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C1
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Slide 1
Tool for DNB Practical
examination in pediatrics
CT in
pediatrics
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Identify:
A
B
C
D
E
F
G
H
I
J
k
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D E
A
B
C
F G
H
I
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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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Meningitis
(tuberculous)
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Meningitis
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Meningitis with
Hydrocephalus
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Subdural Effusion Secondary To Meningitis
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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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TUBERCULOMA
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TUBERCULOMAS
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NEUROCYSTICERCOSIS
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NEUROCYSTICERCOSIS
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NEUROCYSTICERCOSIS
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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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Calcified Granuloma
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A CHILD PRESENTED WITH FEVER
AND ALTERED SENSORIUM. A
PROVISIONAL DIAGNOSIS OF
ENCEPHALITIS WAS MADE.
WHAT ARE CT FINDINGS
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Herpes encephalitis
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Japanese B
Encephalitis
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Meningo-Encephalitis
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HOW DO YOU PROCEED
WITH A SUSPECTED CASE
OF INFARCT?
WHAT WOULD BE THE
INVESTIGATION OF
CHOICE?
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DENSE MCA
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MCA ( 3 diff
patients)
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Acute Infarct
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PROTEIN C DEF.
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PROTEIN C
DEF.
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MOYA MOYA
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Venous sinus thrombosis
PLAIN CECT
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Venous infarct
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I.C.Bleed
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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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Encephalomalacia
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Porencephalic Cyst
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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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HIE
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Hypoxic ischaemic
encephalopathy
Perinatal insult
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PVL
Perinatal insult
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GERMINAL MATRIX HAEMMORAGE
IN A PRETERM INFANT
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BASAL GANGLIA CALCIFICATION- AN
INCIDENTAL FINDING.
IS IT NORMAL OR ABNORMAL?
WHAT CLUES ON NEUROIMAGING WOULD
HELP?
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Basal Ganglia Calcification
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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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TORCH(CMV)
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TORCH(CMV)
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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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Leukodystrophy
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KEY POINTS
HEAD CIRCUMFERENCE
AGE OF ONSET
PATTERN OF INVOLVEMENT
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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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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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Adrenal Leukodystrophy
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Alexander’s Disease
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Canavan’s disease
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LEUKODYSTROPHY
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LEUKODYSTROPHY
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Occurs in highly predictable orderly fashion.
Caudad to cephalad, dorsal to ventral and
central to peripheral.
NORMAL MYELINATION
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Normal Myelination Pattern
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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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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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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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Normal Myelination - Age 3
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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Normal Myelination - Age 13
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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WHAT ARE THE VARIOUS
NEURONAL MIGRATION
ANOMALIES?
WHAT MODALITY OF
NEUROIMAGING WOULD
YOU PREFER?
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Neuronal migration anomalies
Agyria/pachygyria
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Agyria/pachygyria
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Cortical Dysplasia
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Polymicrogyria
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Heterotopia
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Schizencephaly