Basic interpretation of

CT-SCAN HEAD

BY
,

Dr. Muhammad Hassan

HELICAL
CT
SCANNER
IMAGES TO
REMEMBER:
IMAGES TO
REMEMBER:
MR. X
MR.
STAR
MR.SMIL
EY
MR.

SAD
 WORM
S
COFFEE
BEAN
 VASCULAR
TERRITORIES

The anterior ,middle and posterior cerebral arteries grossly supply the
anterior, middle and posterior parts of the brain from Mr. X to Mr. SAD. But
from The WORMS to The COFFEE BEAN level anterior cerebral artery
supplies most of the midline.
PATHOLOG
Y PICKING
 HOW TO READ
THE
CT-
HEAD
•Adequacy of film
•Parenchyma
•Ventricle
•Cisterns
•Cranial bones
 SYSTEMATIC APPROACH

In medical school, we are taught a systematic

technique to interpret ECGs (rate, rhythm, axis,
etc.) so that all aspects are reviewed, and no
findings are missed.
The intent of this session is to introduce
a
sn
i imteilraprrseytsatetmo
i anti,cbmaestehdod

oonftchraenial CT mnemonic…
BLOOD CAN BE VERY BAD

• BLOOD
• CISTERNS
• BRAIN
• VENTRICLES
• BONE
 BRAIN
PARENCHYMA

Compare the parenchyma of one side to the other.

*Tilting of head will effect the symmetry.
Look at the grey matter, white matter, at grey white
junction and the peri-ventricular region.
Reference density is that of brain substance and
CSF.
• Hypodense lesion could have density less than
brain
and CSF.
• Hyperdensity greater than bone.
• Isodensity comparable with brain.
• Heterogenous (mixed density).
 HYPERTENSIVE
BLEED

HEMORRHAGE SUB-ARACHNOID
HEMORRHAGE

EPI-DURAL
HEMATOMA

SUB-DURAL

INFARCTION HEMATOM
A

BRAIN ARTERIAL

PARENCHYM
A
VENOUS
EDEMA

VASOGENIC
EDEMA

CYSTIC LESIONS CYTOTOXIC

EDEMA
 HYPODENSITY ON CT
SCAN

Higher than CSF but lower than brain tissue:

• Evolution infarct.
• Tumor.
• Abscess .
• Resolving hematoma

Iso-density to CSF:
• Chronichematoma.
• Chronic infarct.
• Congenital cyst.
 HYPER-DENSITY
ON CT SCAN

Iso- or higher than bone:

• Ossification.
• Calcification.
• Metallic.
• Iatrogenic.
• Blood pooling.

Less than bone but higher than brain tissue:

• Hemorrhage.
• Compacted cellularity.
HEMORRHAG
E
1st question: Is blood present?
2nd question: If so, where is it?
3rd question: what effect is it
having?
Acute blood is bright white on
CT (once it clots).

Blood becomes iso-dense at

approximately 1 week

Blood becomes hypo-dense

 HYPERTENSIVE
BLEED ON C.T
SCAN HEAD

1. BASAL GANGLIA
2. CEREBELLUM
3. THALAMUS
4. PONS
HEMORRHAGE IN
BASAL GANGLIA
HEMORRHAGE
BASAL
IN GANGLIA
HEMORRHAGE
CEREBELLUM
IN
HEMORRHAGE IN
THE THALAMIC
REGION
PONTINE
HEMORRHAGE
 SUBARACHNOID
HEMORRHAGE

Blood in the cisterns/cortical gyral

surface
•Aneurysms responsible for 75-
80% of SAH
• AVM’s responsible for 4-5%
• Vasculitis accounts for small
proportion (<1%)
• No cause is found in 10-15%
• 20% will have associated
acute
hydrocephalus
SUB-ARACHNOID
HEMORRHAGE
 Epidural
Hematoma

• Lens shaped.

• Does not cross

sutures.

•Classically described
with injury to middle
meningeal artery.

•Low mortality if treated

prior to
unconsciousness
 Subdural
Hematoma

•Crescent shaped.

•Crosses sutures, but

does not cross midline.

