4. Presentation of infection
•Pia or Subarachnoid space and/or dura or arachnoid
•Empyema : epidural or subdural
•Cerebritis :Intraparenchymal early stage of abcess formation
•Intraparenchymal abcess
•Ventriculitis
5. BACTARIAL infections
• ORGANISMS INVOLVED
•
•
•
•
Neonates:GROUP B Streptococcus,E.Coli,Listeria
Young Children:Heamophilus,E.Coli,Nisseria meningitides
Adults:Streptococcous pneumoniae,,N.Meningitidis
Old age:S.pneumoniae,Listeria
7. Meningitis
•Types
•Predisposing Factors(
Sinusitis, Chronic Pulmonary
Infection, Tetrology of Fallot, Transposition of great vessels, other
Cyanotic heart diseases)
Imaging Features:
a. Initially Normal on C.T.
b. Convexity enhancement
c. Basilar enhancement(more common on T.B.M.)
8. COMLICATIONS OF MENINGITIS
1.
2.
3.
4.
5.
6.
Subdural effusion common in infants and children
Empyema
Parenchymal extension (Cerebritis ,Abcess formation)
Hydrocephalous(communicating>non communicating
Ventriculitis
Venous infections secondary to thrombosis
9. Frontal sinusitis, empyema, and
abscess formation in a patient
with bacterial meningitis. This
contrast-enhanced, axial T1weighted magnetic resonance
image shows a right frontal
parenchymal low intensity
(edema), leptomeningitis
(arrowheads), and a lentiformshaped subdural empyema
(arrows).
10. Chronic mastoiditis and
epidural empyema in a patient
with bacterial meningitis. This
axial computed tomography
scan shows sclerosis of the
temporal bone (chronic
mastoiditis), an adjacent
epidural empyema with
marked dural enhancement
(arrow), and the absence of
left mastoid air.
11. Brain Abcess
1. Children:(staphylococcal especially after
trauma,Streptococcuc,Pneumococcus)
2. Adults:mixed aerobic and anaerobic flora
3. Immunosuppression:Toxoplasmosis,Cryptococcus,CandidiasisAspergi
llosis,Nocardiosis,mucormycosis,T.B.Atypical Mycobacteria
• MECHANISM
1.
2.
•
•
•
3.
Hematogenous Spread(I/V drug abuse,Sepsis)
Direct Extension
Sinusitis
Otitis,Mastoiditis
Open trauma(penetrating trauma,Surgery
Idiopathic
12. Cerebral
abscess.
(A) Low-density lesion in occipital region with some mass effect. (B) After contrast
medium, note thin ring of enhancement round the abscess with oedema anteriorly. (C)
Multiple abscesses in frontoparietal area showing capsular enhancemenT
after contrast medium (L34, W75).
16. Acute bacterial meningitis. This
contrast-enhanced, axial T1weighted magnetic resonance
image shows leptomeningeal
enhancement (arrows).
17. Tuberculous Meningitis
•
•
•
•
•
•
•
Most common CNS manifestation of T.B.
Followed by pulmonary T.B.
Intraparenchymal Tuberculoma
Basilar Meningeal involvement
Cranial Nerve Palsies*(commonly Optic nerve)
Hydrocephalous
MRI IS MORE SENSITIVE
18. Imaging Features
•Basilar Meningitis
1. Intense contrast enhancement of basilar Meninges(CT&MRI)
2. Pituitary and parasellar involvement
3. Pituitary or hypothalamic axis involvement
4. T2W hypo intense Meninges
5. Calcification occur late in disease
• Tuberculoma(usually solitary, Nonspecific enhancing mass like
lesion)
• Miliary Form: Multiple tiny Intraparenchymal lesions
19.
20.
21.
22.
23.
24. Enhanced CT of a patient with tuberculous meningitis showing
perivascular inflammatory changes and temporal infarction due to
vasculitis.
