basic tutorial for MBBS final year students

1. Imaging Brain--CT Scan Head
By: DR REKHA KHARE
MD RADIOLOGY

2. When do you need CT scan Head?
• Head injury
• Stroke
• Seizure/ Fit/ epilepsy
• Pyrexia of unknown origin
• Altered consciousness
• Headache- unusual

3. How to perform CT?
• In order to perform a head CT, the patient is placed
on the CT table in a supine position and the tube
rotates around the patient in the gantry
• In order to prevent unnecessary irradiation of the
orbits and especially the lenses, Head CTs are
performed at an angle parallel to the base of the
skull
• Slice thickness may vary, but in general, it is
between 5 and 10 mm for a routine Head CT.

4. How to read CT scan?
• Cranial cross-sectional anatomy is very important to
know prior to analyzing a head CT
• Symmetry is an important concept in anatomy and is
almost always present in a normal head CT unless the
patient is incorrectly positioned
• Intravenous contrast is not routinely used, but may be
useful for evaluation of tumors, cerebral infections, and
in some cases for the evaluation of stroke patients, it is
Radiologist decision

5. Slice 1
A. Orbit
B. Sphenoid Sinus
C. Temporal Lobe
D. External Auditory Canal
E. Mastoid Air Cells
F. Cerebellar Hemisphere

6. Slice 2
A. Frontal Lobe
B. Frontal Bone (Superior Surface
of Orbital Part)
C. Dorsum Sellae
D. Basilar Artery
E. Temporal Lobe
F. Mastoid Air Cells
G. Cerebellar Hemisphere

7. Slice 3
A. Frontal Lobe
B. Sylvian Fissure
C. Temporal Lobe
D. Suprasellar Cistern
E. Midbrain
F. Fourth Ventricle
G. Cerebellar Hemisphere

8. Slice 4
A. Falx Cerebri
B. Frontal Lobe
C. Anterior Horn of Lateral
Ventricle
D. Third Ventricle
E. Quadrigeminal Plate Cistern
F. Cerebellum

9. Slice 5
A. Anterior Horn of the Lateral
Ventricle
B. Caudate Nucleus
C. Anterior Limb of the Internal
Capsule
D. Putamen and Globus Pallidus
E. Posterior Limb of the Internal
Capsule
F. Third Ventricle
G. Quadrigeminal Plate Cistern
H. Cerebellar Vermis
I. Occipital Lobe

10. Slice 6
A. Genu of the Corpus Callosum
B. Anterior Horn of the Lateral
Ventricle
C. Internal Capsule
D. Thalamus
E. Pineal Gland
F. Choroid Plexus
G. Straight Sinus

11. Slice 7
A. Falx Cerebri
B. Frontal Lobe
C. Body of the Lateral Ventricle
D. Splenium of the Corpus
Callosum
E. Parietal Lobe
F. Occipital Lobe
G. Superior Sagittal Sinus

12. Slice 8
A. Falx Cerebri
B. Sulcus
C. Gyrus
D. Superior Sagittal Sinus

13. TRAUMA---Head fracture
Examine bone window carefully for
linear # : more common
depressed # : the fracture fragments are depressed below the
surface of the skull.
• A skull fracture is most clinically significant if the paranasal sinus or skull
base is involved.
• Fractures must be distinguished from sutures that occur in anatomical
locations (sagittal, coronal, lambdoidal) and venous channels.
• Sutures have undulating margins both sutures and venous channels have
sclerotic margins.
• Depressed fractures are characterized by inward displacement of fracture
fragments

14. Skull fracture

15. Extra axial/ Intraaxial haemorrhage
• Extradural
haemorrhage
• Subdural haemorrhage
• Subarachnoid
haemorrhage
• Intraventricular
haemorrhage
• Intracerebral
haemorrhage/
contusion

16. Subarachnoid haemorrhage
• SAH occurs with injury of small arteries or veins on the surface of
the brain. The ruptured vessel bleeds into the space between the
pia and arachnoid matter
• Traumatic cause of SAH occurs over the cerebral convexities or
adjacent to cerebral contusion
• Non traumatic cause of SAH is the rupture of a cerebral aneurysm
particularly in basal cistern ,if so Cerebral Angiography is needed
for further evaluation
• On CT, subarachnoid hemorrhage appears as focal high density in
sulci and fissures or linear hyperdensity in the cerebral sulci.

