and its linings
infection of brain and its linings 103
 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
104infection of brain and its linings
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
infection of brain and its linings
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
infection of brain and its linings
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
infection of brain and its linings
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
108infection of brain and its linings
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
109infection of brain and its linings
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.
110infection of brain and its linings
Patho physiology
111infection of brain and its linings
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.
112infection of brain and its linings
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.
infection of brain and its linings 113
Mucormycosis
infection of brain and its linings
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
infection of brain and its linings 115
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
Imaging of infection of brain and its linings
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
infection of brain and its linings
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
infection of brain and its linings 118
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
infection of brain and its linings
 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
120infection of brain and its linings
121infection of brain and its linings
Intraventricular
cysticercosis
potentially lethal
The cysts can be identified by CSF density or signal
intensity
A thick, ring like enhancement associated with
intraventricular cysticercosis
122infection of brain and its linings
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
123infection of brain and its linings
infection of brain and its linings 124
 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
infection of brain and its linings 125
Imaging of infection of brain and its linings
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.
127infection of brain and its linings
(parieto-occipital
most commonHemispheric infarction
128infection of brain and its linings
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
129infection of brain and its linings
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.
130infection of brain and its linings
Intracranial infections take the following forms
Cerebritis
Abscess
Empyema
Granuloma
Encephalitis
Meningitis
Osteomyelitis
infection of brain and its linings 131
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
infection of brain and its linings
133infection of brain and its linings

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Imaging of infection of brain and its linings

  • 1. MODERATOR: DR R.K. GOGOI Presenter Dr CHARUSMITA CHAUDHARY
  • 2. 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
  • 3. 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
  • 4. Forms of Intracranial infections Cerebritis  Abscess Empyema Granuloma  Encephalitis Meningitis Osteomyelitis 4infection of brain and its linings
  • 5. 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 5infection of brain and its linings
  • 6. 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 6infection of brain and its linings
  • 8. 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 8infection of brain and its linings
  • 9. 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) 9infection of brain and its linings
  • 10. Causative organism 10infection of brain and its linings
  • 11. 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
  • 12. 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
  • 13. 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 13infection of brain and its linings
  • 14. 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 14infection of brain and its linings
  • 16. 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 16infection of brain and its linings
  • 17. 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 17infection of brain and its linings
  • 19. complications Early complications abscess, subdural empyema, ventriculitis, and infarction.  Late complications subdural effusion, encephalomalacia, hydrocephalus, and atrophy 19infection of brain and its linings
  • 20. 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 infection of brain and its linings
  • 21. Grp b streptococcal meningitis Leading cause of newborn meningitis in developed countries Best diagnostic clue: Meningoencephalitis in anewborn 21infection of brain and its linings
  • 22. 22infection of brain and its linings
  • 23. 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. 23infection of brain and its linings
  • 24. 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 24infection of brain and its linings
  • 26. infection of brain and its linings 26 INTRACRANIAL EMPYEMA
  • 27. 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 27infection of brain and its linings
  • 28. 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. 28infection of brain and its linings
  • 29. 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 29infection of brain and its linings
  • 30. Epidural Empyema 30infection of brain and its linings
  • 31. 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 infection of brain and its linings
  • 32. 32infection of brain and its linings
  • 33. 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 33infection of brain and its linings
  • 34. 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). 34infection of brain and its linings
  • 35. 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 35infection of brain and its linings
  • 36. 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 36infection of brain and its linings
  • 37. VIRUSES THAT CAUSE MENINGOENCEPHALITIS cont. Sporadic ; HSV1 and 2, Mumps, EB, adenovirus, rabies etc Epidemic; Arboviruses, influenza, enteroviruses, emerging viruses (Nipah). 37infection of brain and its linings
  • 38. 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 . 38infection of brain and its linings
  • 39. 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→ → 39infection of brain and its linings
  • 40. 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 40infection of brain and its linings
  • 41. 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 infection of brain and its linings 41 DWMRI oIn acute stage- DW may show ↑ or equal lesions compared to conventional MR. In later stages may show less lesions[1,2]
  • 42. 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 42infection of brain and its linings
  • 43. 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 43infection of brain and its linings
  • 44. 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 44infection of brain and its linings
  • 45. CONGENITAL HIV Scattered Ca++ • Hydrocephalus Periventricular Ca++ 45infection of brain and its linings
  • 47. 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. 47infection of brain and its linings
  • 48. Herpes simplex encephalitis  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. 48infection of brain and its linings
  • 49. Herpes simplex encephalitis 49infection of brain and its linings
  • 50. 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 infection of brain and its linings 50 Herpes simplex encephalitis
  • 51. 51infection of brain and its linings
  • 52. Herpes simplex encephalitis Rare paraneoplastic syndrome limbic system, often bilateral Active seizures may disrupt BBB, cause signal abnormalities and enhancement 52infection of brain and its linings
  • 53. 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 53infection of brain and its linings