26. Herpes Simplex Virus Encephalitis
HSV-1,oral herpes
•Children and adults
•Activation of latent virus in trigeminal ganglion
•Altered mental status
•Limbic system, frequently b/l but asymmetrical
HSV-2 genital herpes
•Neonatal torch infection
•Acquired during parturition
•Manifests several weeks after birth
•Diffuse encephalitis(non focal)
27. IMAGING FEATURES
•MRI is superior to CT
•CT & MRI findings are normal initially
•MRI detect changes even 2 to 3 days after disease
•Distribution: limbic system , temporal lobe> cingulate gyrus,subfrontal region
1. Acute Stage
•
Decreased/restricted diffusion in affected areas
Gyral oedema( T1W hypo intense/T2W hyperintense)
No enhancement
2. Subacute stage
Marked increase in edema
bilateral asymmetrical involvement
gyral enhancement
Hemorrhage is common
28.
29.
30. HSE. T2 weighted MRI
showing extensive area of
increased signal in right
temporal lobe and lesser
involvement of the left.
31. Axial proton density–
weighted image in a 62-yearold woman with confusion
and herpes encephalitis
shows T2 hyperintensity
involving the right temporal
lobe.
32. Axial nonenhanced T1weighted image shows
cortical hyperintensity
(arrows) consistent with
petechial hemorrhage. In
general, this is a common
pathologic finding but less
commonly depicted in
herpes encephalitis.
33. Axial gadoliniumenhanced T1-weighted
image reveals
enhancement of the right
anterior temporal lobe
and parahippocampal
gyrus. At the right anterior
temporal tip is a hypo
intense, crescentic region
surrounded by
enhancement consistent
with a small epidural
abscess.
34. Axial diffusion-weighted image
reveals restricted diffusion in
the left medial temporal lobe
consistent with herpes
encephalitis. This patient also
had a positive result on
polymerase chain reaction
assay for herpes simplex
virus, which is both sensitive
and specific. In addition, the
patient had periodic lateralized
epileptiform discharges on
electroencephalogram, which
supports the diagnosis of
herpes encephalitis.
35. hyperintensity in the left temporal
lobe (arrows) in a distribution
similar to the restricted diffusion
abnormality seen in the previous
image. This finding is typical for
herpes encephalitis. In patients
with HHV6 infection, one series
noted that in addition to mesial
temporal lobe
abnormality, abnormal T2
hyperintensity has been seen in the
insular and inferior frontal
region, which may suggest the
diagnosis. There are felt to be 2
typical imaging appearances: one
seen in older adults involves T2
hyperintensity confined to the
medial temporal lobe; in young
adults, a more varied pattern has
been described that includes foci of
restricted diffusion with an
otherwise normal magnetic
resonance, diffuse cortical
necrosis, or small focal regions of
abnormal T2 hyperintensity.
36. Progressive multifocal
leukoencephalopathy
•Papova virus causative organism
•Effect patients with compromised immunity
•Multifocal demyelinating lesion spread in hemispheres often
asymmetrically
•MRI superior to CT
•Spreading areas of low density seen on CT
• Increased signals on T2W & less conspicuous reduced signals on T1W
37. Neurological outcomes of congenital CMV infection. Examples of computed tomography (A) and magnetic
resonance imaging (B and C) of three infants with severe symptomatic congenital CMV infection with CNS
involvement are shown. The classical pattern of injury described with congenital CMV infection involving the CNS is
characterized by periventricular calcifications (panel A, arrow). Other consequences of fetal brain infection include
abnormalities of neuronal migration, leading to polymicrogyria (panel B, arrows) and, in extreme cases, profound
structural defects such as porencephalic cysts with associated schizencephaly (panel C, arrow).
38.
39. Subacute sclerosing panencephalitis.
Figure 1. MRI scans of the brain at the
time of presentation in the neurology
clinic (A and B) and 3 months later (C
and D). Panels A and C are T1weighted images; B and D are T2weighted images. The initial MRI scan
(A and B) reveals a focal abnormality
in the subcortical white matter of the
left frontal lobe, consisting of a
hypointense signal on the T1-weighted
image (arrow in A) and a hyperintense
signal on the T2-weighted image
(arrow in B). In the follow-up scan, the
focal abnormality in the left frontal
lobe is less obvious than previously
(arrow in D), but advanced and diffuse
cortical atrophy is present, signified by
the ventriculomegaly and markedly
enlarged sulci (arrowheads in C).
40. Axial FLAIR images of a
patient with chronic HHV
6 encephalitis showing
patchy signal
hyperintensities in white
matter and cortex.