17. Subarachnoid haemorrhage

18. Acute subdural haematoma
• Deceleration and acceleration or rotational forces that tear
bridging veins can cause an acute subdural hematoma.
• The blood collects in the space between the arachnoid matter
and the dura matter
• The hematoma on CT has the following characteristics:
- Crescent shaped
- Hyperdense, may contain hypodense foci due to serum,
CSF or active bleeding
- Does not cross dural reflections

19. ACUTE SDH

20. Sub acute subdural haematoma
• Subacute SDH may be difficult to visualize by CT because as the
hemorrhage is reabsorbed it becomes isodense to normal gray matter
• A subacute SDH should be suspected when there is shift of midline
structures without an obvious mass
• Giving contrast may help in difficult cases because the interface between
the hematoma and the adjacent brain usually becomes more obvious due
to enhancement of the dura and adjacent vascular structures
• Some of the notable characteristics of subacute
SDH are:- Compressed lateral ventricle
- Effaced sulci
- White matter "buckling"
- Thick cortical "mantle

21. CHRONIC SDH
Chronic SDH becomes
low density as the
hemorrhage is further
reabsorbed
It is usually uniformly
low density but may
be loculated
Rebleeding often
occurs and causes
mixed density and
fluid levels.

22. Subdural haematoma
Acute Chronic

23. Epi/extra dural haematoma
• An epidural hematoma is usually associated with a skull
fracture. The fractured bone lacerates a dural artery or a
venous sinus. The blood from the ruptured vessel collects
between the skull and dura.
• On CT, the hematoma forms a hyperdense biconvex mass. It is usually
uniformly high density but may contain hypodense foci due to active
bleeding.
• Since an epidural hematoma is extradural it can cross the dural
reflections unlike a subdural hematoma.
• However an epidural hematoma usually does not cross suture lines
where the dura tightly adheres to the adjacent skull.

24. Extradural haemorrhage

25. Diffuse axonal injury ---Shear injury
Acceleration, deceleration and rotational forces cause portions of the brain with
different densities to move relative to each other resulting in the deformation and
tearing of axons
Immediate loss of consciousness is typical of these injuries
The CT of a patient with diffuse axonal injury may be normal
despite the patient's presentation with a profound
neurological deficit
With CT, diffuse axonal injury may appear as ill-defined areas
of high density or hemorrhage in characteristic locations.
The injury occurs in a sequential pattern of locations based on the severity of the
trauma -- Subcortical white matter ,Posterior limb internal capsule,
Corpus callosum and Dorsolateral midbrain

26. Diffuse axonal injury

27. Cerebral contusion
Cerebral contusions are the most common primary intra-
axial injury. They often occur when the brain impacts an
osseous ridge or a dural fold. The foci of punctate
hemorrhage or edema are located along gyral crests.
On CT, cerebral contusion appears as an ill-defined
hypodense area mixed with foci of hemorrhage.
Adjacent subarachnoid hemorrhage is common.
After 24-48 hours, hemorrhagic transformation or
coalescence of petechial hemorrhages into a
rounded hematoma is common.

28. Iintraventricular
haemorrhage
Traumatic
intraventricular
hemorrhage is
associated with
diffuse axonal injury,
deep gray matter
injury, and brainstem
contusion. An isolated
intraventricular
hemorrhage may be
due to rupture of
subependymal veins.

29. Contusion Intraventricular
Haemorrhage

30. Cerebro-vascular accidents
STROKE
• Strokes are classified into two major types –
• Hemorrhagic strokes are due to rupture of a cerebral
blood vessel that causes bleeding into or around the
brain.
• Ischemic stroke is caused by blockage of blood flow in
a major cerebral blood vessel, usually due to a blood
clot.
• Ischemic strokes are further subdivided based on
their etiology into several different categories
including thrombotic strokes, embolic strokes, lacunar
strokes and hypoperfusion infarctions.

