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© 2003 By Default!
A Free sample background from www.awesomebackgrounds.com
Slide 1
Tool for DNB Practical
examination in pediatrics
CT in
pediatrics

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Slide 2
Identify:
A
B
C
D
E
F
G
H
I
J
k

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Slide 3

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Slide 4
D E
A
B
C
F G
H
I

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Slide 5

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Slide 6
WHAT IS THE ROLE OF NEUROIMAGING IN
MENINGITIS?
WHAT IS THE ROLE OF NEUROIMAGING IN
DIAGNOSING
EARLY TBM?
WHAT ARE THE FEATURES OF BASAL
EXUDATES ON CT/MRI?

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Slide 7
Meningitis
(tuberculous)

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Slide 8
Meningitis

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Slide 9
Meningitis with
Hydrocephalus

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Slide 10
Subdural Effusion Secondary To Meningitis

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Slide 11
IN CASE OF HEALTHY CHILDREN WITH
SEIZURES ONE SHOULD SUSPECT AN
INTRACRANIAL GRANULOMA.
INTRACRANIAL GRANULOMA- A CLINICAL
DILEMMA.
IS IT A TUBERCULOMA OR
NEUROCYSTICERCOSIS?
HOW WOULD NEUROIMAGING HELP?

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Slide 12
TUBERCULOMA

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Slide 13
TUBERCULOMAS

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Slide 14
NEUROCYSTICERCOSIS

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Slide 15
NEUROCYSTICERCOSIS

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Slide 16
NEUROCYSTICERCOSIS

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Slide 17
NEUROCYSTICERCOSIS
STAGES CT MR
VESICULAR Hypodense lesion with
mural nodule,
edema/enhancement rare.
T1W-hypointense
T2W-hyperintense
COLLOIDAL
VESICULAR
Ring enhancing lesion
with edema.
Hyperintense on
T2W with peripheral
enhancement/edema.
GRANULAR
NODULAR
Isodense cyst with
hyperdense cacified
scolex.Edema/enhanceme
nt +.
Isointense to
hypointense on
T2W.Target or Bull’s
eye appearance.
NODULAR
CALCIFIED
Small calcified nodule.No
edema / enhancement.
Void on T2W.

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Slide 18

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Calcified Granuloma

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Slide 20
A CHILD PRESENTED WITH FEVER
AND ALTERED SENSORIUM. A
PROVISIONAL DIAGNOSIS OF
ENCEPHALITIS WAS MADE.
WHAT ARE CT FINDINGS

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Slide 21
Herpes encephalitis

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Slide 22
Japanese B
Encephalitis

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Slide 23
Meningo-Encephalitis

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Slide 24
HOW DO YOU PROCEED
WITH A SUSPECTED CASE
OF INFARCT?
WHAT WOULD BE THE
INVESTIGATION OF
CHOICE?

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Slide 25
DENSE MCA

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Slide 26
MCA ( 3 diff
patients)

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Slide 27
Acute Infarct

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Slide 28
PROTEIN C DEF.

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Slide 29
PROTEIN C
DEF.

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Slide 30
MOYA MOYA

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Slide 31
Venous sinus thrombosis
PLAIN CECT

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Slide 32
Venous infarct

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Slide 33
I.C.Bleed

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Slide 34
INTRAPARENCHYMAL BLEED
STAGES CT MRI
ACUTE
(De-oxy Hb)
Hyperdense to brain
parenchyma.
T1- HYPERINTENSE
T2- HYPOINTENSE
SUBACUTE
(MethHb)
1 to 6 weeks.
Isodense with adjacent brain
parenchyma.
Peripheral enhancement.
T1- HYPERINTENSE
T2- HYPERINTENSE
CHRONIC
(Haemosiderin)
Hypodense to adjacent
parenchyma.
Fluid –fluid level s/o rebleed.
T1- HYPOINTENSE
T2- MORE
HYPOINTENSE

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Slide 35
Encephalomalacia

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Slide 36
Porencephalic Cyst

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Slide 37
ONE AND A HALF YEAR OLD CHILD – A
CASE OF CEREBRAL PALSY WITH
SPASTIC QUADRIPARESIS,
MICROCEPHALY AND NORMAL VISION,
WHAT WOULD YOU EXPECT TO SEE IN
NEUROIMAGING ?

