CN

Bikash Raj Thapa, MD

Imaging modalities

Simple radiography

-cheap preliminary screening

-accuracy & specificity is low

USG:

Inexpensive; portable; multiplanar-dynamic; no-radiation

Choice in neonates/infants
Computerized tomography- basic choice
hge stroke; head injury; screening
MRI tissue characterization is better
Angiography- mainly for interventional radiology
Radionuclide scan- is superseded by CT & MRI

Positron emission tomography (PET)

-

expensive & available in very advance centre

PET tracer like carbon, nitrogen, oxygen
Demonstrates difference in focal brain metabolism
Major use in oncology

NEUROSONOGRAPHY
NICU
Assist in diagnosis:
PVL; ICH;
hydrocephalous
etc
Monitor
complications and
interventions:
ventriculoperitone
al shunts

CENTRAL NERVOUS SYSTEM

CALCIFICATION, HYDROCEPHALUS
BASICS OF TUMORS, INFARCTS,
INFECTIONS ON CT
SPINE
D/D: COLLAPSE VERTEBRAE: TB
D/D: METASTATIC
SCLEROTIC LESIONS
OSTEOMYELITIS

Hypodense lesions

Hyperdense

1. Infarct
2. Non-haemorrhagic
contusion
3. Tumours
4. Edema
5. Metabolic
encephalopathy
6. Hypertensive
encephalopathy
7. Encephalitis
8. Lipoma

1.
2.
3.

Intracranial calcifications
Infection (TORCH)
Tumors
1. lymphoma
2. medulloblastoma
3. meningioma
4. metatasis
a. mucin-producing
adenocarcinoma
b.
hemorrhagic metatasis:
breast/lung; melanoma/RCC
choriocarcinoma

4.
5.
6.
7.

Cysts: Colloid
Endocrinal:
hypoparathyroidism
Neurocutaneous syndromes
Arteriovenous lesions

Ring enhancing lesions

Metastasis
Abscess
Glioblastoma
Infarction
Contusion
Demylinating disease
Radiation necrosis

INTRACRANIAL
CALCIFICATIONS
Normal intracranial calcificationscan be
defined as all age-related physiologic and
neurodegenerative calcifications that are
unaccompanied by any evidence of disease and
have no demonstrable pathological cause.
PINEAL GLAND: 60% adult; >14mm: neoplasm
HABENULA: 30%
CHOROID PLEXUS: 10%
BASAL GANGLIA
DURA
PETROCLINOID LIGAMENTS
SSS

CRANIOCEREBRAL
TRAUMA

Classification of head injury

Primary injury:
Those occurring as a direct result of
initial traumatic event.

Secondary injury:
These are consequences of primary
injuries
Frequently more devastating than the
primary injury

Primary injuries:
Skull #, scalp hematoma/ lacerations
Extracerebral hemorrhage
Epidural hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage

Intraaxial lesions:

Diffuse axonal injury

Cortical contusions
Deep cerebral gray matter injury
Brainstem injury
Intraventricular/ choroid plexus hemorrhage

Secondary lesions:

Cerebral herniations
Traumatic ischemia, infarction
Diffuse cerebral edema
Hemorrhages

Imaging Strategy
Imaging of acute head trauma is performed
to detect treatable lesions before secondary
neurologic damage occurs.
Currently, this is best performed by CT for
several reasons:
it is quick & widely available
Highly accurate in the detection of acute intraaxial and extra-axial hemorrhage, as well as
skull, temporal bone, facial, and orbital fractures.
Monitoring equipment is easily accommodated.

Skull Fractures:
Types:
Linear #
Depressed #; ping-pong/pond fracture
(newborn)
Comminuted #
Compound #
Growing #: (leptomeningeal cyst)

Can involve:
Cranial vault
Base of the skull
Sutural diastases

Epidural hematoma
1-4% pt imaged for craviocerebral trauma
Etiology- # that lacerates MMA or dural venous sinus
Location:
Between skull & dura (biconvex shape)
Temporoparietal region commonest site
95% unilateral
Do not cross suture
Secondary herniation common

Imaging :
Biconvex extra-axial collection
May be heterogeneous due to hyperdense blood
and hypodense serum or due to active bleeding
Chronic- Peripheral enhancement representing
dura and membrane formation between
hematoma & adjacent brain parenchyma.