31. What is Stroke?

32. HAEMORRHAGIC STROKE
There are two major categories Intracerebral
hemorrhage is the most common, due to rupture of
a cerebral aneurysm
• Intracerebral Hemorrhage non traumatic cause is
hypertensive hemorrhage.
• Other causes include amyloid angiopathy, a ruptured
vascular malformation, coagulopathy, hemorrhage
into a tumor, venous infarction, and drug abuse

33. Hypertensive haemorrhage
• It is commonly due to vasculopathy involving deep
penetrating arteries of the brain.
• It has a predilection for deep structures including
the thalamus, pons, cerebellum, and basal ganglia,
particularly the putamen and external capsule
• It often appears as a high-density
hemorrhage in the region of the basal
ganglia.Blood may extend into the
ventricular system

34. Hypertensive bleed

35. Coagulopathy related ICH
• It can be due to drugs such as coumadin or a
systemic abnormality such as
thrombocytopenia
• On imaging, this hemorrhage often has a
heterogeneous appearance due to
incompletely clotted blood. A fluid level
within a hematoma suggest coagulopathy as
an underlying mechanism

36. Coagulopathic bleed

37. ICH due to arteiovenous
malformation
• An underlying arteriovenous malformation
(AVM) may or may not be visible on a CT scan
• However, prominent vessels adjacent to the
hematoma suggest an underlyingAVM
• In addition, some AVM contain dysplastic
areas of calcification and may be visible as
serpentine enhancing structures after contrast
administration

38. AV malformation haemorrhage

39. Non traumatic SAH
Ruptured Cerebral aneurysm
Cerebral aneurysms are frequently located around the
Circle of Willis
Common aneurysm locations include the anterior and
posterior communicating arteries, the middle
cerebral artery bifurcation and the tip of the basilar
artery
Subarachnoid hemorrhage typically presents as the
"worst headache of life" for the patient

40. SAH due to cerebral aneurysm
• On CT, subarachnoid hemorrhage appears as
focal high density in sulci and fissures or linear
hyperdensity in the cerebral sulci
• Bleed may extend to ventricle may cause
Hydrocephalus

41. Ischaemic stroke
• Causes could be: Thrombosis, Embolism, Hypoperfusion
Lacunar infarctions.
• Thrombotic stroke occurs when a blood clot forms in situ
within a cerebral artery and blocks or reduces the flow of
blood through the artery.
• This may be due to an underlying stenosis, rupture of an
atherosclerotic plaque, hemorrhage within the wall of the
blood vessel, or an underlying hypercoagulable state.
• This may be preceded by a transient ischemic attack and
often occurs at night or in the morning when blood pressure
is low.

42. Ischaemic stroke
Embolic stroke occurs when a detached clot flows into and blocks a cerebral
artery. The detached clot often originates from the heart or from the walls
of large vessels such as the carotid arteries. Atrial fibrillation is also a
common cause
Lacunar infarction occurs when the walls of small arteries thicken and cause
the occlusion of the artery. These typically involve the small perforating
vessels of the brain and result in lesions that are less than 1.5 cm in size
Hypoperfusion infarctions occur under two circumstances. Global anoxia
may occur from cardiac or respiratory failure and presents an ischemic
challenge to the brain. Tissue downstream from a severe proximal
stenosis of a cerebral artery may undergo a localized hypoperfusion
infarction.

