Basic interpretation of

CT-SCAN HEAD

BY,

DR. FAISAL NAWAZ

PGR MEDICAL UNIT-I

MULTI SLICE HELICAL

CT SCANNER

6 ESSENTIAL C.T SCAN IMAGES TO

REMEMBER:

6 ESSENTIAL C.T SCAN IMAGES TO

REMEMBER:

MR. X

MR. STAR

MR.SMILEY

MR. SAD

THE WORMS

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.

PATHOLOGY 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

similar systematic method of cranial CT
interpretation, based on the 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).

HYPODENSITY ON CT SCAN
Higher than CSF but lower than brain tissue:
Evolution infarct.
Tumor.
Abscess .
Resolving hematoma

Iso-density to CSF:
Chronic

hematoma.
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.

HEMORRHAGE

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

at approximately 4 weeks.

COMMON SITES OF HYPERTENSIVE

BLEED ON C.T SCAN HEAD

1. BASAL GANGLIA
2. CEREBELLUM
3. THALAMUS
4. PONS

HEMORRHAGE IN BASAL
GANGLIA

HEMORRHAGE IN BASAL GANGLIA

HEMORRHAGE IN CEREBELLUM

HEMORRHAGE IN THE
THALAMIC REGION

PONTINE HEMORRHAGE

SUBARACHNOID HEMORRHAGE

Blood in the cisterns/cortical gyral

surface
Aneurysms responsible for 7580% of SAH
AVMs 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
( < 20%).

Acute right extra-dural

hemorrhage
(arrowheads).

Right extradural hemorrhage.

The collection is hyperdense
and isodense indicating both acute and
subacute hemorrhage. In addition,
there is evidence of subarachnoid
haemorrhage.

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
tolerated.

Shallow acute left subdural

hematoma (arrows).

Large acute right subdural

hematoma
(arrowheads).

INFARCTION

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 supply
from the anterior cerebral and
posterior cerebral arteries.

RIGHT SIDE INSULAR RIBBON

SIGN AND VANISHING
BASALGANGLIA SIGN

MCA DOT SIGN

HYPERDENSE MCA SIGN

TYPES

Ischemic.
Hemorrhagic.
Hemodynamic.
Lacunar.

FOGGING EFFECT:
In roughly of the cases,the infarct
may change from hypo-dense to
iso-dense. This has been termed
the "fogging effect" on CT and is
usually seen 2-3 weeks post ictus
during the sub-acute phase of
infarction and should resolve on
subsequent imaging. IV contrast
may make the infarct more
conspicuous.

THALMIC INFARCTION

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: Scans pre- and post-contrast.

On the pre-contrast study , hyper-dense material is seen within the sagittal sinus.
This is an unreliable sign for acute thrombus. However, following contrast, the
delta sign is clearly visible.

Venous lesions are

differentiated from arterial by
these facts:
They are usually present in
the superficial slides.
These lesions occur in an
area which is not
characteristic of any arterial
territory.
They dont have any definite
shape.

Venous hemorrhage in
the left
Fronto-parietal cortex

EDEMA

VASOGENIC EDEMA
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) and
Cerebral Abscesses.

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) &
effacement of sulcal space.

RING ENHACNING LESIONS

DIFFERENTIALS
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.
Small (<1-2cm) lesions with thin walls especially if other calcific
foci are present suggest neuro-cysticercosis.

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 relationship.
The presence of the blood.

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 SubArachnoid space.
Adult CSF volume is approx.
150 ccs.
Adult CSF production is
approx. 500-700 ccs per day.

HYDROCEPHALUS
Hydrocephalus results from an excess of CSF, due to an imbalance
between CSF production and absorption, resulting in increased intraventricular pressure.
Communicating hydrocephalus is caused by elevated intraventricular 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
HYDROCEPHALUS

NON-COMMUNICATING HYDROCEPHALUS

Lateral ventricles have three horns each; the frontal, occipital, and
temporal horns.
The frontal and occipital horns are easily identified, but the
temporal horns can be a little bit tricky. They are not always visible.
However, symmetry is the key. If you see one, you should see the
other. They will be located slightly anterior to the petrous ridge, on
approximately the same slice, and are shaped like an L.
Obliteration of these is caused by:
Medial movement of the temporal lobes (secondary to mass effect
or hematoma) tumor, or prior surgery.
Increase in the size of the temporal horns is due to:
Atrophy or Increased CSF ( i.e. Hydrocephalus).

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

(arrowheads) with marked
overlying
soft tissue contusion.

Depressed skull
fracture

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: Acute subdural hemorrhage.

CASE 2

Case 2. Large area of low density, involving both grey and white matter, within
the left middle cerebral artery territory (arrowheads).
Diagnosis: Acute left middle cerebral artery territory infarct.

CASE 3

Case 3. Focal area of hyper-density centered upon the right thalamus and
lentiform nucleus (arrowhead).
Diagnosis: Acute parenchymal hemorrhage. This type of hemorrhage
has a strong association with uncontrolled hypertension.

CASE 4

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

concavity (arrowheads).
Diagnosis: Acute subdural hemorrhage.

CASE 5

Case 5. Subtle linear hyperdensity is seen outlining several sulci within the
left cerebral hemisphere (arrowheads).
Diagnosis: Acute subarachnoid haemorrhage.

CASE 6

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

marginated defects within the left occipital bone (arrowheads).
Diagnosis: Left occipital fracture.

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: Acute Infarction

CASE 8

Case 8.
1. Hyper-dense biconvex collection over the
right temporal lobe (straight
white arrowheads).
2. Linear hyper-density outlining the basal
cisterns (curved arrowheads).
3. Focal parenchymal hyperdensity (black
arrowheads).
Diagnosis: Acute extra-dural hemorrhage
with additional subarachnoid
hemorrhage 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
of the fourth ventricle due to mass effect.
Diagnosis: Acute left cerebellar infarct.

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.
M.R.I done shows a 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: Arterio-venous malformation.

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: Right sided Acute on chronic Sub-dural hematoma.