•Acute subdural is a
marker for severe head
injury. (Mortality
approaches 80%)

•Chronic subdural
usually slow venous
bleed and well
INFARCTI
ON
 SEVEN
STAGES:

• Acute(Entirely normal)
•Loss and blurring of gray white interface seen in
basal ganglion/thalamus/ internal capsule.
(Vanishing Basal ganglia sign).
• Loss of insular ribbon in the temporal lobe.
(Insular ribbon sign).
• Hyper-dense (MCA Dot sign).
•Localized mass effect, effacement of Sulci and
asymmetry of lateral ventricles.
• As edema progresses generalized mass
effect.
• Hypo-density.
 INSULAR
RIBBON
SIGN

The insular ribbon sign refers to

a loss of grey white differentiation
in the lateral margin of the insular
cortex ("insular ribbon") and is
considered an early CT sign of
MCA infarction.

The insular cortex is more

susceptible to ischaemia following
MCA occlusion than other portions
of the MCA territory because it has
the least potential for collateral
RIGHT SIDE INSULAR
supply from the anterior cerebral RIBBON SIGN AND
VANISHING
and posterior cerebral arteries. BASALGANGLIA SIGN
MCA DOT HYPERDENSE MCA SIGN
SIGN
THALMIC
INFARCTIO
N
INFARCTION IN LEFT
MIDDLE
CEREBRAL ARTERY
BASAL GANGLIA
INFARCTION
 CEREBRAL VENOUS
SINUS
THROMBOSIS

•Classically presents with sudden, severe headache,

worsened by coughing and associated with
vomiting.
•Focal neurological deficit may be seen if venous
infarction occurs.
• Cranial nerve palsies are characteristic.
• Seizures may occur.
• Sigmoid sinus thrombosis causes cerebellar signs and
lower
cranial nerve palsies.
• Periorbital oedema and chemosis are seen with
cavernous
sinus thrombosis.
•Fundoscopy may show papilloedema or retinal
vein thrombosis.
Sagittal sinus thrombosis:
• They usually present in the superficial slides.
• The usually occurs in areas which does not
corresponds to any arterial territories.
• They don’t have any definite shapes.
Venous hemorrhage
in the left
Fronto-parietal cortex
EDEM
A
 VASOGENI
EDEMA
C
•In this type of edema, the
blood brain barrier is
disrupted.
Grey-white matter differentiation
is maintained and the edema
involves mainly white matter,
extending in finger-like fashion.

It is most frequently seen

around Brain Tumors (both
primary and secondary).
 CYTOTOXIC
EDEMA
•In this type of edema, the
blood brain barrier is intact.

•It is due to a cellular swelling

from lack of ATP, that is
typically seen in area
of cerebral
ischemia or cerebral
hypoxia.

•Loss of grey white matter

differentiation (as it
mainly affects grey
matter) &
RING ENHACNING
LESIONS
 DIFFERENTI
ALS
1.Cerebral
abscess.
2.Tuberculoma.
3. Metastasis.
4. Toxoplasmosis
5.C.N.S lymphoma (in immuno-compromised
patient). 6.Glioblastoma multiforme.
7. Cystic astrocytoma.
8. Neuro-cysticercosis
9. Sub-acute infarct / hemorrhage / contusion.
10. Demyelination (incomplete ring).
11.Radiation necrosis.
12.Post-operative
change.

Mneumonics for this are TRAGIC M.D / MAGIC D.R

 DIFFERENTIATING
FEATURES
Enhancing wall characteristics:
•Thick and nodular with rough inner margin favors neoplasm.
•Thin and regular with smooth inner margin favors abscess.
•Incomplete ring often opened toward the cortex
favors demyelination.

Surrounding oedema:
• Extensive oedema relative to lesion size favors
abscess.
• Increased perfusion favors neoplasm (metastases or
primary cerebral malignancy).

Number of lesions:
• Similar sized rounded lesions at grey white matter junction
favors
metastases or abscesses.
 A = Metastasis
 B = Abscess
 C = Radiation necrosis
 D = GBM
 E = Demyelination
 F = Contusion
 GLIOBLASTOMA
MUTLIFORME

Irregular thick margins having an irregular hypo-dense centre (representing

necrosis) with marked mass effect and surrounding vasogenic oedema.
 VENTRICLES

Inspect the ventricles

for:
Size.
Shape.
Spatial
relatio
nship.
The
presen
ce of
 C.S.F
PRODUCTION
•Production occurs in the
choroid plexus of the lateral
ventricles Foramen of
Monro  IIIrd Ventricle 
Acqueduct of Sylvius  IVth
Ventricle  Foramen of
Lushka / Magendi  Sub-
Arachnoid space.