43. Role of Imaging in Stroke
• Stroke" is a clinical diagnosis; however imaging is playing an increasingly
important role in its diagnosis and management. The most important
issue to determine when imaging a stroke patient is whether one is
dealing with a hemorrhagic or ischemic event
• This has crucial therapeutic and triage implications.
• Decisions that must be made concerning therapy are dependent on the
diagnosis and may include the following:
- Is the patient a thrombolysis candidate and should thrombolytic therapy
be used?
- Intravenous or intrarterial therapy?
- Neurosurgery or neurology patient?
In addition about 2% of clinically definite "strokes" are found to be a
result of some other pathology such as a tumor, a subdural hematoma or
an infection

44. Why CT scan is preferred?
• There are several advantages to performing a CT scan
instead of other imaging modalitie
• Advantages of CT scan : Is readily available
Is rapid
Allows easy exclusion of
hemorrhage
Allows the assessment of parenchymal damage
Disadvantages of CT:
- Old versus new infarcts is not always clear
- No functional information (yet)
- Limited evaluation of vertebrobasilar system

45. CT Pathophysiology
• After a stroke, edema progresses, and brain
density decreases proportionately. Severe
ischemia results in a 3% increase in
intraparenchymal water within 1 hour. This
corresponds to 7-8 Hounsfield Unit decrease
in brain density. There is also a 6% increase in
water at 6 hours. The degree of edema is
related to the severity of hypoperfusion and
the adequacy of collateral vessels.

46. Common CT signs of ischaemia/
Infarction
One of the first findings to look for is the presence or absence
of hemorrhage.

47. Hyperdense MCA sign

48. Hyperdense Vessel Sign
Dense MCA sign
• A hyperdense vessel is defined as a vessel
denser than its counterpart and denser than
any non-calcified vessel of similar size
• In patients presenting with clinical deficit
referable to the middle cerebral artery
territory, the hyperdense vessel sign is
present 35-50% of the time.
• This sign indicates poor outcome and poor
response to IV-TPA therapy.

49. Basilar thrombosis
• Thrombosis of the basilar artery is a common
finding in stroke patients.
• CT findings include a dense basilar artery
without contrast injection

50. Lentiform Nucleus Obscuration
• Lentiform nucleus obscuration is due to
cytotoxic edema in the basal ganglia. This sign
indicates proximal middle cerebral artery
occlusion, which results in limited flow to
lenticulostriate arteries.
• Lentiform nucleus obscuration can be seen as
early as one hour post onset of stroke

51. Insular ribbon sign
• Loss of the gray-white interface in the lateral
margins of the insula.
• This area is supplied by the insular segment of
the middle cerebral artery and is particularly
susceptible to ischemia because it is the most
distal region from either anterior or posterior
collaterals.

52. Obscured lentiform nucleus
Insular ribbon sign

53. Diffuse Hypodensity and Sulcal
Effacement
• Diffuse hypodensity and sulcal effacement is the
most consistent sign of infarction.
• If this sign is present in greater than 50% of the
middle cerebral artery territory there is, on average,
an 85% mortality rate.
• Hypodensity in greater than one-third of the middle
cerebral artery territory is generally considered to be
a contra-indication to thrombolytic therapy.

54. Acute infarct on CT scan

55. CT scan in subacute infarction
1 -3 days: - Increasing mass effect
- Wedge shaped low density
- Hemorrhagic transformation
After 4 - 7 days: - Gyral enhancement
- Persistent mass effect
In 1-8 weeks: - Mass effect resolves
- Enhancement may persist

56. Enhancement in infarction
• Ninety percent of infarcts enhance on CT
examinations with intravenous contrast at 1 week
after the infarct.
• Faint enhancement begins near the pial surface or
near the infarct margins.
• The enhancement is initially smaller than the area of
infarction. It subsequently becomes gyriform.
• Enhancement is due to breakdown of the blood
brain barrier, neovascularity, and reperfusion of
damaged brain tissue

57. Hyperintensity on MRI =
Irreversible changes

58. Stroke on CT & MRI
Haemorrhage is seen better on CT but can be seen on gradiant
scan

59. MRI Quick Basic sequences
• T2 weighted: Plain axial ( T2 FSE)
• FLAIR sequence: Axial
• Diffusion-weighted imaging (DWI) : Axial
• Susceptibility weighted imaging (SWI): Axial

60. MRI Sequence for stroke
signal intensity

61. HAVE A NICE DAY
THANK YOU