Axial CT scan demonstrates a biconvex, high-attenuation,

extra-axial collection causing mass effect on the right frontal
lobe and mild midline shift (subfalcial herniation). Note how
the epidural hematoma does not extend beyond the right
coronal suture

Subdural Hematoma
Most lethal of all head injuries
Mortality rates upto 50-85%
Stretching and tearing of bridging cortical veins
as they cross sd space common
disruption of penetrating branches of superficial
cerebral arteries less common
Location:

Between dura and arachnoid

Frontoparietal convexities & middle cranial fossa
Widespread than EDH
Crescentic shaped, cross suture, extend into interhemispheric
fissure
Doesnt cross midline
85% unilateral

Sub Arachnoid hemorrhage

Traumatic.
Spontaneous SAH:
Ruptured arterial aneurysm (70-80%)
Arteriovenous malformation (10%)
Other rare causes:

Tumor bleeding
Mycotic aneurysm
Cortical thrombosis
Dural AV fistula
Arterial Dissection

No cause identifiable in angiogram

Noncontrast axial CT scans in two different patients

demonstrate high-attenuation material within the sulci and
right sylvian fissure consistent with subarachnoid
hemorrhage.

Hydrocephalus
Denotes an increase in the volume of CSF
and thus of the cerebral ventricles.
Obstructive and non-obstructive (on
the grounds of whether or not there is
obstruction of CSF pathways in the
ventricles or in the subarachnoid space)
Communicating and noncommunicating (addressing where
theobstructionis located).

Obstructive hydrocephalus
passage of CSF within the ventricular system or in the
subarachnoid space isimpaired at some point
communicating obstructive hydrocephalus
passage of CSF from the ventricular system and into the
subarachnoid space is unimpeded butabsorption of CFS via
arachnoid granulations is impaired
subarachnoid haemorrhageormeningitis
extra-axial CSF spaces (e.g. Sylvian fissures and sulci) are also
distended

non-communicating obstructive hydrocephalus

often merely referred to of asobstructive hydrocephalus
due to obstruction of CSF out flow at any point (e.g.aqueduct
stenosis,colloid cystobstructing the foramen of Monro)
up-stream ventricles are dilated and exert mass effect upon
adjacent brain (e.g. effacement of sulci)

 Non-obstructive hydrocephalus
often referred to asex-vacuo
dilatation of the ventricles
CSF can pass out of the ventricles and
into the basal cisterns without
impediment, and is readily absorbed
ventricles are enlarged due to loss of
adjacent brain parenchyma

Characteristics of
Hydrocephalus
Ventricular enlargement disproportionate to the
degree of sulcal widening
Enlargement of temporal horns
Periventricular fluid secondary to
transependymal CSF permeation
Enlarged 3rd ventricle (outward bowing of the
lateral wall) with large suprapineal and
chiasmatic receses and inferior bowing of the
floor
In children < 2 years the head circumference is
often the best distinguishing feature between
hydrocephalus and atrophy.

MEASUREMENTS
Frontal horns (Monro):
<40 yrs= <12mm
>40 yrs=<15

Ventriculohemispheric ratio:
<33% in adults
<40% in children

Third ventricle
<5mm: children
<7mm: <60yrs
<9mm:>60yrs

Hydrocephalic
Brain

Normal CT Brain

Colloid cyst

STROKE

 On CT 60% of
infarcts are seen
within 3-6 hrs and
virtually all are
seen in 24 hours.
ADV: Hge stroke
(MRI confusing)

MRI- Diffusion
restriction (DWI)
with reduced ADC
has been observed
as early as 30
minutes after the
onset of ischemia.

Imaging protocal
Nonenhanced scanning must be performed as
soon as possible after the stroke is suspected.
and the key role of nonenhanced CT is the
detection of hemorrhage or other possible
mimics of stroke (eg,neoplasm, arteriovenous
malformation).

CT Findings in Infarction
Hyperacute: <12 hrs

Normal 50-60%
Hyperdense artery (dense MCA sign)
Obscuration of the lenticular nucleus
loss of gray-white interfaces (insular ribbon sign

Acute: 12-24 hrs

Low density basal ganglia
sulcal effacement
1 to 3 Days:
Increasing mass effect
Wedge-shaped low density area involving gray and white
matter
Possible hemorrhagic transformation

 Axial unenhanced CT
images in a proximal
segment of the left MCA
in a 53-year-old man (a)
and a distal segment of
the left MCA in a 62year-old woman (b),
obtained 2 hours after
the onset of right
hemiparesis and aphasia,
show areas of
hyperattenuation (arrow)
suggestive of intravascular
thrombi

 Axial unenhanced CT
image obtained in a 53year-old man shows
hypoattenuation and
obscuration of the left
lentiform nucleus (arrows),
which, because of acute
ischemia in the
lenticulostriate distribution,
appears abnormal in
comparison with the right
lentiform nucleus

 Axial unenhanced CT
image, obtained in a 73year-old woman 212 hours
after the onset of left
hemiparesis, shows
hypoattenuation and
obscuration of the posterior
part of the right lentiform
nucleus (white arrow) and
a loss of gray matterwhite
matter definition in the
lateral margins of the right
insula (black arrows).The
latter feature is known as
the insular ribbon sign.