41. AIDS
•A neurotropic Virus
•Can effect brain directly or can predispose to opportunistic infections
•Common HIV –related infections include
1. HIV encephalopathy
2. Toxoplasmosis most common opportunistic infection of CNS
3. Cryptococcosis
4. Progressive multifocal leukoencephalopathy
5. TB
6. Syphilis
7. Varicella
8. CMV
42. HIV ENCEPHALOPATHY
•Progressive sub acute sub cortical dementia secondary to HIV itself.
•60% patients effected
•IMAGING FEATURES
•Atrophy most common finding
•T2W bright WM lesion in frontal & occipital lobe and peri ventricular
location(gliosis, demyelination)
•No enhancement or mass effect of WM lesions
•CT:diffuse white matter low attenuation
•Most of AIDS findings seen are due to associated Viruses
43.
44.
45. Fungal Infections
•Fungal infections of CNS only rarely seen in healthy people
•Common Infections
1. Cryptococcosis
2. Aspergillosis
3. Candidiasis
4. Mucormycosis
• Less common are
Histoplasmosis,coccididomycosis,blastomycosis,cladosporiasis,nocardiosis,actino
mycosis
46. Cryptococcal Infection
•Meningitis spread along perivascular spaces
•Multiple areas of enhanced signals on T2W images of basal
ganglia and brainstem
•Cystic lesions also seen
47. (A,B) Bilateral basal ganglia cryptococcomas, which have a slightly punctuate appearance on the
T 2 -weighted images. On the T, coronal
images, the lesions are slightly hypointense and those on the right exert some mass effect on
the right frontal horn.
48. (C,D) Axial and coronal sections
T2-weighted and T,-weighted show small enhancing abscess impinging on the right ventricle.
50. Coronal T1WI after
gadolinium enhancement.
Patient after bone marrow
transplantation with
aspergillus encephalitis. Ringenhancing lesion with
perifocal edema and mass
effect compressing the lateral
ventricle.
52. Toxoplasmosis
•Toxoplasma Gondi
•Two types(congenital & adult)
•Commonly associated with AIDS
•Congenital:
•Gross degree of venticular dilatation
•Extensive calcification of
a) Basal ganglia
b) Subcortical regions
54. Adult toxoplasmosis
Commonly associated with AIDS
IMAGING FEATURES:
•Single or multiple ring enhancing lesions with surrounding edema
•Target appearance of lesion is common
•Major consideration in D.D. is CNS LYPHOMA
•Periventriclar location and subependymal spread favors lymphoma
•Multiple lesions are suggestive of lyphoma
55. (A) Toxoplasmic encephalitis in a patient with AIDS.Multiple small
abcesses with ring enhancement .A ring enhancing lesion proven to
toxoplasmosis abcess is shown periphally in the left frontal lobe on the
T2 axial(B) and T, coronal postcontrast imaging(C).the appearences are
non-specific and there is a large amount of assosiated vasogenic
edema.Multiple small enhancing nodules are present predominently at
the grey-white matter junction in this T,axial image
57. (E)This patient was known to have Aids And have Multiple
Toxoplasmosis abcesses
58. Cysticercosis
•Taenia solium
•Cysticercus cellulosae is larval stage
•Acute stage shows small rounded low density lesion enhance with CM on CT
•Chronic stage shows punctuate calcifications, obstructive hydrocephalous on CT
•MRI demonstrate lesion well even in very early stage.
62. Manifestation of palsy of
left seventh cranial nerve
in 10-year-old male patient
with recent history of
camping. Transverse T1weighted postcontrast MR
image shows
enhancement of left
seventh cranial nerve
(arrow).
•Borrelia burgdorferi is the
causative agent
63. Right facial
numbness, pain, and
paralysis in 42-year-old
female patient. T1weighted postcontrast
coronal MR images
depict enhancement of
(a) right trigeminal
nerve (arrow)
65. Figure 2a. Sporadic CreutzfeldtJakob disease in a 65-year-old
man 10 weeks after the onset of
dementia, insomnia, and optical
hallucinations and 4 weeks
before the appearance of
periodic synchronous discharges
on the EEG. Diffusion-weighted
image shows bilateral areas of
abnormal high signal intensity in
the cerebral cortex, caudate
nuclei, putamen, and thalamus.