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Slide 38
HIE

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Slide 39
Hypoxic ischaemic
encephalopathy
Perinatal insult

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Slide 40
PVL
Perinatal insult

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Slide 41
GERMINAL MATRIX HAEMMORAGE
IN A PRETERM INFANT

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Slide 42
BASAL GANGLIA CALCIFICATION- AN
INCIDENTAL FINDING.
IS IT NORMAL OR ABNORMAL?
WHAT CLUES ON NEUROIMAGING WOULD
HELP?

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Slide 43
Basal Ganglia Calcification

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Slide 44
CAUSES OF BASAL GANGLIA
CALCIFICATION
COMMON
Idiopathic
Fahr’s Disease
Hypoparathyroidism
Postinflammatory ( TB, CID, toxoplasmosis,
cysticercosis, congenital HIV )
UNCOMMON
Congenital ( Tuberous sclerosis, Downs syndrome,
MELAS/MERRF, Cockayne syndrome )
Post anoxic/toxic ( carbon monoxide poisoning,
chemotherapy and radiation therapy)

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Slide 45
TORCH(CMV)

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Slide 47
WHICH ARE THE
NEURODEGENERATIVE DISORDERS
THAT SHOW POSITIVE
NEUROIMAGING FINDINGS?
HOW MANY CASES HAVE YOU SEEN
SO FAR?
WHAT ARE SPECIFIC OBSERVATIONS
ON IMAGING?

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Slide 51
Normal head circumference
Central to peripheral pattern
Metachromatic leukodystrophy (onset: 4 to 8 years)
Krabbe's disease (onset: before 4 years)
Pelizaeus-Merzbacher disease (onset: 4 to 8 years,
boys)
Dorsal to ventral pattern
Adrenoleukodystrophy* (onset: 4 to 8 years)
Increased head circumference
Peripheral to central pattern
Canavan's disease (onset: infancy)
Ventral to dorsal pattern
Alexander's disease* (onset: infancy)
*Enhances with gadolinium.

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Slide 52
DISTINCTIVE FEATURES OF
LEUKODYSTROPHIES
COMPLETE OR NEAR LACK OF MYELINATION
Canavan Disease
Pelizaeus-Merzbacher Disease
FRONTAL WHITE MATTER MOST INVOLVED
Alexander Disease
OCCIPITAL WHITE MATTER MOST INVOLVED
Adrenoleukodystrophy
THICK MENINGES
Hurler Syndrome

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Slide 58
 Occurs in highly predictable orderly fashion.
 Caudad to cephalad, dorsal to ventral and
central to peripheral.
NORMAL MYELINATION

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Slide 60
BIRTH
Medulla, Dorsal midbrain, Cerebellar peduncles, Posterior limb of
internal capsule.
ONE MONTH
Deep cerebellar white matter, Corticospinal tracts, Pre/postcentral
gyrus, optic nerves and tracts.
THREE MONTHS
Brachium pontis, ventral brainstem, optic radiations, anterior limb
of internal capsule, corpus callosal splenium.
SIX MONTHS
Corpus callosum genu, paracentral subcortical U fibres, centrum
semiovale.
EIGHT MONTHS
Centrum semiovale, Subcortical U fibres.
EIGHTEEN MONTHS
Essentially like adult.

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Slide 61
Normal Myelination - Age 1 Day
On T2-weighted images the white matter has a higher signal intensity than the gray
matter except. Low–signal intensity myelin is seen in the ventrolateral thalamus,
dorsal pons, and rolandic and perirolandic gyri.

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Slide 62
Normal Myelination - Age 1
Month
T2-weighted images show further deposition of myelin in the
ventrolateral thalamus, posterior limb of the internal capsule, and
rolandic and perirolandic gyri. Note the small amount of myelin in the
optic radiations.

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Slide 63
Months
On T2-weighted images, myelin deposition is seen throughout the
posterior limb of the internal capsule and in the optic radiations
and the white matter of the central semiovale adjacent to the
precentral and postcentral gyri. The entire medulla and the central
cerebellar white matter are now myelinated.

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Slide 64
Months
On T2-weighted images the white matter now has
a lower signal intensity than the gray matter (early
adult pattern).

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Slide 65
WHAT ARE THE VARIOUS
NEURONAL MIGRATION
ANOMALIES?
WHAT MODALITY OF
NEUROIMAGING WOULD
YOU PREFER?

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