•Adult CSF volume is

approx.
150 cc’s.
Adult CSF production is
approx. 500-700 cc’s per
 HYDROCEPHAL
US
Hydrocephalus results from an excess of CSF, due to an imbalance
between CSF production and absorption, resulting in increased
intra- ventricular pressure.

Communicating hydrocephalus is caused by elevated intra-

ventricular pressure secondary to obstruction of CSF flow beyond
the outlet of 4th ventricle.
This may be due to impeded CSF flow over the cerebral
convexities and/or impeded re-absorption of CSF by the
Arachnoid Villi.

Non-communicating hydrocephalus is caused by blockage of

CSF flow within the ventricular system, with dilatation proximal
to the obstruction.
Often referred to as obstructive hydrocephalus.
COMMUNICATING
HYDROCEPHALU
S
NON-COMMUNICATING HYDROCEPHALUS
Lateral
ventricles
 BONE

•Look at the scout film as it is a free lateral skull

plain radiograph.
•The bone windows should be examined for
evidence of fracture as a clue to underlying
intracranial pathology. Be sure to inspect the soft
tissues for swelling and defects (i.e.
lacerations).
•Determine if there are any depressed fractures,
or pieces of bone missing (i.e. previous surgery).
Left parietal bone fracture Depressed skull
(arrowheads) with marked fracture
overlying
soft tissue contusion.
Complex vault fracture Bilateral temporal bone
fractures
 CISTERNS

Cisterns are CSF collections, jacketing the brain.

Four key cisterns must be examined for blood,

asymmetry and effacement (as with increased ICP.
These are:
1. Circum-mesencephalic / Ambient: ring around
the
midbrain.
2. Supra-sellar: Star shaped at circle of willis
3. Sylvian cistern: between temporal and
frontal lobe.
4. Quadrigeminal: W shaped ay the top of
midbrain
 BLOOD CAN BE
VERY
BAD

•If no blood is seen,

• All cisterns are present and open,
•The brain is symmetric with
normal
gray-white differentiation,
•The ventricles are symmetric
without dilation,
• And there is no bony fracture,
•Then there is no emergent
diagnosis from the CT scan.
SELF
ASSESSMENT
 CASE
1

Case 1. A shallow hyper-dense collection is seen over the right

frontal lobe(arrowheads).
Diagnosis:
 CASE
2

Case 2. Large area of low density, involving both grey and white matter, within

Diagnosis:
 CASE
3

Case 3. Focal area of hyper-density centered upon the right thalamus

and lentiform nucleus (arrowhead).
Diagnosis: Acute parenchymal hemorrhage.
 CASE
4

Case 4. A shallow hyper-dense collection is seen over the left

cerebral concavity (arrowheads).
Diagnosis:
 CASE
5

Case 5. Subtle linear hyperdensity is seen outlining several sulci within

the left cerebral hemisphere (arrowheads).
Diagnosis: .
 CASE
6

Case 6. Axial scan viewed on ‘bone windows’, demonstrating sharply

marginated defects within the left occipital bone (arrowheads).
Diagnosis:
 CASE
7

Case 7. Insular ribbon sign in the left insular cortex and in the
immediately adjacent cortical and sub-cortical portions of the left
temporal region.
Diagnosis:
 CASE
8

Case 8.
1.Hyper-dense biconvex collection over the
ght temporal lobe (straight
white arrowheads).
2.Linear hyper-density outlining the
basal cisterns (curved arrowheads).
3.Focal parenchymal hyperdensity
(black rrowheads).
Diagnosis: Acute extra-dural hemorrhage
with additional subarachnoid
emorrhage and parenchymal
contusions.
 CASE
9

Case 9. Large area of low density, involving both grey and white matter,
within the left cerebellar hemisphere (arrowheads). Associated
compression

Diagnosis:
 CASE
10

Case 10. Hyper-dense focus within the fourth ventricle

(arrow). Diagnosis: Acute intra-ventricular hemorrhage.
 CASE
11

Case 11. This plain CT scan of the head shows a cerebellar vermian mass
with associated vasogenic edema and moderate cerebral atrophy.
ring enhancing lesion
Differentials:
 CASE
12

Case 12. This CT scan of the head shows mixed density lesion composed
of coarse calcification, and faintly hyper-dense vessels (arrowhead).
Marked enhancement post-contrast.
Differentials:
 CASE
13

Case 13: Mixed density crescent shaped area over the right cerebral
concavity with peri-focal edema and prominent sulci gyri on left side.
Diagnosis: