Great presentation on CT imaging of brain. Must for physicians.

1. CT Imaging (Brain) in
Clinical Practice
Dr Vaibhav Yawalkar
MD

2. Imaging in ER
 Cranial computed tomography (CT) is an extremely useful
diagnostic tool used routinely in the care of ER patients.
 The attending physician needs to be able to accurately
interpret and act upon certain CT findings without
specialist (e.g., radiologist) assistance, because many
disease processes are time dependent and require
immediate action.
 It has been shown that even a brief educational
intervention can significantly improve the physician’s ability
to interpret cranial CT scans.

3. PRINCIPLE
 Collimated X-rays are passed through the patient
and information is obtained with a detector on
the other side.
 The X-ray source and the detector are
interconnected and rotated around the patient
during scanning period.
 Digital computers then assemble the data that is
obtained and integrate it to provide a cross
sectional image (tomogram)

5.  A 2D image is obtained at
each level by 360 degree
rotation of Xray source and
detectors around the patient,
which gives information about
inside of tissue.
 Sequential 2D images can be
combined to obtain full 3D
image.

6.  X-rays are absorbed to different degrees by different
tissues. Dense tissues such as bone absorb the most x-
rays, and hence allow the fewest passing through the
body part being studied to reach the film or detector.
 This ability to block x-rays as they pass through a
substance is known as attenuation.
 In CT, these attenuation coefficients are mapped to an
arbitrary scale between −1000 hounsfield units [HU] (air)
and +1000 HU (bone)

7.  Imagine a CT film to be bright grey(silver
coloured) to start with and the xrays
falling on it makes that particular area
darker.
 More the exposure to xrays darker will
be the area.

9. DIFFERENT SHADES OF GREY
 The reference density for comparison is the brain,
being the largest component inside the skull. Anything
of the same density as the brain is called ISODENSE.
 Anything of higher density (whiter) than the brain is
called HYPERDENSE, and the skull is the best example
of a hyperdense.
 Similarly, anything of lower density (darker tone) than
brain is described as HYPODENSE. The cerebrospinal
fluid (CSF) is the typical example of a hypodense
structure in the brain CT scan. Air is also hypodense
and surrounds the regular outline of the skull in CT.

11. DESCRIPTION Approx. HU DENSITY
Calcium > 1000 Hyperdense
Acute blood 60-80 Hyperdense
Grey matter 38 (32-42) Hyperdense
White matter 30 (22-32) Isodense
CSF 0-10 HYPODENSE
Fat -30 to - 100 Hypodense
Air - 1000 Hypodense

12. INDICATIONS
 To diagnose CNS infections and their
complications
 Stroke: to distinguish infarct from hemorrhage
 Acute changes in mental status
 Focal neurologic findings
 Trauma
 Suspected SAH
 CNS tumors or ICSOLs
 Ct angiography before thrombolysis
 Ct venogram for cerebral venous thrombosis(cvt)

13. CT
 Advantages –
 Easy availability / Low cost
 Fast
 Better for bone and acute haemorrage,
lesions of skull base and calvarium
 Calcification
 Less limited by patient factors
 Disadvantages-
 High radiation
 Poor visualisation of posterior fossa lesions

14. Viewing Planes
 Axial
 Coronal
 Sagittal

16. INTERPRETATION OF CT
BRAIN
 1-GENERAL INFORMATION
 2-EXTRACRANIAL TISSUE
 3-CRANIAL BONE
 4-BLOOD
 5-CSF FLOW
 A-VENTRICULAR SYSTEM
 B-CISTERNS
 6-BRAIN TISSUE
 A-MASS LESIONS
 B-SULCI & GYRI
 C-GRY & WHITE DIFFERENTIATION

17. A
C
B
D
E
F
G

18. A
C
B
D
E
F
G

19. A
C
B
D
E
F

20. A
C
B
D
E
F
G
I
H

21. A
C
B
D
E
F
G

22. A
C
B
D
E
F
G

23. A
C
B
D

24. IDENTIFYING CNS PATHOLOGY ON
CRANIAL CT SCANS
 First step is to simply compare one half of the
scan against the other half. If there are
significant differences (for instance if the
right and left halves are not the same), then
the scan is abnormal.
SYMMETRY–MIRROR IMAGE

25. IDENTIFYING CNS PATHOLOGY ON
CRANIAL CT SCANS
 Radiologists use a “center-out” technique, in which the examiner
starts from the middle of the brain and works outward.
 Clinicians advocate a problem-oriented approach, in which the
clinical history directs the examiner to a particular portion of the
scan.
 A preferred method, one that has been demonstrated to work in
the ER is to use the mnemonic “blood can be very bad”.
 In this mnemonic, the first letter of each word prompts the
clinician to search a certain portion of the cranial CT scan for
pathology.
 The clinician is urged to use the entire mnemonic when
examining a cranial CT scan because the presence of one
pathologic state does not rule out the presence of other.

26. What to look for:
“ Blood Can Be Very Bad”
 Blood
 Cisterns
 Brain
 Ventricles
 Bone

27. Blood
 Blood is the most common hyperdense
abnormality found on a brain CT scan. So if a
hyperdense appearance is not in the right
location for bone then it must be blood, until
proven otherwise.
 So the rule of thumb is that ‘anything white in
the CT scan is either blood or bone’.

28. Exceptions:
 There are two common exceptions to this rule.
 The Pineal gland is a little Calcified speck in the
middle of the CT scans of most adults.
 The second exception is the calcified choroid
plexus, which is located in the body of each
lateral ventricle

29. Calcified Pineal
gland
Calcified
Choroid plexus

30. Physiologic calcifications
 Choroid plexus- rare before 10yrs
 Basal ganglia- rare before 40ys
 Pineal gland- common after 30 year
 Falx
 Dentate nuclei

31.  Blood—Acute hemorrhage appears hyperdense
(bright white) on CT. This is due to the fact that the
globin molecule is relatively dense and hence
effectively absorbs x-ray beams.
 As the blood becomes older and the globin breaks
down, it loses this hyperdense appearance,
beginning at the periphery and moving towards
centre.
 Localization of the blood is as important as
identifying its presence.

32.  On the CT scan, blood will become isodense with the brain at 1 to
2 weeks, depending on clot size, and will become hypodense with
the brain at approximately 2 to 3 weeks.

33. Peidural hematoma
Convex shape
Subdural hematoma
Cresent shape

34. Intra parenchymal hemorrhage
in putamen
Sub arachnoid hemorrhage
( hyperdensities in sylvian fissure, basal cysterns)

35. Intraparenchymal haemorrhage
with intraventricular extension

36. Infarcts
 Infarctions can be seen as early as 2 to 3 hours following the
event, but most will not begin to be clearly evident on the CT scan
for 12 to 24 hours. Infact immediate CT scans may be completely
normal in these cases.
 The earliest change seen in areas of ischemia is loss of gray-white
differentiation, due to influx of water into the metabolically active
gray matter.
 The release of osmotically active substances (arachidonic acid,
electrolytes, lactic acid) from the necrotic brain tissue
causes cerebral edema. This is aggravated by vascular injury and
leakage of proteins in the interstitial space. By 3-4 days, interstitial
fluid accumulates in the infarct and around it.

37.  The key principle behind successful use of the CT scan
in dealing with ischemic stroke is KNOWING WHERE TO
LOOK, AND WHAT TO LOOK FOR! And WHEN TO LOOK!
 The golden rule with stroke as with most of emergency
neurosurgery or neurology is that, the clinical symptoms
reign supreme.
Infarcts

38. Non-contrast CT scan of a 61-year-old male with sudden onset right
hemiplegia two and a half hours prior to the CT scan. He is
diabetic and hypertensive.
The CT findings are often only as important as the question it was
intended to answer! What was the clinical question in requesting a CT scan
Here?

39. Non-contrast CT scan of the same patient after 8 hours now
showing the obvious left basal ganglia infarct
Justifying the need of follow up scans.

40.  One specialized type of stroke frequently
identified on CT imaging is a lacunar infarction,
which are small, discrete nonhemorrhagic
lesions usually secondary to hypertension and
found in the basal ganglia region.
 They frequently are clinically silent.

41. Lacunar infarct in
Basal ganglia.

42. Infarcts
Anterior cerebral
artery infarct

43. Middle cerebral artery infarct Hyper dense MCA sign
Internal cerebral artery infarct
ACA+MCA

44. Posterior cerebral artery infarct

45. Cisterns
 Cisterns are potential spaces formed
where there is a collection of CSF
surrounding the Brain.
 There are four key cisterns that the
physician needs to be familiar with in
order to identify increased intracranial
pressure as well as the presence of
blood in the subarachnoid space.

46. Cisterns
 Circummesencephalic: Hypodense CSF ring around
the midbrain; most sensitive marker for increased
intracranial pressure; will become effaced first with
increased pressure and herniation syndromes.
 Suprasellar: Star-shaped hypodense space above the
sella and pituitary; location of the circle of Willis, hence
an excellent location for identifying aneurysmal
subarachnoid hemorrhage.
 Quadrigeminal: W-shaped cistern at the top of the
midbrain; can be a location for identifying traumatic
subarachnoid hemorrhage, as well as an early marker
of increased intracranial pressure.
 Sylvian: Bilateral CSF space located between the
temporal and frontal lobes of the brain; another good
location to identify subarachnoid haemorrhage.

48. CT appearance of increased intracranial pressure:
A: normal intracranial pressure
B: elevated intracranial pressure.
A B

49. Ventricles:
 Pathologic processes can cause either dilation
(hydrocephalus) or compression/shift of the ventricular
system.
 Hydrocephalus frequently is first evident in dilation of
the temporal horns, which are normally small with a slit-
like morphology.
 It is likely that enlargement is the result of brain volume
loss rather than the increased ventricle size, particularly
in older ages.
 Conversely, if the ventricles are large, but the brain
appears “tight” with sulcal effacement and loss of
sulcal space, then the likelihood of hydrocephalus is
high.

50. Increasing degrees of temporal horn
Dilatation in worsening hydrocephalus

51. Gross hydrocephalus, showing dilatation of frontal horns,
body and occipital horns.

52. Effacement of sulci due to raised
ICP

53. Evan’s Index for Hydrocephalus
 Maximum transverse diameter of Frontal Horns divided
by Maximum internal transverse diameter of cranium
If Index is > 0.3 , suggests
Hydrocephalus.

54. CNS infections
 Meningitis:
Radiological signs:
 Meningeal enhancement
 Cerebral edema
 To look for fractures of skull base
and other complications.

55.  In cases of suspected bacterial meningitis with
clouded consciousness, an immediate cranial CT is
recommended before lumbar puncture to rule out
causes for swelling that might lead to herniation.
CT findings are mostly normal. Contrast-enhanced CT
may show beginning meningeal enhancement,
which becomes more accentuated in later stages of
disease.
CT is important and sufficient to define pathology of
the base of skull that may be causative and require
rapid therapeutic intervention and surgical
consultation.

56. Meningeal enhancement in case of meningitis

57. Space occupying lesions
(SOL)
 Brain Abscess
 Primary Tumors
 Metastases

58. Space occupying lesions
 Such lesions will present with one or more of the following
clinical problems:
 Features of raised ICP
 Convulsions
 Headache
 Focal neurological deficits
 With/without altered level of consciousness.
 Fever in brain abscesses.
 Slow-growing tumours may give rise to a longer duration of
symptoms.

59. Points to be considered to
study ICSOLs
 Mass effect
 Enhancement on contrast
 Appearance
 Location

60. Mass effect
 The side with a tumour or abscess is more likely to have the sulci
squeezed (effaced) and often the lateral ventricle on that side is
also compressed ,and in more severe cases there is midline shift
towards the normal side.
 This is often the first clue that there may be a lesion ,prompting
the intravenous injection of contrast to see if the lesion takes up
contrast and become brighter.
 Most brain tumours will declare their presence by a significant
mass effect from their size or by the severe oedema around them

61. Non-contrast CT scan showing alterations of the normal
sulcal pattern as evidence of mass effect from an
 A) isodense meningioma
 B) a low-density glioma
 C) hyperdense meningioma

62. Enhancement
 “Enhancement simply means it is appearing clearer” that is
higher density compared to the pre-contrast scan.
 When injected intravenously the contrast material concentrate
in vascular areas of the brain including tumours and abscess
walls thereby making them appear hyperdense and hence
easier to see.
 Meningiomas and lymphomas tend to enhance uniformly and
intensely whereas malignant gliomas and abscesses may show
an intermediate degree of enhancement in which there is an
outer enhancing ring surrounding a core of non-enhancing low
density (necrotic centre), which fails to take up the contrast.
 Abscesses typically show THIN UNIFORM enhancing wall
surrounding the pus whereas the ring of enhancement in
gliomas is thicker with more solid tumour in the wall

63.  In general abscesses have a thinner and
smoother enhancing ring with no chunk of
enhancing tumour along the wall.
 Whereas the enhancing ring in malignant
gliomas and metastatic tumours tends to be
thicker and irregular and there may be an
asymmetric large chunk of enhancing tumour
as part of the wall.
 Hypodensities in INFARCTIONS will have DIFFUSE
margins as compared to SMOOTHER margins in
above lesions.

64.  Tumours such as Meningiomas are obvious
and call for little differential diagnosis.
Pre- and post-contrast CT scans of a 22-year-old male that presented
with seizures. Effect of contrast is obvious.

65. Contrast-enhanced CT scan showing a brain abscess
in a patient on immunosuppression therapy for SLE.
Lesions show smooth outline of the rings of enhancement.
Brain Abscess

66. Contrast-enhanced brain CT scan illustrating a uniformly enhancing
left parafalcine meningioma. It is solid and very Unlikely an abscess.
It is benign and carries a good prognosis

67.  Malignant gliomas and metastatic tumours share the
property of ring enhancement with abscesses and are
therefore the subject of much clinical controversy.
 A patchy irregular enhancement will suggest a partially
solid and cystic tumour like a glioma, and a ring
enhancing, circular lesion with central hypodensity will
suggest an abscess with the important differential
diagnosis of a metastasis.

68. Contrast CT scan showing a left frontal irregularly enhancing tumour
with solid and cystic components.
This is a typical appearance for a high-grade glioma usually
glioblastoma.

69. Cystic, solid and partially calcified with Irregular enhancement
Glioblastoma multiforme

70. Location
 A uniformly enhancing tumour with a broad based
attachment to the dura, it is a meningioma until
proven otherwise.
 A ring-enhancing lesion located deep in the white
matter, is most likely
 A Glioblastoma (if soild/cystic/ irregularly enhancing) or
 An abscess (if thin ring enhancement and hollow core)
 A metastasis (if multiple)

71. Thin Ring of Abscess Thick ring of glioma

72. Lesions mimicking abscess, but multiple lesions and
clinical history if available favours METASTASIS

73. Metastasis

74. DDs for multiple ring
enhancing lesions
 Tuberculoma
 Neurocysticerosis
 CNS cryptococcosis
 Metastasis
 Abscess
 Glioblastoma
 Granulomas
 Toxoplasmosis / Lymphoma (common in AIDS)
 Neurosarcoidosis

75. Ring Enhancing Lesions
with Perilesional Edema
 TUBERCULOMA
VS
 NEUROCYSTICERCOSIS

76.  Cysticerci are usually round in shape, 20 mm or less in
size with ring enhancement or visible scolex, and
cerebral edema severe enough to produce midline shift
and focal neurological deficit is not seen.
 Tuberculomas are usually irregular, solid and greater
than 20 mm in size. They are often associated with
severe perifocal edema and focal neurological deficits.
 A lesion greater than 20 mm is likely a Tuberculoma.
 Visualization of an enhancing or a calcified eccentric
dot which represented the scolex, could be considered
a definite imaging feature of cysticercus etiology

77. Tuberculomas with perilesional Edema

78. Multiple NCC

79. Multiple NCC in Vesicular stage:
scolex can be seen inside cysts

80. Contrast Nephropathy
 Rise in serum creatinine level of at least 1 mg/dL
within 48 hours of contrast administration.
 Incidence more when used Ionic contrast material.
 Mechanism of Injury:
 Renal Tubular Obstruction
 Endothelial cell damage
 Immunological Reactions
 There is favourable prognosis and creatinine levels
return to normal in 1-2 weeks.

81. Risk Factors:
 Age > 80 Years
 Pre-existing renal disease [Creatinine > 2 mg/dL]
 Solitary Kidney
 DM / Dehydration / Paraproteinemia
 Patients on Nephrotoxic Medications

82. Prevention
Using non-ionic contrast
Using low dose of contrast
Prior Hydration
Using bicarbonate and
acetylcysteine

83. Allergic Reactions to
contrast
 Incidence 0.04 % with Non-ionic contrast.
 History of Atopy, bronchial asthma or other allergies are at
more risk.
 If patient has history of prior contrast allergy and if contrast
absolutely required:
Premedicate with:
 12 Hours before administration: Prednisolone 50 mg PO
 2 Hours before: Prednisolone 50 mg + Cimetidine 300 mg
 Just before administration : IV Diphenhydramine 50 mg