Drawings (top) illustrate the territories(blue) of the ACA, middle cerebral artery (MCA)
, and posterior cerebral artery. CT scans (bottom) show established infarctions of
these arteries

CVA

Intracerebral
hematoma
basal nuclei
region with
mass effect

INFECTIONS

 Congenital / neonatal infections

Meningitis
Pyogenic parenchymal
infections
Encephalitis
Tubercular and fungal infections
Parasitic infections

 CMV
DNA virus
Most common cong. CNS infection
(also cause cardiac anomalies, hepatosplenomegaly)
Predilection for periventricular subependymal germinal matrix
Widespread periventricular tissue necrosis and subsequent
dystrophic calcification.
Plain film microephaly with egg shell- like periventricular
calcification
US/CT/MRI encephaloclastic lesions, periventricular ca++,
subependymal paraventicular cyst, ventriculomegaly
MRI- delayed myelination, encephalomalacia, migrational
disorder (lissencephaly, polymicrogyria, pachygyria)

Periventricular calcification in CMV infection

Fink K R et al. Radiographics 2010;30:1779-1796

2010 by Radiological Society of North America

 TOXOPLASMOSIS

T. gondii, obligate intracellular parasite

Multifocal, scattered lesions (basal ganglia,
cortex, periventricular location and white
matter)
No migrational disorder
Triad (imaging)
hydrocephalus (due to ependymitis-leads to
periaqueductal necrosis-aqueductal
stenosis)
b/l chorioretinitis
intracranial calcifications

Axial unenhanced CT image

reveals a peripherally
calcified lesion (arrow) in the
right caudate head that is a
sequela of previous
toxoplasmosis infection. The
low-attenuation mass lesion
with surrounding edema in
the region of the left basal
ganglia is from a new focus
of toxoplasmosis.

MENINGITIS

Role of CT in meningitis
toidentify contraindicationsof a lumbar puncture
to identify complicationsthatrequire prompt
neurosurgical interventions such assymptomatic
hydrocephalus, subdural empyema, and cerebral abscess.
CT scans may reveal the cause of meningeal infection.
Otorhinologic structures and congenital and posttraumatic
calvarial defects can also be evaluated
CT cisternography may depict CSF leaks, which may be the source
of infection in cases of recurrent meningitis

Nonenhanced CT scan findings

may be normal (>50% of patients)
effacement of basilar & convexity cisterns by inflammatory
exudates
mild ventricular dilatation and effacement of sulci
cerebral edema and focal low-attenuating lesions.

Contrast-enhanced CT scans
Meningeal & ependymal enhancement
Help in detecting complications of meningitis, such as
subdural empyema
Venous thrombosis, infarction
Cerebritis/abscess
Ventriculitis.

Unenhanced axial CT image

shows high-attenuation
material in the basilar
cisterns

Cerebritis and developing

abscess formation in a
patient with bacterial
meningitis . This contrastenhanced, axial computed
tomography scan shows a
small, ring-enhanced,
hypoattenuating lesion in
the left basal ganglia and
a left subdural fluid
collection with enhanced
meninges.

Abscess in a patient with

bacterial meningitis. This
contrast-enhanced
computed tomography
scan shows a ringenhancing,
hypoattenuating mass
(abscess) with peripheral
edema and mass effect.

Bilateral subdural
empyema in a patient
with bacterial meningitis.
This computed
tomography scan
demonstrates the
important diagnostic
features of meningitis:
prominent enhancement
of the margin and
increased attenuation of
the empyema.

CNS tuberculosis
Hematogenous dissemination usually from pulmonary
infection
Meningitis- most common manifestation
Parenchymal lesions
Caseating granuloma
Usually solitary, multiple in 1/3
Cortical, subcortical, basal ganglia lesions. Cerebellum in
children
Tubercular abscess
indistinguishable from caseating granuloma/ pyogenic
abscess
thinner & smoother wall
multiloculated
larger(>3cm)
surrounding edema is less than that in pyogenic abscess

Multiple bilateral ring-enhancing lesions

(tuberculomas) in the frontal and parietal lobes

Parasitic infections

NCC
Echinococcosis
Amebiasis
Paragonimiasis
Spargonimiasis
Malaria

Neurocysticercosis
Larval form of T. solium
Most common CNS parasite
location
Brain parenchyma- corticomedullary junction
Intraventricular in 20-50% cases
Subarachnoid space

Dying larva incite host inflmm rxn &

calcifies later

CT scan of the brain

In parenchymal NCC, the various stages are as follows:
Vesicular stage is characterized by a small, rounded, low-density area
in the brain parenchyma, without edema or enhancement with contrast.
Sometimes the scolex can be seen as a hyperdense dot inside the
hypodensity.