  • 54. 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 54infection of brain and its linings
  • 55. 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++, 55infection of brain and its linings
  • 56. 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 infection of brain and its linings
  • 57. 57infection of brain and its linings
  • 59. 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). 59infection of brain and its linings
  • 60. Pathology 1)Tiroumourougane. Postgrad. Med. J. 2002; 78: 205 60infection of brain and its linings Some neurons have specific receptors with strong affinity for JEV [1
  • 61. 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 61infection of brain and its linings Imaging
  • 62. Evolution of lesions in JE 62infection of brain and its linings
  • 63. 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 63infection of brain and its linings
  • 64. infection of brain and its linings 64 T2 DWI PATTERN 1 DWI>T2 [1]
  • 65. 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 65infection of brain and its linings
  • 66. 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. 66infection of brain and its linings
  • 67. infection of brain and its linings 67 co-infection
  • 68. 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 68infection of brain and its linings
  • 69. 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 69infection of brain and its linings
  • 70. 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 70infection of brain and its linings
  • 71. 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 71infection of brain and its linings
  • 72. Dengue infection of brain and its linings 72 From. Muzaffar. Sing Med J 2006;47:975 Imaging studies have shown cerebral edema, lesions in the hippocampus and temporal lobes
  • 73. 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. 73infection of brain and its linings
  • 74. infection of brain and its linings 74
  • 75. 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 75infection of brain and its linings
  • 76. 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 infection of brain and its linings 76
  • 77. 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. 77infection of brain and its linings
  • 78. 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. 78infection of brain and its linings
  • 79. 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 79infection of brain and its linings
  • 80. infection of brain and its linings 80  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
  • 81. 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. 81infection of brain and its linings
  • 82. 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] 82infection of brain and its linings
  • 83. 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. 83infection of brain and its linings
  • 84. 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 84infection of brain and its linings
  • 85. 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. 85infection of brain and its linings
  • 86. 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. 86infection of brain and its linings
  • 87.  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 87infection of brain and its linings Cytomegalovirus Encephalitis
  • 88. Cerebritis and Abscess 88infection of brain and its linings
  • 89. 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 infection of brain and its linings 89
  • 90. 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 infection of brain and its linings 90
  • 91. infection of brain and its linings 91 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
  • 92. 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. infection of brain and its linings 92 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
  • 93. infection of brain and its linings 93 Abscess treated conservatively with antibiotics.
  • 94. infection of brain and its linings 94 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
  • 95. 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 95infection of brain and its linings 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
  • 96. 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 infection of brain and its linings 96
  • 97. infection of brain and its linings 97  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.
  • 98.   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 98infection of brain and its linings
  • 100. 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 100infection of brain and its linings
  • 101. TBM pathology Penetration of meningeal vessel walls by haematogenous spread • Rupture of subependymal or subpial granulomata into the CSF 101infection of brain and its linings
  • 102. 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 102infection of brain and its linings
  • 103. infection of brain and its linings 103  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.
  • 104. Tuberculous meningitis differential diagnosis includes fungal meningitis, sarcoid and carcinomatous meningitis 104infection of brain and its linings
  • 105. 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 infection of brain and its linings
  • 106. 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 infection of brain and its linings
  • 107. 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 infection of brain and its linings
  • 108. 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 108infection of brain and its linings
  • 109. 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 109infection of brain and its linings 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
  • 110. 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. 110infection of brain and its linings
  • 111. Patho physiology 111infection of brain and its linings
  • 112. 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. 112infection of brain and its linings
  • 113. 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. infection of brain and its linings 113
  • 114. Mucormycosis infection of brain and its linings 114
  • 115. 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 infection of brain and its linings 115 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
  • 117. 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 infection of brain and its linings 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)
  • 118. 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 infection of brain and its linings 118
  • 119. 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 infection of brain and its linings
  • 120.  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 120infection of brain and its linings
  • 121. 121infection of brain and its linings
  • 122. Intraventricular cysticercosis potentially lethal The cysts can be identified by CSF density or signal intensity A thick, ring like enhancement associated with intraventricular cysticercosis 122infection of brain and its linings
  • 123. 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 123infection of brain and its linings
  • 124. infection of brain and its linings 124  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
  • 125. 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 infection of brain and its linings 125
  • 127. 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. 127infection of brain and its linings
  • 129. 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 129infection of brain and its linings
  • 130. 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. 130infection of brain and its linings
  • 131. Intracranial infections take the following forms Cerebritis Abscess Empyema Granuloma Encephalitis Meningitis Osteomyelitis infection of brain and its linings 131
  • 132. 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 infection of brain and its linings
  • 133. 133infection of brain and its linings