Colloidal vesicular stage is characterized by a hypodense or isodense

lesion with edema and a ring-enhancing pattern after administration of
contrast. This is the "acute encephalitic form," manifested as a reaction by
the host.

Granular nodular stage-NECT shows isodense cyst with hyperdense

calcified scolex .

Nodular Calcified stage is characterized by a dead cysticercus. In

NECT, a small calcified nodule without mass effect or enhancement
is typical. However, perilesional edema may occur around already
calcified cysts (may be upto 5 yrs) and is related to symptom relapse.

Transitional stages between these stages also can be seen; the

pattern on CT scan is a combination of 2 stages.

NCC

Brain tumors

Classification by histology

A)Glial tumors-

Astrocytomas
Oligodendroglioma
Ependymal
Choroid plexus tumors-CPP/CPC

B) Neuronal and mixed neuronal/glial tumorsganglioma

gangliocytoma
central neurocytoma

C) Meningeal and mesenchymal tumorsmeningioma

hemangioblastoma
hemangiopericytoma

D) Pineal cell tumorspineoblastoma

pineocytoma

E) Embryonal tumorsneuroblastoma
retinoblastoma
PNETS

F) Hematopoetic tumorslymphoma
leukaemia
plasmacytoma

G) Pitutary tumors
H) Cyst and tumor like lesions

Revised WHO classification

Subdivides into 4 grades (IIV) based
on specific histologic features of
tumor such as cellularity, nuclear
atypia, mitotic activity,
pleomorphism, vascular hyperplasia,
and necrosis.

BRAIN TUMOURS

Most common

CNS tumor in adult: Metastasis

Primary CNS neoplasm: GBM
Non-glial: Meningioma
Neonates: Teratoma
Germ cell tumor: Germinoma
Site of Schwonnoma: Vestibular division of VIII NV
Sellar/parasella: Pituitary adenoma
Posterior fossa tumor in adult: Metastases
Tumor to calcify: Oligodendroglioma
Spinal extradural tumor: Metastasis
Benign spinal neoplasm: Vertebral hemangioma
Intramedullary spinal tumors in adults : ependymoma
Intramedullary spinal tumors in children: Astrocytoma

 In diagnosis of brain tumors following

points are importantage
anatomic location
character of tumor
perilesional edema
CT density and MR signal
characteristics
contrast enhancement

GLIOMA/NEUROGLIAL
Tumours
Glial cells: 5-10X (trillion) neurons
Among Primary brain tumours :
approx are glioma
Among glioma: > are astrocytoma

Glioblastoma multiforme
Most common and malignant of all
primary intracranial tumours ( 50%
astrocytomas)
Rapidly enlarging malignant
astrocytic tumor characterized by
necrosis and neovascularity
Common in older age >50yrs; Rare
below 30yrs
Location:
o Supratentorial white matter most
common
Frontal, temporal, parietal lobes
Occipital lobes relatively spared
o Cerebral hemispheres> brainstem >
cerebellum
o Brainstem, cerebellum - common in
children
Worst prognosis

 CT: Marked
intratumoral
heterogenicity with
central low density
region (s/o necrosis or
cyst form) is present in
95% of all GBM
Hemorrhage & peripheral
oedema (Fingers of
edema) is common
Enhancement is strong &
inhomogenous with thick
irregular rim
enhancement
MR: T1 shows poorly
delineated mixed signal
mass with necrosis or cyst
formation with marked
inhomogenous
enhancement
T2 shows heterogenous
mass with mixed signal,
central hemorrhage &
necrosis

Thick, irregular-enhancing rind

of neoplastic tissue surrounding
necrotic core

Spread of GBM:

Viable tumor extends far beyond

signal abnormalities!
Common
Along compact white matter tracts- corona
radiata, corticospinal tracts, corpus callosum
(Butterfly glioma) and hippocampal
commissures
Around ventricular ependyma
Into leptomeninges
CSF seeding of subarachnoid space
Uncommon
Dural invasion
Rare
Extracerebral metastasis

 SPINE

SPINE
D/D: Collapsed vertebra
1. Vascular: hemangioma, ABC
2. Infective
3. Neoplastic:
1. Metastatic
2. MM/Plasmocytoma

4.
5.
6.
7.

Drug/metabolic: osteoporosis
LCH
Traumatic
Pagets

Tubercular spine

common in NEPAL

1-3% -osseous involvement

>50% affects spinal column

commonest form of skeletal TB.

Dorsal spine - most commonly

involved

Most Common first 3 decades.

RADIOLOGY
Plain radiography
signs :
Reduced disc space
Blurred paradiscal
margins
Destruction of bodies
Loss of trabecular
pattern
Increased
Prevertebral soft
tissue shadow
Subluxation/dislocatio
n
Decreased Lordosis/
kyphosis

Roentgen triad: primary vertebral lesion,

disc space narrowing and paravertebral
abscess

Tuberculous
Spondylitis

Pyogenic
Spondylitis

Onset

Insidious/ chronic

Acute

Progress

Slow

Rapid

Site

Thoraco-lumbar

Lower lumbar

X ray changes

At presentation

2-3 wks aft

presentation

Bone sclerosis

Lack sclerosis

Present

Periosteal reaction

Little or absent

Present

Multifocal
involvement

Multiple contiguous
vertebrae

Two or one

Disc involvement

Late

Early

Posterior element
inv

More frequent

Less

Subligamentous
spread

common

+/-

Paraspinal mass

Large

Small

Calcification

Hallmark

Rare

Spinal deformity

Common (kyphosis)

Not so

Spinal tuberculosis
A destructive bone
lesion associated with
a poorly defined
vertebral body
endplate, with or
without a loss of disk
height.
Better prognosis

Metastatic tumor
A destructive bone
lesion associated with a
well preserved disk
spaces with sharp end
plates s/o neoplastic
infiltrates.
Bad prognosis

Good disc , bad news;

Bad disc, good news

Vertebral Metastasis

General Information
Metastatic disease is the most common
tumor affecting the spinal column.
Approximately 70% of all spinal tumors
are metastatic in nature.
Primary carcinoma of the prostate,
breast, lung, thyroid gland or intestinal
tract.

Two types of spinal

metastases

1. Osteoclastic / Osteolytic (destruction of bone)

Frequently associated with vertebral body collapse.

May be mistaken for plasma cell myeloma.

2. Osteoblastic (formation of bone)

Hard and ivory like appearance to the bone.

Prostate; carcinoid; stomach
May be mistaken for osteopetrosis, osteoslerotic anemia,
Hodgkins disease or syphilis.

Osteolytic destruction is present in 75% of spinal

metastases.

Both osteolytic and osteoblastic types may be present

within the spinal column and even within the same
vertebrae.

Vertebral Metastases of C5

Differential diagnosis for ivory

vertebral body:
- Metastases
- Lymphoma
- Paget disease
- Less common: Infection (low grade
i.e. TB) or Idiopathic segmental
sclerosis

Conventional Radiographs
Conventional radiography is relatively insensitive to bone
metastases.
50% destruction of the bone mineral content is necessary
for detection, thus it is not apparent on conventional
radiographs the early stages of disease.
As a rule, lesions need to be 2 cm to be detected.
Conventional radiography is still the preferred imaging
method to determine behavior (i.e.) sclerotic, osteolytic or
mixed.
Osteolytic metastases can mimic:
o OA, Subchondral cysts or Schmorl nodes of the spine

Sclerotic metastases may mimic other sclerotic bone lesions

such as:
o Tuberous sclerosis, Mastocytosis or Osteopoikilosis

Sclerotic metastases of L2
Common signs of spinal
metastases found on
conventional radiographs
include:
Destruction of the
pedicle
Associated soft-tissue
mass

MRI
Imaging method of choice for evaluating
suspected metastatic spinal pathology.
Apparent diffusion coefficient (ADC)
values calculated from diffusion-weighted
MR images is a reliable factor to
distinguish vertebral metastases
from normal vertebrae.
MRI can also help detect metastatic
lesions before changes in bone
metabolism make the lesions detectable
on bone scintiscans

Criteria

Infection

Tumour

No & pattern of
vertebral involve

At least 2 around
affected disc

Isolated/ non contiguous

Portion of
vertebral involve

Mostly
endplates; post
elements relatively
spared

Body, typically pedicles

Disc involvement

Yes

Spared (exception: Prostate

ca)

Marrow signal

T1 low, T2 high,
normal diffusion

T1 low, T2 high, restricted

diffusion

Epidural
component

Granulation tissue;
extends several
levels above &
below

Focal mass; limited to level

affected (exception: lymphoma)